Mutant dragons displayed evidence of scale patterns, despite the absence of fully formed scales. This shows that there are factors other than the anatomical placode at play in scale formation.

there is an active correlation between the populations of prey and predators, when the camouflage groupers aggregate in order to spawn. This increase in prey is what attracts the sharks. MSARS , WT & YS

The study showed that overall, there was a higher number of sharks observed that spent most of their time in the pass than there were that spent less of their time in the pass. YS & WT

The authors used 5 measures for replication success to check to what extent the 100 original studies could be successfully replicated.

The authors wanted to know if successfully replicable studies differed from studies that could not be replicated in a systematic way. As the criterion for replication success, they used their first approach (significance testing). They found that studies from social psychology and studies from social psychology journals were less likely to replicate than those stemming from cognitive psychology and cognitive psychology journals. Moreover, studies were more likely to replicate if the original study reported a lower p-value and a larger effect size, and if the original finding was subjectively judged to be less surprising. However, successfully replicated studies were not judged to be more important for the field or conducted by more experienced research teams.

From this study, we can conclude that the efforts made to reduce the influence of the researchers involved in the replication studies on replication success seemed merited. Importantly, replication success was less influenced by the characteristics of the replication team than by how strong the results of the original study were. Stronger evidence for the effect the original study investigated was related to a successful replication.

For the fourth measure, the authors combined the original and replication effect sizes and calculated a joint estimation of the effects. They wanted to see how many of the studies that could be analyzed this way would show an effect that was significantly different from zero if the evidence from the original study and that of the replication study was combined.

Results showed that 68% of the studies analyzed this way indicated that an effect existed. In the remaining 32% of the studies, the effect found in the original study, when combined with the data from the replication study, could no longer be detected.

A second way to evaluate the replication success was to compare the sizes of the effects of the original studies and those of the replication studies using confidence intervals (CIs). They checked if the effects size of the original study was a value that was also among the range of values revealed as good estimates of the true effect size in reality, which was calculated from the size of the effect in the replication study.

Using this measure, they found that slightly fewer than half the replications were successful.

The authors first checked how many replications "worked" by analyzing how many replication studies showed a significant effect with the same direction (positive or negative) as the original studies.

Of the 100 original studies, 97 showed a significant effect. Based on their ability to replicate the original studies, the authors expected around 89 successful replications. However, results showed that only 35 studies were successfully replicated.

The shape of corals has a strong influence on how much they are damaged because shape directly affects how much force flowing water exerts on the coral's skeleton. Thinly branching corals are especially susceptible to breaking, whereas corals with thicker, leaflike, encrusting, and head forms experience much less mechanical stress during a storm.

I would love to see you submit this to the new DigiSoc@VCU Medium.com page. You would need to strengthen the conclusions. You discuss is so very powerful up until the end. The it falls a bit flat. What are the implications of this new form of digital social capital? Are there other ways of mapping and measuring it? How can SNA advance this literature? What research questions come out of the alt-right study? These are the type of questions you should explore in your conclusions.

The R2 value indicates how much of the variation in a trait can be explained by the genetic markers identified. If R2 is not 100% than other locations in the genome or environmental factors are influencing the trait being analysed.

In this case the SNPs associated with survival in Finland were much more important in influencing plant survival than the SNPs associated with survival in England.

The biggest molecule, in this experiment KDM5B, took the longest to translate.

Most polysomes translated the FLAG tagged and HA tagged proteins independently; however, a few interacted with one another, suggesting that translation of some proteins might be co-regulated.

The translational elongation rate was consistent for each of the translated proteins and was between 8-12 amino acids per second.

Like the process of transcription, the start of the translation process is random and there is no memory of previous initiations.

Polysomes used for translation are constructed like a big ball rather than an elongated structure.

Polysomes showed a lot variation in movement through the cell. Proteins that were moving into the nucleus generally moved by diffusion while beta actin polysomes showed a slower pattern of movement, suggesting that the newly translated protein might be interacting with other cellular proteins.

After tracking the mRNA going through translation, it was concluded that polysomes are variable.There can be one ribosome present for on average every 200 mRNA bases, but a ribosome can be present every 900 mRNA bases.

The results suggested that there are multiple ribosomes per RNA being translated. The number of ribosomes/mRNA varied from 3-5 and seemed to correlate with the length of the mRNA.

Because the spots became brighter after addition of cycloheximide (which allows more ribosomes to load onto each mRNA) and because their were fewer spots after addition of puromycin, it can be concluded that the fluorescent spots in the cell are sites of translation.

With the addition of puromycin, the number fluorescent spots decreased, suggesting that the spots were sites of translation.

The RCP2.6 scenario, the pathway that is likely to limit warming to the 2.0°C threshold targeted by the Paris Agreement, would result in changes that are just within the most extreme variation of the Holocene. This pathway is considered highly ambitious as it would require achieving even more emissions reductions than are currently proposed.

The pathway developed by the authors to meet the 1.5° threshold, RCP2.6L, is the only one that would keep the ecosystem changes within the Holocene variation.

This analysis indicates that for the Mediterranean region, there will likely be significantly larger impacts if the global temperature increase reaches the threshold of 2.0°C rather than being limited to 1.5°C.

The current scenario for global greenhouse gas emissions, taking into account all the voluntary emission reductions targets set by countries as part of the United Nations Framework Convention on Climate Change, matches best with RCP4.5. This analysis shows that the climate change associated with that pathway would likely result in changes in the Mediterranean ecosystems by the end of the century that go far beyond what was seen in the past 10,000 years.

Even though the Atlantic pine forests and the Mediterranean vegetation types are different, the BIOME4 model is not able to sort the two types into separate categories.

Lewis and colleagues made a genetically modified mouse with a mutated APP gene and a mutated tau gene.

These double mutants had plaques like other hAPP mice, but they also had tangles that were more severe than in other mice, showing that problems with amyloid and tau can interact and cause symptoms of Alzheimer’s disease.

This work started as a side project and eventually became a pillar of Dr. Roberson’s later work on mouse models of Alzheimer’s disease. It has been credited with "sparking the research community’s interest in the role of tau in the pathogenesis of Alzheimer’s disease.”

Read more in Neurology Today:

http://journals.lww.com/neurotodayonline/_layouts/15/oaks.journals.mobile/post.aspx?blogId=1&postId=520

Lowering tau even in normal mice (those without the hAPP gene, who would not get Alzheimer’s disease) was beneficial in making mice less prone to seizures when injected with an seizure-inducing drug.

This means that in healthy mice, normal tau may be involved in modulating excitation in neurons, reducing the overall risk of seizures.

(Seizures are a result of abnormally high electrical activity in the brain that occurs when certain neurons are excessively excited.)

Like humans with Alzheimer’s disease, many mice used as models of the disease have a tendency to get seizures, including the hAPP mice used in this study.

However, hAPP mice without tau or with reduced tau had fewer seizures than those with the normal amount of tau.

Eliminating tau in hAPP mice prevented memory and cognitive problems, but it didn’t prevent the neurons from becoming damaged and impaired.

The removal of tau must therefore work in an unrelated way to improve cognition in these mice.

All hAPP mice, independent of the amount of tau, had neurons whose axons and dendrites were withering away in regions near amyloid plaques.

These results show that this type of damage in Alzheimer’s disease can happen even without tau being present.

Reducing tau in hAPP mice protected those mice against the cognitive impairments seen in Alzheimer’s disease.

The authors looked at hAPP mice with normal amounts of tau to see how the tau became abnormal later in life. They compared these changes with abnormal tau measured in other mouse models of Alzheimer’s disease.

The connection between tau and amyloid-β in this model isn’t clear and may involve multiple types of tau or tau stored in various locations (or pools) within the cell.

The authors examined the brains of hAPP mice with different levels of tau. They found that, at all levels of tau, the amount of amyloid plaques and the amount of floating amyloid-β were the same in all hAPP mice.

Thus, the reduction of tau, which had improved memory, didn’t alter the amyloid-β or plaque levels, suggesting that amyloid-β or plaque levels alone are not responsible for memory loss.

hAPP mice are known to die young, as a result of the induced Alzheimer’s disease. But if hAPP mice had a reduced amount of tau, they lived much longer.

Additionally, hAPP mice with normal levels of tau were hyperactive even into middle age, whereas hAPP mice with no tau were not.

Mice with the hAPP gene usually do poorly in the water maze because of their impaired memory. However, hAPP mice that have only half the amount of normal tau did remember where the platform was after additional training.

hAPP mice with no tau performed similar to normal, healthy mice, showing good memory on this test.

Thus, removal of all the normal tau seems to prevent memory problems. Even removing just half the normal tau already has some memory benefits.

Evidence from this study and following studies showing the importance of lowering tau has led researchers to target tau with their experimental new treatments, including vaccines that use the body’s own immune system to fight off the problematic tau proteins.

http://www.medicaldaily.com/alzheimers-disease-tau-protein-vaccine-391883

Almost 10 years after this paper was published, no good treatments for Alzheimer’s disease exist, but more and more of the new drugs in clinical trials are targeting the tau protein, as a result of early laboratory research such as this.

http://www.bloomberg.com/news/articles/2016-06-27/after-190-tries-are-we-any-closer-to-a-cure-for-alzheimer-s

The negative phase of a blast wave follows the initial shock, and sucks items back toward the center of the blast source. Here, the authors consider the possibility that this negative phase could contribute to injury.

They use underwater sonar as a standard. Tissue damage results from repeated negative pressure of ~100 kilopascal generated by sonar waves. Because the blast pressure wave used in this experiment is only a single compressive wave and the negative pressure is far below the positive pressure, the authors discount negative pressure as a possible cause of injury.

Lithotripsy is a procedure that uses sound waves to break apart kidney stones without damaging normal tissue. These waves have positive pressures of around 40 megapascal. Because the waves created by blast pressure are much smaller in amplitude than those used in lithotripsy, it is unlikely they would cause damage.

Mouse tau protein is resistant to pathogenic aggregation like that seen in humans. Therefore, it is not surprising that the authors did not observe neurofibrillary tangles (NFTs) in the brains of blast-exposed mice).

However, the authors were surprised to see pretangles (early-stage NFTs) and elevated levels of abnormally phosphorylated tau protein in the brains of blast-exposed mice. The observation of both of these abnormalities in wild-type mice strongly supports the link between blast exposure and CTE.

Alternatively, the authors could have used genetically modified (transgenic) mice that overexpress human tau protein. These mouse strains show aggressive tau protein aggregation leading to mature NFTs.

Regardless of the magnitude of the signal immediately after the blast, the post-tetanic response in the blast-exposed mice falls off sharply over the 1-hour period following the stimulus. This means that the brain pathway and processes by which new memories are formed is impaired in blast-exposed mice.

Post-tetanic potentiation (PTP) is the change in potential that occurs after a tetanus, or a series of stimuli that occur in a short period. It is thought to be involved in synaptic plasticity, which is important to learning and memory.

The authors observed that blast-exposed mice had a reduced potential that is consistent with impaired hippocampal function. The deficit remained for at least 1 month.

This is an unexpected and important finding. Wild-type C57BL/6 mice with murine tau protein do not normally develop the neurofibrillary pretangles seen in this figure panel. The authors confirmed this finding in Figure 5.

The authors also observed this in the human cases in Figure 1. This is a surprising result, because the CP13 antibody detects hyperphosphorylated human tau protein (not mouse), and phosphorylated tau abnormalities had not been observed in nontransgenic mouse models.

Because the authors saw CTE-linked tau abnormalities in the mouse model but not in mice in the control group, they concluded that blast exposure is linked to brain abnormalities associated with CTE.

Using more sensitive methods (light microscopy, electron microscopy, protein immunoblotting, neurophysiology, and behavioral testing), the authors found that a single blast exposure was sufficient to cause significant brain injury, CTE-related abnormalities, and cognitive deficits in mice.

There were no significant differences between the pressure in the brains of living mice compared to decapitated mice. This led the authors to reject the hypothesis that there is a thoracic-vascular contribution to TBI (the water hammer effect).

This result also suggested there must be a different way that blast exposure causes brain injury, which motivated the authors' investigation of other hypotheses.

The authors report several findings linking blast exposure to CTE:

-A correlation between blast exposure and CTE in human brains (identical to the CTE seen in athletes' brains).

-A causal link between blast exposure and CTE in a mouse model.

-A causal link between blast exposure and cognitive problems commonly seen in blast-exposed military veterans.

-Cognitive problems can be prevented by restricting head movement during a blast.

We can see this in Table S3 in the Supplementary Materials.

A continental effect indicates that the shifts in elevation are predictably different depending which continent the species is on.

Positioning of the mountains could cause this.

As we can see in Figure 1C, species in southern areas have seen their southern range limits shift by as much as 300 km on average.

Canada and northern Europe have very different histories of land-use. If land-use were an important factor behind declines in bumblebee ranges, than there likely would have been a difference in bumblebees' ability to track climate change between North America and Europe.

The authors did not see this, and conclude that land-use is likely not an important factor driving these range declines.

The authors conclude that while neonicotinoids and other pesticides do kill bumblebees, they are likely not responsible for the large-scale declines in range sizes that are observed.

Bumblebees evolved in cool, temperate conditions, and did not need to evolve tolerances to high temperatures. Considering this, it's not surprising that they are dying out from the regions of their ranges that reach the hottest temperatures.

The e coli strain engineered by the authors is behaving as they predicted.

The authors concluded that writing skills do not affect the chance of receiving grant funding from NIH.

Microstimulation of deep layers of the somatosensory cortex is sufficient to trigger tickling-associated vocalizations.

The response to tickling is different than the general response to being touched. It is dependent on the type of touch, the location of touch, and the emotional state of the rat.

There are two pieces of evidence that show the link between mood and ticklishness in rats:

First, the initial round of tickling seems to predispose rats to both play behaviors and to an increased tickling response in subsequent interactions.

Second, anxiety suppresses the rats' responses to tickling.

Neural activity in the trunk cortex was greater during tickling than during gentle touch.

There is a strong correlation between the production of tickle-related USVs and activity in the somatosensory cortex.

Tickling and the anticipation of tickling are both associated with activity in the somatosensory cortex.

"Priming" the rats by tickling them prior to microstimulation increases the number of USVs produced.

Stimulation of somatosensory neurons (in the absence of tickling) is sufficient to cause the production of USVs.

This shows a direct causal link between the increased neural activity and the increased production of USVs.

Neural firing rates in the deeper layers of the cortex have a stronger relationship to USVs than rates in the surface layers of the cortex.

The firing rate of neurons is highest just before and during USV production. This shows that these two events are correlated.

There was also increased activity in the somatosensory cortex during hand-chasing, despite the fact that the rats were not being touched.

This was interesting, because the primary function of the somatosensory cortex is to detect touch.

Rats produce USVs during play behavior, even if they are not currently being tickled.

The ventral (belly) region of the rat is more ticklish than the dorsal (back) or tail regions.

The authors used 5 measures for replication success to check to what extent the 100 original studies could be successfully replicated.

Nosek and colleagues summarize eight standards for transparency and openness in research that focus on citations, data accessibility, accessibility of computational resources, making research materials like participant instructions available and giving access to the design and analyses, study and analysis plan pre-registration, and the use of replication studies overall.

They argue that journals should require and enforce adherence to transparency guidelines, and that the submission of replication studies, in particular in the Registered Report format, should be an option.

The fifth and final conclusion of the paper addresses the big-picture takeaway of the results.

On one hand, the authors recognize that research is a process where new ideas have to be explored and sometimes might turn out not to be true. Maximum replicability is therefore not desirable, because it would mean that no more innovations are being made.

On the other hand, the authors also conclude that there is room for improvement: stronger original evidence and better incentives for replications would form a stronger foundation for psychological research.

Because there is some uncertainty about how exactly the replication success rate in psychological research should be determined, the authors go about the interpretation of the results of this study very conservatively.

This very careful interpretation of the data is that the replication studies yielded largely weaker evidence for the effects studied than the original studies.

It is difficult to say exactly how many original studies were successfully replicated. The precise conclusions drawn from this paper depend a lot on which of the 5 measures used to determine replication success you think is the most appropriate measure. The results of one measure indicate a replication success rate as low as 36%, while another measure suggests a success rate of 68%. Perhaps some researchers would even say that another measure not included in this study would have made it possible to draw more meaningful conclusions. The scientific community has so far not agreed on what measure should be used to evaluate replication success rates.

Moreover, there are other limitations on this approach to studying reproducibility (see paragraph "Implications and limitations")that make it difficult to generalize the findings of this study not only psychological research, but other disciplines. It is also difficult to evaluate from the findings in this study whether the evidence indicates a specific effect is true or does not exist.

Therefore, the first conclusion of this paper is that all interpretations of the data are only an estimation of how reproducible psychological research is, not an exact answer.

Finally, the authors used the subjective rating as an indicator of replication success. Out of 100 replication teams, only 39 reported that they thought they had replicated the original effect.

With this third measure for replication success, the authors further compared the sizes of the original and replicated effects. They found that the original effect sizes were larger than the replication effect sizes in more than 80% of the cases.

The way that physical forces affected corals depended heavily on their form, since form affects how organisms are influenced by mechanical forces. Different species have different shapes and sizes, so the impact of the storm depends on the species.

The energy within waves is released most violently in shallow waters. Corals at greater depths were less likely to be damaged.

The authors report that their results confirm previous evidence connecting the ZIKV outbreak in Brazil to an increase in cases of microcephaly.

The authors used models that allowed them to study early stages of brain development. They suggest there is more work to be done to determine the effects of ZIKV infection on later stages of fetal development.

Summarizing the results, the authors conclude that in their model of early brain development, ZIKV causes severe damage.

Because DENV2 did not reduce cell growth or affect morphology, the researchers concluded that those effects are unique to ZIKV and not characteristic of the flavivirus family (to which both DENV2 and ZIKV belong).

Zika virus induces the expression of caspase 3/7, indicating a cell is preparing to die.

Dengue virus 2, on the other hand, did not increase caspase 3/7.

Brain organoids infected with Zika virus were, on average, 40% smaller.

Summing up all results, we can say that previous work or elite affiliations do not "close the door" for new ideas in research.

The authors' findings suggest that peer reviewers are good at identifying innovative and ground-breaking projects.

The authors show that peer review scores are good predictors of scientific productivity when differences in field of research, year, and applicant qualifications are removed. This suggests that peer reviewers have the necessary expertise to choose good applicants.

The authors conclude here that regardless of gender, ethnicity, or institutional prestige, when the peer-review score lowers by one standard deviation, we can observe a corresponding decrease of the number of publications and citations of an author.

Again, controlling for the variable of a PI's research background does not eliminate the relationship the authors originally found.

The authors' adjustments to control for various external effects did not change their original findings.

The authors found that there is a lot of variation in the research output of projects that receive grants. They conclude that it would be useful to find a way to accurately screen applications to determine their potential.

Based on an analysis conducted by the authors, biomedical research is valued highly by individuals, governments, foundations, and corporations. Research is seen as a source of more effective treatments and preventive measures and as a route to policy, new commercial products, and economic development.

As a result, investments in biomedical research are the highest of all sectors.

In addition to the observations and findings of this study, the physical instruments and experimental protocols that were developed will likely be very useful for further research and development of diagnostics, therapies, rehabilitation strategies, and preventative measures.

The work here will help military service personnel and others at risk for developing neurotrauma-related disease.

All of these are known to affect how susceptible a patient is to mild forms of neurotrauma and related effects. They can also affect how these are expressed.

The authors suggest that blast exposure may be more damaging than sports-related impact because they were able to observe substantial neural abnormalities after a single blast exposure.

In the case of impact-induced head injury, mild cases typically require repetitive impacts to cause neural abnormalities.

A possible alternative hypothesis is that the structure of the head and the brain would cause the blast wave to bounce around inside the brain, causing damage.

The authors' observations of roughly equal pressures both inside and outside the skull suggest that this is not a likely cause of injury. Furthermore, the magnitude of the pressure wave is far below the threshold that causes damage to tissues.

The results of this study suggest that pressure from the blast wave is not enough to cause brain injury. The data and calculations show that the brain rapidly adapts to the changing pressure, and that the pressure inside and outside the skull during the blast wave is comparable.

Thus, blast wave pressure alone is not responsible for TBI.

This statement is based on the authors' human findings from the human case studies. They observed identical paterns in head-injured athletes and blast-exposed military veterans, which has important implications for our undersetanding of traumatic brain injury and CTE.

To test the "bobblehead effect," the authors performed the same experiments on mice whose heads had been held still during blast exposure and mice whose heads were allowed to move freely.

Mice whose heads were allowed to move freely were exposed to both the blast wave (the pressure of the blast) and the blast wind (the wind following a blast wave). Mice whose heads were restrained were only exposed to the blast wave.

The authors hypothesized that blast neurotrauma and the resulting cognitive deficits were the result of the acceleration of the head during a blast (i.e., the blast wind), meaning that mice whose heads were restrained would not show any abnormalities.

The results reported here support the authors' hypothesis that head acceleration is a major contributor to traumatic brain injury following blast exposure.

Astrocytes support blood vessels and interact with other types of brain cells to control the blood-brain barrier (BBB), a membrane that protects the brain from disruptive changes in the blood.

Using the electorn microscopic images in Figure 4 and Supplementary Figures 11 to 16, the authors saw that a single blast exposure can damage not only are the smallest blood vessels but the astrocytic "feet" that wrap around and encase these blood vessels.

Because these blood vessels are critical for gas and fluid exchange, damage to them can disrupt many metabolic processes.

Choline acetyltransferase (ChAT) is an enzyme that produces the neurotransmitter acetylcholine.

Reduced ChAT concentrations are associated with Alzheimer's disease and amyotrophic lateral sclerosis (ALS).

Decreased ChAT following blast TBI suggests similarities between Alzheimer's, ALS, and TBI.

The authors also observed other key signs of CTE, such as the presence of activated microglia near small blood vessels (perivascular microgliosis).

This finding is consistent with traumatic microvascular injury and reactive microgliosis, which are signs of chronic inflammation in the brain.

The authors also calculated how the blast pressure wave would travel through the brain tissue. They found that, as with the skull, the pressure wave moved too quickly through the brain to cause injury.

The authors conclude that the head may be treated as a "lumped element," meaning that the blast pressure wave travels through it as if it were a single body.

The authors next investigated how the blast pressure wave interacted with the mice's skulls. They calculated the speed of the shockwave by taking pressure measurements with multiple sensors at different locations and measuring the time delay between recordings. Using the distance between sensors and the time delay, they were able to record the "speed" of the wave as it traveled down the shock tube.

By comparing the wave speed with the width of the mice's heads, the authors concluded that the wave traveled too quickly to create a pressure gradient large enough to cause injury. Based on these results, they were able to rule out skull compression as a cause of TBI.

Mice that were exposed to blasts had memory and learning problems. Additionally, axons in their brain showed reduced function and they had defective activity-dependent long-term potentiation, which is thought to be important to learning and memory.

In this case, these defects were all correlated but not necessarily caused by one another.

Some of the environmental damage caused by human actions is too far along to be repaired, including species loss and, to some extent, climate change. Because we cannot undo some of our environmental alterations, we must adapt to them. We already know a great deal about how to adapt to climate change, and in many places around the world, particularly cities, communities are making the adaptive changes needed to deal with extreme weather and other climate change–related impacts.

Human society is on an unsustainable trajectory. Because environmental degradation is ultimately a human behavior problem, human behavior must change. Adjustments in resource consumption must happen at both an individual level as well as across societies. The industrial systems and infrastructure that currently serve human needs must change as well, to dramatically lower their impact on natural systems.

Generally people build their own worldview over time through trial and error, listening to elders, going to school and religious services, and general experience. There has been very little experimental research done about how people can transform quickly from an unsustainable worldview, such as the modern-industrial worldview, to a more ecologically-grounded worldview.

We are surrounded by systems that define how we behave, including neighborhoods, households, schools, religions, and the economy.

The government is one example of a system that defines rules about how groups of people act (for instance, when and for how long people can water their lawns), interact together (whether roads are built to accommodate pedestrians, bikes, buses, trains, and cars), and how we share resources (such as community composting sites).

It is important to remember that a system such as a government is run by people, so individual people need to start the process of changing the systems by voting, running for office, or through work as government employees.

The situation is a powerful driver of human behavior. Therefore we must create situations that drive behavior toward sustainability rather than against it. This means that, among other things, situations, tasks, and activities have to engage people's needs to feel competent, have choices, and to feel like they belong.

There is very little research studying how to change worldviews. Yet, people in developed countries will not be able to make ecologically appropriate decisions if they keep thinking the same way they do now.

There are many tools that psychologists have developed for other purposes that can be applied to facilitating worldview change. For instance, educational psychologists, who are experts about how people learn, and industrial/organizational psychologists, who regularly develop employee training programs, can apply what they know about teaching knowledge, skills, and abilities to teaching worldview principles.

There are physical laws that govern how ecosystems work. Only when leaders better understand this will they be able to make sustainable decisions. Because the path from ecosystem to organization is often long, this connection between individuals' decisions and the state of the planet is very hard to see. Therefore, decision-makers have to add "understanding how ecosystems work" to the knowledge, skills, and abilities they develop to do their jobs.

Psychologists have studies individuals' motivations for volunteering for many decades. The reasons people volunteer, or join collective efforts to help others, include:

• To do something new
• To feel good about themselves
• To learn a new skill
• To help others, the community, or the larger world
• To live their values, in particular religious values

An important insight from evolutionary psychology is that all human beings carry with them certain inherited behavioral tendencies. One of these is a tendancy to be short-term thinkers.

According to Van Vugt, Grisckevicius, and Schultz (2014), early humans were more likely to survive if they focused on immediately available benefits rather than thinking about possible future needs. In contrast, solving complex environmental issues such as climate change requires reducing, or even eliminating, current fossil fuel–intensive behaviors (for example, commuting alone in a personal car) in order to ensure a healthy climate in the future.

Before modern times, people lived in small groups, hunting and foraging for food. By necessity, they were very tuned in to their surroundings, and likely believed that other species were their neighbors and family.

Over the past couple of centuries, humans have become more and more disconnected from the natural world, treating it as something that exists for us—as resources to be used, abused, and discarded.

Human beings throughout most of the world need to work together to dramatically change the way we meet our everyday needs for food, clean water, energy, shelter, and transportation.

There is very little published research about how to help organizational leaders (CEOs, religious clergy, elected officials) understand the importance of their role in creating sustainable systems.

Additionally, with just a few exceptions, most research about developing a realistic understanding of the earth's systems is aimed at children. For adults there is an additional challenge of having to unlearn assumptions that are deeply embedded in the way they think about the world.

Since working toward sustainability of large systems, including organizations, will lead to faster and more expansive change, more research needs to be done on how to effectively increase the knowledge and motivation of these leaders.

The environmental degradation we face is much larger than what individual change can effectively address. To solve issues such as climate change, loss of biodiversity, and other global environmental issues, we must change the larger systems that meet our needs for energy, food, water, transportation, and goods. These systems are not going to change on their own; instead, it will take the efforts of many, many people working together to demand change and to be persistent in those demands.

One's identity and social group affiliations appear to be among the most important determinants of whether a person takes pro-environmental action. If an individual does not identify as someone who cares about the environment, then it feels very uncomfortable and awkward to take actions typical of environmentalists. In addition, if one's social group does not express environmental concern, then taking environmental action in front of them can feel very risky as they may notice and express disapproval.

Community-Based Social Marketing (CBSM) programs have been applied around the world to change behaviors that are most environmentally impactful: agricultural practices, transportation, home energy use, water use, overall resource consumption and waste, and toxic chemical production and use.

When humans do not interact directly with the natural world it is hard to know that we completely depend on it to live. For instance, when we buy food at the supermarket, we may not think about where that food was grown, how long it took to grow, and what kind of soil and weather conditions were required. We may not think about how drought and changes in climate are likely to change the food that is available to us. A direct experience with nature such as caring for some food plants helps us understand how long it takes and how challenging it is to grow what we need to eat.

The shapes of corals has a strong influence on how much they are damaged because shape directly affects how much force flowing water exerts on the coral's skeleton. Branching corals have large flat exposed areas that are especially susceptible to breaking, while corals with leaf-like, encrusting and head forms experience much less mechanical stress during a storm.

The way that physical forces affected corals depended heavily on their form, since form affects how organisms are influenced by mechanical forces. Different species have different shapes and sizes, so the impact of the storm depends on the species.

The energy within waves is released most violently in shallow waters. Corals at greater depths were less likely to be damaged.

Third, from this study we can conclude that the precautions the authors took against replication success depending on the team of researchers who conducted the replication study were quite successful: there is no evidence that characteristics of the replication team influenced the outcomes of the replication attempt.

Rather than replication-team-specific differences that influenced the replication outcome, there were systematic differences between successfully replicated and non-replicable studies based on characteristics of the original study. Therefore, the fourth conclusion of this paper is that original studies which showed stronger evidence for the effect they investigated were also more likely to be successfully replicated.

The fifth and final conclusion of the paper regards the question what psychologists and other researchers should take from these results regarding their overall research practices. The conclusion is mixed. On the one hand, the authors recognize that research is a process where new ideas have to be explored and sometimes might turn out not to be true. Maximum replicability is therefore not desirable, because it would mean that no more innovations are being made. On the other hand, the authors also conclude that there is room for improvement: stronger original evidence and better incentives for replications would put progress in psychological research on a stronger foundation.

Because there is some uncertainty about how exactly the replication success rate in psychological research should be determined, the authors go about the interpretation of the results of this study very conservatively. This very careful interpretation of the data, and the second conclusion of this study, is that the replication studies yielded largely weaker evidence for the effects studied than the original studies.

The discussion section begins with a cautionary sentence reminding the reader that it is difficult to say exactly how many original studies were successfully replicated. The precise conclusions drawn from this paper depend a lot on which of the 5 measures used to determine replication success you think is the most appropriate measure. The results of measure indicate a replication success rate as low as 36%, while another measure suggests a success rate of 68%. Perhaps some researchers would even say that another measure not included in this study would have made it possible to draw more meaningful conclusions. The scientific community has so far not agreed on what measure should be used to evaluate replication success rates.

Moreover, there are other limitations to this approach to studying reproducibility (see paragraph "Implications and limitations"), which make it difficult to generalize the findings of this study to psychological research in general, or even to other disciplines. It is also difficult to evaluate from the findings in this study whether the evidence indicates a specific effect is true or does not exist.

Therefore, the first conclusion of this paper is that all interpretations of the data are only an estimation of how reproducible psychological research is, not an exact answer.

The carbon dioxide (CO₂) released from surface water as calculated in this paper only accounts for 20% to 40% of the estimated CO₂ release from all arctic freshwater.

Other possible sources of CO₂ include CO₂ released directly from water in the ground and CO₂ produced by organisms living in the sediment at the bottom of lakes, rivers, and streams.

The authors report that their results confirm previous evidence connecting the ZIKV outbreak in Brazil to an increase in cases of microcephaly.

Summarizing the results, the authors conclude that in their model of early brain development, ZIKV causes severe damage.

Because DENV2 did not reduce cell growth or affect morphology, the researchers concluded that those effects are unique to ZIKV and not characteristic of the flavivirus family (to which both DENV2 and ZIKV belong).

Zika virus induces the expression of caspase 3/7, indicating a cell is preparing to die.

Dengue virus 2, on the other hand, did not increase caspase 3/7.

The authors' findings suggest that peer reviewers are good at identifying innovative and ground-breaking projects.

The authors show that peer review scores are good predictors of scientific productivity when differences in field of research, year, and applicant qualifications are removed. This suggests that peer reviewers have the necessary expertise to choose good applicants.

The authors conclude here that regardless of gender, ethnicity, or institutional prestige, when the peer-review score lowers by one standard deviation, we can observe a corresponding decrease of the number of publications and citations of an author.

The authors concluded that writing skills does not affect the chance of receiving grant funding from the NIH.

The authors found that there is a lot of variation in the research output of projects that receive grants. They conclude that it would be useful to find a way to accurately screen applications to determine their potential.

Based on an analysis conducted by the authors, biomedical research is valued highly by individuals, governments, foundations, and corporations. Research is seen as a source of more effective treatments and preventive measures and as a route to policy, new commercial products, and economic development.

As a result, investments in biomedical research are the highest of all sectors.

Lewis and colleagues made a genetically modified mouse with a mutated APP gene and a mutated tau gene.

These double mutants had plaques like other hAPP mice, but they also had tangles that were more severe than in other mice, showing that problems with amyloid and tau can interact and cause symptoms of Alzheimer’s disease.

This work started as a side project and eventually became a pillar of Dr. Roberson’s later work on mouse models of Alzheimer’s disease. It has been credited with "sparking the research community’s interest in the role of tau in the pathogenesis of Alzheimer’s disease.”

Read more in Neurology Today:

http://journals.lww.com/neurotodayonline/_layouts/15/oaks.journals.mobile/post.aspx?blogId=1&postId=520

This work was covered by AlzForum, a leading advocacy group for Alzheimer’s research and patients.

Read more at AlzForum:

http://www.alzforum.org/news/research-news/app-mice-losing-tau-solves-their-memory-problems

Lowering tau even in normal mice (those without the hAPP gene, who would not get Alzheimer’s disease) was beneficial in making mice less prone to seizures when injected with an seizure-inducing drug.

This means that in healthy mice, normal tau may be involved in modulating excitation in neurons, reducing the overall risk of seizures.

(Seizures are a result of abnormally high electrical activity in the brain that occurs when certain neurons are excessively excited.)

Like humans with Alzheimer’s disease, many mice used as models of the disease have a tendency to get seizures, including the hAPP mice used in this study.

However, hAPP mice without tau or with reduced tau had fewer seizures than those with the normal amount of tau.

Eliminating tau in hAPP mice prevented memory and cognitive problems, but it didn’t prevent the neurons from becoming damaged and impaired.

The removal of tau must therefore work in an unrelated way to improve cognition in these mice.

All hAPP mice, independent of the amount of tau, had neurons whose axons and dendrites were withering away in regions near amyloid plaques.

These results show that this type of damage in Alzheimer’s disease can happen even without tau being present.

Reducing tau in hAPP mice protected those mice against the cognitive impairments seen in Alzheimer’s disease.

The authors looked at hAPP mice with normal amounts of tau to see how the tau became abnormal later in life. They compared these changes with abnormal tau measured in other mouse models of Alzheimer’s disease.

The connection between tau and amyloid-β in this model isn’t clear and may involve multiple types of tau or tau stored in various locations (or pools) within the cell.

The authors examined the brains of hAPP mice with different levels of tau. They found that, at all levels of tau, the amount of amyloid plaques and the amount of floating amyloid-β were the same in all hAPP mice.

Thus, the reduction of tau, which had improved memory, didn’t alter the amyloid-β or plaque levels, suggesting that amyloid-β or plaque levels alone are not responsible for memory loss.

hAPP mice are known to die young, as a result of the induced Alzheimer’s disease. But if hAPP mice had a reduced amount of tau, they lived much longer.

Additionally, hAPP mice with normal levels of tau were hyperactive even into middle age, whereas hAPP mice with no tau were not.

Mice with the hAPP gene usually do poorly in the water maze because of their impaired memory. However, hAPP mice that have only half the amount of normal tau did remember where the platform was after additional training.

hAPP mice with no tau performed similar to normal, healthy mice, showing good memory on this test.

Thus, removal of all the normal tau seems to prevent memory problems. Even removing just half the normal tau already has some memory benefits.

Evidence from this study and following studies showing the importance of lowering tau has led researchers to target tau with their experimental new treatments, including vaccines that use the body’s own immune system to fight off the problematic tau proteins.

http://www.medicaldaily.com/alzheimers-disease-tau-protein-vaccine-391883

Almost 10 years after this paper was published, no good treatments for Alzheimer’s disease exist, but more and more of the new drugs in clinical trials are targeting the tau protein, as a result of early laboratory research such as this.

http://www.bloomberg.com/news/articles/2016-06-27/after-190-tries-are-we-any-closer-to-a-cure-for-alzheimer-s

the authors are demonstrating that not only the signalling pathway but also the anatomical placode are required for reptiles to develop scales properly.

The insertion of the jumping DNA caused a mutation. This mutation affected splicing, a process where the DNA is edited to ultimately produce the correct protein.

This incorrect splicing resulted in a shortened non-functional protein.

Because the same patterns in development of chicken feathers and lizard scales are similar, it can be assumed that they are related.

The placode is crucial in the formation of all the different skin appendages (hair, feathers, scales), and all of them develop with the same molecules.

This shows that they are homologous- thus closely related.

The authors have found that the placode and the placode's signalling molecules are highly conserved - meaning it is found across many species.

This study shows that the placode is responsible for the formation of many different structures in the various species, such as feathers, scales and hair.

Homozygous means that they have two copies of the exact same gene.

Co-dominant means that two different genes that are present in the same individual will both be expressed and blended together.

In this case, the gene which causes a scaleless mutant must have two copies of the mutant gene. If there is one copy, there will be partial formation of scales.

Similar disease symptoms can be observed in other animals with a mutation in the same gene.

Even though the mutant does not have scales as a result of a non functional protein, it still shows the beginnings of a pattern for scales.

This means that there are other elements that are not part of the anatomical placode which contribute to the formation of scales

Eels always check if there is living prey by sending two fast electric signals (doublet). Only after the eels feel the movement of the fish, which they induced by their double shock, they attack the fish by really strong shocks.

The fish did not behave differently. Thus, the eel's shock activates "decentralised" motor neurons of the fish.

This study revealed that Eels, through the process of evolution and survival for the fittest, have developed a very efficient system of prey detection and capture. The Eel's electrical powers work much like the way a TV remote control does. Using electrical pulses Eels turn off their prey's nervous system the same way a remote control turns off a tv screen. This happens because the electric pulses take advantage of the mechanism through which the Prey's nervous system works by hacking into it and telling it to freeze.

The eel's electric shock contracts the fish's muscles, which paralyses it.

The eel's shock affects the nervous system (motor neurons) of the fish.

The authors identified small deletions in the genome of the family in genes coding for various proteins that are highly expressed in the brain. However, it has not been proven that all these deletions play a role in the disease.

In consanguineous families, the authors observed that the proportion of affected women amongst the affected children was higher as well as the number of de novo CNVs was reduced.

This could mean that families with related parents present more recessive causes for autism. The authors will now try to determine what these causes are and where they are located on the genome.

After the experiments, the data was analyzed in order to determine the proportion of de novo copy number variants in each subject in comparison with a reference set of unaffected and affected subjects as well as the rates of de novo CNVs inherited from their parents.

The data showed that de novo CNVs were much less frequent in consanguineous families (both simplex and multiplex) and the amount of inherited CNVs is high.

The low rate of de novo copy number variant suggests that abnormalities in autistic patients' genomes comes from defective genes that were already present in the parents, rather than healthy genes that mutated before or shortly after fertilization.

A second big deletion was identified on the chromosome. This codes for a protein that allows for neuron, and more specifically axon, growth.

This deletion completely removes a protein-coding gene called c3orf58, and a large section of possible regulatory regions of another gene called NHE9. SK

The authors focused on one pedigree in this paragraph: the family of patient AU-3101. A first deletion removes an entire gene, coding for a protein present in the Golgi Apparatus, as well an upstream region of the gene coding for NHE9, an ion exchanger.

The authors noticed that in some cases, there were deletions of certain long sequences present on both chromosomes of the affected individuals. These huge deletions could cause symptoms of autism in certain cases.

The abnormalities in autistic patient's chromosomes were not shared between families. This suggests that autism can have many different genetic origins.

The authors observed that the proportion of women affected doubles in consanguineous multiplex compared to the whole HMCA and is almost tripled compared to simplex families.

The authors found that large deletions of genes that are regulated by neuronal activity were associated with autism symptoms. This is an interesting finding, because autism symptoms often develop later in development.

Summing up all results we can say that previous work or elite affiliations do not "close the door" for new ideas in research.

One of the goals of fear learning research is to be able to improve therapies for people suffering from fear and anxiety disorders.

The fear extinction process is impaired in many of these patients, so identifying molecular targets may aid in drug development.

Changes that occur following fear conditioning, such as a reduction in hippocampal BDNF, may be corrected by BDNF treatment.

The effects that infused BDNF has on extinction are mediated by NMDA receptors in the IL mPFC.

Activation of these receptors may stimulate neurons in this region, and this could explain why infusion of BDNF results in reduced freezing even when the animals do not go through extinction training.

This research furthers our understanding of fear learning by describing extinction using both a systems level approach (hippocampus to IL-mPFC pathway) and a molecular mechanism (BDNF-mediated NMDA activation).

When infused into the hippocampus, BDNF can induce extinction in the absence of extinction training.

This suggests that activation of this pathway is a key component of the fear extinction process.

Blocking BDNF activity in the IL mPFC inhibits the effects of BDNF infused into the hippocampus.

The fact that BDNF infusion into the hippocampus results in similar fear reduction to infusion into the IL mPFC supports the hypothesis that the hippocampus supplies BDNF to the IL mPFC.

The role of NMDA receptors in fear acquisition has been previously established.

By showing that rats receiving an NMDA antagonist do not respond to BDNF, the authors show that these receptors are also required for BDNF-induced fear reduction.

Based on the fact that unsignaled footshocks can reinstate freezing after extinction, the authors conclude that BDNF does not degrade the original memory.

When testing the behavioral effects of a treatment, it is important to rule out nonspecific interaction with other regions of the brain that may similarly affect behavior through an alternative route.

The amygdala is known to be involved in fear acquisition, so if the BDNF was nonspecifically acting on the amygdala it would be apparent during conditioning or open-field anxiety testing.

The purpose of extinction training is to subject the animals to the tone enough times to allow them to form a new memory. They realize that the tone is not followed by a shock and therefore is not associated with a threat. This concept forms the basis of exposure therapy, which is used to treat humans with anxiety disorders by progressively re-exposing them to a traumatic memory while in a safe environment.

In this experiment, the BDNF animals show reduced freezing prior to extinction training. This allows the authors to conclude that at least some of the effects that BDNF infusion has on fear expression occur regardless of whether the animals receive extinction training.

Extinction memory is tested on the third day, when the animals are subjected to another round of tones without footshocks. If the animals freeze less in response to the tones, it means that they have successfully extinguished their perceived association between the conditioned stimulus (tone) and unconditioned stimulus (footshock).

BDNF infusions reduced freezing relative to controls, indicating that the extinction memory in these animals was strengthened.

The latency to door opening as well as the likelihood of door opening to free a trapped cagemate were used as readouts for empathy. Based on these criteria the authors conclude that rats are capable of feeling empathy and will act on those feelings.

Here is a nice summary video of the authors' work, narrated by one of the authors, Dr. Peggy Mason.

[https://www.youtube.com/watch?v=3jkOwYKBJEI]

Rats took about 6 days to learn to open the chocolate containing restrainer. In the earlier experiment with the trapped cagemate, the rats took about 7 days to open the restrainer.

The length of time it takes for the rats to master this door-opening maneuver indicates that this action took some effort and didn't come naturally.

Once rats learned to open the door, they were just as likely to open the door to the chocolate-containing restrainer as to the restrainer holding their cagemate.

The helper rats' motivation to set their trapped cagemates free does not depend on social contact with their freed cagemates.

This is evidenced by the fact that helper rats freed their trapped cagemates even when there was no possibility of interaction after freeing.

Rats that showed bolder traits may be more likely to act to help their fellow rat. The second panel of figure S1 shows this. However, although a trend is there, it did not reach statistical significance. http://www.sciencemag.org/content/suppl/2011/12/07/334.6061.1427.DC1/Bartal.SOM.pdf

The rats that displayed more boldness, (as measured by a shorter time to emerge from a half-opened cage) were the ones who freed their cagemates.

http://www.sciencemag.org/content/suppl/2011/12/07/334.6061.1427.DC1/Bartal.SOM.pdf

When their cagemate was trapped in the restrainer, female rats moved around the arena faster than males and also opened the door of their trapped cagemates quicker than males.

The trapped rats emitted ultrasonic alarm calls, which is a measure of stress in rats.

Rats in an arena with a trapped cagemate:

A. moved more frequently around the arena

B. moved faster around the arena

C. spent a longer time in the arena center near the<br> restrainer

D. moved more after the restrainer was opened and the previously confined rat was freed

All these findings point toward the movement and activity of the free rat being linked to the presence of a rat in the restrainer.

The authors rule out the alarm calls as an indicator of stress and the source for door opening.

QUESTION: What other criteria could the trapped rat use to communicate its distress to the helper rat?

The amount of time the helper rat remained frozen after door opening significantly decreased by day 6.

This suggests the helper rat expected the door to fall as a result of its action.

The free rat moved around much more quickly after the door opening that freed the trapped rat. The authors interpret this increase in activity as an indication of the importance of the freeing event in the mind of the rescuing rat.

Since 2006, most ivory poaching occurred in just two key areas.

Poaching activity is highest in a few key regions.