Category: Science News

{Memories formed in one part of the brain are replayed and transferred to a different area of the brain during rest, according to a new UCL study in rats.}

The finding suggests that replay of previous experiences during rest is important for memory consolidation, a process whereby the brain stabilises and preserves memories for quick recall in the future. Understanding the physiological mechanism of this is essential for tackling amnesiac conditions such as Alzheimer’s disease, where memory consolidation is affected.

Lead researcher, Dr Freyja Ólafsdóttir (UCL Cell & Developmental Biology), said: “We want to understand how a healthy brain stores and accesses memories as this will give us a window into how conditions such as Alzheimer’s disease disrupt the process. We know people with Alzheimer’s have difficulty recalling the recent past but can often readily remember childhood memories, which seem more resilient.

The parts of the brain we studied are some of the first regions affected in Alzheimer’s and now we know they are also involved in memory consolidation.”

The study, published in Nature Neuroscience and funded by the Wellcome Trust and Royal Society, investigated the role of sleep in memory consolidation by simultaneously studying two areas of the brain as the rats rested following activity.

Six rats each ran for 30 minutes on a six metre long track before resting for 90 minutes. During rest, the team studied the responses of place cells in the hippocampus, where memories are formed, and grid cells in the entorhinal cortex, where the memories were found to transfer to.

The response of the place cells showed that the rats re-ran the track in their minds as they rested but did so at speeds 10-20 times faster than they experienced in reality. The same replay happened almost simultaneously, with a 10 millisecond delay, in grid cells located in a different part of the brain, suggesting that the rats’ memories transferred from one part of the brain to another.

Study supervisor, Dr Caswell Barry (UCL Cell & Developmental Biology), said: “This is the first time we’ve seen coordinated replay between two areas of the brain known to be important for memory, suggesting a filing of memories from one area to another. The hippocampus constantly absorbs information but it seems it can’t store everything so replays the important memories for long term storage and transfers them to the entorhinal cortex, and possibly on to other areas of the brain, for safe-keeping and easy access.”

The scientists plan to investigate memory transfer to other areas of the brain and replay in rats with Alzheimer’s disease to better understand the memory consolidation mechanism and the link between quality of sleep and amnesiac conditions.

{An unexpected discovery has led to a rechargeable battery that’s as inexpensive as conventional car batteries, but has a much higher energy density. The new battery could become a cost-effective, environmentally friendly alternative for storing renewable energy and supporting the power grid.
}

A team based at the Department of Energy’s Pacific Northwest National Laboratory identified this energy storage gem after realizing the new battery works in a different way than they had assumed. The journal Nature Energy published a paper today that describes the battery.

“The idea of a rechargeable zinc-manganese battery isn’t new; researchers have been studying them as an inexpensive, safe alternative to lithium-ion batteries since the late 1990s,” said PNNL Laboratory Fellow Jun Liu, the paper’s corresponding author. “But these batteries usually stop working after just a few charges. Our research suggests these failures could have occurred because we failed to control chemical equilibrium in rechargeable zinc-manganese energy storage systems.”

{{Chemically inclined}}

After years of focusing on rechargeable lithium-ion batteries, researchers are used to thinking about the back-and-forth shuttle of lithium ions. Lithium-ion batteries store and release energy through a process called intercalation, which involves lithium ions entering and exiting microscopic spaces in between the atoms of a battery’s two electrodes.

This concept is so engrained in energy storage research that when PNNL scientists, collaborating with the University of Washington, started considering a low-cost, safe alternative to lithium-ion batteries — a rechargeable zinc-manganese oxide battery — they assumed zinc would similarly move in and out of that battery’s electrodes.

After a battery of tests, the team was surprised to realize their device was undergoing an entirely different process. Instead of simply moving the zinc ions around, their zinc-manganese oxide battery was undergoing a reversible chemical reaction that converted its active materials into entirely new ones.

{{Attractive alternative}}

Liu and his colleagues started investigating rechargeable zinc-manganese batteries because they are attractive on paper. They can be as inexpensive as the lead-acid batteries because they use abundant, inexpensive materials (zinc and manganese). And the battery’s energy density can exceed lead-acid batteries. The PNNL scientists hoped they could produce a better-performing battery by digging deeper into the inner workings of the zinc-manganese oxide battery.

So they built their own battery with a negative zinc electrode, a positive manganese dioxide electrode and a water-based electrolyte in between the two. They put small, button-sized test batteries through the wringer, repeatedly charging and discharging them. As others had found before them, their test battery quickly lost its ability to store energy after just a few charging cycles. But why?

{{Detailed investigation}}

To find out, they first performed a detailed chemical and structural analysis of the electrolyte and electrode materials. They were surprised to not find evidence of zinc interacting with manganese oxide during the battery’s charge and discharge processes, as they had initially expected would happen. The unexpected finding led them to wonder if the battery didn’t undergo a simple intercalation process as they had previously thought. Perhaps the zinc-manganese battery is less like a lithium-ion battery and more like the traditional lead-acid battery, which also relies on chemical conversion reactions.

To dig deeper, they examined the electrodes with several advanced instruments with a variety of scientific techniques, including Transmission Electron Microscopy, Nuclear Magnetic Resonance and X-Ray Diffraction. The instruments used were located at both PNNL and the Environmental Molecular Sciences Laboratory (EMSL), a DOE Office of Science user facility located at PNNL. Combining these techniques revealed manganese oxide was reversibly reacting with protons from the water-based electrolyte, which created a new material, zinc hydroxyl sulfate.

Typically, zinc-manganese oxide batteries significantly lose storage capacity after just a few cycles. This happens because manganese from the battery’s positive electrode begins to sluff off, making the battery’s active material inaccessible for energy storage. But after some manganese dissolves into the electrolyte, the battery gradually stabilizes and the storage capacity levels out, though at a much lower level.

{{A simple fix}}

The team used the new knowledge to prevent this manganese sluff-off. Knowing the battery underwent chemical conversions, they determined the rate of manganese dissolution could be slowed down by increasing the electrolyte’s initial manganese concentration.

So they added manganese ions to the electrolyte in a new test battery and put the revised battery through another round of tests. This time around, the test battery was able to reach a storage capacity of285 milliAmpere-hours per gram of manganese oxide over 5,000 cycles, while retaining 92 percent of its initial storage capacity.

“This research shows equilibrium needs to be controlled during a chemical conversion reaction to improve zinc-manganese oxide battery performance,” Liu said. “As a result, zinc-manganese oxide batteries could be a more viable solution for large-scale energy storage than the lithium-ion and lead-acid batteries used to support the grid today.”

The team will continue their studies of the zinc-manganese oxide battery’s fundamental operations. Now that they’ve learned the products of the battery’s chemical conversion reactions, they will move on to identify the various in-between steps to create those products. They will also tinker with the battery’s electrolyte to see how additional changes affect its operation.

This research was supported by DOE’s Office of Science and used resources at the Environmental Molecular Sciences Laboratory (EMSL), a DOE Office of Science user facility located at PNNL.

{Women in the U.S. who live in homes surrounded by more vegetation appear to have significantly lower mortality rates than those who live in areas with less vegetation, according to a new study from Harvard T.H. Chan School of Public Health and Brigham and Women’s Hospital. The study found that women who lived in the greenest surroundings had a 12% lower overall mortality rate than those living in homes in the least green areas.}

The study suggests several mechanisms that might be at play in the link between greenness and mortality. Improved mental health, measured through lower levels of depression, was estimated to explain nearly 30% of the benefit from living around greater vegetation. Increased opportunities for social engagement, higher physical activity, and lower exposure to air pollution may also play an important role, the authors said.

The study will be published online April 14, 2016 in the journal Environmental Health Perspectives.

“We were surprised to observe such strong associations between increased exposure to greenness and lower mortality rates,” said Peter James, research associate in the Harvard Chan School Department of Epidemiology. “We were even more surprised to find evidence that a large proportion of the benefit from high levels of vegetation seems to be connected with improved mental health.”

Previous studies have suggested that exposure to vegetation was related to lower mortality rates, but those studies were limited in scope, and some had contradictory findings. The new study is the first to take a nationwide look at the link between greenness and mortality over a period of several years.

The study incorporated data on 108,630 women enrolled in the Nurses’ Health Study across the United States in 2000-2008. The researchers compared the participants’ risk of mortality with the level of vegetation surrounding their homes, which was calculated using satellite imagery from different seasons and from different years. The researchers accounted for other mortality risk factors, such as age, socioeconomic status, race and ethnicity, and smoking behaviors.

When the researchers looked at specific causes of death among the study participants, they found that associations between higher amounts of greenness and lower mortality were strongest for respiratory-disease and cancer mortality. Women living in areas with the most vegetation had a 34% lower rate of respiratory disease-related mortality and a 13% lower rate of cancer mortality compared with those with the least vegetation around their homes. These more specific findings were consistent with some of the proposed benefits of greener areas, including that they may buffer air pollution and noise exposures and provide opportunities for physical activity.

“We know that planting vegetation can help the environment by reducing wastewater loads, sequestering carbon, and mitigating the effects of climate change. Our new findings suggest a potential co-benefit–improving health–that presents planners, landscape architects, and policy makers with an actionable tool to grow healthier places,” said James.

{How long-term memory is formed is not well understood, and remains a central question of inquiry in neuroscience. Now researchers report they may have an answer to this question.}

Research strongly suggests that sleep, which constitutes about a third of our lives, is crucial for learning and forming long-term memories. But exactly how such memory is formed is not well understood and remains, despite considerable research, a central question of inquiry in neuroscience.

Neuroscientists at the University of California, Riverside report in the Journal of Neuroscience that they now may have an answer to this question. Their study provides for the first time a mechanistic explanation for how deep sleep (also called slow-wave sleep) may be promoting the consolidation of recent memories.

During sleep, human and animal brains are primarily decoupled from sensory input. Nevertheless, the brain remains highly active, showing electrical activity in the form of sharp-wave ripples in the hippocampus (a small region of the brain that forms part of the limbic system) and large-amplitude slow oscillations in the cortex (the outer layer of the cerebrum), reflecting alternating periods of active and silent states of cortical neurons during deep sleep. Traces of episodic memory acquired during wakefulness and initially stored in the hippocampus are progressively transferred to the cortex as long-term memory during sleep.

Using a computational model, the UC Riverside researchers provide a link between electrical activity in the brain during deep sleep and synaptic connections between neurons. They show that patterns of slow oscillations in the cortex, which their model spontaneously generates, are influenced by the hippocampal sharp-wave ripples and that these patterns of slow oscillations determine synaptic changes in the cortex. (Change in synaptic strength is widely believed to underlie learning and memory storage in the brain.) The model shows that the synaptic changes, in turn, affect the patterns of slow oscillations, promoting a kind of reinforcement and replay of specific firing sequences of the cortical neurons — representing a replay of specific memory.

“These patterns of slow oscillations remain even without further input from the hippocampus,” said Yina Wei, a postdoctoral researcher and the first author of the research paper. “We interpret these results as a mechanistic explanation for the consolidation of specific memories during deep sleep, whereby the memory traces are formed in the cortex and become independent of the hippocampus.”

Study results appear in the Journal of Neuroscience.

Wei explained that according to the biologically realistic network model the researchers used, input from the hippocampus reaches the cortex during deep sleep and influences how the slow oscillations are initiated and propagated in the cortical network.

“Input from the hippocampus — the sharp-wave ripples — determines the spatial and temporal pattern of these slow oscillations,” she said. “By influencing the nature of these oscillations, this hippocampal input activates selective memories during deep sleep and causes a replay of specific memories. During such memory replay, the corresponding synapses are strengthened for long-term storage in the cortex. These results suggest the importance of the hippocampal sharp-wave ripple events in transferring memory information to the cortex.”

Normal sleep, during which brain activity remains high, is made up of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. NREM and REM sleep alternate in each of the 4-5 cycles during an eight-hour sleep period. Each cycle consists of NREM sleep followed by REM sleep, and roughly lasts 90-110 minutes. NREM sleep has three stages, Stage 3 being deep sleep. Deep sleep, which makes up at least 20 percent of a person’s total sleep time, occurs mostly in the first third of the night.

“In our model, even weak and spatially localized input from the hippocampus influenced the spatiotemporal pattern of slow oscillations and led to a persistent change of synaptic efficacy between neurons,” Wei said. “Further, our model makes predictions that can be tested experimentally, including specific interventions to suppress or augment memory consolidation processes.”

{If you think you know your animal facts very well, you may be in for a major shocker after you read this post.}

There are a lot more to animals than you know, as this post will show/tell you. See for yourself.

1. In China, it’s criminal to kill a panda. Pandas are one of the many protected animals in China, poaching and killing them can attract a death sentence.

2. When you have more than 2 owls gathered in a place, it’s called a ‘parliament’. This is because owls are usually solitary, so they’re considered of great disposition when they’re done together in a group.

3. Bees are known to feed and live off sweet nectar on flowers, however, there is a specie of bee that do not feed on nectar; they feed on human tears. This specie of bees is called the Lisotrigona, and they’re mostly found in Thailand.

4. Bats can fly, but they just can’t walk. This is owing to their very tiny legs, which cannot support their frame.

5. The appropriate name for a flock of parrots is called Pandemonium, and a group of peacocks is called ostentation.

6. Human beings are not the only animals that suffer menopause; elephants also do.

7. All dogs bark, except the Basenji. They are a unique specie of dogs that do not bark, and that is why most people refer to them as the ‘soundless dog’.

8. Mayflies have a lifespan of roughly 8 hours. This means that if a mayfly is given birth to by 8 in the morning, it has from then till 4 in the evening that same day to: grow, mature, mate and eventually die.

9. Tardigrades are a special kind of microscopic animals. They can live and survive under any sort of condition –.cold, radiations, etc, and live comfortably in space or vacuum

10. The Angler fish is a rare creature; it reproduces by an interesting form of attachment. When a male angler fish sees a female, it attaches itself to the female and gradually becomes an organ of the female I.e a part of her body. So the male totally ceases to exist, and the female now has a new organ (a testes) and hence reproduction can occur. Talk about amazing. Lol.

So now, you know a few more things about animals than you did before now; whoever said knowledge could be exhausted? Lol.

{Sometimes forgetting can be harder than remembering. When people forced themselves to forget a recently seen image, select brain activity was higher than when they tried to remember that image.}

Forgetting is often a passive process, one in which the memory slips out of the brain, Tracy Wang of the University of Texas at Austin said April 2 at the annual meeting of the Cognitive Neuroscience Society. But in some cases, forgetting can be deliberate.

Twenty adults saw images of faces, scenes and objects while an fMRI scanner recorded their brains’ reactions to the images. If instructed to forget the preceding image, people were less likely to remember that image later. Researchers used the scan data to build a computer model that could infer how strongly the brain responds to each particular kind of image. In the ventral temporal cortex, a part of the brain above the ear, brain patterns elicited by a particular image were stronger when a participant was told to forget the sight than when instructed to remember it.

Of course, everyone knows that it’s easy to forget something without even trying. But these results show that intentional forgetting isn’t a passive process — the brain has to actively work to wipe out a memory on purpose.

{Research undergone by Brandeis University shines new light on what goes on in the brain when we’re not awake. Contrary to the generally accepted theory of why we sleep, the new work shows that homeostatic rebalancing doesn’t occur during sleep; instead, it happens exclusively when animals are awake and active, leading to the question of what actually happens, then, when we are sleeping.}

Even though slumber consumes about a third of the day for many life forms, we know very little about why it’s needed. The need for sleep remains one of the great mysteries of biology.

A leading theory posits that sleep may provide the brain with an opportunity to “rebalance” itself. In this model, waking experiences are associated with powerful processes of learning and development that, over time, result in the saturation of our brains’ ability to strengthen connections. Not only would this prevent further learning, but this unbounded increase in connectivity would destabilize the brain, leading to “overexcitation” of neural networks. A leading theory suggests that the core function of sleep is “neuronal homeostasis,” the processes whereby neurons self-tune their excitability to restore balanced activity to brain circuits.

Brand new research conducted in the lab of Brandeis neurobiologist Gina Turrigiano suggests this theory isn’t true. In a paper published in the March 24th issue of the journal Cell, the Turrigiano lab showed that when the activity of neurons is suppressed in rats, homeostatic rebalancing doesn’t occur during sleep; instead, it happened exclusively when animals were awake and active.

This research poses as many questions as it answers. For example, why is homeostasis inhibited during sleep? Turrigiano suggests that homeostatic plasticity may interfere with a sleep-dependent process that strengthens memories. Using behavioral states such as sleep and wake to temporally segregate distinct forms of plasticity may alleviate this interference problem.

Gina Turrigiano is the Joseph J. Levitan Chair in Visual Sciences at Brandeis, and was elected to the National Academy of Sciences in 2013. In 2000, at the age of 37, she won a MacArthur Fellowship, or ‘genius’ award. Her groundbreaking work has focused on the cellular processes that allow neuronal circuits in the brain to change and adapt. Her lab has played a major role in identifying the key mechanisms underlying homeostatic plasticity, or a neuron’s ability to dynamically seek stability despite changes induced by learning or development.

This latest research in Cell, led by postdoctoral fellow Keith Hengen, broke new ground as it explored neuronal homeostasis in the context of freely behaving rats (most research in the past has relied upon cell cultures or anesthetized animals). In this work, rats with occlusion of vision from one eye were observed over nine days during sleep and wake periods. Electrodes inserted in the animals’ visual cortex recorded the firings of many individual neurons; these neurons were then followed for nine days, producing a total of six terabytes of data. Algorithms developed in Turrigiano’s lab with the help of Brandeis assistant professor Steven Van Hooser enabled the analysis of these enormous and complex datasets.

Turrigiano expects these computational methods to open new avenues of research for her lab, enabling far longer observation of rats’ brains and with greater precision.

Some of the key questions arising from the study include:

• What it is about sleep that impedes homeostasis?

• How is it possible for the brain to quickly shift in and out of periods of homeostasis depending on the sleep state?

• What is it about being awake that incites and necessitates the activation of homeostatic regulation?

{New cancer-fighting nanoparticles deliver results — and status reports. }

Tiny biochemical bundles carry chemotherapy drugs into tumors and light up when surrounding cancer cells start dying. Future iterations of these lab-made particles could allow doctors to monitor the effects of cancer treatment in real time, researchers report the week of March 28 in the Proceedings of the National Academy of Sciences.

“This is the first system that allows you to read out whether your drug is working or not,” says study coauthor Shiladitya Sengupta, a bioengineer at Brigham and Women’s Hospital in Boston.

Each roughly 100-nanometer-wide particle consists of a drug and a fluorescent dye linked to a coiled molecular chain. Before the particles enter cells, the dye is tethered to a “quencher” molecule that prevents it from lighting up. When injected into the bloodstream of a mouse with cancer, the nanoparticles accumulate in tumor cells and release the drug, which activates a protein that tears a cancer cell apart. This cell-splitting protein not only kills the tumor cell, but also severs the link between the dye and the quencher, allowing the nanoparticles to glow under infrared light.

Previous techniques could track drugs entering tumors, but that “doesn’t necessarily tell you whether the drug is working or not,” says study coauthor Ashish Kulkarni, a bioengineer at Brigham and Women’s and at Harvard Medical School.

The team tested the nanoparticles in mice that each had two types of tumor: one resistant to the drug in the particles and one responsive to the drug. Drug-sensitive tumors glowed around five times as intensely as the resistant tumors. Results were swift, with tumors lighting up in eight to 12 hours.

Replacing the particles’ cancer drug with antibodies that summoned the body’s tumor-fighting defenses allowed the team to test the nanoparticles as immunotherapy agents. In this case, tumors lit up after five days, reflecting an initial lag time of immunotherapy compared with chemotherapy.

These nanoparticles are a proof of concept, Sengupta says. Next steps include redesigning the nanoparticles using clinically approved materials and dyes that would be easier to track in the human body with the use of an MRI machine. But such imaging chemicals can be toxic, which could pose a problem for the nanoparticle design, says cancer nanotechnologist Mansoor Amiji of Northeastern University in Boston.

Dyes should be cleared from the body as quickly as possible, while the drug they’re paired with might take weeks to work. But the study’s focus on detecting drug performance in real time is very important, and demands further study, Amiji says. “There’s tremendous need, especially as we think about personalizing cancer therapies.”

{Some people infected with HIV naturally produce antibodies that effectively neutralize many strains of the rapidly mutating virus, and scientists are working to develop a vaccine capable of inducing such “broadly neutralizing” antibodies that can prevent HIV infection.}

An emerging vaccine strategy involves immunizing people with a series of different engineered HIV proteins as immunogens to teach the immune system to produce broadly neutralizing antibodies against HIV. This strategy depends on the ability of the first immunogen to bind and activate special cells, known as broadly neutralizing antibody precursor B cells, which have the potential to develop into broadly neutralizing antibody-producing B cells.

A research team has now found that the right precursor (“germline”) cells for one kind of HIV broadly neutralizing antibody are present in most people, and has described the design of an HIV vaccine germline-targeting immunogen capable of binding those B cells. The findings by scientists from The Scripps Research Institute (TSRI), the International AIDS Vaccine Initiative (IAVI) and the La Jolla Institute for Allergy and Immunology were published in Science on March 25.

“We found that almost everybody has these broadly neutralizing antibody precursors, and that a precisely engineered protein can bind to these cells that have potential to develop into HIV broadly neutralizing antibody-producing cells, even in the presence of competition from other immune cells,” said the study’s lead author, William Schief, TSRI professor and director, Vaccine Design of the IAVI Neutralizing Antibody Center at TSRI, in whose lab the engineered HIV vaccine protein was developed.

The body’s immune system contains a large pool of different precursor B cells so it can respond to a wide variety of pathogens. But that also means that precursor B cells able to recognize a specific feature on a virus surface are exceedingly rare within the total pool of B cells.

“The challenge for vaccine developers is to determine if an immunogen can present a particular viral surface in a way that distinct B cells can be activated, proliferate and be useful,” said study co-author Shane Crotty, professor at the La Jolla Institute. “Using a new technique, we were able to show — well in advance of clinical trials — that most humans actually have the right B cells that will bind to this vaccine candidate. It is remarkable that protein design can be so specific as to ‘find’ one in a million cells, demonstrating the feasibility of this new vaccine strategy.”

The work offers encouraging insights for a planned Phase 1 clinical trial to test a nanoparticle version of the engineered HIV vaccine protein, the “eOD-GT8 60mer.” “The goal of the clinical study will be to test safety and the ability of this engineered protein to elicit the desired immune response in humans that would look like the start of broadly neutralizing antibody development,” Schief said. “Data from this new study was also important for designing the clinical trial, including the size and the methods of analysis.”

In June, scientists from TSRI, IAVI and The Rockefeller University reported that the eOD-GT8 60mer produced antibody responses in mice that showed some of the traits necessary to recognize and inhibit HIV. If the eOD-GT8 60mer performs similarly in humans, additional boost immunogens are thought to be needed to ultimately induce broadly neutralizing antibodies that can block HIV.

The new work also provides a method for researchers to assess whether other new vaccine proteins can bind their intended precursor B cells. This method is a valuable tool in the design of more targeted and effective vaccines against AIDS, providing the ability to vet germline-targeting immunogens before testing them in large, time-consuming and costly clinical trials.

Looking at blood donated by healthy volunteers, the scientists found B cells that were capable of creating “VRC01-class” antibodies that recognized a critical surface patch, or epitope, of HIV. VRC01-class broadly neutralizing antibodies are a group of antibodies isolated from different individuals that appear to have developed in a very similar way, and it has been hypothesized that the starting VRC01-class B cells were very similar in the different people. The eOD-GT8 60mer is designed to engage these precursor B cells to initiate HIV broadly neutralizing antibody development.

{If you are earning less than you think you should, it just might be certain physical traits you have.}

According to a study published in the scientific journal BMJ, being a genetically overweight woman or a short man is correlated with a lower salary.

The researchers found that for every 2.5 inches of “genetically determined” extra height in men, men earned around $1,611 more per year and were 12 percent more likely to work in high-status jobs.

While for every 4.6-point increase in BMI for women, they earned an average of $4,200 less per year.

119,669 men and women were used for the study.

It’s really sad that the society places way too much importance on looks.