1. Last 7 days
    1. The console pod does not run under a service account named migration-console. The chart uses migration-console-access-role.

      Can be rephrased to make it more clear. I believe this is an example issue. But to tther reader it may be a bit confusing.

    1. exp 溢出、除零、消减或长归约误差

      溢出:exp指数超出float 除零错误 消减误差:大数相减,小精度丧失 长规约误差:多个小数相加,后面的小数省略产生误差。

    2. 广播、转置或非连续 stride

      广播:多个变量访问一块内存 转置:矩阵转置 stride是矩阵的访问步长,矩阵元素在gpu中连续存储,用stride控制如何访问(如访问第几行第n个元素),当stride和尺寸不一致,访问不连续

    3. 理论最小访存量

      这个问题分析:一个 kernel 到底是算力瓶颈还是内存瓶颈。 假设矩阵A(MK),B(KN),C(MN),则共需要读写MN+MK+KN次。 好的kernel希望一次加载,多次复用,计算强度AI=FLOPS/memory. 优化后一个tile,可以供多个计算步骤使用。

    4. 能否分块?

      分块 tileling 不能分块的情况: (1). 前面一个对后面一个存在强依赖关系,前面结果是后面的输入 (2) 数据量太小,分块后通信开销比不分块大 (3)计算需要全局信息。分块后前面信息丢失,无法计算完整结果

    5. 分布式均值

      每个GPU计算的样本数量不一定相同,每个GPU有一个均值计算所有GPU就要分布式均值。将一个batch切分,放到多个GPU上并行运行。accuracy,loss等都需要所有batch计算后的整体均值

    6. Online Softmax 的分块合并

      把大块attention切分成小块attention减少显存开销。 原来大块attention需要保存S^2矩阵在显存中,计算小块attention,不用保存完整attention.用完就丢,节省显存

    7. Dh\sqrt{D_h}Dh​

      每个head的Q,K维度为S*D, attention score =QK^T,每个token和哪个token有关。

      QK^T得到矩阵维度为S*S,但每个元素的长度都是Dh,由Dh次乘法加法得到,用于归一化

    8. X

      X乘权重W,维度是W(H,H),乘完后Q,K,V维度为BSH。 1. 因为Transformer使用多头注意力机制,有N个头,每个都维度为D。所以BSND 2. 因为attention需要计算QK^T, 希望每个head单独计算,因此希望维度为BNSD。(每个head单独计算的Q,K维度为S*D).因为一次batch和head.都希望作为并行维度,所以前面要再乘B,N.

      使用transpose可以交换指定轴的维度transpose(1,2),交换1,2维维度

    1. 只有通过发达的工业,也就是以私有财产为中介,人的激情的本体论本质才能在其总体上、在其人性中存在

      工业的发展,一方面创造了许多东西,这些东西反映了人的本质力量, 也就是人的激情,扩大了人的能力,另一方面也产生异化

    2. 如果人的感觉、激情等等不仅是在〔狭隘〕意义上的人本学的规定,而且是对本质(自然)的真正本体论的肯定

      就是说,人的各种感觉反映的是人作为人的能力,而不只是被动地接受刺激

    3. 分工和交换是私有财产的形式,这一情况恰恰包含着双重证明:一方面人的生命为了本身的实现曾经需要私有财产;另一方面人的生命现在需要消灭私有财产。

    4. 因此,利息的减少只有当它是资本的统治正在完成的征兆,也即当它是异化正在完成因而加速其扬弃的征兆的时候,才是资本的扬弃的征兆。

      翻译一下就是:只有当社会愈发受到资本的完全控制,只有当异化进行的愈发彻底时,利息(即资本所带来的利润)的减少才能成为资本的扬弃(即超越资本,超越异化)的征兆。问题:如何衡量控制程度?如何确定什么时候才符合呢?

    5. 异化的扬弃总是从作为统治力量的异化形式出发

      大致理解:要将人从异化中解放,就要首先抓住那个异化形式,从批判这种形式出发

    6. 甚至从主观方面来说,这一点部分地表现在:产品和需要的范围的扩大,要机敏地而且总是精打细算地屈从于非人的、精致的、非自然的和臆想出来的欲望。私有制不懂得把粗陋的需要变为人的需要。它的理想主义不过是幻想、任意的奇想、突发的怪想;没有一个宦官不是厚颜无耻地来向自己的君主献媚,并力图用卑鄙的手段来刺激君主的痲木不仁的享乐能力,以骗取君主的恩宠;工业的宦官即生产者则更下贱地用更卑鄙的手段来骗取银币,从自己的按照基督教教义说来应该爱的邻人的口袋里诱取黄金鸟(每一个产品都是人们想用来诱骗他的人的本质即他的货币的诱饵;每一个现实的或可能的需要都是把苍蝇诱向黏竿的弱点;对共同的人的本质的普遍利用,正像人的每一个缺陷一样,对人来说是同天国连结的一个纽带,是使僧侣能够接近人心的途径;每一项急需都是一个机会,使人能够摆出一副格外殷勤的面孔来接近自己的邻人并且向他说:亲爱的朋友,你需要什么,我给你,而必不可缺的先决条件,你是知道的;你应当用什么样的墨水给我写字据,你也是知道的;既然我给你提供了享受,我也要敲诈你一下),-工业的宦官投合消费者的最下流的意念,充当他和他的需要之间的牵线人,激起他的病态的欲望,窥伺他的每一个弱点,然后要求对这种殷勤的服务付报酬

      有种诉诸道德的味道,但描述的挺精彩的

    7. 正像现实生活是人的不再以私有财产的扬弃即共产主义为中介的积极的现实一样

      这里应该是指,那个时候的现实生活里的人不需要先经过“共产主义”这个革命阶段,才能成为真正的人,或者说,不是为了共产主义,而是为了人的自由发展,在这里,它和无神论坐一桌

    8. 但是,社会主义作为社会主义,已经不再需要这样的中介;它是从把人和自然界看作本质这种理论上和实践上的感性认识开始的。

      就是说,不在围绕人和神的关系来确认人的地位,而是直接从人的现实的生活出发,确认人的地位

    9. 所以,关于某种异己的存在物,关于凌驾于自然界和人之上的存在物的问题,即包含着对自然界和人的非实在性的承认的问题,实际上已经成为不可能的了。

      就是说,我们能够直观地了解到人是怎么从自然界产生的,怎么由动物变化成人的,但是关于这个世界,关于人的诞生是否是某个超脱自然界和人的存在创造的,这个是无法回答的,也不能回答的

    10. 对人民意识来说是不能理解的,因为这种存在是同实际生活的一切明摆着的事实相矛盾的。

      马克思在这里想要表达的观点是:人和自然本身就是现实存在,不需要借助一个外在创造者来解释。

    11. 如果我的生活不是我自己的创造,那末,我的生活就必定在自身之外有这样一个根源。所以,创造是一个很难从人民意识中排除的观念。

      宗教,神,上帝的来源

    1. if you were an academic researcher in 2010 and you talked about AI systems getting smarter than humans and becoming catastrophically misaligned, you were a crank who didn’t actually understand the technology.”

      I think today you are still a crank.

    1. Whole exome sequencing identifies a novel splice-site mutation in IMPG2gene causing Stargardt-like juvenile macular dystrophy in a northIndian family

      PMID:35973334

      Gene: ABCA4

      HGNC ID: 34

      Case#: the youngest sister II.7, aged 12 years, was the least affected

      Variant splice-site variant NC_000003.11(NM_016247.3):c.1239 + 1G > T [Chr3:100972539C > A

      FammilyInfo two-generation north Indian family with three members affected with Stargardt-like macular dys trophy

      CasePresentingHPOs:ow vision and difficulty in night vision, with symptoms starting in the early second decade of life, which progressed slowly over time

      PedrigreeIn the results section is mentioned

      CaseHPOFreeText:NA

      CaseNotHPOs:Na

      CaseNotHPOFreeText:NA

      Genotyping Method:2.3. Validation of identified variant by Sanger sequencing

      PreviouslyPublished:NA

    1. ABCA4-retinopathy

      Case#: 1 male, 24 years old, from consanguineous parents, Somali ancestry.

      DiseaseAssertion: ABCA4-related retinopathy Stargardt disease

      FamilyInfo: Single affected individual consanguineous parents, Somali ancestry. No additional information about family is provided in text.

      CasePresentingHPOs: HP:0000572- reduced central vision, HP:0001102- Angioid streaks, HP:0007980- retinal pigment epithelium atrophy, HP:0007401- Macular atrophy, HP:0000630- Abnormal retinal arterial/arteriolar morphology

      CaseHPOFreeText: Presents with reduced central vision, Fundus autofluorescence (FAF) showed angioid streaks, reduced signal in the central macula indicative of retinal pigment epithelium atrophy. Electrophysiological testing showed severe macular dysfunction with generalized retinal involvement.

      CaseNotHPOs: HP:0200070- Peripheral retinal atrophy

      CaseNotHPOFreeText: Peripheral retina appears unaffected after ultra-widefield FAF imaging

      Genotyping Method: PCR-amplification and Sanger sequencing of ABCA4 on Exon 42, Stargardt/Macular dystrophy SmartPanel v5; Molecular Vision Laboratory, Hillsboro, Oregon tested DNA for mutations which confirmed findings of ABCA4, with no additional pathogenic mutations found.

      PreviouslyPublished: PMID: 22261738, 1 male, 24 years old, from consanguineous parents, Somali ancestry presenting with reduced vision.

      Variant: NM_000350.3(ABCA4):c.5882G>A (p.Gly1961Glu)

      ClinVar: Variation ID: 7888

      CAID: N/A

      SupplementalData: N/A

    1. 20/28/2/18/
female CRD c.1654 G>A
c.4363 T>C 35, 35 38,
34 52,
57 4,
5 45.0,
42.5 1.0,
0.7

      Case#: Subject 20, 28yo, 18yo at first ffERG, Sweden, female

      DiseaseAssertion: CRD, group 2

      FamilyInfo: n/a

      CasePresentingHPOs:

      CaseHPOFreeText: extensive atrophies in the posterior pole. peripheral pigmentations. few peripapillary changes. Normal thickness of the most central segment recorded on OCT. total absence of the PIL (photoreceptor integrity line) and RPE atrophy on the OCT B-scans. ETDRS VA score= 35, 35. Rod
ffERG= 38, 34 Ampl
(µV). Combined ffERG= 52, 57 Ampl
(µV). Cone
ffERG= 4, 5; 45.0, 42.5 Amp IT
(µV; ms). mERG sum= 1.0, 0.7 Ampl (µV). Group 2 with larger central scotomas from 10° to 35°

      CaseNotHPOs:

      CaseNotHPOFreeText:

      GenotypingMethod: Sequence analysis of the entire coding region of the ABCA4 gene was performed.

      PreviouslyPublished: n/a

      Variant: c.1654G>A; c.4363T>C

      CAID: CA239745

      SupplementalData: n/a

    1. Sixteen patients from 13 families with signs of Stargardt macular dystrophy/fundus flavimaculatus and known mutations on both alleles of the ABCA4 gene (15 compound heterozygous, one homozygous) were characterized by clinical examination, fundus autofluorescence, psychophysics (color vision, kinetic and two-color dark- and light-adapted static threshold perimetry), and electrophysiology (Ganzfeld, multifocal ERG, EOG).

      Article is a PDF, so annotating here.

      ClinVar assertion listed this paper; however looking at the genotype table, none of the variants appear to match the variant in question.

    1. Patient 2

      Case#: 39 Year Old Female, India Punjab

      DiseaseAssertion: EORSD

      FamilyInfo: Family history for other disease was negative, husband was first cousin and their son had normal vision

      CasePresentingHPOs: HP:0007401, HP:0007913

      CaseHPOFreeText: Macular atrophy and pigmentation, yellowish flecks

      CaseNotHPOs: N/a

      CaseNotHPOFreeText: N/a

      Genotyping Method: BGISeq-500 2 x 100-bp paired-end module, Burrows-Wheeler Aligner and Genome Analysis Tooklit HaploptypeCaller

      PreviouslyPublished: N/a

      Variant: NM_000350.3(ABCA4):c.6729+5_6729+19del

      ClinVar: 283573

      CAID: CA501163

      SupplementalData: Confirmed that she had never seen properly or normally, marked horizontal nystagmus and poor pupil reaction to light

    Annotators

    1. In Fig 2B, the spectrum for DENV3 (and to a lesser extent DENV4) does not seem to resemble a protein. It seems like the two broad peaks are consistent with a phosphate buffer, which perhaps was used in the protein purification.

      Is there any evidence that plasmonic enhancement is occurring? If the claim is that SERS is being performed, it would be valuable to demonstrate a spectrum of the protein on the Al surface, and one without the surface. If enhancement is happening, the spectrum of protein of Al should be several times higher than the protein alone.

    1. Fig 3: it's not immediately evident from the caption that the ng/mL values correspond to BMP4 concentrations. it may be good to restate that somewhere.

      Figure S2: I assume the blue color is the 2940 intensity but it does not seem to be on the colormap. The colormaps are also difficult to read. It would also be useful to see a brightfield image -- it's hard to orient oneself to where the cells are.

      The study would benefit from controls / ground truth experiments to ensure that the slight differences being observed in the Raman spectra actually correlate with the biological interpretation. For example, it would be useful to image cells with known high-protein or high-lipid phenotypes to confirm that the interpretation in Figure 4 is consistent with reality. Alternatively, or in addition, it would be useful to actually correlate Raman peaks with gold-standard techniques for measuring lipids, proteins, and DNA in cells (staining and imaging or blots).

      I think the claim "Raman spectroscopy revealed concentration dependent spectral differences and enabled discrimination between differentiating condition within individual hiPSC lines" is slightly speculative. The PCA results show some cases of spectra clustering with, but it would be important to rule out batch effects by performing multiple end-to-end biological replicates. It's also unclear why many BMP4 effects are non-monotonic (e.g. Figure 4B -- the peak height increases and then decreases as concentration increases).

      I appreciate the work the authors put into getting the results! Looking forward to follow-up studies.

    1. "Each region was embedded using the corresponding genomic language model. Token-level representations were then pooled by masked averaging over the region of interest only, excluding padding tokens. This yielded a single vector representation per region."

      This is the standard approach for pooling over positions and is deservedly the focus of analysis, but I am curious if you had considered more complex pooling approaches like the reduced-dimension covariance probe (flattened to a vector) from the Goodfire EVEE paper. This captures pairwise interactions across base-pair positions and enables improved pathogenicity prediction. Obviously this also requires something like training an additional classifier layer, but it would be interesting to see how well these much more compact models perform on ClinVar with this pooling approach that preserves more of the regional representation.

      https://www.biorxiv.org/content/10.64898/2026.04.10.717844v4

    1. Dear authors, I was quite shocked that you did not reference our 2019 Nature paper, entitled “Intestinal infection triggers Parkinson’s disease-like symptoms in Pink -/- mice” where we developed the model of infecting mice with a PD-related mutation with Citrobacter rodentium four times at one month intervals to trigger motor symptoms.

      Given the striking similarities between the approaches and results, I can only assume that not citing us was an oversight on your part.

      For your information, our paper can be found here: https://www.nature.com/articles/s41586-019-1405-y

      Sincerely, on behalf of the four corresponding authors of the 2019 paper.

    1. • Broaden the sampling or narrow the claims of representativeness. The bacterial collection was derived from only 12 floor-laid eggs obtained from four backyard keepers, rather than from commercial production systems. Although 50 isolates were identified and eight species were selected for detailed analysis, this sampling frame is insufficient to support broad conclusions about eggshell-associated microbial diversity or commercial egg processing. The authors should ideally include eggs from multiple commercial flocks or production batches. If additional sampling is not feasible, the study should be clearly presented as preliminary and the conclusions restricted to the isolates and backyard eggs examined.

      • Clarify the detection limit and avoid equating loss of culturability with complete killing. PAW efficacy was assessed exclusively by CFU enumeration, yet the precise limit of detection is not reported. Statements such as “complete inactivation” should therefore be replaced with wording such as “no culturable cells were recovered above the assay detection limit.” The authors should report the exact detection limit and acknowledge that culture-based enumeration cannot exclude viable-but-non-culturable cells. An independent viability measurement, such as membrane-integrity staining combined with microscopy or flow cytometry, would strengthen the bactericidal claim.

      • Validate PAW directly on eggshells. Despite the proposed application, the PAW experiments used biofilms formed on plastic microtitre plates, with SEM experiments conducted on plastic coverslips. The authors should test PAW against biofilms established directly on eggshell fragments or intact eggs, preferably incorporating realistic organic contamination and an exposure time relevant to commercial washing, which the manuscript describes as approximately 30 seconds. A comparison with an established eggshell sanitiser would further improve the practical relevance. If these experiments cannot be added, claims regarding application in egg production should be substantially moderated.

    1. • Improve structure and separation of sections: Reorganize the Results into clear subheadings and restrict it to direct experimental observations. Move mechanistic interpretation, literature context, and clinical implications to the Discussion. New findings belong in Results, but new background concepts should be introduced earlier or discussed later.

      • Correct all in-text references and presentation details: Align figure and table citations with the actual numbering (e.g., Figures 1–7 and Table 1) and standardize supplementary references, units, labels, and terminology throughout. Figure legends should describe the experiment and data without interpreting the mechanism.

      • Strengthen the Discussion and future-work section: Avoid repeating the Results. Instead, discuss the significance, limitations, alternative explanations, and strength of the mechanistic evidence. Future work should validate the heme and beta-lactamase mechanisms directly, test clinical isolates and wound-like models, and compare turbidity-based MICs with CFU, time-kill, and bactericidal endpoints.

    1. • Appropriate carrier controls and lipid-dose reporting Include an empty-LNP control, prepared and purified using the same procedure, at lipid doses matched to each AuNCs@LNP group in the principal in vitro and in vivo experiments. The final lipid concentration, injected lipid mass, and animal exposure in mg/kg should also be reported.

      • Statistical analysis and reporting Strengthen the statistical reporting by providing the prespecified direct comparison between the 75 and 150 µg AuNCs@LNP groups, together with exact adjusted p-values, effect sizes, and 95% confidence intervals. The meaning of all significance symbols should be defined. The discrepancy between the Dunnett tests stated in the Figure 2 and Figure 3 legends and the Bonferroni procedure reported in the Methods should also be resolved.

      • Consistency of Methods, figure legends, and assay controls Systematically reconcile the Methods and figure legends regarding doses, replicate numbers, controls, and statistical procedures. In particular, appropriate background controls should be included for the ROS and XTT assays to exclude optical interference. The normalization procedure and the use of separate parallel wells should also be clearly described and justified.

    1. • Statistical analysis and reporting: Distinguish biological from technical replicates, present the results from all independent experiments, describe the statistical methods and their limitations, and avoid claims of statistical significance where a test could not be performed. Exact p-values or appropriate measures of variability should be provided where possible.

      • Interpretation of mechanism: The current data support an interaction-associated change in the C. jejuni phenotype but do not establish the underlying molecular mechanism. Proposed roles for direct contact, microcolony formation, altered protein expression, or the cmeABC efflux system should either be experimentally investigated or clearly identified as hypotheses.

      • Controls and causal validation: Please provide full information on assay controls and replication. Reconstruction of the matched purified C. jejuni–Enterococcus pairs at controlled starting ratios, followed by testing against multiple relevant antibiotics, would substantially strengthen the conclusion that the associated enterococci are sufficient to produce the observed phenotype.

    1. I find it interesting that before the removal of the circuit, the RQ70 strain was slightly slower than the MG70 control. Do you think that's from the burden of the circuit or the format of the culture that you see making a large difference later in the results, or a mixture of the two? Since the culture format changed the rankings between the strains so much, I wonder how much the format of the culture during the selection would change the results. Excited to see if you look into the specific genetic changes you saw in RQ70 in the future!

    1. Das bleibt Information und Orientierung, keine medizinische Behandlung.

      make this: Eine solche Analyse dient zur Information und Orientierung, sie ist und ersetzt keine medizinische Behandlung.

    2. taugt also als Beleg für individuelle Unterschiede, nicht als Regel für jeden Einzelfall.

      make this: für eine Verallgemeinerung des Befundes braucht es mehr und größer angelegte Studien.

    3. Supplementen, wobei ein Nahrungsergänzungsmittel rechtlich ein Lebensmittel bleibt, kein Arzneimittel.

      make this: Supplementen. Ein Nahrungsergänzungsmittel ist rechtlich ein Lebensmittel, kein Arzneimittel.

    4. aus und stellen daraus eine auf deine Werte abgestimmte Formel zusammen, statt von einem Durchschnitt auszugehen, der für alle gleich sein soll.

      make this: aus. Daraus stellen sie eine auf deine Werte abgestimmte Formel zusammen, statt von einem Durchschnitt auszugehen, der für alle gleich sein soll.