Discovery

 

Mom’s Mitochondria Affect

Pup Longevity Mitochondrial mutations inherited from the mother can shorten a mouse’s lifespan.  lifespan.  

A person’s lifespan may be determined in part before they are even born, if research published today (October 9) in Scientific Reports translates from mice to humans. The new study shows that mitochondrial DNA mutations in the mother’s eggs can shorten her pups’

lives by approximately one third.  “The overriding importance importance of this kind of work work is the demonstration that that the mitochondrial

DNA, which is maternally inherited, carries the genetic information that can be critical for longevity,” said  said Douglas Wallace, Wallace, a professor of pathology and laboratory l aboratory medicine at the Children’s Hospital of Philadelphia. Wallace was not involved in the new study, but

has independently shown  has  shown that maternally inherited mitochondrial mutations can influence aging, longevity, and cancer. The new paper follows up on a  a  study published last year  year in Nature, which showed, among other results, that mutated mitochondrial DNA from mom is sufficient to cause premature aging in an otherwise wild-type mouse—a finding that  that Gerald Shadel, Shadel, a professor of pathology and genetics at Yale University, described as “a real breakthrough.”   But because of the hurry to publish the novel findings, “what we didn’t know at the time ti me was whether or not their lifespan was going to be affected,” said the Karolinska Institute’s Jaime Ross, Ross, lead author of both the Scientific Reports and Nature papers. That

would take another year or so of waiting for the animals to die. Now those results are in. The mice that inherited i nherited mutant mitochondrial DNA showed an average lifespan of 100 weeks compared with 141 weeks for control mice.  mice.  Douglas Turnbull, Turnbull,  a professor of neurology at Newcastle University in the U.K. who was not involved in the research, described the result as “interesting “i nteresting but not surprising” because animals that age

prematurely would be expected to die young. What is not yet known is how mitochondrial DNA lifespan. Dysfunctional mitochondria could impair cellular metabolism andmutations lead to a shorten variety of problems, such as the accumulation of damaging reactive oxygen species, reduced vitality of stem cells, and reduced DNA repair, leading to the accumulation of damage to the genome in the nucleus.  “Aging is a complex process process and involves so so many different facets,” facets,” said Ross, “so “so maybe it’s a little bit of everything that together keeps on beating down the organism a little at a time.”  

But regardless of the mechanism, or mechanisms, by which damaged mitochondria mit ochondria affect aging, the finding that such mutations can cause transgenerational effects has reproductive implications. For example, mitochondrial mutations tend to accumulate with age in a person’s somatic tissues, and it is i s thought that this also occurs in the egg, said Wallace. If so, older mothers could be passing on more mitochondrial mutations than younger mothers.  “If, in theory, we were able able to measure these mutations, mutations, we could say say to ourselves, OK, if they get higher than this threshold in the mom’s egg, what can we do about it?” Ross said.  “Maybe there are interventions.” interventions.” Pharmaceutical Pharmaceutical or nutritional approaches approaches may help, she said, as might three-parent in vitro fertilization —a technique that enables a woman carrying

severe disease-causing mitochondrial mutations to avoid passing the disease to her offspring by injecting a nucleus from one of her h er eggs into a healthy woman’s egg, which

carries unaffected mitochondria. The technique is  is  expected to be available in the U.K. in a years.  few years.

 

As for the rest of us who may worry about the state of the mitochondria we’ve inherited ,

there is evidence that in mitochondrial mutation-carrying mice prone to premature aging exercise can slow the aging process. “We can change our fate, that’s the good news,” said

Ross.

 

Beneficial Brew Drinking green tea appears to boost the activity of DNA repair enzymes.

EDITOR'S CHOICE IN CELL & MOLECULAR BIOLOGY  The paper  C.K. Ho et al., “Effects of single dose and regular intake of green tea (Camellia ( Camellia sinensis) on DNA damage, DNA repair, and heme oxygenase-1 expression in a randomized controlled human supplementation study,”  Mol Nutr Food Res,doi:10.1002/mnfr.201300751, 2014. The context  Researchers have long reported that green tea drinkers have better health outcomes, but why that is has been unclear. To get to the cellular roots of these observations, Iris Benzie of the Hong Kong Polytechnic University and her colleagues monitored the activity of DNA repair enzymes in lymphocytes shortly after people drank a cup of green tea and after a week of drinking two cups of tea each day. The findings  An enzyme critical for fixing DNA damage from oxidation, hOGG1, and another that protects against such damage, heme oxygenase-1 (HMOX-1), were more active after the 16 study participants drank tea, compared to when they drank water. The team also found 30 percent less DNA damage in lymphocytes 60 minutes after a cup of tea. Benzie says the finding “opens up a whole new avenue to look at the molecular mechanisms” of green tea’s effect on cells.   The mechanism  Genes coding for hOGG1 and HMOX-1 did not show an increase in expression. The authors speculate -lives or their ability to that green tea triggers posttranslational changes that prolong the enzymes’ half -lives protect and repair DNA. There’s also the possibility that increased HMOX -1 could be a sign of oxidative stress induced by green tea that prompts antioxidant defense and enhanced DNA repair. Another cup   “It’s a good preliminary study,” says Sus Susanne Henning of the University of California, Los Angeles. She recommends studying animal models for a clearer understanding of the molecular mechanism in all tissue types. It also remains to be seen whether the changes Benzie observed actually correspond to any health benefits.

 

Cone Cell Correctors In mice, adult cone cell outer segments and their visual functions deteriorate if two microRNAs are not present.

The paper  V. Busskamp et al., “miRNAs 182 and 183 are necessary to maintain adult cone photoreceptor outer segments and visual function,”  Neuron, 83:586-600, 2014. The background  In retinal photoreceptors, the conversion of light to an electrical signal occurs in an organelle known as the outer segment. Malfunctioning outer segments are linked to cone cell diseases and blindness. Previous studies have shown microRNAs (miRNAs)—noncoding RNAs that repress gene expression— are essential to normal cone cell development, but how they operate in adult retinas was unclear. The experiment  Botond Roska of the Friedrich Miescher Institute for Biomedical Research in Switzerland and his colleagues developed knockout mice and in vitro models in which all miRNAs were depleted in fully formed retinas. Lacking miRNAs, cone cells lost their outer segments and showed reduced responses to light, but the cells did not degenerate. “Finding a phenotype where the cells lose the outer segment but stay absolutely intact was very unexpected,” says Roska. Reexpressing two of the most abundant cone miRNAs, miR-182 and miR-183, restored outer segments and normal light responses in cultured retinal cells. The functions  These two miRNAs are thought to play a role in lipid metabolism within cells. Roska speculates that they may help regulate a supply of lipids and other molecules to cone cells’ apical membranes to renew outer segments.

 

Protein Helps Cells Adapt— or Die Scientists show how cell stress both prevents and promotes cell suicide in a study that’s equally divisive.

A cellular stress pathway called the unfolded-protein-response (UPR) both activates and degrades death receptor 5 protein (DR5), which can promote or prevent cell suicide, according to a paper published in Science today (July 3). The theory is that initial stress blocks cell suicide, or apoptosis, to give the cell a chance to adapt, but that if the stress persists, it eventually triggers apoptosis.  “This work has made the most beautiful simplification of of all this big complex mess.

Basically, they identified and pinpointed the specific protein involved in i n the switching decision and explain how the decision is made,” said  Alexei Korennykh, Korennykh, a professor of molecular biology at Princeton University, who was not involved in the work. But Randal Kaufman  But  Kaufman of the Sanford-Burnham Medical Research Institute in La Jolla, California, was not impressed. He questioned the physiological relevance of the experiments supporting the authors’ main conclusions about this key cellular process.  Protein folding in a cell takes place largely in the endoplasmic reticulum (ER), but if the process goes awry, unfolded proteins accumulate, stressing the ER. This triggers the UPR, which shuts down translation, degrades unfolded proteins, and increases production of protein-folding machinery. If ER stress is not resolved, however, the UPR can also induce apoptosis. Two main factors control the UPR—IRE1a and PERK. IRE1a promotes cell survival by activating the transcription factor XBP1, which drives expression of cell-survival genes. PERK, on the other hand, activates a transcription factor called CHOP, which in turn drives expression of the proapoptotic factor DR5. Peter Walter  Walter of the University of California, San Francisco, and his colleagues have now confirmed that CHOP activates DR5, showing that it isdegrading a cell-autonomous cell -autonomous process. aBut process. they have also found that IRE1a suppresses DR5, directly its mRNA through process called regulated IRE1a-dependent degradation (RIDD). Inhibition of IRE1a in a human cancer cell line undergoing ER stress both prevented DR5 mRNA decay and increased apoptosis. However, in an e-mail to The Scientist , Kaufman expressed concern that “the significance of RIDD has not been demonstrated in a physiologically-relevant context.”   Walter insisted that the evidence for RIDD’s existence is “crystal clear.” His only concession was that “the effects aren’t 100 percent,” he said, because “RIDD degrades mRNA by a few fold,” making it difficult to measure. 

This RIDD debate aside, the researchers have also sparked a rumpus with their finding that IRE1a expression switches off just 24 hours after ER stress initiation, leaving PERK to drive the cell toward apoptosis. “We and others have evidence that suggests another model,”

said  Scott Oakes, said Oakes, a professor of pathology at the University Uni versity of California, San Francisco,  “which is that both PERK PERK and IRE1a under under high stress will send out out death signals.”   Whether IRE1a promotes or inhibits apoptosis under extreme stress “is controversial,” said  Ira Tabas, a professor at Columbia University in New York City. But it’s essential that said scientists figure it out. Cell death from ER stress is a pathological process in many major diseases, Tabas said, and there are IRE1a inhibitors in pharmaceutical development. “ It is

 

very important because under high stress you have two different views here,” said Oakes.  “One is that you want want to keep IRE1a on, the other other is that you want to shut it off.”   Because ER stress is central to many diseases, “a lot of people are passionate about it,” said Tabas, explaining the polemic views. “Who’s right? . . . I think it depends on the context in which the experiments are done—one pathway may be important in some settings, and another pathway may be important in different settings,” he su ggested. What might help to resolve the issues, he said, will be “in vivo causation studies using actual disease models.”   Researchers will continue to debate. So, said Walter, “we’ll have to see what holds -up five years from now.”  

 

Heritable Histones Scientists show how roundworm daughter cells remember the histone modification patterns of their parents.

After DNA replication and division, cells generally remember which of their genes should be active and which repressed—but how? A study in worms published today (September 18) in Science reveals that part of the mechanism involves divvying up modified histones— molecular tags that label active or repressed genes —between daughter chromosomes at replication. Researchers from the University of California, Santa Cruz and Indiana University, Bloomington, found that although the tags in each chromosome are reduced as a result of division, subsequent recruitment of histone-modifying enzymes reestablishes the full tag quota, thus preserving the memory of modifications for the next round of division. divi sion.  “They show very elegantly elegantly using their system system that modified histones can can be inherited through multiple rounds of cell division and can be passed on . . . to the next generation,”

said  Shiv Grewal, said Grewal, an epigenetics and chromatin researcher at the National Cancer Institute who was not involved in the work. “That’s quite remarkable.”  

Histones, the proteins around which DNA is wrapped to form chromatin, can be modified modifi ed by the addition a various moieties. And such modifications are thought to represent —and even influence—the transcriptional activity of associated genes. Although the presence of these modifications at given genomic locations can be inherited from a parent cell to its daughters, exactly how this landscape of histone modifications is reestablished after DNA replication—when the histones are temporarily evicted from DNA —was unclear.  “There’s been a lot of of debate about whether histone modifications modifications can be heritable,” heritable,” said Bill

Kelly,, a biologist at Emory University in Atlanta, Georgia, who was not involved in the study. Kelly  “When you replicate the DNA you have to replicate repli cate the histones . . . and de novo synthesized histones don’t have marks put there by transcription or repression,” he

explained. There have been two theories as to how histone modification patterns might be remembered, said Santa Cruz’s Susan Strome, Strome, the professor of molecular, cell, and developmental biology who led the new study. One theory suggests “histone modifications

on the original mother chromosome get split between the two daughter chromosomes and probably diluted,” she said. An opposing theory, however, suggests “histone modifications

are not passed through DNA replication. . . [Instead], the enzyme is passed on and it restores modifications on the two daughter chromosomes.”   Luckily, said Strome, she and her colleagues “were in a position positi on to directly test those two models.” Her team generated Caenorhabditis elegans eggs that lacked an enzyme called

Polycomb repressive complex 2 (PRC2), a histone-modifying enzyme that methylates lysine 27 of histone H3 (H3K27me) —a mark associated with transcriptiona transcriptionall repression. Fusing these roundworm eggs with wild-type sperm resulted in a single-celled si ngle-celled embryo with one set of chromosomes (paternal) dusted with H3K27me marks, and another (maternal) that was not. Because the sperm cannot contribute PRC2 itself, the embryos lacked the enzyme altogether, allowing Strome and colleagues to clearly visualize the fate of the existing H3K27me marks. With each cell division the H3K27me marks became dimmer until, until , by approximately the 48cell stage, they were “below the detection of the microscope,” said Strome. But, importantly, what the researchers could see was that, “histone modifications are indeed passed to the daughter chromosomes—the chromosomes derived from the initial sperm chromosomes—and the oocyte chromosomes, which did not have the mark to begin with, do not acquire it,” she added.  

 

The team then performed a reverse experiment in which the male chromosomes were unmarked and the oocytes contained both H3K27me marks and PRC2. This time the signal did not become dimmer with each division, because PRC2 was able to reestablish the mark. But, said Strome, “what was really remarkable for us to see was that, even wit h active enzyme, the H3K27me marking was restricted to the parent-of- origin chromosome.” This ability to recreate marks only at their original chromosome locations was, said Strome, “the hallmark of memory.”   According to Kelly, the results suggest “that af ter ter replication there is sufficient information there that it can be targeted by the maintenance system”—the histone-modifying enzymes.

Indeed, the mammalian PRC2 is capable of both binding to H3K27me as well as creating the mark, explained Strome. The findings have implications not only for cellular inheritance of epigenetic marks but also transgenerationall inheritance, which “a lot of people transgenerationa p eople suspect,” said Grewal, but for which  “there is not much evidence.” evidence.” Indeed, added Strome: Strome: “We’re starting to get get a molecular handle on what it means to pass epigenetic information from parent to child —both at the organism and cell level—and our work provides a little window into that.”  

 

Giant DNA Origami Researchers create the largest 3-D DNA structures to date, many times bigger than previously constructed origami shapes.

DNA origami, a strategy devised eight years ago by Paul Rothemund’s group at Caltech,

allows researchers to link DNA scaffolds with smaller bits of the nucleic acid called staples to create desired shapes. The technique is now being used to develop drug-delivery systems and other molecular machines. But the most common technique—using an M13 bacteriophage to generate single-stranded DNA scaffolds of up to 7 kilobases —has restricted the size of the products to tens of square nanometers. Double-stranded DNA could be produced at longer lengths, but was limited limi ted in its ability to fold at a researchers’

will. Now, Thomas LaBean of North Carolina State University and colleagues have devised a solution: using a hybrid virus for DNA production, the researchers can generate scaffolds of up to 51 kilobases kil obases—and they’ve used these to create DNA structures that are hundreds of square nanometers in size, size,Chemical & Engineering News  (C&EN ) reported.  “They’ve achieved something something people have been trying to do for a while,” Rothemund Rothemund told C&EN .

To fold giant pieces of DNA, D NA, LaBean’s team used more than 1,600 staples. According to C&EN , such a task would have cost $7,000 using conventional DNA synthesis. So to reduce the cost, the team repurposed an ink-jet printer to synthesize the DNA, using reusable templates and chips with polymer micropillars, then amplified the produces using PCR.  “We had to do two things to make this viable,” lead lead author Alexandria Alexandria Marchi of Duke

University said in apress release. “First we had to develop a custom scaffold strand that contained 51 kilobases. . . . Second, in order to make this economically feasible, we had to find a cost-effective way of synthesizing staple strands—because we went from needing 220 staple strands to needing more than 1,600.”   Using these two DNA components, the team constructed notched rectangles with surface areas seven times bigger than similar structures made with traditional, M13 phageproduced scaffolds. The researchers reported their results this month (September 1) in  Nano Letters.  in  “These origami can be customized for use in everything from studying studying cell behavior to creating templates for the nanofabrication of electronic components,” LaBean said in the

release.

 

How Hummingbirds Taste Nectar Hummingbirds perceive sweetness through a receptor with which other vertebrates taste Hummingbirds savory foods.

Birds lack the classical vertebrate sweet taste receptor, but evolution has fashioned a new one for hummingbirds from an ancestral savory, or umami, receptor, according to a report published inScience today (August 21). This repurposed receptor has enabled hummingbirds to glug plant nectar while their closest relatives eat insects. i nsects.  “It’s long been a puzzle as as to how hummingbirds detect sweetness and and these investigators, using a whole bunch of different techniques, have pretty much . . . nailed the answer,”

said Gary Beauchamp, said  Beauchamp, director of the Monell Chemical Senses Center in Philadelphia, who was not involved in the work. On the tongues of most vertebrates, the receptor that binds sugars and conveys the sense of sweet taste consists of two subunits called T1R2 and T1R3. When T1R3 is i s paired with the subunit T1R1, on the other hand, savory flavors from meat, cheese, and fish are sensed. The subunit T1R2 is therefore thought to be largely l argely responsible for sweet taste perception. Indeed, mammals that are solely carnivorous have lost the gene encoding T1R2 and mice genetically engineered to lack T1R2 cannot perceive sweetness. Birds have varied diets—seeds, insects, fish, fruits, and nectars are all on the avian menu— but they lack the gene for f or T1R2. “This raised a very interesting mystery as to how these animals can detect sugar,” said  Stephen Liberles, Liberles, a professor of cell biology at Harvard

Medical School, who led the new study. To solve the mystery, Liberles turned to perhaps the most sweet-toothed bird of all —the hummingbird. His team cloned taste receptors from hummingbirds —which consume more than their own body weight in nectar each day—as well as from their closest relative, the insect-eating chimney swift, and the sugar-insensitive chicken. The researchers also examined taste receptors in the available genomes of 10 other bird bi rd species. Although none of the birds possessed T1R2, they all possessed T1R1 and T1R3. And in the hummingbird, these genes revealed mutations that appeared to be under positive selection —that is, the proportion of protein-altering mutations were greater than expected by chance. The team expressed the hummingbird, chimney swift, and chicken T1R1-T1R3 receptors in cultured cells and discovered that while the swift and chicken receptors responded robustly to amino acids—as would be expected for the savory taste receptor —the hummingbird receptor did not. Instead it produced a strong response to sugars. The team then made chimeric T1R1-T1R3 receptors—using parts from the hummingbird genes and parts from the chicken genes —and found widespread mutations over both T1R1 and T1R3 that conveyed the switch from savory to sugar detection. “[The paper] does a very nice job of putting a molecular explanation on to a very specific type of ecological and behavioral response in hummingbirds—their very specific diet,” said Steven Munger, Munger,  associate director of the Center for Smell and Taste at the University of Florida, Gainesville, who was not involved in the work.  “It’s a really nice example example of how a change in one receptor can drive a complex behavioral phenotype and ultimately drive the evolution of a new species,” added Liberles, who

explained that the acquisition of nectar-eating behavior in hummingbirds had allowed them to expand into a novel ecologi cal niche. These birds have undergone “massive radiation,” he

 

added—there are more than 300 species of hummingbird throughout North and South America. One outstanding question is whether evolution has come up with the same solution for other sweet-toothed birds. “I’m sure people, the day after this is published, will madly start trying to answer [that],” said Beauchamp. 

 

Rare Fat Keeps Fly from Freezing Researchers report the first evidence e vidence of cryopreservation by an overwintering insect in which stores of an uncommon lipid are critical.

During the North American winter, when most animals try to escape the cold, the t he Goldenrod gall fly (Eurosta solidaginis) stays put and freezes nearly solid. But pockets of liquid li quid life remain within the fly, allowing the insect i nsect to resume its activities come spring. According to a study published today (April 30) in  in  The Journal of Experimental Biology , E. solidaginis possesses a secret antifreeze weapon —a rare lipid. Until now, only one type of lipid was thought to have antifreeze properties, according to study coauthor  coauthor Brent Sinclair  Sinclair from the Western University in Ontario: “antifreeze glycolipids, [which were] discovered a few years ago by Jack Duman and colleagues at University of Notre Dame.”  

The parasitic fly preys on a specific plant host —the Canada goldenrod, Solidago canadensis, a relative of the sunflower. Adult gall flies mate and lay eggs at the tips of emerging goldenrod stems. Larvae burrow into the stems, inducing galls via plant growth hormonemimicking substances in their saliva. The larvae mature by late summer and over-winter inside the galls, later to emerge unscathed from temperatures as low as -80°C. Overwintering larvae store carbohydrates and lipids in special fat body cells, which survive intracellular freezing. This first amazed the late  late Reginald Salt  Salt at the Canadian Agricultural Research Station at Alberta in 1959, while he was studying E. solidaginis in the field—he observed clear lipid droplets inside the larval insects’ fr ozen fat body cells. Eager to determine the contents of these droplets, Western’s  Katie Marshall  Marshall and her

colleagues collected galls from goldenrod plants from fields in nearby London, Ontario, O ntario, during the 2011-12 winter. The researchers ground up insects, dissolved them in organic solvents, and separated the lipids according to molecular weight using thin layer l ayer chromatography/flame chromatogra phy/flame ionization detection. Most animals store fats as long-chain triacylglycerols (lcTAGs), lipids made of three fatty acid chains bound together by glycerol. But in the gall fly larvae collected before winter, the researchers found that common lcTAGs made up hardly a quarter of the lipids. Nearly 46 percent were rare lipids—acetylated triacylglycerols (acTAGs), which are triglycerides with an acetyl group attached to one of the fatty-acid chains. The acetyl group in acTAGs changes the way the molecules interact with water—they don’t repel it as much as lcTAGs do, allowing the lipids to interact with other cellular components. And acTAGs lower the cell’s overall freezing temperature.  Marshall and her colleagues were the first to report finding an animal with a lipid pool dominated by acTAGs.  “We have two hypotheses hypotheses at the moment about how acTAGs prevent tissue damage: the

acetyl group might help the molecule to function like an antifreeze, or it may just be that acTAGs remain liquid enough to reduce the mechanical damage that happens during cytoplasmic freezing,” Marshall explained in an e-mail to The Scientist . Because of low temperature-induced freezing stress, the gall fly starts producing acTAGs in early autumn, while the levels of lcTAG remain constant. During spring, the process reverses: in their analysis, the researchers for that the amount of lcTAG increased while the amount of acTAG decreased, both by the same relative amounts. This caused the team to

 

speculate that the fly was converting lcTAGs into acTAGs during winter and then back to lcTAGs in spring.  “Modification of lcTAGs to produce acTAGs with their unique stereochemistry would be quite complicated based on what we know about TAG synthesis,” said biochemist  Timothy

Durrett  from Kansas State University, who studies acTAGs in plants but was not involved in Durrett the study. “If the authors’ claim about the method of acTAG synthesis in the gall fly fl y is correct, it will be extremely interesting to isolate the enzymes involved in that process.”  

John Ohlrogge, Ohlrogge, a plant biologist at Michigan State University, University, was more cautious cautious about the authors’ interpretations. “I feel the evidence that the insects produce acTAG is a very important observation,” he wrote in an e -mail. “But there is no direct di rect evidence to support the freezing hypothesis, or the biosynthesis from lcTAG.”  

Nevertheless, the researchers maintained that their study serves to enhance researchers’ understanding of lipids for cryopreservation. “We speculate that the unique conditions of Eurosta fat body cells—lots of lipid, intracellular freezing —may have made acTAGS selectively advantageous,” said Sinclair. “Possibly, this is the only species to have evolved this molecule for this purpose.”    “If we could find a biological biological way to make lcTAGs lcTAGs into acTAGs, like fermentation, fermentation, it would make it relatively easy to make acTAGs which stay liquid in i n the cold,” he added. “This will make them more useful as biofuels in cold places.”  

 

Artificial Blood Is PatientReady In the midst of news that engineered organs are being implanted into animals and people, researchers announce the creation of artificial blood for transplant.

A new source of blood could be just around the corner: red blood cells grown from fibroblasts that have been reprogrammed into mature red blood cells in the lab. The blood, developed by researchers at the University of Edinburgh and the Scottish Scotti sh National Blood Transfusion Service (SNBTS), would be Type O negative, also known as universal donor blood, which currently comprises just 7 percent of the blood donor pool.  “We have made red blood blood cells that are fit to go in a person’s body,” project project leader Marc Turner, medical director at SNBTS, told  told Forbes Forbes.. “Before now, we haven’t really had that.”  

The blood is created by dedifferentiating fibroblasts from an adult donor and reprogramming them into induced pluripotent stem cells (iPSCs), which are then cultured in a bone-marrowlike environment for a month. Blood cells are then extracted from the cell culture. If the technique can be scaled up to industrial i ndustrial levels (which is no trivial task), beyond potentially supplying an endless supply of life-giving blood, the artificial blood would consist entirely of young, healthy, and infection-free cells, avoiding the issues of pathogen contamination that have in the past plagued the donor blood bl ood supply.  “Although similar research research has been conducted conducted elsewhere, this is the first time anybody has

manufactured blood to the appropriate quality and safety standards for transfusion into a human being,” Turner told  told The Telegraph.  The artificial blood could be transfused into patients in a clinical trial setting as early as 2016, likely for three patients suffering from a genetic g enetic disorder called thalassaemia, in which the body makes unusually low levels of hemoglobin —a problem that is treated frequent transfusions.

 

Exercise Can Erase Memories Running causes rodents to forget their fears in part because of increased hippocampal neurogenesis, a study shows.

Adult mice that exercised on a running wheel after experiencing an event were more likely than their inactive mates to forget the experience, according to a paper from researchers at the University of Toronto, published in  in  Science today (May 8). The results suggest that the production of new neurons —neurogenesis—prompted by the exercise wiped out the mice’s mi ce’s memories. They might also explain why human infants, whose brains exhibit abundant neurogenesis, do not have long-term memories.  “In general, hippocampal hippocampal neurogenesis has been thought to be the basis basis for memory and they’re suggesting that it’s the basis for amnesia,” said Thomas Insel, Insel, director of the National Institute of Mental Health. “That’s a very controversial and provocative concept.”  

Infantile amnesia is common to all humans. Children typically do not develop long-term memories until age three or four. But why is i s that?  that? Sheena Josselyn  Josselyn and her husband  husband Paul Frankland,, who are both neuroscientists at the University of Toronto, pondered precisely Frankland that question after noticing that their two-year-o t wo-year-old ld daughter could easily remember things that happened within a day or two, but not several months in the past. More specifically, they wondered whether it might have something to do with neurogenesis in the hippocampus—a brain region involved in learning and memory. Hippocampal neurons are produced rapidly during infancy, but neuronal generation in the region slows to a trickle t rickle in adulthood. “This inverse relationship between the levels of neurogenesis and the ability to form a long-term memory got us thinking that maybe one is i s due to the other,” said

Josselyn. Running is known to boost neurogenesis in mice. So, to test whether neurogenesis might impair memory, Josselyn and Frankland first taught mice to fear a particular environment— the researchers placed the animals in a distinctive box and gave them electric el ectric shocks—and then provided them with access to a running wheel or let them remain sedentary. When the mice were returned to the box after a day or a week, both groups of animals tended to recognize the now-familiar environment and freeze —a fear response. But if the mice mi ce were returned to the box after two weeks or more, only the sedentary mice froze. The exercisers seemed to have forgotten their fears. Running imposes physiological changes aside from neurogenesis, of course, but the team saw the same failure in memory recall when they specifically increased neurogenesis pharmacologically in the mice. They also found that inhibiting neurogenesis in exercising mice and in infant mice made the animals better at remembering. The team also showed that rodents such as guinea pigs, which have reduced neurogenesis in infancy compared with mice, tended to remember a fearful experience for much longer than did infant mice. And boosting the guinea pigs’ neurogenesis caused them to forget their fears more readily. As Insel pointed out, previous studies have indicated that neurogenesis in adults is beneficial to learning and memory—a finding that seems at odds with Josselyn and Frankland’s. However, said René Hen, Hen, a professor at the Kavli Institute for Brain Science at Columbia University in New York, “previous findings have mostly been dealing with the role of neurogenesis in encoding novel information”—that is, learning and remembering something new. “Now, in the Frankland study, they are looking not at the ability of encoding

 

novel information, but at forgetting older information. So one way to reconcile the two is to think of it as a trade-off: if you get better at acquiring acqui ring new stuff it maybe at the detriment of keeping old stuff.”   Should the results of this study on rodents cause people to worry that training for a marathon might make them forgetful? “People do always say that r unning clears your mind,” said Josselyn, “and in a sense I would say that’s true.” But clearing one’s mind is not necessarily detrimental, she added. “For instance, I don’t want to remember where I parked my car two weeks ago because that’s going to interf ere ere with me remembering where I

parked it today. . . . We think that neurogenesis and forgetting is an iimportant mportant part of healthy memory. We don’t want to remember absolutely everything.”  

 

 

Ang dengue fever ay isa sa mga karaniwang sakit na natatagpuan sa mga bansang tropica, katulad ng pilipinas. Hindi gaya ng mga malaria, ang kaso ng Dengue Fever sa mga kalunsuran at kasing-dami rin ng mga kaso sakanayunan. Ano nga ba ang solusyon dito? May nagiikot na kampanya sa iwas dengue. Kabilang sa programa ay ang patuloy paglilinis sa lahat ng barangy sa lungsod,pagtrap lungsod,pa gtrap sa mga lamok, information at education materials at paglalagay ng ibapang pangontrol sa pagdami ng lamok sa mga kanal a estero.II. Mas mabuting panatilihin umanong malinis at tuyo ang kapaligiran upang hindi mabigyang daan ang pangingitlog ng dengue lamok sa lahat ng oras dahil ikinukunsindera din ng DOH na year-round threat ang dengue lamok sa bansa. Bukod sa paglilinis, tiyakin na napapalitan ang flower vase ng tubig dahil ang dengue lamok ay sa malinaw at malinis na tubig na ngingitlog. Huwag ding ipagwalang-bahala kung nakakaranas ng paglalagnat,pananakit ng ulo at tiyan at pagkakaroon ng rashes sa balat, Dapat umanongmagkons umanongmagkonsulta ulta sa doctor para sa tiyak na kaligtasan.

Ang lamok na tagadala ng Dengue Virus ay nangingitlog sa mga nakaimbak na tubig. Alisin ang tubig o linisin ang mga lugar o bagay na pinangingitluga pinangingitlugan n ng lamok. Karaniwan dito ay ang mga lumang gulong, paso, alulod, lata, bao ng niyog at kung anu-ano pa. Huwag mag-imbak ng basura. Isa sa mga dahilan ng pagdami ng lamok ay mga basura.Takpan lahat ang mga tubig na iniimbak dahil gusto ng mga lamok na mangitlog sa malinis na tubig. Gumamit ng kulambo sa pagtulog o lagyan ng mga screen ang bintana at pinto. Kung may nararamdamang sintomas, ipagbigay-alam agad sa inyong mga doktor upang malunasan ng maaga ang karamdamang ito.