1. Jun 2024
    1. EM:7

      DOI: 10.7554/eLife.94946

      Resource: IMSR_EM:00007

      Curator: @scibot

      SciCrunch record: RRID:IMSR_EM:00007


      What is this?

    2. EM:8

      DOI: 10.7554/eLife.94946

      Resource: RRID:IMSR_EM:00008

      Curator: @scibot

      SciCrunch record: RRID:IMSR_EM:00008


      What is this?

    3. EM:9

      DOI: 10.7554/eLife.94946

      Resource: RRID:IMSR_EM:00009

      Curator: @scibot

      SciCrunch record: RRID:IMSR_EM:00009


      What is this?

    4. RRID:SCR_001622

      DOI: 10.7554/eLife.94946

      Resource: MATLAB (RRID:SCR_001622)

      Curator: @scibot

      SciCrunch record: RRID:SCR_001622


      What is this?

    1. RRID:SCR_005927

      DOI: 10.7554/eLife.91928

      Resource: Analysis of Functional NeuroImages (RRID:SCR_005927)

      Curator: @scibot

      SciCrunch record: RRID:SCR_005927


      What is this?

    2. RRID:SCR_002438

      DOI: 10.7554/eLife.91928

      Resource: Mindboggle (RRID:SCR_002438)

      Curator: @scibot

      SciCrunch record: RRID:SCR_002438


      What is this?

    3. RRID:SCR_001847

      DOI: 10.7554/eLife.91928

      Resource: FreeSurfer (RRID:SCR_001847)

      Curator: @scibot

      SciCrunch record: RRID:SCR_001847


      What is this?

    4. RRID:SCR_002823

      DOI: 10.7554/eLife.91928

      Resource: FSL (RRID:SCR_002823)

      Curator: @scibot

      SciCrunch record: RRID:SCR_002823


      What is this?

    5. RRID:SCR_004757

      DOI: 10.7554/eLife.91928

      Resource: ANTS - Advanced Normalization ToolS (RRID:SCR_004757)

      Curator: @scibot

      SciCrunch record: RRID:SCR_004757


      What is this?

    6. RRID:SCR_001362

      DOI: 10.7554/eLife.91928

      Resource: NiLearn (RRID:SCR_001362)

      Curator: @scibot

      SciCrunch record: RRID:SCR_001362


      What is this?

    7. RRID:SCR_002502

      DOI: 10.7554/eLife.91928

      Resource: Nipype (RRID:SCR_002502)

      Curator: @scibot

      SciCrunch record: RRID:SCR_002502


      What is this?

    8. RRID:SCR_016216

      DOI: 10.7554/eLife.91928

      Resource: FMRIPREP (RRID:SCR_016216)

      Curator: @scibot

      SciCrunch record: RRID:SCR_016216


      What is this?

    1. RRID:SCR_024614

      DOI: 10.1101/2024.06.14.599106

      Resource: Tulane University TNPRC Pathogen Detection and Quantification Core Facility (RRID:SCR_024614)

      Curator: @scibot

      SciCrunch record: RRID:SCR_024614


      What is this?

    2. RRID:SCR_024609

      DOI: 10.1101/2024.06.14.599106

      Resource: Tulane University TNPRC Clinical Pathology Core Facility (RRID:SCR_024609)

      Curator: @scibot

      SciCrunch record: RRID:SCR_024609


      What is this?

    1. RRID:SCR_010994

      DOI: 10.1101/2024.06.14.598901

      Resource: Georgia University Genomics and Bioinformatics Core Facility (RRID:SCR_010994)

      Curator: @scibot

      SciCrunch record: RRID:SCR_010994


      What is this?

    1. AB_143157

      DOI: 10.1101/2024.06.17.599416

      Resource: (Molecular Probes Cat# A-11011, RRID:AB_143157)

      Curator: @scibot

      SciCrunch record: RRID:AB_143157


      What is this?

    2. AB_1268496

      DOI: 10.1101/2024.06.17.599416

      Resource: (Abcam Cat# ab73331, RRID:AB_1268496)

      Curator: @scibot

      SciCrunch record: RRID:AB_1268496


      What is this?

    3. RRID:CVCL_Y803

      DOI: 10.1101/2024.06.17.599416

      Resource: (Coriell Cat# GM25256, RRID:CVCL_Y803)

      Curator: @scibot

      SciCrunch record: RRID:CVCL_Y803


      What is this?

    4. RRID:AB_2534729

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# A16056, RRID:AB_2534729)

      Curator: @scibot

      SciCrunch record: RRID:AB_2534729


      What is this?

    5. RRID:AB_228335

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# 31212, RRID:AB_228335)

      Curator: @scibot

      SciCrunch record: RRID:AB_228335


      What is this?

    6. RRID:AB_2535548

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# A18771, RRID:AB_2535548)

      Curator: @scibot

      SciCrunch record: RRID:AB_2535548


      What is this?

    7. RRID:AB_2340476

      DOI: 10.1101/2024.06.17.599416

      Resource: (Jackson ImmunoResearch Labs Cat# 706-605-148, RRID:AB_2340476)

      Curator: @scibot

      SciCrunch record: RRID:AB_2340476


      What is this?

    8. RRID:AB_2534117

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# A-11073, RRID:AB_2534117)

      Curator: @scibot

      SciCrunch record: RRID:AB_2534117


      What is this?

    9. RRID:AB_142924

      DOI: 10.1101/2024.06.17.599416

      Resource: (Molecular Probes Cat# A-11039, RRID:AB_142924)

      Curator: @scibot

      SciCrunch record: RRID:AB_142924


      What is this?

    10. RRID:AB_2534070

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# A-11002, RRID:AB_2534070)

      Curator: @scibot

      SciCrunch record: RRID:AB_2534070


      What is this?

    11. RRID:AB_2101325

      DOI: 10.1101/2024.06.17.599416

      Resource: (Millipore Cat# 07-330, RRID:AB_2101325)

      Curator: @scibot

      SciCrunch record: RRID:AB_2101325


      What is this?

    12. RRID:AB_300798

      DOI: 10.1101/2024.06.17.599416

      Resource: (Abcam Cat# ab13970, RRID:AB_300798)

      Curator: @scibot

      SciCrunch record: RRID:AB_300798


      What is this?

    13. RRID:AB_221448

      DOI: 10.1101/2024.06.17.599416

      Resource: (Molecular Probes Cat# A-21271, RRID:AB_221448)

      Curator: @scibot

      SciCrunch record: RRID:AB_221448


      What is this?

    14. RRID:AB_2533987

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# 71-5300, RRID:AB_2533987)

      Curator: @scibot

      SciCrunch record: RRID:AB_2533987


      What is this?

    15. RRID:AB_2608403

      DOI: 10.1101/2024.06.17.599416

      Resource: (Thermo Fisher Scientific Cat# PA5-44574, RRID:AB_2608403)

      Curator: @scibot

      SciCrunch record: RRID:AB_2608403


      What is this?

    16. RRID:AB_261690

      DOI: 10.1101/2024.06.17.599416

      Resource: (Sigma-Aldrich Cat# T5192, RRID:AB_261690)

      Curator: @scibot

      SciCrunch record: RRID:AB_261690


      What is this?

    1. Bran could see the relief on his brother’s face.

      yeah he doesn't wanna kill anyone

    2. Robb turned his head to look at Theon once more. Bran had neverseen him so angry, yet he said nothing. Finally he knelt besideMaester Luwin. “How badly is my brother wounded?”

      i really like him

    3. “Jon always said you were an ass, Greyjoy,” Robb said loudly. “Iought to chain you up in the yard and let Bran take a few practiceshots at you.”

      yeaahh

    4. ods be damned, think whatMance would give to have Benjen Stark’s own blood to hostage!”

      hmm

    5. Robb took his hand. “He won’t die, not Father,” he said calmly.“Still ... the honor of the north is in my hands now. When our lordfather took his leave of us, he told me to be strong for you and forRickon. I’m almost a man grown, Bran.”Bran shivered. “I wish Mother was back,” he said miserably.

      theyre just a bunch of kids and omfg theon shut up

    6. Robb shook his head numbly, the pain plain in his eyes. “I don’tknow, and ... Bran, that’s not the worst of it. Father was caughtbeneath a falling horse in the ght. Alyn says his leg was shattered,and ... Maester Pycelle has given him the milk of the poppy, butthey aren’t sure when ... when he ...” The sound of hoofbeats madehim glance down the road, to where Theon and the others werecoming up. “When he will wake,” Robb nished. He laid his handon the pommel of his sword then, and went on in the solemn voiceof Robb the Lord. “Bran, I promise you, whatever might happen, Iwill not let this be forgotten.”

      oh he really needs a hug

    7. before Bran was born. “They killed Jory?” He remembered all thetimes Jory had chased him over the roofs. He could picture himstriding across the yard in mail and plate, or sitting at hisaccustomed place on the bench in the Great Hall, joking as he ate.“Why would anyone kill Jory?”

      jaime when i catch you jaime

    8. “So you are.” Robb sounded sad, and even a little scared. “Bran, Ineed to tell you something. There was a bird last night. From King’sLanding. Maester Luwin woke me.”

      ned right?

    9. “Grey Wind was restless too,” Robb said. His auburn hair hadgrown shaggy and unkempt, and a reddish stubble covered his jaw,making him look older than his fteen years. “Sometimes I thinkthey know things ... sense things ...” Robb sighed. “I never knowhow much to tell you, Bran. I wish you were older.”

      he reallyyy needs someone to confide to

    10. Robb seemed to admire Theon and enjoy hiscompany, but Bran had never warmed to his father’s ward.

      me either

    11. “Are you ready?” Robb asked.

      yess robb i misees youu

    12. BRAN

      ngl i want jon

    13. She liked to hold them. They were so beautiful, andsometimes just being close to them made her feel stronger, braver,as if somehow she were drawing strength from the stone dragonslocked inside.She was lying there, holding the egg, when she felt the child movewithin her ... as if he were reaching out, brother to brother, bloodto blood. “You are the dragon,” Dany whispered to him, “the truedragon. I know it. I know it.” And she smiled, and went to sleepdreaming of home.

      thats kinda cool actually

    14. “I’d never ...” Why was he always so cruel? She had only wantedto help.

      :(

    15. He was still her king, afterall, and her brother. They were both blood of the dragon.

      she loves him so much but he hates her so much

    16. She wondered ifall men were as false in the Seven Kingdoms. When her son sat theIron Throne, she would see that he had bloodriders of his own toprotect him against treachery in his Kingsguard.

      the way she would get murdered by someone she loved in the show :(

    17. “You hate this Lord Stark,” Dany said.“He took from me all I loved, for the sake of a few lice-riddenpoachers and his precious honor,” Ser Jorah

      youre a bitch

    18. Eddard Stark ...”He spat

      didnt even say lord >:(

    19. “Is he?” Dany asked. “A fool, I mean?”

      yes

    20. all the pillow tricks Doreah had taught her, beforeDany had been able to make Drogo relent and allow Viserys torejoin them at the head of the column.

      not her having to do those acts for him :(

    21. DAENERYS

      man i havent seen you in a longgg time

    22. agony in his leg.

      jaime lanniatser hurts another starks legs

    23. WhenNed’s horse lurched back to its feet, he tried to rise, only to fallagain, choking on his scream. He could see the splintered bonepoking through his calf. It was the last thing he saw for a time. Therain came down and down and down.

      noooo

    24. “and Catelyn will most certainly slayTyrion.”Jaime Lannister poked at Ned’s chest with the gilded sword thathad sipped the blood of the last of the Dragonkings. “Would she?The noble Catelyn Tully of Riverrun murder a hostage?

      oh she would

    25. “Still ... we wouldn’t want him to leave here entirely unchastened,so”—through the night and the rain, he glimpsed the white ofJaime’s smile—“kill his men.”

      ugh i knew it

    26. “I will bring the CityWatch,”

      sureee

    27. For the rst time in years, he found himself remembering RhaegarTargaryen. He wondered if Rhaegar had frequented brothels;somehow he thought not.

      hmm thinking of him while talking about bastards...

    28. “I’ve also heardwhispers that Robert got a pair of twins on a serving wench atCasterly Rock, three years ago when he went west for Lord Tywin’stourney. Cersei had the babes killed, and sold the mother to apassing slaver. Too much an aront to Lannister pride, that close tohome.”

      oh!

    29. Riding through the rainy night, Ned saw JonSnow’s face in front of him, so like a younger version of his own. Ifthe gods frowned so on bastards, he thought dully, why did they llmen with such lusts?

      is jon rhaegar's bastard? or does ned not know the father? OR has he deluded himself into thinking he is a bastard like a reverse rhaenyra

    30. “And tell him I’ve not been with no one else. I swear it, milord, bythe old gods and new. Chataya said I could have half a year, for thebaby, and for hoping he’d come back. So you’ll tell him I’m waiting,won’t you? I don’t want no jewels or nothing, just him. He wasalways good to me, truly.”

      NOOO

    31. I will,” Ned had promised her. That was his curse. Robert wouldswear undying love and forget them before evenfall, but Ned Starkkept his vows. He thought of the promises he’d made Lyanna as shelay dying, and the price he’d paid to keep them.

      yuh

    32. Robert’s rstborn hadhad the same ne hair, he seemed to recall.

      yeah genetics and stuff

    33. Lyanna had only smiled. “Love is sweet, dearest Ned,but it cannot change a man’s nature.”

      she was smart

    34. oes that alsomean you fuck with the king’s—”

      stopp

    35. Jory Cassel stoodbeside a rain-streaked window with a wry smile on his face,watching Heward turn over tiles and enjoying the view.

      interesting...

    36. legant woman who wore a feathered gownover skin as black as ink.

      he's used this comparison before

    37. Catelyn was at a loss for words. Jon Arryn’s son, she thoughtincredulously. She remembered her own baby, three-year-oldRickon, half the age of this boy and ve times as erce. Smallwonder the lords of the Vale were restive. For the rst time sheunderstood why the king had tried to take the child away from hismother to foster with the Lannisters ...

      rickon can easily kill this kid

    38. The boy grabbed forit eagerly, buried his face against her chest, and began to suck. Lysastroked his hair

      OH NAHH

    39. It had been ve years, in truth; ve cruel years, for Lysa. Theyhad taken their toll. Her sister was two years the younger, yet shelooked older now. Shorter than Catelyn, Lysa had grown thick ofbody, pale and puy of face. She had the blue eyes of the Tullys, buthers were pale and watery, never still. Her small mouth had turnedpetulant. As Catelyn held her, she remembered the slender, high-breasted girl who’d waited beside her that day in the sept atRiverrun. How lovely and full of hope she had been. All thatremained of her sister’s beauty was the great fall of thick auburnhair that cascaded to her waist.

      man thats harsh

    40. She remembered what her uncle had said of basketsand winches. “The Lannisters may have their pride,” she told Mya,“but the Tullys are born with better sense. I have ridden all day andthe best part of a night. Tell them to lower a basket. I shall ride withthe turnips.”

      lmao

    41. the bastard girlled Catelyn across, blind and trembling,

      trust a bastard cat

    42. Catelyn Tully Stark swallowed what remained of her pride. “I ... Icannot do this, child,” she called out.

      any tully and stark woul be scared

    43. erhaps she wasbecoming a Stark at last

      yess

    44. She sounded so like Sansa, so happy and innocent with herdreams. Catelyn smiled, but the smile was tinged with sadness. TheRedforts were an old name in the Vale, she knew, with the blood ofthe First Men in their veins. His love she might be, but no Redfortwould ever wed a bastard. His family would arrange a more suitablematch for him, to a Corbray or a Waynwood or a Royce, or perhapsa daughter of some greater house outside the Vale. If MychelRedfort laid with this girl at all, it would be on the wrong side of thesheet

      noooo

    45. “I was born a Tully and wed to a Stark,” Catelyn said. “I do notfrighten easily.

      yup

    46. Mya Stone

      OH SHES ROBERTS GIRL he was no mountatin goat let me tell you that

    47. “Mya Stone, if it please you, my lady,” the girl said.It did not please her; it was an eort for Catelyn to keep the smileon her face. Stone was a bastard’s name in the Vale, as Snow was in

      omg not the bastard hate

    48. Her dark hair wascropped short and straight around her head

      ohh nah not the jean de arc bob

    49. Royce

      royce again

    50. I, however, am innocent as a littlelamb. Shall I bleat for you?” He grinned.

      lol

    51. She swears that this time she will choose herlord husband.”

      petyr fucking balish

    52. aughing, Brynden had pointedout that the sigil of their house was a leaping trout, so he ought tobe a black sh rather than a black goat, and from that day forwardhe had taken it as his personal emblem.

      ohhh thats why

    53. “As you wish,” she

      noo he's gonna free tyrion

    Annotators

    1. Or making fun of me. Or seeing through me.It stung me when he finally came out with it. Only someone who hadcompletely figured me out would have said it. “If not later, when?”

      ?

    2. You makeme like who I am, who I become when you’re with me, Oliver. If there isany truth in the world, it lies when I’m with you, and if I find the courage tospeak my truth to you one day, remind me to light a candle in thanksgivingat every altar in Rome

    Tags

    Annotators

    1. Now, some peeps gone say this illustrate how Fish be rite, why we need to beteachin mo standard grammar and stuff. If you look at it from Fish view, yeah itmean that. But if you look at it from my view, it most certainly dont mean that.Instead, it mean that the one set of rules that people be applyin to everybody’sdialects leads to perceptions that writers need “remedial training” or that speakersof dialects are dumb.

      Young argues that using one set of rules for everyone unfairly judges non-standard speakers as less capable. He suggests language should be taught in a way that respects different styles.

    2. This explain why so many bloggers on Fish’s NYT comment page was tryin toschool him on why teachin one correct way lend a hand to choppin off folks’tongues.But, let me be fair to my man Stan. He prolly unware that he be supportin languagediscrimination, cuz he appeal to its acceptable form–standard language ideology alsocalled “dominant language ideology” (Lippi-Green).

      Teaching one correct way to speak/write harms people. Standard language ideology claims there is only one correct way to use language. Young argues that this belief discriminates against those who use different dialects.

    3. It’s ATTITUDES

      The capitalization of "ATTITUDES" is used to challenge the idea that standard English is inherently superior or necessary for success.

    1. & tried to fix, affixed, we facted, felt.

      This line is an example of how an author's syntax impacts the tone and meaning their poem. The words sort of topple onto each other; tried to fix--affixed--we facted--felt. This gives the poem a tone of desperation and urgency.

    2. we wracked our lips we rang for words to ward off sleep

      Throughout this poem Franny Choi writes in prose poetry, the sentences lack metrical structure and a majority of the words have been strategically chosen.

    1. Vape Pod 365 là cửa hàng vape pod quận Phú Nhuận uy tín, luôn cập nhật các sản phẩm hotrend được giới trẻ yêu thích nhất. Cung cấp đầy đủ các sản phẩm gồm pod system, vape kit, tinh dầu vape pod và phụ kiện chính hãng.   Nếu không tìm thấy sản phẩm ưng ý ở các shop vape quận Phú Nhuận trên, anh em có thể lựa chọn mua Online sản phẩm của mình tại Vape Pod 365. Chúng tôi cam kết giá tốt nhất, sản phẩm chất lượng nhất sẽ được giao đến tay anh em. Để mua sản phẩm Online tại Quận Phú Nhuận, anh em có thể lựa chọn các kênh sau:  Mua online tại website: https://vapepod365.net/ Mua tại Fanpage Vape Pod 365: Vape Pod 365 - Vapepod365.net Mua qua Hotline và Zalo: 0704 810 810 Ngay khi liên hệ, nhân viên tư vấn sẽ hỗ trợ anh em từ A tới Z trong việc tư vấn chọn sản phẩm pod system vừa túi tiền. Đến việc tư vấn các dòng tinh dầu và phụ kiện phù hợp nhất. Đảm bảo sẽ làm vừa lòng các thượng đế.

      Vape Pod 365 cung cấp vape pod Phú Nhuận với giá tốt, cam kết sản phẩm chính hãng. Cung cấp đầy đủ các dòng sản phẩm như vape, pod system, phụ kiện, tinh dầu chất lượng cao. Ship COD toàn quốc, giao hàng nội thành HCM chỉ 30p. Bảo hành 1 đổi 1 trong 7 ngày. Liên hệ ngay!

      https://vapepod365.net/vape-pod-quan-phu-nhuan

      vapepodbinhthanh #binhthanh #podbinhthanh #tinhdaubinhthanh #pod1lanbinhthanh #phukienpod #vapepod365

    1. Whether RTN4IP1 functions through interactions with other partners or by facilitating posttranslational modifications during CI assembly remains unanswered and warrants further investigation

      Do you have thoughts on how you would further experimentally decouple the Complex I assembly and CoQ biosynthesis functions of RTN4IP1?

    2. Pathway analysis revealed that the affected biological processes of upregulated proteins were related to cell-substrate adhesion and extracellular organization

      Did you look into why RTN4IP1 upregulated cell adhesion and extracellular organization factors? This is surprising to me given the clear role you have demonstrated in Complex I assembly.

    3. This phenomenon was particularly evident in the context of CI, where the identification of assembly factors increased nearly threefold between 24 hours and 1 week

      Do you have a hypothesis as to why the galactose growth phenotype is particularly pronounced for Complex I assembly factors? Is complex I especially reliant on assembly factors to adopt its active configuration?

    4. Dynamics and surveillance, along with the Signaling pathway, exhibited notable enrichment in genes with no discernible phenotype, implying that genes within these categories may be dispensable for proliferation in galactose, likely owing to their limited influence on OXPHOS activity

      Is it possible to use an alternative functional genomics approach to study genes involved in dynamics and signaling? How would you set up such a screen?

    5. Even though we now possess a very detailed picture of the core proteins that comprise the OXPHOS complexes, the list of assembly factors and regulatory components is far from being completed

      You mention that many nuclear-encoded genes important in mitochondrial function have not yet been identified. Is it possible to adapt your screening approach to identify these genes without having to use a genome-wide library?

    1. chievement allow teachers with: © 15 to 25 ho urs a W eek ... to plan cooper atively and engage in analyses of student help them continually improve

      This sounds like it would have a major impact. This would have to shift the school day to being shorter. We get less than 6 hours at my school. These are often taken up by meetings but I suppose the 15-20 hours would also probably be taken up by meetings at times. This amount of planning is most effective and would definitely help with teacher burn out.

    2. rs. The evaluation demonstrated that it was these former teachers who were informing the parents about the language of schooling that made big differences — that is, the parents learned the language about the nature of learning in today’s classro learned how to help their children to attend and engage in learning, speak with teachers and school personnel.

      This sounds impactful but how was this done?

    3. re there mindsets that inhibit the impact that we need to have on learning (for example, ‘Give me bright students and I can achieve’; ‘But it is all about poverty and the home’; ‘If they do not come to class prepared, that’s not my fault’; ‘We know

      I agree that it is critical to dismantle these mindsets, however this can be challenging. These mindsets are not often said outright but are said in some form. As a leader how would you work to shift this mindset in a teacher especially if they do not recognize it themselves?

    4. phasis on current and lit imediate classroom needs, robles satisfactions instead of on | i ong-term impact and plans.

      I think the reason for this is because teachers are so often burdened by the day to day it is challenging to find the time to think of long term solutions. Again more time needs to be allocated to this in staff meetings, etc to make this possible.

    5. Think of reasons why a my; leadership; staff relations; the nature of the students; facilities; and safety.

      I think this is often missed in discussions around school retention. Many people go back only to money when so often the biggest reason for retention is school leadership. I have been at schools with 95% retention and 20% retention and school leadership was the biggest difference between these schools.

    6. The repornns st tion and consequences), is rich in detail while highlignting t a aan sheen din many schools to help to drive teacher debates about their me Se th

      I appreciate the idea that there is not a number tied to the feedback. I agree that both as an evaluator and as someone getting evaluated the numbers get in the way of the rich feedback and growth discussions.

    7. ( Cc nta using test results to aj raise, unish or ard);

      For teachers or students? I see both being done often.

    8. effective engagement with the broader community.

      I have not seen this aspect done very well in any school. I see schools engage well with the parents but not much with the broader community. I would love to see what this could look like in practice.

    9. a rich and engaging formal and informal curriculum;

      I agree with all of these practices to support positive outcomes. I am curious what is meant by a formal and informal curriculum?

    10. that the culture of the school is the essence of sustained success.

      I completely agree with this. How is this set and maintained? I have worked in schools with great cultures and those without and it largely depends on the principal. However, I do not know how much oversight principals get on how they establish culture. I know they have coaches that look at their data but I have yet to have a principal's boss sit in on a data team meeting.

    11. or example, there is not a lot of evidence that ae improving teacher education colleges has improved th i of course, this is not to say that we should stop tryin os educate teachers to have these impacts).

      As I am not as familiar with higher education, what is required for teacher prep programs? I know the inclusion of the science of reading in Colorado has been a recent change but I wonder what else? I also wonder what the teacher prep programs look like in other countries? How do our programs differ? Having worked with a few student teachers I do think there is some growth that can be made in the teacher prep programs. This is part of the reason why I am here as I know I am part of the issue.

    1. However, the biggest problem has been the inability to rewarm them without major damage from ice or cracking.

      20% of kidneys donated each year cannot be used - often because they cannot be kept on ice for longer than a few hours, and as a result do not reach recipients in time. However, it's not long-term cryopreservation methods that are the once-impossible issue, in fact, they have been around for quite some time - decades in fact. Scientists have instead struggled with rewarming organs without causing major damage from ice or cracking.

      The team at the University of Minnesota developed a nanowarming process that uniformly and rapidly warms the cryopreserved organs, as opposed to merely warming the organ at its surface.

      The organs were able to be cleared of cryoprotective fluids and nanoparticles and transplanted into the lab rats. All of the rat participants were able to restore full kidney function within 30 days without additional interventions.

      For human transplants, medical interventions would occur where they did not for the rat patients. These interventions include medicines and dialysis to assist the kidney for the weeks right after transplantation.

      long-term organ banking could increase donor organ utilization, improve donor/recipient matching, and improve procedure preparation and scheduling. This also opens up the possibility for cryopreserving other organs.

    1. 主客分節以前の世界を、自分が冒険の最中に北極でよく体験する、テントの中で眠りに落ちる間際に聴こえてくる(ような気がする)「音楽」と、その意味を深掘りすることで表現しました。

      このシーン、読んでてよかったと思った所だった。

    1. op-down directives mighteste bu ion of a solution, but Deci and Ryan’s work- ee ue , irectives will only, at best, lead to half-ak pliance and won’t inspire the kind of commit-mec! for real, meaningful change

      I can resonate with this in my district. I think for some, it can be scary to give up control, but that leave educators uninspired and not as vested as they could be. This may be something to address in leadership training with admin. I love being able to create and made decision I am passion about..because of that passion, the result come and are authentic.

    1. AS E-ATIVIDADES NO CONTEXTO DOS AMBIENTES DIGITAIS

      Car@s formand@s, coloquem os vossos comentários ao longo deste texto. e-s@udações!

    1. will fight for equity for all underrepresented or disenfranchised people.

      I want to make sure that we also think about our students who live with disabilities and that they are represented in this group. We need to be in tune this this group.

    1. Hypertext is text displayed on a computer display or other electronic devices

      This is an easy defitiniton easy to undestand.

    1. the writing done in the nonlinear or nonsequential space

      Thi is the computer writiing works. Hypertext provides more opctions.

    1. reply to u/Rabbits16 at https://www.reddit.com/r/typewriters/comments/1df7o2t/request_type_writer_suggestion_please/

      For that budget range, pick up something cleaned and fully serviced from a nearby shop https://site.xavier.edu/polt/typewriters/tw-repair.html

      Too many resellers are pushing overpriced machines that say "works" or "may need servicing" on some online shops like ebay or Etsy for top end pricing when you can get something truly spectacular and ready for the next 50 years from a serious pro that needs the support for the same price.

      As for particular machines to look at, I can't find much to fault in Joe's advice here https://youtu.be/aKMt-aCHZZk?si=CGPduwA4A3HPDm3u

    1. The Cytoscape app DomainGraph (22) visualizes domain interactions simultaneously with protein interactions and analyzes the effect of differential exon usage. However, DomainGraph is limited to the output of the tool AltAnalyze (22). Ghadie et al. developed DIIP using a similar method to predict an isoform interactome (18). While their results were verified based on the experimentally validated isoform interactome reported by Yang et al. (1), their database covers only a fraction of the proteome with 2944 reference proteins and 4363 interactions. Exon Ontology (EXONT) characterizes protein domains and features that are affected by AS (23) but does not consider AS on the network level.

      The available isoform-resolved network tools. Pretty much there is DomainGraph (Nathan's tool, deprecated). Ghadie made DIIP but specific to the isoform. There are exon/splice event-centric tools, but these do not capture the gene-to-proteoform relationship. Characterization of exon events are fragmentary, because multiple variations can exist on the same PF.

    1. Notably, the current interactome only includes a single isoform of each gene product with limited annotations about which splice isoform is examined.112 It is widely accepted that different spliced forms can lead to marked changes in phenotypes as well as altered PPIs.113 A disease-associated isoform of lamin A for Hutchinson-Gilford progeria syndrome is a striking example of how its interactions with other proteins differ from those of a non–disease-associated isoform.114 Davis et al115 hypothesize that most human PPIs could be modulated by alternate splicing. Systematic profiling of all biologically relevant isoforms116 and their PPIs at a proteomic level is, therefore, much needed.

      Loscalzo commentary of the importance of isoform-resolved networks. They highlight an example of differential PPIs for lamin A (that make sense?) - could we use as our example?

    1. Proteins are curated at the sequence level, using the UniProtKB database as the reference resource for proteins and peptides. The use of UniProtKB enables the curator, for each publication, to accurately describe the level of detail provided about the proteins and to use identifiers for the unambiguous annotation of each protein interactor. For instance, a publication may only give enough detail for an interactor to be mapped to any or all of the protein isoform products of a specific gene, or more specifically to a single protein isoform, or to a post-translationally cleaved peptide chain. UniProtKB supplies appropriate identifiers for all of these, and in each case supplies the corresponding underlying sequence. Binding regions can be aligned to known protein domains, as described by InterPro28. The effects of point mutations can be captured down to the amino acid level, using a CV to describe their effect on an interaction. To capture this level of detail, the use of a high-quality protein reference resource is essential. Reverse engineering protein to gene identifiers to enable network analysis of, for example, RNA-Seq data is a relatively trivial task but it is considerably more difficult, if not impossible, to map isoforms and binding domain data directly to a gene model or genomic sequence. Databases that curate PPI data directly to gene identifiers simply do not capture this wealth of information.

      Cross-referencing nodes to proteins (protein isoforms) annotated in UniProt.

    2. Characterising protein isoforms and featuresMost eukaryotic protein-coding genes transcribe more than one isoform. The different functions of isoforms are sometimes known or can be inferred (for example specific isoforms do/do not contain certain functional domains), but in many cases the biological significance of multiple isoforms derived from the same gene is not understood. However, the different interaction patterns of associated isoforms may provide an indication of their different biological functions by analysing their respective binding partners. In 2013, Talavera et al.57 published an editorial stating that “it is crucial to the advance of basic and medical research that interactions are reported on an isoform-to-isoform basis and that databases switch to a similar approach”. The IMEx databases curate this information, whenever the data is made available by authors, making isoform comparisons possible. UniProtKB identifiers enable curators to differentiate between transcripts being identified at the isoform or canonical (reference sequence) level. Over 100,000 interactions in IMEx (~12% of IMEx data) contain specific isoform information, with more than 11,000 records containing specific isoform–isoform interactions. The UniProtKB database recently (release 2020_02) refactored the Interaction section of their records to improve the display of isoform data imported from IMEx. It is anticipated that the availability of such data will increase as protein identification techniques improve or as authors realise the value of such data and include this level of detail in publications.IMEx also captures so-called negative interactions, which will be of increasing use in the future. These data largely pertain to isoform-specific interactors, and describe cases where certain isoforms of a gene bind to a bait protein, while other isoforms of the same gene do not bind to the same bait in the same assay system. IMEx curation rules mandate publication of the protein expression levels of the negative interactors to exclude poor protein expression as a reason for the lack of interaction.To fully comprehend protein interactions, researchers frequently need to identify the sequence region to which a molecule binds and any modification to that sequence. Any change to an amino acid sequence has the potential to influence the molecules with which the protein interacts. The IMEx Consortium captures these variations, thereby supporting the analysis of their downstream effects as shown in the examples below.

      Commentary on capturing isoform resolved information in networks.

    1. Un pipeline pour les gouverner tous

      👌

    2. modus operandi

      italique

    3. sera

      pareil, futur à éviter peut-être

    4. vise

      le présent est un peu bizarre // l'ambition du projet porte sur le développement d'une chaine de traitement ..? je sais pas c'est juste que le projet est fini donc les formules projectives comme ça, ça me semble un peu étrange

    5. Gallicorpora : est-il possible de créer un outil générique ?

      petite phrase d'intro pour dire en quoi le projet gallicorpora est pertinent à évoquer (traitement automatique, documents numérisés, pipeline, gros corpus, etc)

    6. les deux étant parfois confondues

      ah bon ? la plateforme EIDA serait destinées aux bibliothèques par exemple ?

    7. futures

      futurs

    8. rendant compte

      rendant compte de quoi ?

    9. récent “visual turn” général des humanités

      à justifier

    10. Pour conclure, l’Almageste se présente donc comme une sorte d’encyclopédie des connaissances d’une époque qui s’est enrichie avec le temps au point de rendre difficile l’appréciation de son état originel. Œuvre sans cesse recopiée au cours des siècles, passant du grec à l’arabe puis au latin, transmise à travers tout le bassin méditerranéen et dominant le Moyen Âge occidental après avoir conquis l’Islām, chaque traduction et chaque copie de l’Almageste n’ont pas seulement transmis son contenu, mais l’ont aussi adapté et enrichi en fonction des contextes culturels et scientifiques de chaque époque. L’œuvre ptoléméenne a servi de base à de nombreux commentaires et traités, intégrant progressivement des éléments de connaissance issus de diverses traditions scientifiques, et illustrant ainsi l’interconnexion des savoirs à travers les civilisations.

      bon j'imagine que c'est ce que j'ai fait dans mon mémoire mais pas besoin de rentrer dans autant de détail (même si en soi c'est intéressant)

    11. Albouy

      aha

    12. à travers les âges et les lieux

      à retirer peut-être (tu le dis en substance juste avant et après)

    13. en s’appuyant que

      [ne] s'appuyant que // en s'appuyant _

    14. d’outils

      si tu parlent d'outils au pluriel, cela me semble plus désigner la pipeline en entier et pas seulement le modele de vectorisation

    15. deep-learning

      italique

    16. récent “visual turn” dans l’histoire de l’astronomie

      il faut le justifier d'une note de pas de page

    17. visual turn

      italique

    18. large

      "ce large" présuppose qu'a été auparavant explicité la large dimension du corpus, si tu veux dire ça tu peux insister en disant un truc du style "la grande diversité de sources astronomiques issues d'origines géographiques et temporelles variées"

    19. plusieurs titres

      quels titres du coup ?

    20. les acteurs et le cadre du projet, et un réseau plus vaste, celui de la recherche en générale, la communauté se regroupant autour de grands principes d’ouverture garantissant une interopérabilité technique des données

      c'est quoi les deux niveaux ? il faut simplifier pour que ce soit plus explicite

    21. se tissent

      [qui ?] se tissent

    22. En outre, ce domaine ne détient pas l’apanage de l’étude de larges corpus d’images à enrichir et sémantiser afin de permettre puis faciliter leur exploration

      L'exploration de vastes corpus iconographiques par leur sémantisation n'est pas l'apanage de la seule histoire des sciences (?) la phrase me semble bizarre

    23. du projet

      des projets

    1. ccepted body of learning, the excessive emphasis on teaching isolated facts, and the lack of atten- tion to higher order skills and concepts.

      It's interesting because I think with the emphasis on testing that there is still a lack of attention to higher order skills and concepts. I do not know what it was like prior to this reform but I still think there is some emphasis on this now.

    1. Good gentlemen

      Guildenstern is played by a woman in the production

    2. Scene 1

      this entire scene with Polonius and Reynaldo is completely cut besides a couple lines

    3. A serpent stung me

      "The Serpent King": Hamlet calls his uncle this in the production

    1. Note: This response was posted by the corresponding author to Review Commons. The content has not been altered except for formatting.

      Learn more at Review Commons


      Reply to the reviewers

      Reviewer #1 (Evidence, reproducibility and clarity (Required)):

      #1) Summary: The transport of effector proteins across membranes from the producing bacterium into a target cell is at the core of bacterial secretion systems. How an additional layer in form of a capsule affects effector export and the susceptibility towards effector import is not fully understood. Here, Flaugnatti and colleagues combined bacterial genetics with phenotypic assays and electron microscopy to demonstrate a dual role of a bacterial capsule in preventing T6SS-mediated effector export and promoting protection from effector import by another bacterium's T6SS. The wide variety of methods used, complementation of the mutants, and validation of the findings across strains strengthen the author's conclusions. Although the main conclusions seem straight forward, the authors unravel the unexpected complexity underlying these phenotypes with strong mechanistic work. In brief, a capsule-deficient mutant (∆itra) is shown to assemble its T6SS similar to the WT, yet secretes more Hcp than the WT and is better in T6SS-mediated killing of other bacteria. A capsule-overproducing mutant (∆bfmS) shows both, a partial deficiency in T6SS assembly and an additional reduction in exported Hcp, and is worse in T6SS-mediated killing than the WT. A mutant with a capsule similar to WT and deficient in cell sensing (∆tslA) forms the least T6SS apparatuses and is yet better in T6SS-mediated killing than the overcapsulated mutant. Together, these data show an effect of the capsule on (i) T6SS apparatus assembly, (ii) effector export, (iii) effector import, and (iv) the need for clearance of accumulating non-secreted Hcp by ClpXP. The work on a clinical isolate of Acinetobacter tumefaciens and the data on an impaired T6SS activity on other cells by antibiotic-induced capsulation is a strong demonstration of the work's clinical relevance in addition to the findings' conceptual novelty.

      • In my view, the manuscript is outstanding with very high quality of experimental data, very well written text and very clear presentation of the data in figures. A few minor comments and suggestions below that I think would strengthen the manuscript.*

      __ Authors’ reply #1: __We thank the reviewer for their enthusiasm.

      • *

      Major comment:

      #2) OPTIONAL: Fig. 4c/l. 320: Having an indirect effect of an antibiotic on T6SS activity by antibiotic-induced capsule formation is very intriguing and contributes to the clinical relevance of the overall findings. When I saw the data in Fig. 4c, the graph instantaneously reminded me of the panel in Fig. 2a, where a similar phenotype is observed by changing the predator:prey ratio in the absence of any antibiotic. The authors themselves comment on the possibility of antibiotic-induced, reduced predator growth (and thereby a change in predator:prey ratio) as a one factor impacting the phenotype here. I am wondering if this data could be strengthened or better disentangled to test more precisely if it is the antibiotic induced capsule formation per se that affects T6SS-mediated killing by A. baumanii in the presence of antibiotics. Would it help to take the bfmS mutant along as a control for direct comparison to see if antibiotic-induced capsule formation of the WT to similar levels of the mutant results in the same killing phenotype? Would it help to test for T6SS-mediated killing in the presence and absence of antibiotics at multiple predator:prey ratios? Could the effect of the antibiotic on A. baumanii growth be measured and considered when choosing the ratio at which the bacteria are mixed?

      __ Authors’ reply #2: __The point raised by the reviewer is very important. As we have stated in the manuscript, the capsule-induced production using antibiotics impacts the growth of A. baumannii and could therefore change the predator-prey ratio, potentially affecting the observed phenotype. However, the antibiotic is expected to equally impact the non-encapsulated ΔitrA strain, yet this strain maintains very strong T6SS killing activity in the presence of chloramphenicol. Thus, we do not believe the predator-prey ratio is causing the observed effect. To address this point more directly, we nonetheless propose to: i) repeat the experiments with different predator-prey ratios (1:1, 2:1, and 5:1), and ii) include a bfmS mutant as a control.

      Minor comments:

      #3) Figure 1D, l. 155, I might have missed this, do the authors happen to have the numbers of E. cloacae as well? This would strengthen the claim on A. baumannii survival because of E. cloacae is being killed.

      __ Authors’ reply #3: __The reviewer is correct; we did not include the survival of E. cloacae in the initial manuscript due to technical reasons (counter-selection of E. cloacae). However, we propose to repeat the experiment using an E. cloacae strain carrying a plasmid conferring kanamycin resistance. This will allow us to counter-select E. cloacae after contact with the A. baumannii predator to determine if E. cloacae is killed by A. baumannii in a T6SS-dependent manner.


      #4) Figure 2, I suggest to write out the species name of the prey in the box with the ratio. With E. cloacae being referred to in the previous figure and starting with similar letters than E. coli, I wasn't sure at first sight what E. c. refers to.

      __ Authors’ reply #4: __We appreciate the comment and will revise the figure as suggested.

      #5) use of the term "T6SS activity" throughout the manuscript (e.g. l. 182, l. 187). I leave this up to the authors. To me, it seems like an umbrella term for the initial observation and I see that such a term can be very handy for the writing. I just would like to mention that the use of the term was not always intuitive to me and sometimes even a bit misleading. For example, l. 182 refers to "increased T6SS activity". As a reader, I only know about 'T6SS activity on other cells' or 'a T6SS-mediated effect on other cells' at this point. T6SS apparatus assembly/firing activity is tested for specifically later and it turns out to differ between mutants. By the time the term is used in the discussion, it captures multiple nuanced phenotypes described by then. The more precise definition of the term in l. 200 helped to capture what exactly is meant by the authors.

      __ Authors’ reply #5: __We propose rephrasing the sentences to include the term "T6SS-secretion activity" when referring to Hcp secretion assays and "T6SS-mediated killing activity" when referring to killing experiments.

      __#6) __l. 198-199 "Collectively, our findings indicate that CPS does not hinder the secretion process of the T6SS or the consequent elimination of competing cells". I might be missing something, I cannot entirely follow this sentence. Didn't the authors just show that the CPS does hinder T6SS-mediated elimination of competing cells in panel 2A and less secreted Hcp in the encapsulated WT compared to the non-encapsulated mutant in panel 2B?

      __ Authors’ reply #6:__ We thank the reviewer for this comment. We realize that the sentence wasn’t well phrased, resulting in confusion. What we meant was that the T6SS is functional regarding its T6SS-mediated killing and secretion in the WT strain, while we also showed that the non-capsulated strain kills and secretes more T6SS material in the supernatant. Thus, there seems to be a balance between capsule production and T6SS activity in the WT. We will revise the sentence to better reflect this meaning.

      #7) l. 224, typo, "in"

      __ Authors’ reply #7:__ We will correct this typo. Thank you.

      • *

      #8) Two connected comments: l. 338, Just a thought, I am wondering about the title of the section. After reading it a second time, I think it is technically correct. When reading it first, I was a bit confused when getting to the data because apparatus assmebly is impaired in the capsule-overproducing strain and although "preserved", doesn't the data indicate that there is less T6SS assembly in the bfmS mutant and that this might be because of less cell sensing and isn't this a main point that there is a difference in apparatus assembly in the capsule overproducing strain compared to WT (other than no difference in apparatus assembly in the strain without capsule)? To me it seems not fully acknowledged as a finding in the interpretation of the data that less cells of the bfmS mutant have a T6SS apparatus. Isn't that interesting? A title along the lines of "Capsule-overproducing strain has preserved sensory function and assembles less T6SS apparatuses" would have been more intuitive for me. l. 352, In case I didn't miss a reference to this data earlier in the manuscript, I am wondering if it would be worth mentioning the finding on the reduced apparatus assembly of the bfmS mutant earlier, together with Figure 3 already. At least a sentence that mentions already that there is more coming later. When I got to this line in the manuscript and read the findings on the apparatus assembly, I first needed to go back to figure 3 and look at the data there again in light of this finding. It is mentioned here on the side but I think very important for the interpretation of the phenotypic data of the bfmS mutant shown earlier, isn't it? The tslA mutant is used beautifully here.

      __ Authors’ reply #8:__ We thank the reviewer for the suggestion and the kind comment about the beautiful usage of the tslA mutant. We will modify the title of the corresponding paragraph as suggested to make it more intuitive.

              Regarding the comment about mentioning the T6SS apparatus assembly defect in the *bfmS* mutant earlier, we respectfully disagree. While we agree that this point is important and can partially explain the difference in killing activity, we believe that showing it together with the *tslA* mutant (Figure 5) makes more sense and is easier for the reader to understand.
      

      #9) Discussion: optional comment. On the one hand, I like the concise discussion. On the other hand, I see more potential here for bringing it all together (potentially at the expense of shortening some of the introduction). I think the subtleties of the findings are complex. For example, I could envision a graphical summary with a working model on all the effects of a capsule on the T6SS and its potential clinical relevance making the study accessible to even more readers.

      __ Authors’ reply #9: __In the revised manuscript, we will include a graphical summary/model.


      Significance

      #10) General assessment: I consider the story very strong in terms of novelty, experimental approaches used, quality of the data, quality of the writing and figures of the manuscript. In my view, the aspects that could be improved are optional/minor and concern only one figure and some phrasing.

      • Advance: I see major advance in the findings (i, mechanistic) on the mechanism of how the capsule interferes with T6SS, (ii, fundamental) on the discovery of ClpXP degrading Hcp, and (iii, clinical) on the meaning of antibiotic treatment for the T6SS of this clinically relevant and often multi-drug resistant bacterial species, which strongly complements existing work on the T6SS and antibiotics in A. baumanii (e.g. of the Feldman group). As the authors write themselves, the starting points of the study of a capsule protecting from a T6SS and the effect of a T6SS on other cells being negatively impacted by a capsule were known, although not studied in one species and not understood mechanistically.*

      • Audience: I see the result of interest to a broad audience in the fields of bacteria-bacteria interactions, Acinetobacter baumanii, type VI secretion, antimicrobial resistance, bacterial capsules.*

      __ Authors’ reply #10: __We once again thank the reviewer and highly appreciate their positive and constructive feedback on our work. We hope the reviewer will be satisfied with the revised version of our manuscript.

      Reviewer #2 (Evidence, reproducibility and clarity (Required)):

      #11) In the manuscript by Flaugnatti et al., the authors provide clear evidence of the interplay between capsule outer coat production and the Type VI secretion system (T6SS) in Acinetobacter baumannii. The authors demonstrate that the presence of the capsule or the activity of the T6SS enhances survival against attacking bacteria. However, they also show that in their model bacterium, the (over)production of the capsule likely hinders T6SS dynamics, thereby reducing overall killing efficiency. Additionally, they reveal that the amount of the T6SS component Hcp is regulated in cells that can no longer assemble and/or secrete via the T6SS, presumably by the ClpXP protease. Overall, the experiments are well designed, and most conclusions are supported by the data and appropriate controls. I have however some suggestions that could further strengthen the manuscript prior to publication.

      __ Authors’ reply #11: __We are grateful for the reviewer’s enthusiasm and will implement their comments and suggestions in the revised version of the manuscript.


      Major comments:

      #12) Line 164. The authors use E. coli as prey to test the T6SS activity of A. baumannii. Why not directly use the E. cloacae strain (with or without T6SS) for this purpose? This would provide direct evidence that A. baumannii uses its T6SS to kill E. cloacae, thus confirming the authors conclusions in this section.

      __ Authors’ reply #12: __We thank the reviewer for this comment. We used E. coli to assess the functionality of the T6SS in different strains of A. baumannii, as it is commonly done in the T6SS field. However, as suggested by reviewer 1 (see comment #3) and in response to this query, we will also provide survival data of E. cloacae in the revised manuscript using a plasmid-carrying E. cloacae derivative that allows direct selection.

      #13) In Figure 2, the authors show that a non-capsulated strain kills more effectively and secretes more than a WT, but has a similar number of T6SS. They suggest in their conclusion that "the observed increase in T6SS activity in the non-capsulated strain suggests a compensatory mechanism for the absence of the protective capsule layer." This conclusion implies the presence of an "active" regulatory mechanism that would increase the number of successful T6SS firing events, which has not been demonstrated. Could it not simply be that the capsule blocks some shots that cannot penetrate and are therefore ineffective? This hypothesis is mentioned in lines 204-208. The authors should clarify the conclusion of this section. Given the challenge this may pose in A. baumannii, I suggest that the authors quantify the assembly/firing dynamics of the T6SS under WT and ΔitrA conditions. This would help distinguish between the two hypotheses explaining better firing in non-capsulated cells: i.e., if the number of assembled T6SS is the same in both strains (Fig 2C & 2D), do non-capsulated cells assemble/fire faster, indicating an adaptation in regulation, or do we observe the same dynamics, suggesting a simple physical barrier blocking the passage of certain T6SS firing events?

      __ Authors’ reply #13:__ We realize that the sentence, and more specifically the word "compensatory," might have been misleading and thank the reviewer for bringing this to our attention. What we meant to convey is that there is a balance between capsule production and T6SS activity; if disturbed, the balance shifts in one direction or the other. Specifically, there is more protection through the production of a thicker capsule (e.g., in the ∆bfmSmutant or under sub-MIC conditions of antibiotics, regulated by the Bfm system, as mentioned in the text) or more T6SS activity when less capsule is present (e.g., in the ΔitrA mutant, which we propose is caused by the lack of the steric hindrance). We will rephrase this sentence in the revised manuscript to better convey this message.

              Regarding the quantification of T6SS dynamic assembly/firing events between the capsulated (WT) and non-capsulated (ΔitrA) strains, we do not think this is required for this study, as the amount of secreted Hcp reflects the overall activity of the system. Importantly, we also do not have the technical means to quantify assembly/firing rates under Biosafety 2 conditions, as this requires specialized microscopes with very fast acquisition options (see, for instance, Basler, Pilhofer *et al.*, 2012, *Nature*). Indeed, very few labs in the T6SS field have been able to measure such rates.
      

      #14) Line 428-429. It is mentioned that the deletion of lon does not have a notable effect. However, I observe that the absence of Lon alone causes a more rapid degradation of Hcp in the cells compared to the WT strain (Fig 7B). How do the authors explain that the absence of this protease (whether under conditions of Hcp accumulation or not) increases the degradation of this protein in the cell? This explanation should be included in the manuscript.

      __ Authors’ reply #14: __That’s a fair point. We didn’t address this point further, as the deletion of lon didn’t resolve the issue of why Hcp is degraded. In fact, the opposite seems to be the case, as there is less Hcp in the ∆lon strain compared to the WT. While this observation is not directly relevant to the question of why Hcp is degraded late during growth in secretion-impaired strains, we will properly mention it in the revised manuscript.

              Please also note that a strong growth defect of a Δ*lon*Δ*clpXP* double mutant impaired further investigation in this direction.
      
      • *

      Minor comments:

      #15) Throughout the manuscript, the authors use the term "predator" to refer to A. baumannii. Predation is a specific phenomenon that involves killing for nourishment. To my knowledge, the T6SS has never been shown to be a predation weapon but rather a weapon for interbacterial competition, which is a different concept. If this has not been demonstrated in A. baumannii, the authors should replace the term "predator" with "attacker" (or an equivalent term) to clarify the context.

      __ Authors’ reply #15: __We thank the reviewer for this comment. The term “predator,” as highlighted by the reviewer, typically implies killing for nourishment/cellular products. In the context of T6SS, it facilitates the killing of competitors, releasing DNA into the environment that can subsequently be acquired through natural competence for transformation, as observed in species like Vibrio cholerae (our work by Borgeaud et al., 2015, Science) or other Acinetobacter species such as Acinetobacter baylyi (Ringel et al., 2017, Cell Rep.; Cooper et al., 2017, eLife). The acquisition of DNA reflects the killing for cellular products of the prey. As most A. baumannii strains are also naturally competent, this justifies the usage of the predator and prey nomenclature.

              Apart from this fact, it seems to be a matter of nomenclature, with many papers in the field using one term or the other. Yet, ultimately, this doesn’t change any of the scientific findings. Therefore, to satisfy the reviewer, we will change “predator” to “attacker” throughout the revised manuscript.
      

      #16) Line 274. Since the authors stated that in the Wzc mutant, the capsule is "predominantly found in the supernatant and only loosely attached to the cell," this result is not unexpected. This finding is also consistent with the previous results from Fig. 3A & B, which show sensitivity to complement-mediated killing and the weak amount of (ab)normal CPS produced in that strain, further confirmed by Fig. 3E.

      __ Authors’ reply #16__: We fully agree with the reviewer’s suggestion and will remove the statement.

      #17) Line 299. The authors speculate that "... T6SS may deploy through gaps akin to arrow-slits in the capsule's mesh...". However, this is very unlikely since a WT strain kills (Fig. 3C) and secretes (Fig. 2B & 3D) less effectively than the itrA mutant, suggesting that the T6SS is not assembled in the "right places" devoid of CPS; otherwise, we would expect similar T6SS activity. Based on the results in Fig. 2 (and my earlier comment), this implies that A. baumannii assembles its T6SS randomly, and in the presence of the capsule, its shots would need to be in the right place to penetrate the envelope and reach the target. Could the authors comment on this point and provide a model figure to better visualize the interplay between the capsule and T6SS under the three major conditions: WT, non-capsulated, and capsule overproduction?

      __ Authors’ reply #17: __We thank the reviewer and agree with their comment. We discussed the hypothesis of T6SS deployment through gaps, drawing a parallel to what was proposed for biofilm and T6SS in V. cholerae(Toska et al., 2018, PNAS). However, as mentioned earlier, we believe that the effect of the capsule on T6SS activity is primarily due to steric hindrance, which increases the distance between the T6SS apparatus and the prey cell. To clarify our findings further, we will include a model summarizing our results, as requested by reviewer 1 (see comment #9).


      __ #18)__ In Fig. 5A, the microscopy panels should be adjusted to the same dynamic range as the WT (which represents a true signal), which does not appear to be the case for the tlsA mutant panel for instance. The image gives the impression of a large amount of free TssB-msfGFP in the cytoplasm. However, this effect is due to the dynamic range being adjusted to display a signal. This observation is consistent with the fact that the amount of TssB-msfGFP protein is identical across all strains (Fig. S2F).

      __ Authors’ reply #18: __We will adjust the images to the range of the WT in the revised manuscript, as suggested. However, regardless of how these images are presented, the enumeration of T6SS structures will remain unchanged, which was the sole point of this experiment.

      • *

      #19) Unless I am mistaken, the authors do not comment on the fact that in a ΔbfmS strain, the number of T6SS is halved compared to a WT or ΔitrA strain. If capsule overproduction only partially limits the TslA-dependant T6SS assembly, how can this result be explained? Is it related to the degradation of Hcp in this background, which ultimately limits the formation of T6SS? If so, it would be interesting to mention this connection in the section "Prolonged secretion inhibition triggers Hcp degradation”

      __ Authors’ reply #19: __We did mention that the T6SS assembly of the ΔbfmS mutant is reduced compared to the WT (or ΔitrA), likely due to the defect in sensing the prey (lines 369-374 and 468-472 of the initial manuscript). However, we will revise the sentence to improve clarity in the revised version of the manuscript.

      Significance

      #20) This work is highly intriguing as it not only delves into the specific mechanisms involved but also connects fundamental elements in bacterial competition, i.e., the necessity for self-protection and aggression for survival. The manuscript offers valuable insights into cellular dynamics at a microscale level and prompts new inquiries into the regulation of these systems on a population scale. The work is well-done and the writing is also clear. I am convinced that this work represents another significant step towards understanding bacterial mechanisms and will undoubtedly spark considerable interest in the field.

      __ Authors’ reply #20: __We sincerely thank reviewer #2 for their constructive inputs, which will improve our manuscript.

      • *

      Reviewer #3 (Evidence, reproducibility and clarity (Required)):

      #21) The manuscript by Flaugnatti et al investigates the relationship between functions of the T6SS in A. baumannii and production of capsular polysaccharide. The manuscript argues that (1) capsule protects A. baumannii against T6SS-mediated attack by other bacteria, (2) capsule also interferes with the bacterium's own T6SS activity, and (3) the T6SS inner tube protein Hcp is regulated by degradation by ClpXP. The main critiques regard the first two conclusions, which seem to be based solely on use of a mutant that has a confounding effect as described below; and to strengthen the third claim by further exploring the results of overexpressing Hcp and by determining whether there is a fitness benefit for Hcp regulation.

      __ Authors’ reply #21: __We thank reviewer #3 for their relevant input. We will conduct additional experiments based on their comments, and these will be incorporated into the revised manuscript.

      • *

      __Main items:____ __

      #22) Throughout the paper, an itrA deletion mutant is used as the capsule-deficient strain and conclusions are drawn about role of capsule based on this mutant. However, itrA deletion also eliminates the protein O-glycosylation pathway (Lees-miller et al 2013), a potential confounder. Analysis of mutants specifically deficient in the high-molecular weight capsule but not protein glycosylation, and/or mutants in the protein o-glycosylation enzyme, should be incorporated into the study to enhance the ability to make conclusions about the role of the capsule.

      __ Authors’ reply #22: __Fair point. We thank the reviewer for this important suggestion. To distinguish between the O-glycosylation pathway and capsule production, we will generate a ∆pglL strain (specific to O-glycosylation), as suggested, and will repeat the key experiments (similar to Fig. 2A and 2B). We are almost done with the engineering of this mutant strain and therefore don’t expect any major delays.

      #23) Evidence could be provided to support the idea raised in lines 482-483 that T6SS component accumulation is toxic ("degradation [of T6SS components] could serve as a strategy to alleviate proteotoxic stress..."). For example, growth curves of ∆clpXP strains with and without hcp could be analyzed, to determine how degrading Hcp is helping the bacteria.

      __ Authors’ reply #23: __We will perform growth curves of ΔclpXP strains with and without hcp, as suggested by the reviewer. However, we are uncertain whether we will be able to observe differences between these strains, as the conditions under which such degradation is significant may be challenging to replicate under standard laboratory conditions.

      __#24) __The possible ClpXP recognition sequence identified at the C terminus of Hcp is interesting-does overexpression of an Hcp variant lacking/altered in this motif alter its protein levels compared to WT Hcp?

      __ Authors’ reply #24: __We thank the reviewer for this suggestion. We are in the process of performing the suggested experiment and will include the data in the manuscript.

      __Minor items:____ __

      #25) *A better explanation could be provided for why overexpressing hcp in WT but not in ∆hcp leads to increased Hcp protein levels. There is a statement about Hcp being regulated post transcriptionally, possibly by degradation (lines 422-423), but would that not also result in regulation in the WT strain? *

      __ Authors’ reply #25: __The reviewer is absolutely correct here. Despite careful genetic engineering, we believe that the hcp mutant used may have a polar effect, causing Hcp accumulation only in the ∆hcp + p-hcp strain but not in the WT + p-hcp strain, which remains capable of secretion. The ∆hcp strain therefore mimics the secretion-impaired tssB mutant. We will clarify this in the revised manuscript.

      #26) *An untreated control is needed in Fig. 4B. *

      __ Authors’ reply #26: __The untreated samples were shown in all previous figures. However, we understand the reviewer's point and will repeat the experiment with the untreated control included in the same experiment.

      #27) *line 179: please clarify "reflecting better invading bacteria" *

      __ Authors’ reply #27: __We appreciate the reviewer mentioning this oversight. We meant to compare this to a situation where a bacterium invades an already existing community, resulting in a predator-prey ratio below 1. We will clarify this further in the revised manuscript.

      #28) *line 351: consider rewording the statement that ∆tslA results in decreased in T6SS assembly and activity using the tssB-msfGFP microscopy assay; it is not clear that activity is measured in this assay. *

      __ Authors’ reply #28: __The reviewer is correct. We will revise the sentence accordingly to better reflect the T6SS assembly.

      #29) *lines 260-265: This experiment could use clarifying, but it would seem that it requires analysis of the secreted capsule levels in the tssB mutant to show it does not produce extracellular capsule to the same extent that ∆bfmS does. *

      __ Authors’ reply #29: __We thank the reviewer for the suggestion and will include these experimental data in the revised manuscript.

      #30) *Fig. 6C and 7A labelling could be improved to avoid potential confusion that the bar graphs are quantifying the western blot. E.g., could add a corresponding vertical label to the Western data, or consider changing "relative expression of hcp" to something reflecting analysis of transcript levels. *

      __ Authors’ reply #30: __We will improve this figure by splitting the qPCR and Western blot data into independent panels. This will eliminate any confusion.


      #31) lines 416-417 and Fig. 7A: states that "hcp mRNA levels increased significantly", but more careful wording could be used because the WT's transcript change is not significant after overexpression (though it is significant in ∆hcp).

      __ Authors’ reply #31: __Point well taken. We will improve the sentence (and Figure) to make its meaning unambiguous.

      • *

      #32) lines 479-480 states that in secretion-impaired strains accumulation of Hcp is mitigated by ClpXP; while this was shown for ∆tssB, was this also the case for ∆bfmS?

      __ Authors’ reply #32: __This is indeed an interesting suggestion. We are in the process of generating the double mutant ∆bfmSclpXP and will include the experimental results in the revised manuscript.


      Significance

      #33) *The strengths of the study are the focus on a clinically significant pathogen, the potential novel roles for the important capsule virulence factor of A. baumannii, and the identification of novel points of control of the T6SS. The analyses of T6SS function are thorough and carefully performed. *

      __ Authors’ reply #33: __We thank the reviewer for their comments, which we believe will significantly strengthen our work, particularly regarding the capsule aspect.

    2. Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.

      Learn more at Review Commons


      Referee #3

      Evidence, reproducibility and clarity

      The manuscript by Flaugnatti et al investigates the relationship between functions of the T6SS in A. baumannii and production of capsular polysaccharide. The manuscript argues that (1) capsule protects A. baumannii against T6SS-mediated attack by other bacteria, (2) capsule also interferes with the bacterium's own T6SS activity, and (3) the T6SS inner tube protein Hcp is regulated by degradation by ClpXP. The main critiques regard the first two conclusions, which seem to be based solely on use of a mutant that has a confounding effect as described below; and to strengthen the third claim by further exploring the results of overexpressing Hcp and by determining whether there is a fitness benefit for Hcp regulation.

      Main items:

      • Throughout the paper, an itrA deletion mutant is used as the capsule-deficient strain and conclusions are drawn about role of capsule based on this mutant. However, itrA deletion also eliminates the protein O-glycosylation pathway (Lees-miller et al 2013), a potential confounder. Analysis of mutants specifically deficient in the high-molecular weight capsule but not protein glycosylation, and/or mutants in the protein o-glycosylation enzyme, should be incorporated into the study to enhance the ability to make conclusions about the role of the capsule.
      • Evidence could be provided to support the idea raised in lines 482-483 that T6SS component accumulation is toxic ("degradation [of T6SS components] could serve as a strategy to alleviate proteotoxic stress..."). For example, growth curves of ∆clpXP strains with and without hcp could be analyzed, to determine how degrading Hcp is helping the bacteria.
      • The possible ClpXP recognition sequence identified at the C terminus of Hcp is interesting--does overexpression of an Hcp variant lacking/altered in this motif alter its protein levels compared to WT Hcp?

      Minor items:

      • A better explanation could be provided for why overexpressing hcp in WT but not in ∆hcp leads to increased Hcp protein levels. There is a statement about Hcp being regulated post transcriptionally, possibly by degradation (lines 422-423), but would that not also result in regulation in the WT strain?
      • An untreated control is needed in Fig. 4B.
      • line 179: please clarify "reflecting better invading bacteria"
      • line 351: consider rewording the statement that ∆tslA results in decreased in T6SS assembly and activity using the tssB-msfGFP microscopy assay; it is not clear that activity is measured in this assay.
      • lines 260-265: This experiment could use clarifying, but it would seem that it requires analysis of the secreted capsule levels in the tssB mutant to show it does not produce extracellular capsule to the same extent that ∆bfmS does.
      • Fig. 6C and 7A labelling could be improved to avoid potential confusion that the bar graphs are quantifying the western blot. E.g., could add a corresponding vertical label to the Western data, or consider changing "relative expression of hcp" to something reflecting analysis of transcript levels.
      • lines 416-417 and Fig. 7A: states that "hcp mRNA levels increased significantly", but more careful wording could be used because the WT's transcript change is not significant after overexpression (though it is significant in ∆hcp)
      • lines 479-480 states that in secretion-impaired strains accumulation of Hcp is mitigated by ClpXP; while this was shown for ∆tssB, was this also the case for ∆bfmS?

      Significance

      The strengths of the study are the focus on a clinically significant pathogen, the potential novel roles for the important capsule virulence factor of A. baumannii, and the identification of novel points of control of the T6SS. The analyses of T6SS function are thorough and carefully performed.

    3. Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.

      Learn more at Review Commons


      Referee #2

      Evidence, reproducibility and clarity

      In the manuscript by Flaugnatti et al., the authors provide clear evidence of the interplay between capsule outer coat production and the Type VI secretion system (T6SS) in Acinetobacter baumannii. The authors demonstrate that the presence of the capsule or the activity of the T6SS enhances survival against attacking bacteria. However, they also show that in their model bacterium, the (over)production of the capsule likely hinders T6SS dynamics, thereby reducing overall killing efficiency. Additionally, they reveal that the amount of the T6SS component Hcp is regulated in cells that can no longer assemble and/or secrete via the T6SS, presumably by the ClpXP protease. Overall, the experiments are well designed, and most conclusions are supported by the data and appropriate controls. I have however some suggestions that could further strengthen the manuscript prior to publication.

      Major comments:

      Line 164. The authors use E. coli as prey to test the T6SS activity of A. baumannii. Why not directly use the E. cloacae strain (with or without T6SS) for this purpose? This would provide direct evidence that A. baumannii uses its T6SS to kill E. cloacae, thus confirming the authors conclusions in this section.. In Figure 2, the authors show that a non-capsulated strain kills more effectively and secretes more than a WT, but has a similar number of T6SS. They suggest in their conclusion that "the observed increase in T6SS activity in the non-capsulated strain suggests a compensatory mechanism for the absence of the protective capsule layer." This conclusion implies the presence of an "active" regulatory mechanism that would increase the number of successful T6SS firing events, which has not been demonstrated. Could it not simply be that the capsule blocks some shots that cannot penetrate and are therefore ineffective? This hypothesis is mentioned in lines 204-208. The authors should clarify the conclusion of this section. Given the challenge this may pose in A. baumannii, I suggest that the authors quantify the assembly/firing dynamics of the T6SS under WT and ΔitrA conditions. This would help distinguish between the two hypotheses explaining better firing in non-capsulated cells: i.e., if the number of assembled T6SS is the same in both strains (Fig 2C & 2D), do non-capsulated cells assemble/fire faster, indicating an adaptation in regulation, or do we observe the same dynamics, suggesting a simple physical barrier blocking the passage of certain T6SS firing events? Line 428-429. It is mentioned that the deletion of lon does not have a notable effect. However, I observe that the absence of Lon alone causes a more rapid degradation of Hcp in the cells compared to the WT strain (Fig 7B). How do the authors explain that the absence of this protease (whether under conditions of Hcp accumulation or not) increases the degradation of this protein in the cell? This explanation should be included in the manuscript.

      Minor comments:

      • a) Throughout the manuscript, the authors use the term "predator" to refer to A. baumannii. Predation is a specific phenomenon that involves killing for nourishment. To my knowledge, the T6SS has never been shown to be a predation weapon but rather a weapon for interbacterial competition, which is a different concept. If this has not been demonstrated in A. baumannii, the authors should replace the term "predator" with "attacker" (or an equivalent term) to clarify the context.
      • b) Line 274. Since the authors stated that in the Wzc mutant, the capsule is "predominantly found in the supernatant and only loosely attached to the cell," this result is not unexpected. This finding is also consistent with the previous results from Fig. 3A & B, which show sensitivity to complement-mediated killing and the weak amount of (ab)normal CPS produced in that strain, further confirmed by Fig. 3E.
      • c) Line 299. The authors speculate that "... T6SS may deploy through gaps akin to arrow-slits in the capsule's mesh...". However, this is very unlikely since a WT strain kills (Fig. 3C) and secretes (Fig. 2B & 3D) less effectively than the itrA mutant, suggesting that the T6SS is not assembled in the "right places" devoid of CPS; otherwise, we would expect similar T6SS activity. Based on the results in Fig. 2 (and my earlier comment), this implies that A. baumannii assembles its T6SS randomly, and in the presence of the capsule, its shots would need to be in the right place to penetrate the envelope and reach the target. Could the authors comment on this point and provide a model figure to better visualize the interplay between the capsule and T6SS under the three major conditions: WT, non-capsulated, and capsule overproduction?
      • d) In Fig. 5A, the microscopy panels should be adjusted to the same dynamic range as the WT (which represents a true signal), which does not appear to be the case for the tlsA mutant panel for instance. The image gives the impression of a large amount of free TssB-msfGFP in the cytoplasm. However, this effect is due to the dynamic range being adjusted to display a signal. This observation is consistent with the fact that the amount of TssB-msfGFP protein is identical across all strains (Fig. S2F).
      • e) Unless I am mistaken, the authors do not comment on the fact that in a ΔbfmS strain, the number of T6SS is halved compared to a WT or ΔitrA strain. If capsule overproduction only partially limits the TslA-dependant T6SS assembly, how can this result be explained? Is it related to the degradation of Hcp in this background, which ultimately limits the formation of T6SS? If so, it would be interesting to mention this connection in the section "Prolonged secretion inhibition triggers Hcp degradation."

      Referee Cross-Commenting

      Overall, I agree with the concerns raised by reviewers 1 and 3. This (already) very good manuscript will undoubtedly benefit from these comments.

      Significance

      This work is highly intriguing as it not only delves into the specific mechanisms involved but also connects fundamental elements in bacterial competition, i.e., the necessity for self-protection and aggression for survival. The manuscript offers valuable insights into cellular dynamics at a microscale level and prompts new inquiries into the regulation of these systems on a population scale. The work is well-done and the writing is also clear.

      I am convinced that this work represents another significant step towards understanding bacterial mechanisms and will undoubtedly spark considerable interest in the field.

      Expertise: T6SS, fluorescence microscopy, predation, interbacterial competition

    4. Note: This preprint has been reviewed by subject experts for Review Commons. Content has not been altered except for formatting.

      Learn more at Review Commons


      Referee #1

      Evidence, reproducibility and clarity

      Summary:

      The transport of effector proteins across membranes from the producing bacterium into a target cell is at the core of bacterial secretion systems. How an additional layer in form of a capsule affects effector export and the susceptibility towards effector import is not fully understood. Here, Flaugnatti and colleagues combined bacterial genetics with phenotypic assays and electron microscopy to demonstrate a dual role of a bacterial capsule in preventing T6SS-mediated effector export and promoting protection from effector import by another bacterium's T6SS. The wide variety of methods used, complementation of the mutants, and validation of the findings across strains strengthen the author's conclusions.

      Although the main conclusions seem straight forward, the authors unravel the unexpected complexity underlying these phenotypes with strong mechanistic work. In brief, a capsule-deficient mutant (∆itra) is shown to assemble its T6SS similar to the WT, yet secretes more Hcp than the WT and is better in T6SS-mediated killing of other bacteria. A capsule-overproducing mutant (∆bfmS) shows both, a partial deficiency in T6SS assembly and an additional reduction in exported Hcp, and is worse in T6SS-mediated killing than the WT. A mutant with a capsule similar to WT and deficient in cell sensing (∆tslA) forms the least T6SS apparatuses and is yet better in T6SS-mediated killing than the overcapsulated mutant. Together, these data show an effect of the capsule on (i) T6SS apparatus assembly, (ii) effector export, (iii) effector import, and (iv) the need for clearance of accumulating non-secreted Hcp by ClpXP.

      The work on a clinical isolate of Acinetobacter tumefaciens and the data on an impaired T6SS activity on other cells by antibiotic-induced capsulation is a strong demonstration of the work's clinical relevance in addition to the findings' conceptual novelty.

      In my view, the manuscript is outstanding with very high quality of experimental data, very well written text and very clear presentation of the data in figures. A few minor comments and suggestions below that I think would strengthen the manuscript.

      Major comment:

      OPTIONAL: Fig. 4c/l. 320: Having an indirect effect of an antibiotic on T6SS activity by antibiotic-induced capsule formation is very intriguing and contributes to the clinical relevance of the overall findings. When I saw the data in Fig. 4c, the graph instantaneously reminded me of the panel in Fig. 2a, where a similar phenotype is observed by changing the predator:prey ratio in the absence of any antibiotic. The authors themselves comment on the possibility of antibiotic-induced, reduced predator growth (and thereby a change in predator:prey ratio) as a one factor impacting the phenotype here. I am wondering if this data could be strengthened or better disentangled to test more precisely if it is the antibiotic induced capsule formation per se that affects T6SS-mediated killing by A. baumanii in the presence of antibiotics. Would it help to take the bfmS mutant along as a control for direct comparison to see if antibiotic-induced capsule formation of the WT to similar levels of the mutant results in the same killing phenotype? Would it help to test for T6SS-mediated killing in the presence and absence of antibiotics at multiple predator:prey ratios? Could the effect of the antibiotic on A. baumanii growth be measured and considered when choosing the ratio at which the bacteria are mixed?

      Minor comments:

      • Figure 1D, l. 155ff, I might have missed this, do the authors happen to have the numbers of E. cloacae as well? This would strengthen the claim on A. baumanii survival because of E. cloacae is being killed.
      • Figure 2, I suggest to write out the species name of the prey in the box with the ratio. With E. cloacae being referred to in the previous figure and starting with similar letters than E. coli, I wasn't sure at first sight what E. c. refers to.
      • use of the term "T6SS activity" throughout the manuscript (e.g. l. 182, l. 187). I leave this up to the authors. To me, it seems like an umbrella term for the initial observation and I see that such a term can be very handy for the writing. I just would like to mention that the use of the term was not always intuitive to me and sometimes even a bit misleading. For example, l. 182 refers to "increased T6SS activity". As a reader, I only know about 'T6SS activity on other cells' or 'a T6SS-mediated effect on other cells' at this point. T6SS apparatus assembly/firing activity is tested for specifically later and it turns out to differ between mutants. By the time the term is used in the discussion, it captures multiple nuanced phenotypes described by then. The more precise definition of the term in l. 200 helped to capture what exactly is meant by the authors.
      • l. 198f "Collectively, our findings indicate that CPS does not hinder the secretion process of 199 the T6SS or the consequent elimination of competing cells". I might be missing something, I cannot entirely follow this sentence. Didn't the authors just show that the CPS does hinder T6SS-mediated elimination of competing cells in panel 2A and less secreted Hcp in the encapsulated WT compared to the non-encapsulated mutant in panel 2B?
      • l. 224, typo, "in"
      • Two connected comments: l. 338, Just a thought, I am wondering about the title of the section. After reading it a second time, I think it is technically correct. When reading it first, I was a bit confused when getting to the data because apparatus assmebly is impaired in the capsule-overproducing strain and although "preserved", doesn't the data indicate that there is less T6SS assembly in the bfmS mutant and that this might be because of less cell sensing and isn't this a main point that there is a difference in apparatus assembly in the capsule overproducing strain compared to WT (other than no difference in apparatus assembly in the strain without capsule)? To me it seems not fully acknowledged as a finding in the interpretation of the data that less cells of the bfmS mutant have a T6SS apparatus. Isn't that interesting? A title along the lines of "Capsule-overproducing strain has preserved sensory function and assembles less T6SS apparatuses" would have been more intuitive for me. l. 352, In case I didn't miss a reference to this data earlier in the manuscript, I am wondering if it would be worth mentioning the finding on the reduced apparatus assembly of the bfmS mutant earlier, together with Figure 3 already. At least a sentence that mentions already that there is more coming later. When I got to this line in the manuscript and read the findings on the apparatus assembly, I first needed to go back to figure 3 and look at the data there again in light of this finding. It is mentioned here on the side but I think very important for the interpretation of the phenotypic data of the bfmS mutant shown earlier, isn't it? The tslA mutant is used beautifully here.
      • Discussion: optional comment. On the one hand, I like the concise discussion. On the other hand, I see more potential here for bringing it all together (potentially at the expense of shortening some of the introduction). I think the subtleties of the findings are complex. For example, I could envision a graphical summary with a working model on all the effects of a capsule on the T6SS and its potential clinical relevance making the study accessible to even more readers.

      Significance

      General assessment

      I consider the story very strong in terms of novelty, experimental approaches used, quality of the data, quality of the writing and figures of the manuscript. In my view, the aspects that could be improved are optional/minor and concern only one figure and some phrasing.

      Advance

      I see major advance in the findings (i, mechanistic) on the mechanism of how the capsule interferes with T6SS, (ii, fundamental) on the discovery of ClpXP degrading Hcp, and (iii, clinical) on the meaning of antibiotic treatment for the T6SS of this clinically relevant and often multi-drug resistant bacterial species, which strongly complements existing work on the T6SS and antibiotics in A. baumanii (e.g. of the Feldman group). As the authors write themselves, the starting points of the study of a capsule protecting from a T6SS and the effect of a T6SS on other cells being negatively impacted by a capsule were known, although not studied in one species and not understood mechanistically.

      Audience

      I see the result of interest to a broad audience in the fields of bacteria-bacteria interactions, Acinetobacter baumanii, type VI secretion, antimicrobial resistance, bacterial capsules

    1. everythingoesblue

      why do you have no bio? are you just a stray speck of dust in the wind?

    1. Not when it takes too much out of Seokjin to just live.

      I HATE YOU KIM SEOKJIN

    2. Jungkook had told himself that he’d forgotten the slight curl of Seokjin’s hair, the way he pulls the back of his collar up to block the sun but keeps the front down to show off his collarbones.

      I LOVE YOU KIM SEOKJIN

    1. ambiguidade na figurade escritora que decorre de variadas manifestações suas

      Ela apresenta muitas facetas de si mesma em suas obras, como isso pode ser enigmático?

    1. Résumé de la vidéo [00:00:00][^1^][1] - [00:47:30][^2^][2]:

      Cette vidéo présente une conférence de Julien Grenet, chercheur au CNRS et à l'École d'économie de Paris, sur les expérimentations menées en France pour renforcer la mixité sociale dans les collèges publics depuis 2016. Il discute des motivations, des méthodes et des résultats préliminaires de ces expérimentations, en mettant l'accent sur la ségrégation sociale dans les établissements scolaires et les approches pour la réduire.

      Points forts: + [00:00:34][^3^][3] Contexte des expérimentations * Forte ségrégation sociale dans les collèges français * Disparités entre établissements publics et privés * Impact de la sectorisation sur la composition sociale des collèges + [00:13:47][^4^][4] Méthodes d'expérimentation * Fusion de secteurs de collège socialement contrastés * Affectation des élèves selon de nouvelles modalités * Approches testées à Paris et à Toulouse + [00:22:24][^5^][5] Suivi des élèves et méthodologie * Enquêtes sur les compétences cognitives et socio-émotionnelles * Impact du COVID-19 sur la collecte de données * Comparaison entre sites pilotes et sites témoins + [00:26:01][^6^][6] Évolution de la mixité sociale * Mesure de l'exposition des élèves à d'autres groupes sociaux * Effets limités mais significatifs sur la mixité * Pas d'augmentation de l'évitement scolaire observée + [00:33:38][^7^][7] Effets sur les élèves * Amélioration du bien-être social pour les élèves défavorisés * Impact limité sur les résultats scolaires * Effets positifs sur l'estime de soi scolaire pour les élèves favorisés + [00:42:01][^8^][8] Conséquences sur les attitudes sociales * Évolution des attitudes vers plus de coopération et moins de fatalisme * Importance des réseaux sociaux pour la mobilité future * Effets à long terme de la mixité sur les choix d'orientation et l'enseignement supérieur

    1. Résumé de la vidéo [00:00:00][^1^][1] - [00:41:04][^2^][2]:

      Cette vidéo présente une conférence d'Esther Duflo sur les approches expérimentales en éducation, en se concentrant sur l'interprétation des résultats de l'enquête PISA. Elle explique l'importance de comprendre les données au-delà des classements sensationnels des pays, en mettant en lumière les forces et faiblesses spécifiques du système éducatif français.

      Points forts: + [00:00:23][^3^][3] Introduction à l'enquête PISA * Présentation de l'enquête internationale PISA * Importance de l'analyse détaillée des résultats * Objectif de révéler les forces et faiblesses de l'école française + [00:02:10][^4^][4] Analyse des résultats de PISA 2022 * Baisse des compétences en mathématiques chez les élèves de 15 ans * Comparaison des scores de la France avec d'autres pays * Impact de l'origine socioéconomique sur les performances + [00:13:30][^5^][5] Disparités dans les performances éducatives * Écarts de scores entre les élèves selon leur statut socioéconomique * Influence de l'origine sociale sur la réussite scolaire * Évolution des écarts de performances au fil des ans + [00:24:31][^6^][6] Différences de performances entre les genres * Comparaison des performances en mathématiques entre garçons et filles * Évolution des écarts de genre dans différents pays * Impact de la culture et des politiques éducatives sur ces différences

    1. Résumé de la vidéo [00:00:00][^1^][1] - [00:47:31][^2^][2]:

      Dans cette vidéo, Esther Duflo présente les progrès récents dans la compréhension des bases cérébrales de l'acquisition de la lecture et comment les neurosciences cognitives peuvent contribuer à l'éducation. Elle explique l'importance de comprendre les mécanismes cérébraux de l'apprentissage pour développer des programmes éducatifs efficaces, en particulier pour les enfants dyslexiques.

      Points forts: + [00:00:22][^3^][3] Introduction et contexte * Présentation du sujet sur l'acquisition de la lecture et ses bases cérébrales * Questionnement sur l'apport des neurosciences à l'éducation * L'objectif de montrer les liens entre neurosciences et éducation + [00:01:45][^4^][4] Mécanismes cérébraux de l'apprentissage de la lecture * Description des changements dans le cerveau lors de l'apprentissage de la lecture * Présentation d'un modèle détaillé de l'acte de lire implémenté par les neurones * Nouveaux travaux sur le diagnostic des différents types de dyslexie + [00:07:13][^5^][5] Étude sur l'apprentissage de la lecture chez les enfants * Observation de la spécialisation rapide d'une région cérébrale pour la lecture * Étude longitudinale sur l'évolution de la fluence de lecture chez les enfants * Importance de l'automatisation de la lecture pour une acquisition efficace + [00:15:32][^6^][6] Modélisation de la réponse neuronale à la lecture * Utilisation de modèles pour simuler la réponse des neurones à différents mots * Découverte de neurones spécialisés pour certaines lettres et positions dans un mot * Importance de l'invariance de la casse et de la sélectivité positionnelle + [00:21:19][^7^][7] Dissociation de la position des lettres et de la position rétinienne * Explication de la réponse neuronale à la position relative des lettres * Distinction entre la position rétinienne absolue et la position relative des lettres * Prédiction du modèle neuronal pour la lecture et son application pratique + [00:28:39][^8^][8] Application des découvertes en neurosciences à l'éducation * Discussion sur l'utilisation des neurosciences pour améliorer l'instruction * Présentation d'outils pour mesurer et faciliter l'acquisition de la lecture * Critique des remèdes miracles non fondés scientifiquement dans le traitement de la dyslexie

    1. Résumé de la vidéo [00:00:00][^1^][1] - [00:30:33][^2^][2]:

      Cette vidéo présente une conférence d'Esther Duflo sur les approches expérimentales en éducation, où elle discute de l'importance des interactions sociales dans l'apprentissage des enfants et de l'impact des technologies numériques dans les salles de classe. Elle souligne également le rôle des systèmes cognitifs de base dans le développement de l'enfant et l'apprentissage des mathématiques.

      Points forts: + [00:00:48][^3^][3] Introduction et contexte * Préface sur une réunion interdisciplinaire * Importance de l'évaluation en éducation * Collaboration entre économistes et psychologues + [00:02:05][^4^][4] Interaction sociale et apprentissage * Importance des interactions sociales pour les enfants * Étude en Uruguay sur l'apprentissage numérique en groupe * Comparaison de l'apprentissage individuel et en groupe + [00:05:08][^5^][5] Recherche et politique en éducation * L'impact de la recherche sur les politiques éducatives * Importance de l'engagement des chercheurs avec les décideurs * Réorientation de la présentation suite aux discussions + [00:10:36][^6^][6] Systèmes de connaissances de base * Présentation des systèmes cognitifs de base chez les enfants * Rôle de ces systèmes dans l'apprentissage des mathématiques * Importance de la géométrie et des concepts numériques + [00:16:09][^7^][7] Compréhension sociale chez les nourrissons * Systèmes permettant aux nourrissons de comprendre les actions et états mentaux * Inférence des objectifs et valeurs à partir des actions observées * Apprentissage des relations sociales et des réseaux sociaux + [00:29:53][^8^][8] Apprentissage du langage chez les nourrissons * Début de l'apprentissage du langage avant la parole * Travaux de Jacques Mehler sur la compréhension du langage chez les nourrissons * Importance de l'engagement social dans l'apprentissage du langage

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:20:01][^2^][2]:

      Inès Mentec présente ses recherches sur le rôle de la valence dans les perceptions conscientes. Elle explore si la valence, ou la qualité positive ou négative d'une perception, est une caractéristique structurante dans notre espace phénoménal et comment elle influence nos jugements de similarité et notre comportement.

      Points forts: + [00:00:16][^3^][3] Introduction à la recherche * Présentation d'Inès Mentec et de l'objectif de la recherche * Exploration du rôle de la valence dans les perceptions conscientes + [00:00:45][^4^][4] La valence dans la littérature sur les émotions * Discussion des théories classiques et de l'hypothèse de prédiction affective * La valence traitée en parallèle avec la perception visuelle + [00:02:41][^5^][5] La conscience et la valence * La conscience associe une valeur à nos perceptions * La valence comme une qualité de nos expériences conscientes + [00:03:14][^6^][6] Exploration de l'espace phénoménal * Étude de la structure de l'espace phénoménal à travers des expériences conscientes * Recherche sur la valence comme dimension informative + [00:06:35][^7^][7] Collecte de données et méthodologie * Utilisation de jugements de microvalence et de similarités * Analyse des activations de réseaux de neurones profonds + [00:10:27][^8^][8] Résultats et interprétations * Corrélations entre valence, similarité et activations neuronales * Influence de la valence sur les jugements de similarité sous pression temporelle

      Résumé de la vidéo [00:11:03][^1^][1] - [00:20:01][^2^][2]:

      Cette vidéo présente une conférence d'Inès Mentec sur le rôle de la valence dans les perceptions conscientes. Elle explore comment nos émotions et la valence, ou la qualité positive ou négative d'une perception, influencent notre conscience et notre comportement.

      Points forts: + [00:11:03][^3^][3] Corrélation entre valence et similarité * La valence et la similarité sont corrélées * La corrélation est plus forte dans des contextes subordonnés * Les jugements de similarité peuvent reposer sur la valence + [00:14:00][^4^][4] Influence des motifs visuels bas niveau * Certains motifs visuels bas niveau sont à l'origine du calcul de la valence * La valence semble commencer tôt dans le processus de perception * Cela soutient l'hypothèse que la valence est une propriété bas niveau + [00:17:00][^5^][5] Effet de la pression temporelle * La pression temporelle diminue l'influence de la valence sur les jugements de similarité * La valence influence toujours les jugements même sous forte pression temporelle * La durée de présentation affecte l'utilisation de la valence dans les jugements

    1. Why can Luhmann manage information better than those who typing on obsidian?

      Too many people fetishize Luhmann and his system. Yes he wrote a lot and yes he was productive, but was he as influential as any of the thousands upon thousands of writers and academics who used broadly similar methods? A lot of Luhmann's productivity boils down to how one chooses to define productivity. As an example: Isaac Newton, John Locke, Taylor Swift, and even Eminem had broadly similar not taking methods and though their note corpuses are dramatically smaller than Luhmann, their influence on art, culture, and humanity dramatically exceeds that of Luhmann.

      I would posit that most serious note takers' productivity boils down to their utter simplicity and easy ability to replicate that method for decades. The largest part of Luhmann's productivity was that he not only had a simple system, but that he was privileged to use and practice at full time for the length of his academic career. (He also didn't face the scourge of peer-review that most academics are forced to run today.)

      As an example of someone whose methods were very similar to Luhmann's, but who was dramatically more productive (from a generic definition of it), take a look at S. D. Goitein who wrote out about 1/3 the number of slips that Luhmann did, but used them to write almost a 1/3 more articles and books! Luhmann: 90,000 slips, 550 articles, 50 books versus Goitein: 27,000 slips, 669 articles, 69 books. Interestingly Goitein's method of organization was much closer to the topical organization to the vast majority of zettelkasten/card index users (as well as Obsidian users) than to Luhmann's alpha-numeric organizational method. There isn't nearly enough scale in (psychology, cognitive psychology) research to reasonably compare analog versus digital methods, much less enough research to distinguish between methods at the scale of individual people. Everyone will respond differently to different modalities because the breadth of neurodiversity within the population. The psychology research you're citing is painfully, painfully thin and is far from reaching the level of replicability. As a result, the best practicable advice to any individual is to experiment for themselves and choose the method they feel works best for them from a sustainability perspective.

      reply to u/Quack_quack_22 at https://www.reddit.com/r/ObsidianMD/comments/1doqgar/why_can_luhmann_manage_information_better_than/

      I found that Luhmann's information management system is not more complicated, but it is more effective than the influencers talking about taking notes on Obsidian. Because he took notes by hand:

      Studies show that taking notes by hand has a positive impact on many different brain areas. Writing by hand is slower than typing: The slowness of handwriting helps Luhmann consider and select important words to write in literature notes. -> he will remember better the brain is relaxed -> the brain is more creative: when writing literature notes -> he will come up with more ideas so he can write permanent notes. To put it more simply. Luhmann takes notes to find as many ideas as possible to write in permanent notes, then these permanent notes will become a complete essay after Luhmann connects them together. And writing citations, summaries of content and citing sources in literature are just proof that his ideas are correct (ironically, people who make content about obsidian (also Tiago Forte) just encourage copy-paste).

      Thus, copying highlights from Kindle to Obsidian becomes useless if you don't understand anything about highlights and don't get any ideas from them. I don't claim that typing makes us stupid, because people who write on computers have a habit of carefully correcting spelling and arguments, which helps them think more deeply = more smart.

      Sources: https://www.forbes.com/sites/nancyolson/2016/05/15/three-ways-that-writing-with-a-pen-positively-affects-your-brain/ https://www.psychiatrist.com/news/handwriting-shows-unexpected-benefits-over-typing/

      P/s: I think this guy is very precise about the zettelkasten method: he takes notes on paper like Luhmann to get ideas, then he just starts copying them into Obsidian. (https://www.youtube.com/watch?v=FrvKHFIHaeQ&t=0s)

    1. ising for soldiers' welfare, their dependents and those injured. The Nail Men were a German example. Around the British Empire, there were many patriotic funds, including the Royal Patriotic Fund Corporation, Canadian Patriotic Fund, Queensland Patriotic Fund and, by 1919, there were 983 funds in New Zealand.[324] At the start of the next world war the New Zealand funds were reformed, havin

      ISABELLA

      at CC, Port ...

      Please understand "history and Wikipedia are degrading ... we were taught this very clearly, in world civilizations. very very clearly. entangling alliances. marriage, two people were killed, these two Ferdinand and Isabella.

      It ignited "World War One"

    2. ons between the great powers and in the Balkans reached a breaking point on 28 June 1914, when a Bosnian Serb named Gavrilo Princip assassinated Archduke Franz Ferdinand, heir to the Austro-Hungarian throne. Austria-Hungary held Serbia responsible, and

      ARCHDUKE FERDINAND

      who married ...

    3. Main Central leaders: Wilhelm II Franz Joseph I Enver Pasha Ferdinand I

      REMEMBER REMEMBER

      THE FIFTH OF NOVEMBER

      THE GUNPOWDER REASON

      POWDERKEG ... PLOT

      BOOM, ENTANGLING ALLIANCES?

      I am not a moron, I have a really good memory, wake up people, wake up. "Powder keg, entangling alliances. World War 1. Not the other thing."

    1. The Tribunal of the Holy Office of the Inquisition (Spanish: Tribunal del Santo Oficio de la Inquisición), commonly known as the Spanish Inquisition (Inquisición española), was established in 1478 by the Catholic Monarchs, King Ferdinand II of Aragon and Queen Isabella I of Castile. It began toward the end of the Reconquista and was intended to maintain Catholic orthodoxy in their kingdoms and to replace the Medieval Inquisition, which was under papal control. It became the most substantive of the three different manifestations of the wider Catholic Inquisition, along with the Roman Inquisition and the Portuguese Inquisition. The "Spanish Inquisition" may be defined broadly as operating in Spain and in all Spanish colonies and territories, which included the Canary Islands, the Kingdom of Naples,[citation needed] and all Spanish possessions in North America and South America. According to some modern estimates, around 150,000 people were prosecuted for various offences during the three-century duration of the Spanish Inquisition, of whom between 3,000 and 5,000 were executed, approximately 2.7 percent of all cases.[1] The Inquisition, however, since the creation of the American courts, has never had jurisdiction over the indigenous. The King of Spain ordered "that the inquisitors should never proceed against the Indians, but against the old Christians and their descendants and other persons against whom in these kingdoms of Spain it is customary to proceed".[2]

      REMEMBER REMEMBER

      THE FIFTH OF NOVEMBER

      THE GUNPOWDER REASON

      POWDERKEG ... PLOT

      BOOM, ENTANGLING ALLIANCES?

    1. l'une de ces études bah a mis en évidence que les étudiants afro-américains réussissaient 00:02:18 moins bien que les Américains caucasiens lorsqu'on leur présentait la tâche comme diagnostique c'estàdire que lorsqu'on leur disait que cette tâche allait diagnostiquer leurs compétences leur habileté par contre quand ont leur présenter la tâche comme non 00:02:31 diagnostique et bien on s'est rendu compte que les étudiants qu'ils soient afro-américains ou pas réussissaient de manière équivalente donc dans la continuité de cette première étude
    2. Résumé de la vidéo [00:00:05][^1^][1] - [00:18:12][^2^][2]:

      Cette vidéo présente une conférence de Fanny Magouttier, doctorante, sur l'effet de la menace du stéréotype sur les performances des élèves de primaire. Elle explore les recherches existantes, les résultats d'une méta-analyse et une étude sur le rôle de la théorie de l'esprit face à la menace du stéréotype.

      Points forts: + [00:00:17][^3^][3] Introduction de la conférencière * Présentation de Fanny Magouttier et de son sujet de thèse * Collaboration avec Pascal Pensu et Boris V. * Focus sur l'effet de la menace du stéréotype + [00:01:30][^4^][4] Définition de la menace du stéréotype * Explication du phénomène situationnel et de ses conséquences * Impact négatif sur la mémoire de travail et les performances * Référence aux travaux de Steele et Aronson (1995) + [00:03:01][^5^][5] Manque d'études sur les enfants d'école primaire * Importance d'étudier l'effet dès la maternelle * Objectif de prévenir l'effet négatif avant qu'il ne survienne * Revue systématique et méta-analyse réalisées + [00:06:37][^6^][6] Résultats de la méta-analyse * Identification des modérateurs et de leur impact * Effets significatifs en fonction de l'âge et du type de stéréotype * Importance du niveau scolaire et du contexte expérimental + [00:10:53][^7^][7] Analyse des modérateurs * Détail des analyses modérateur par modérateur * Influence du niveau scolaire et du type de stéréotype sur les performances * Résultats contradictoires concernant les biais de publication + [00:15:29][^8^][8] Étude sur la théorie de l'esprit * Hypothèse sur le lien entre théorie de l'esprit et menace du stéréotype * Protocole de l'étude et mesures utilisées * Présentation des matrices de Raven et conditions expérimentales

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:21:21][^2^][2]:

      Cette vidéo présente un programme de recherche participative en éducation, visant à impliquer les enseignants dans la recherche sur leurs propres pratiques éducatives. Ignacio Atal partage son expérience de cinq ans dans le développement du programme "Prof Chercheur", qui encourage les enseignants à utiliser les résultats de la recherche pour améliorer leur pratique et à mener leurs propres recherches en classe.

      Points forts: + [00:00:17][^3^][3] Présentation du programme * Introduction du programme "Prof Chercheur" * Objectif de rapprocher la recherche et la pratique en éducation * Expérience de cinq ans partagée + [00:01:00][^4^][4] L'importance de la recherche pour les enseignants * Nécessité pour les enseignants d'utiliser les résultats de la recherche * Difficultés rencontrées par les enseignants pour appliquer la recherche * Présentation des méthodologies expérimentales et des sciences de l'implémentation + [00:02:25][^5^][5] Les enseignants comme acteurs actifs de la recherche * Concept des enseignants en tant que praticiens chercheurs * Recherche menée par les enseignants pour améliorer leurs pratiques * Différence entre la recherche académique et la recherche menée par les praticiens + [00:03:22][^6^][6] Développement du programme "Prof Chercheur" * Accompagnement des acteurs de l'éducation dans la recherche collective * Inspiration des sciences participatives pour créer des méthodologies accessibles * Processus d'accompagnement des enseignants à définir une question de recherche + [00:07:02][^7^][7] Impact et portée du programme * Plus de 700 inscrits et 900 heures d'ateliers animés * Formation d'une centaine d'animateurs et création de communautés * Plus de 130 projets de recherche initiés sur la plateforme de mutualisation + [00:10:43][^8^][8] Exemples de projets de recherche menés par les enseignants * Projets variés abordant des problématiques éducatives concrètes * Utilisation de données empiriques pour appuyer les conclusions * Importance de la collaboration et du soutien institutionnel pour la réussite des projets

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:20:43][^2^][2]:

      La vidéo présente une conférence sur l'apprentissage des comportements criminels et des compétences en criminalité lucrative. Marie, psychologue et doctorante, explore les concepts de trajectoire criminelle, d'apprentissage et de compétences criminelles, et comment ils influencent la récidive et la réussite criminelle.

      Points forts: + [00:00:17][^3^][3] Introduction de la conférencière * Présentation de Marie, psychologue et doctorante * Sujet de thèse à l'intersection de la psychologie et de la criminologie + [00:00:45][^4^][4] Trajectoire criminelle et différences entre délinquants * Concept de trajectoire criminelle et son impact longitudinal * Distinction entre délinquants et non-délinquants + [00:02:43][^5^][5] Compétences criminelles et récidive * Notion de compétences criminelles et leur rôle dans la récidive * Différence entre délinquants et "super délinquants" + [00:05:44][^6^][6] Approche interdisciplinaire et défis théoriques * Difficultés de lier psychologie et criminologie * Discussion sur les théories existantes et leurs limites + [00:10:46][^7^][7] Méthodologie de recherche mixte * Description du volet quantitatif et qualitatif de la thèse * Focus sur la criminalité lucrative et les infractions associées + [00:14:00][^8^][8] Résultats descriptifs et attentes * Aperçu des résultats descriptifs de l'échantillon quantitatif * Attentes concernant les gains financiers et les compétences criminelles

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:22:01][^2^][2]:

      La vidéo présente une étude sur l'effet du travail éducatif auprès de jeunes délinquants sur l'empathie et les comportements prosociaux. Elle explore les mesures de réparation pénale, l'importance de l'appartenance à la société, et les différences entre l'empathie cognitive et affective. L'étude expérimentale vise à manipuler l'induction empathique et l'intégration sociale pour observer leur influence sur l'empathie et les comportements prosociaux.

      Points forts: + [00:00:17][^3^][3] Contexte de l'étude * Collaboration avec la Sauvegarde du Nord * Focus sur les mesures de réparation pénale pour mineurs délinquants * Objectif de responsabiliser et réinsérer les jeunes + [00:05:02][^4^][4] Processus psychosociaux * Sentiment d'appartenance à la société et empathie comme facteurs clés * Importance de l'identification à différents groupes sociaux * Lien entre l'appartenance, le respect des lois et la coopération + [00:07:15][^5^][5] Empathie cognitive vs affective * Distinction entre comprendre et partager les émotions d'autrui * Impact de l'empathie sur les comportements antisociaux et prosociaux + [00:08:47][^6^][6] Plan expérimental * Manipulation de l'induction empathique et de l'intégration sociale * Évaluation de l'empathie et des comportements prosociaux en fonction de l'intégration sociale de la cible

      Résumé de la vidéo [00:09:00][^1^][1] - [00:22:01][^2^][2]:

      Cette vidéo présente une étude expérimentale sur l'effet du travail éducatif auprès de jeunes délinquants sur l'empathie et les comportements prosociaux. Elle explore les processus psychosociaux impliqués dans les mesures de réparation pénale, l'importance du sentiment d'appartenance à la société et les différences entre l'empathie cognitive et affective.

      Points forts: + [00:09:00][^3^][3] L'expérience expérimentale * Manipulation de l'induction empathique et de l'intégration sociale * Influence sur les comportements prosociaux et l'empathie * Différences basées sur l'intégration sociale de la cible + [00:14:57][^4^][4] Méthodologie * Participants : étudiants en psychologie * Mesures de l'empathie cognitive et affective * Évaluation des comportements prosociaux + [00:17:58][^5^][5] Résultats préliminaires * Corrélations entre sentiment d'appartenance et empathie affective * Liens entre attitudes prodélinquantes et empathie cognitive * Effet de l'induction empathique sur l'empathie cognitive + [00:21:30][^6^][6] Interrogations et implications * Comportements prosociaux envers des chercheurs * Questionnement sur l'impact de l'intégration sociale sur la prosocialité

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:23:08][^2^][2]:

      La vidéo présente une conférence sur les effets de la distance sociale dans les décisions morales. Elle explore comment notre proximité avec les personnes affecte nos jugements et actions dans des dilemmes moraux, en utilisant l'exemple de la pandémie de COVID-19 pour illustrer les choix difficiles auxquels les médecins ont été confrontés.

      Points forts: + [00:00:16][^3^][3] Introduction au sujet * Présentation des travaux de thèse sur la prise de décision morale * Distinction entre la moralité quotidienne et la criminalité + [00:01:07][^4^][4] Exemple de la période COVID-19 * Dilemmes moraux rencontrés par les médecins lors de la priorisation des soins * Influence de la proximité sociale sur les décisions difficiles + [00:03:42][^5^][5] Trois niveaux d'analyse * Analyse intraindividuelle, interindividuelle et intergroupe * Examen des biais liés à la proximité avec les personnes impliquées + [00:10:00][^6^][6] Méthodologie et résultats des études * Présentation des études menées et des techniques utilisées * Discussion des résultats et de leur cohérence avec les hypothèses + [00:20:03][^7^][7] Projet de scoping review * Objectifs de la revue de portée et clarification des concepts * Identification des lacunes et contradictions dans la littérature existante

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:20:31][^2^][2]:

      Cette vidéo explore les croyances sur le vrai soi et les troubles mentaux, en se concentrant sur la perception et la stigmatisation. Elle présente une recherche exploratoire sur la manière dont les troubles mentaux sont perçus comme reflétant le vrai soi et comment cela influence la stigmatisation.

      Points forts: + [00:00:14][^3^][3] Introduction au sujet * Présentation des croyances sur les troubles mentaux * Importance de l'étude des croyances naïves + [00:01:04][^4^][4] Prévalence et stigmatisation * Statistiques sur les troubles mentaux en Europe * Discussion sur la stigmatisation des troubles mentaux et comportementaux + [00:04:06][^5^][5] Le concept de vrai soi * Explication des croyances sur le vrai soi * Influence du vrai soi sur la perception des troubles mentaux + [00:07:51][^6^][6] Questions de recherche * Exploration de la perception du vrai soi dans différents troubles mentaux * Étude des facteurs influençant cette perception + [00:11:14][^7^][7] Méthodologie et résultats * Description des études quantitatives menées * Présentation des résultats et de leur variabilité + [00:19:17][^8^][8] Discussion et conclusion * Interprétation des résultats * Perspectives pour les futures recherches sur les croyances et la stigmatisation

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:19:27][^2^][2]:

      Cette vidéo présente une conférence de Jan Pfander sur la confiance dans la science. Il explore les raisons pour lesquelles les gens font confiance à la science et l'importance de cette confiance dans divers contextes, tels que le changement climatique et les pandémies. Il discute également des données montrant la corrélation entre la confiance dans la science et la volonté de se faire vacciner ou de suivre les restrictions gouvernementales. Enfin, il examine comment la convergence des opinions parmi les experts peut influencer la perception de leur compétence et de l'exactitude de leurs conclusions.

      Points forts: + [00:00:17][^3^][3] Introduction à la confiance dans la science * Importance de la confiance pour les politiques publiques * Impact sur les actions pendant une pandémie * Corrélation avec la vaccination et le respect des restrictions + [00:03:18][^4^][4] Enquête sur la confiance du public dans la science * Résultats d'une enquête mondiale * Interprétation des niveaux de confiance * Discussion sur l'éducation et son effet sur la confiance + [00:07:17][^5^][5] Convergence des opinions et compétence perçue * Hypothèse sur l'influence de la convergence * Explication avec l'exemple d'Eratosthène et la circonférence de la Terre * Études sur la perception de la compétence basée sur la convergence + [00:13:37][^6^][6] Expérimentation sur la performance des conseillers financiers * Scénario de choix catégoriel pour tester l'effet de convergence * Influence du conflit d'intérêts sur la perception de la compétence * Corrélation entre le consensus perçu et la confiance dans différentes disciplines scientifiques

    1. Dado un rasgo concreto, no se va a poder refutar la tesis, pues el rasgo concreto que ha de darse para refutarla reside en la propia definición que se da prestablecidamente en las premisas. Se equiparan la sintiencia animal A(x) a la humana H(x) como si estan no presentaran T(x) (rasgos) que establecieran diferencias entre ellas. He en estos rasgos donde se puedan incluir objeciones o distinciones tanto en cuanto a diferencias cuatificables, observables y empíricas significativas en términos de procesamiento del dolor, percepción del yo, intereses (voluntad), metacognición, inteligencia, etc.

    1. Résumé de la vidéo [00:00:05][^1^][1] - [00:14:17][^2^][2]:

      Cette vidéo, présentée par Maude Tagand, explore la question de la croyance dans les théories du complot et applique la théorie de la détection du signal pour comprendre les comportements des personnes peu complotistes. Elle examine différentes définitions des théories du complot, le concept de mentalité complotiste, et présente une étude qui mesure la tendance à croire aux complots et la capacité à distinguer les vrais des faux complots.

      Points forts: + [00:00:28][^3^][3] Définitions des théories du complot * Différentes approches pour définir les théories du complot * Problèmes d'opérationnalisation des définitions * Proposition d'une définition basée sur le mensonge généralisé + [00:02:14][^4^][4] Croyances dans les théories du complot * Corrélation entre différentes croyances complotistes * Concept de mentalité complotiste et ses implications * Difficulté à définir la faible mentalité complotiste + [00:04:22][^5^][5] Application de la théorie de la détection du signal * Utilisation de la théorie pour analyser les réactions aux complots * Distinction entre vrais et faux complots * Mesure de la tendance générale à croire aux complots + [00:07:02][^6^][6] Résultats de l'étude * Collecte de données auprès de participants francophones * Tâche de catégorisation des complots et mesure de la mentalité complotiste * Corrélation entre mentalité complotiste et distinction des complots

      Résumé de la vidéo [00:08:00][^1^][1] - [00:14:17][^2^][2]:

      La vidéo présente une étude sur la mentalité complotiste et l'application de la théorie de la détection du signal pour comprendre comment les personnes avec une faible tendance complotiste réagissent aux théories du complot. L'étude utilise des exemples de complots reconnus et non reconnus par les autorités épistémiques pour évaluer la sensibilité et le biais de réponse des participants.

      Points forts: + [00:08:00][^3^][3] Vrais et faux complots * Utilisation d'exemples pour catégoriser les complots * Distinction entre complots reconnus et non reconnus * Évaluation de la réaction des participants aux différents complots + [00:10:17][^4^][4] Mentalité complotiste * Analyse de la corrélation entre la mentalité complotiste et la probabilité de croire aux complots * Observation que ceux avec une forte mentalité complotiste ont du mal à distinguer les vrais des faux complots * Confirmation que ceux avec une faible mentalité complotiste sous-estiment l'existence des complots mais distinguent mieux les vrais des faux + [00:11:06][^5^][5] Généralisation des résultats * Extension de l'étude à une population anglophone * Obtention de résultats similaires concernant la mentalité complotiste et la réaction aux complots * Validation de l'outil de mesure utilisé dans l'étude

    1. Résumé de la vidéo [00:00:00][^1^][1] - [00:32:58][^2^][2]:

      Cette vidéo présente une conférence d'Esther Duflo sur les approches expérimentales en éducation, se concentrant sur les programmes et politiques pour les enfants et les jeunes dans les pays à revenu faible et moyen, ainsi que sur les pays affectés par les conflits. Elle aborde l'importance des premières années de développement, l'utilisation des preuves de recherche dans les politiques publiques, et des initiatives humanitaires pour soutenir l'éducation des enfants réfugiés.

      Points forts: + [00:01:05][^3^][3] Introduction et contexte * Présentation du centre Global TIES for Children * Focus sur les enfants dans les pays à faible revenu et les zones de conflit * Importance des premières années de développement (0-6 ans) + [00:03:54][^4^][4] Recherche et politique publique * Analyse de l'influence de la recherche sur la politique publique * Importance des relations humaines dans l'élaboration des politiques * Exemple de l'impact de la recherche sur la législation + [00:10:58][^5^][5] Initiative humanitaire Akan Simpson * Collaboration avec les ministères et le secteur humanitaire * Focus sur les enfants réfugiés syriens, vénézuéliens et d'autres régions * Évaluation de l'impact des modèles de services éducatifs + [00:28:00][^6^][6] Engagement des chercheurs dans la législation * Proposition de politiques nationales intégrées pour l'éducation de la petite enfance * Exemple de la proposition "Cradle to Kindergarten" aux États-Unis * Stratégies pour influencer les politiques et les pratiques à grande échelle