chromoscience OP t1_ix5qptl wrote

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Spending time doing nothing helps artificial neural networks learn faster

Humans require 7 to 13 hours of sleep every night, depending on their age. Numerous things take place during this period, including changes in hormone levels, the body relaxing, and variations in heart rate, respiration, and metabolism. Not much happens in the brain.

The University of California San Diego School of Medicine’s Maxim Bazhenov, PhD, professor of medicine and a sleep researcher said that the brain is quite busy when we sleep, reiterating what we have learnt throughout the day. Sleep aids in memory reorganization and delivers memories in their most effective form.

Bazhenov and colleagues have described how sleep strengthens rational memory, the capacity to retain arbitrary or indirect relationships between things, persons, or events, and guards against forgetting past memories in earlier published work.

The architecture of the human brain is used by artificial neural networks to enhance a wide range of technologies and systems, from fundamental research and health to finance and social media. However, they fall short in one crucial area. When artificial neural networks learn sequentially, new input overwrites existing knowledge, a process known as catastrophic forgetting. In other areas, they have exceeded human performance, such as computing speed.

Conversely, according to Bazhenov, the human brain continually learns and integrates new information into existing knowledge, and it normally learns best when fresh instruction is combined with intervals of sleep for memory consolidation.

Senior author Bazhenov and colleagues describe how biological models may help reduce the risk of catastrophic forgetting in artificial neural networks, increasing their usefulness across a spectrum of research interests. Their article will appear in the PLOS Computational Biology journal on November 18, 2022.

The researchers employed spiking neural networks, which artificially imitate natural brain systems by transmitting information as discrete events (spikes) at certain times rather than continually.

They discovered that catastrophic forgetting was reduced when the spiking networks were taught on a new task but with sporadic off-line intervals that mirrored sleep. The networks may repeat previous memories while “sleeping,” just like the human brain, according to the study’s authors, without explicitly requiring prior training data.

In the human brain, patterns of synaptic weight—the force or amplitude of a link between two neurons—represent memories.

According to Bazhenov, neurons fire in a precise order as we acquire new information, which increases the number of synapses between them. The spiking patterns we learnt while awake are automatically replicated when we sleep. Reactivation or replay is the term used.

Synaptic plasticity, the ability to change or shape synapses, is still present during sleep and can further increase synaptic weight patterns that represent the memory, helping to avoid forgetting or enabling the transfer of information from old to new activities.

This method was used to prevent catastrophic forgetting in artificial neural networks, as discovered by Bazhenov and coworkers.

It implied that these networks may continue to learn, much like people or animals. Improving memory in humans may be made easier by having a better understanding of how the brain processes information when we sleep. Improving sleep patterns can improve memory.

In other studies, we employ computational tools to create the best plans for applying stimulation while we sleep, such audio tones that promote learning and sleep patterns. This may be crucial in situations where memory isn’t functioning at its best, such when it deteriorates with age or under certain medical illnesses like Alzheimer’s disease.


Golden R, Delanois JE, Sanda P, Bazhenov M (2022) Sleep prevents catastrophic forgetting in spiking neural networks by forming a joint synaptic weight representation. PLoS Comput Biol 18(11): e1010628.


chromoscience OP t1_iwk3nws wrote

Under their shells, armadillos hide a secret: when exposed to the bacterium that causes leprosy in humans, their livers expand considerably. This oddity, which was discovered in a recent study, might offer insights into how the body regulates liver regeneration and how to speed up the process in humans.

Hepatologist Alejandro Soto-Gutiérrez of the University of Pittsburgh School of Medicine, who was not involved in the study, calls the discovery quite cool. He points out that since mice and rats make up the majority of animal research on liver regeneration, it is “refreshing” that researchers are studying a different species that might offer fresh perspectives.

The liver is the body’s master of regeneration, having the capacity to recover from illnesses and traumas. When a kidney is donated, a replacement does not grow in its place. However, the remaining portion of a donor’s liver will grow back into a full-sized organ even if two thirds of it are removed for transplantation. Scientists are unsure how to start this rejuvenation in people whose livers are deteriorating due to cirrhosis or other diseases, though.

Almost 10 years ago, regeneration biologist Anura Rambukkana of the University of Edinburgh and colleagues discovered leprosy-causing bacteria infect cells known as Schwann cells that embrace neurons. Once the bacteria have established themselves in their new environment, they encourage the cells to revert to a more immature developmental state and resemble stem cells.

However, those tests were done on mouse cells in a dish. Would the same procedure take place in a real animal?

Because leprosy bacteria do not thrive in mice or other common lab animals, Rambukkana claims that this question kept him up at night. Then he remembered that the study’s germs originated from a laboratory in Louisiana where scientists were raising them in nine-banded armadillos, which are an ideal host for the bacterium.

Rambukkana phoned a scientist at the facility to inquire whether he had observed anything strange about the organs of sick armadillos because the germs thrive in the animals’ livers. The researchers constantly see that the liver is enlarged.

The new research supports that finding. Rambukkana and colleagues report today in Cell Reports Medicine that the livers of armadillos afflicted with leprosy bacteria are roughly one-third larger than those of their uninfected counterparts. Furthermore, the liver does not just swell uncontrollably in animals. The larger organs preserve their distinctive structure, including the precise number of lobes and the unusual honeycomb-like arrangement of subunits. Researchers may be able to comprehend the mechanics of regeneration in the human liver by studying how the livers of animals continue to grow.

Patients with infections or other liver diseases may develop tumors and collect scar tissue, which can impair the function of the organ. The armadillos, however, showed no indication of either issue, according to the researchers. Furthermore, their examination of a number of liver proteins revealed that the organs were functioning appropriately.

Rambukkana and colleagues assessed gene activity in infected and uninfected rats to elucidate how the liver bulks up. The liver cells in armadillos that contained the bacteria changed to resemble stem cells, just like the Schwann cells in their earlier research. The pattern of gene activity in the liver of an infected animal matched that of the liver of a developing human.

According to Rambukkana, these small microorganisms know how to build a working liver. He also said that a larger liver is probably helpful for the microorganisms since it offers more living area. Scientists might be able to use this process to help liver disease sufferers regenerate their organs.

However, according to George Michalopoulos, a liver regeneration researcher also at the Pitt School of Medicine, the study leaves a lot of uncertainties. For example, he claims that the researchers must demonstrate that the liver infected armadillos is not simply enlarged because it becomes filled with bacteria.

Researchers will also need to find a solution to another problem before this anatomical abnormality can be used to create viable treatments. According to liver researcher Udayan Apte of the University of Kansas Medical Center, the bacteria have found out how to trick the liver cells into giving them refuge. He also asked h ow can the bacteria prevent the cells from dying and instead cause them to divide?

Apte claims that despite these difficulties, he is enthusiastic about the approach’s potential. The study demonstrates that”the liver can remain functioning, divide, and regenerate at the same time.



chromoscience OP t1_iw6dih0 wrote

From wolves to bees, all animals and insects depend on their capacity to locate the source of odors, which is difficult when wind disperses and hides their source. According to earlier studies, animals and insects find these targets by smelling the strength of the odors and then tracing back in the opposite direction of the wind.

For the same reason that smoke from a chimney disperses and its trail does not necessarily lead back to its source, following the wind alone, however, can misdirect them. Scientists at Yale University led by Thierry Emonet and Damon Clark questioned whether flies were capable of detecting the movements of odor packets without the aid of the wind.

The Emonet and Clark laboratories used their knowledge of motion detection and smell navigation to create experiments to test this theory for a new study. They found that, contrary to popular belief, flies are capable of detecting the motion of odor packets on their own, independent of the wind.

The researchers genetically altered the fly antennae to sense light in order to accomplish this finding. They then made fictive odor packets out of light and observed how the flies reacted to these signals in both windless and windy conditions. They discovered that the fly antennae worked to detect the motion of odor packets, enabling flies to change their route solely based on signals from odor packets. The article was released in the journal Nature on November 9.

According to the researchers, this information will help not just public health (how mosquitoes seek people) and agriculture (how bees locate flowers), but also the creation of robots that can detect threats like landmines.


Nirag Kadakia et al. (2022). Odor motion sensing enhances navigation of complex plumes, Nature. DOI: 10.1038/s41586-022-05423-4


chromoscience OP t1_ivd3bkz wrote

The Devils Hole pupfish inhabits a very horrific environment, as its name suggests.

263 of the pupfish are confined to a single deep limestone cave in the Mojave Desert of Nevada, where the water temperature is almost constantly around 93 degrees Fahrenheit, food is so scarce that they are constantly on the verge of starvation, and oxygen levels are so low that most other fish would die right away. Of all known vertebrates, the pupfish Cyprinodon diabolis inhabits the tiniest habitat.

The significant impact that these severe and isolated settings have had on this fish’s genetic diversity is now supported by new studies.

University of California, Berkeley biologists reveal the first complete genome sequencing of eight species of pupfish from the American Southwest—30 individuals in total, including eight Devils Hole pupfish—in a paper that was published this week in the journal Proceedings of the Royal Society B. Surprisingly, the Devils Hole pupfish has undergone such intense inbreeding that, on average, 58% of the genomes of these eight individuals are identical.

According to lead researcher Christopher Martin, an associate professor of integrative biology at UC Berkeley and curator of ichthyology in the campus Museum of Vertebrate Zoology, “high levels of inbreeding are associated with a higher risk of extinction, and the inbreeding in the Devils Hole pupfish is equal to or more severe than levels reported so far in other isolated natural populations, such as the Isle Royale wolves in Michigan, mountain gorillas in Africa, and Indian.” The researchers were unable to test fitness directly, the increased inbreeding in these pupfish probably causes a significant decline in fitness.

The researchers discovered that other pupfish species are likewise inbred, but only 10% to 30% of their genomes are identical.

The Devils Hole pupfish exhibit an amount of inbreeding comparable to what would occur if four to five generations of siblings interbred, according to graduate student David Tian, the study’s lead author. As a result, dangerous mutations are more likely to be fixed rather than eliminated, potentially driving a population to extinction through a mutational meltdown. Although populations of Devils Hole pupfish in the wild and in captivity, or “refuge” populations, are currently thriving, the species’ low genetic diversity could cause problems if climate change and human influences increase.

The new genome sequences will assist researchers and conservationists in evaluating the health of native pupfish populations in the face of these potential threats and, if necessary, intervening in refuge populations to increase the genetic diversity of these species—the Devils Hole pupfish in particular.

With the help of the new genomic data, Tian said, “there is a lot of potential to look at not just genetic diversity and how these species are related to one another phylogenetically, but also look at inbreeding and mutation load to get an idea of what their current status is, how evolutionary history may have influenced their current genetic variation, and think about where the population is going and what we should do, if anything, to preserve these species.”

Pupfish species are dispersed over the world and frequently found in remote lakes and springs with harsh conditions that most fish would not be able to survive. Warm, saline desert springs and streams in California and Nevada are home to about 30 different species. Martin has researched a number of pupfish populations, including a few in the Bahamas’ San Salvador Island, to better understand the genetics underlying their capacity to survive in harsh environments and specialized ecological niches.

Martin said that the Devils Hole pupfish is special due to its restricted range and precarious existence, which makes environmentalists concerned about its varying wild population.

The possibility that these declines may be related to the population’s genetic health is one of the questions surrounding them. The decreases are caused by deleterious mutations that, because the population is so small, have gotten fixed.

Martin pointed out that human intrusions into their habitat had contributed to the reduced number. In the 1960s and 1970s, local ranchers and developers tapped groundwater in the area, substantially lowering the water level in Devils Hole and causing a population decline. Devils Hole and its inhabitants were preserved by a 1976 Supreme Court decision allowing the federal government to prohibit groundwater extraction, and the endangered species was protected by captive breeding at a nearby 100,000-gallon pool at the Ash Meadows National Wildlife Refuge. However, a reduction in the 1990s brought the wild population to a low of 35 individuals in 2013. Since then, the wild population has returned, but the refuge population has grown to be about 400, which is double the wild number.

However, not all of the genetic variety in the Devils Hole pupfish can be attributed to humans. The genome of a pupfish that was captured in 1980 and kept at the University of Michigan was also sequenced by the UC Berkeley researchers. It displayed inbreeding and a lack of genetic variety similar to those observed in newly captured individuals, the majority of whom passed away naturally. This suggests that over hundreds or even thousands of years, the pupfish population has probably experienced frequent bottlenecks.

Martin and Tian discovered that 15 genes have completely vanished from the Devils Hole pupfish genome as a result of this. Five of them appear to play a role in adjusting to life in hypoxic or low-oxygen settings.

“Because this is a habitat where you’re most exposed to hypoxia,” Martin said, “these deletions are a paradox.” The researchers said that it might have something to do with the habitat’s long-term stability. However, it appears that the hypoxic pathway is damaged. It doesn’t really matter if you break more genes in that regulatory pathway after you disrupt one gene. The researchers’ upcoming task is to investigate what these deletions accomplish in detail. Are they able to tolerate hypoxia better? Do they reduce the body’s tolerance to hypoxia? Both of those situations, in their opinion, are currently equally likely.

The researchers suggested that selective breeding could assist the promotion of diversity and possibly prevent the extinction of the Devils Hole pupfish species. Additionally, CRISPR genome editing could re-add missing genes to the body.

The finding that the fish gathered in 1980 had a genome that was roughly as inbred as fish today is perhaps excellent news, in that the population has traditionally been extremely inbred with very low genetic diversity, suggesting that the recent decrease in the ’90s—with population bottlenecks to only 35 fish in 2013 and 38 fish in 2007—doesn’t appear to have much of an effect.

Tian is currently examining 150 full genome sequences from nine species of American pupfish in order to have a better understanding of the harmful mutations and gene deletions that have occurred in the distinct populations of the Southwest. He views the findings as a demonstration of what conservation genomics may accomplish for globally threatened and possibly inbred populations.

In terms of collecting genomic data and applying it to conservation, the researchers are on a very exciting cusp, especially in a period when it’s an issue that’s likely only to get worse with changing climate, more habitat fragmentation, and just manmade changes.”

However, Tian is wary of genetic treatments because it is unclear how genes affect a species’ physical and behavioral traits and how this relates to fitness and adaption to a particular environment. Still, conservation need to be a top focus.

The solution is still more money for these populations, safeguarding ecosystems, pursuing legal means of protecting these species, and figuring out methods for people and these endangered animals to cohabit on this earth.


David Tian et al. (2022). Severe inbreeding, increased mutation load and gene loss-of-function in the critically endangered Devils Hole pupfish, Proceedings of the Royal Society B: Biological Sciences. DOI: 10.1098/rspb.2022.1561


chromoscience OP t1_iu2oe3c wrote

Smoking has been linked to non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease is a condition where excessive fat is stored in the liver of non-alcoholic drinkers.[1]

Some people with non-alcoholic fatty liver disease can develop steatohepatitis, an aggressive form of fatty liver disease, which may progress to cirrhosis and liver failure.[1]

Researchers discovered that nicotine may accumulate in the intestine of a smoker and activates intestinal AMPKα.

Researchers found that the bacterium Bacteroides xylanisolvens can degrade intestinal nicotine in mice.

Additionally, AMPKα was found to increase intestinal ceramide formation which helps the progression of non-alcoholic fatty liver disease into steatohepatits.

The results highlight the effect of intestinal nicotine accumulation and the discovery of a bacterium that can eliminate intestinal nicotine which reduces liver disease.


Chen, B., Sun, L., Zeng, G., Shen, Z., Wang, K., Yin, L., Xu, F., Wang, P., Ding, Y., Nie, Q., Wu, Q., Zhang, Z., Xia, J., Lin, J., Luo, Y., Cai, J., Krausz, K. W., Zheng, R., Xue, Y., Zheng, M. H., … Jiang, C. (2022). Gut bacteria alleviate smoking-related NASH by degrading gut nicotine. Nature, 610(7932), 562–568.