Moms Mitochondria Affect

Pup Longevity
Mitochondrial mutations inherited from the mother can shorten a mouses lifespan.

A persons 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 mothers eggs can shorten her pups
lives by approximately one third.
The overriding importance of this kind of work is the demonstration that the mitochondrial
DNA, which is maternally inherited, carries the genetic information that can be critical for
longevity, said Douglas Wallace, a professor of pathology and laboratory medicine at the
Childrens Hospital of Philadelphia. Wallace was not involved in the new study, but
has independently shown that maternally inherited mitochondrial mutations can influence
aging, longevity, and cancer.
The new paper follows up on a study published last 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 mousea finding that Gerald 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 didnt know at the time
was whether or not their lifespan was going to be affected, said the Karolinska
Institutes Jaime 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 mutant mitochondrial DNA showed an
average lifespan of 100 weeks compared with 141 weeks for control mice. Douglas Turnbull,
a professor of neurology at Newcastle University in the U.K. who was not involved in the
research, described the result as interesting but not surprising because animals that age
prematurely would be expected to die young.
What is not yet known is how mitochondrial DNA mutations shorten lifespan. Dysfunctional
mitochondria could impair cellular metabolism and lead to a 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 and involves so many different facets, said Ross, so maybe
its 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 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
persons somatic tissues, and it is 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 to measure these mutations, we could say to ourselves, OK, if
they get higher than this threshold in the moms egg, what can we do about it? Ross said.
Maybe there are interventions. Pharmaceutical or nutritional approaches may help, she
said, as might three-parent in vitro fertilizationa 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 eggs into a healthy womans egg, which
carries unaffected mitochondria. The technique is expected to be available in the U.K. in a
few years.
As for the rest of us who may worry about the state of the mitochondria weve 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, thats 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 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 teas effect on cells.

The mechanism
Genes coding for hOGG1 and HMOX-1 did not show an increase in expression. The authors speculate
that green tea triggers posttranslational changes that prolong the enzymes half-lives or their ability to
protect and repair DNA. Theres 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
Its a good preliminary study, says 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 thats
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 all this big complex mess.
Basically, they identified and pinpointed the specific protein involved in the switching
decision and explain how the decision is made, said Alexei Korennykh, a professor of
molecular biology at Princeton University, who was not involved in the work.
But Randal 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 UPRIRE1a 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 of the University of California, San Francisco, and his colleagues have now
confirmed that CHOP activates DR5, showing that it is a cell-autonomous process. But they
have also found that IRE1a suppresses DR5, directly degrading its mRNA through a 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 RIDDs existence is crystal clear. His only concession
was that the effects arent 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, a professor of pathology at the University of California, San Francisco,
which is that both PERK and IRE1a under high stress will send 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 its essential that
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 to keep IRE1a on, the 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. Whos right? . . . I think it depends on the context in
which the experiments are doneone pathway may be important in some settings, and
another pathway may be important in different settings, he suggested. 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, well 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 repressedbut 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 genesbetween 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.
They show very elegantly using their system that modified histones can be inherited
through multiple rounds of cell division and can be passed on . . . to the next generation,
said Shiv Grewal, an epigenetics and chromatin researcher at the National Cancer Institute
who was not involved in the work. Thats quite remarkable.
Histones, the proteins around which DNA is wrapped to form chromatin, can be modified by
the addition a various moieties. And such modifications are thought to representand even
influencethe 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
replicationwhen the histones are temporarily evicted from DNAwas unclear.
Theres been a lot of debate about whether histone modifications can be heritable, said Bill
Kelly, a biologist at Emory University in Atlanta, Georgia, who was not involved in the study.
When you replicate the DNA you have to replicate the histones . . . and de novo
synthesized histones dont 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 Cruzs Susan 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 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 transcriptional repression. Fusing
these roundworm eggs with wild-type sperm resulted in a single-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, by approximately the 48-
cell 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 chromosomesthe chromosomes derived from the initial sperm
chromosomesand 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 with 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 after replication there is sufficient information
there that it can be targeted by the maintenance systemthe 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
transgenerational inheritance, which a lot of people suspect, said Grewal, but for which
there is not much evidence. Indeed, added Strome: Were starting to get a molecular
handle on what it means to pass epigenetic information from parent to childboth at the
organism and cell leveland 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 Rothemunds 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 techniqueusing an M13
bacteriophage to generate single-stranded DNA scaffolds of up to 7 kilobaseshas
restricted the size of the products to tens of square nanometers. Double-stranded DNA
could be produced at longer lengths, but was limited 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 kilobasesand theyve used these to create DNA structures that are hundreds of
square nanometers in size,Chemical & Engineering News (C&EN) reported.
Theyve achieved something people have been trying to do for a while, Rothemund
told C&EN.
To fold giant pieces of DNA, LaBeans 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 author 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 strandsbecause 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 phage-
produced scaffolds. The researchers reported their results this month (September 1)
in Nano Letters.
These origami can be customized for use in everything from 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
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.
Its long been a puzzle as to how hummingbirds detect sweetness and these investigators,
using a whole bunch of different techniques, have pretty much . . . nailed the answer,
said Gary 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 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 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 dietsseeds, insects, fish, fruits, and nectars are all on the avian menu
but they lack the gene for T1R2. This raised a very interesting mystery as to how these
animals can detect sugar, said Stephen 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 allthe
hummingbird. His team cloned taste receptors from hummingbirdswhich consume more
than their own body weight in nectar each dayas 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 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 selectionthat 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 acidsas would be expected for the savory taste receptorthe hummingbird
receptor did not. Instead it produced a strong response to sugars.
The team then made chimeric T1R1-T1R3 receptorsusing parts from the hummingbird
genes and parts from the chicken genesand 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 hummingbirdstheir very specific diet, said Steven Munger,
associate director of the Center for Smell and Taste at the University of Florida, Gainesville,
who was not involved in the work.
Its a really nice 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 ecological niche. These birds have undergone massive radiation, he
addedthere 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. Im 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 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 Goldenrod
gall fly (Eurosta solidaginis) stays put and freezes nearly solid. But pockets of liquid life
remain within the fly, allowing the insect to resume its activities come spring. According to a
study published today (April 30) in The Journal of Experimental Biology, E.
solidaginis possesses a secret antifreeze weapona rare lipid.
Until now, only one type of lipid was thought to have antifreeze properties, according to
study coauthor Brent 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 hostthe 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 hormone-
mimicking 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 -80C.
Overwintering larvae store carbohydrates and lipids in special fat body cells, which survive
intracellular freezing. This first amazed the late Reginald Salt at the Canadian Agricultural
Research Station at Alberta in 1959, while he was studying E. solidaginis in the fieldhe
observed clear lipid droplets inside the larval insects frozen fat body cells.
Eager to determine the contents of these droplets, Westerns Katie Marshall and her
colleagues collected galls from goldenrod plants from fields in nearby London, Ontario,
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
chromatography/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 lipidsacetylated 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 waterthey dont repel it as much as lcTAGs
do, allowing the lipids to interact with other cellular components. And acTAGs lower the
cells 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 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
the study. If the authors claim about the method of acTAG synthesis in the gall fly is
correct, it will be extremely interesting to isolate the enzymes involved in that process.
John Ohlrogge, a plant biologist at Michigan State University, was more 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 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 cellslots of lipid, intracellular freezingmay 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 way to make lcTAGs into acTAGs, like fermentation, it would
make it relatively easy to make acTAGs which stay liquid in the cold, he added. This will
make them more useful as biofuels in cold places.


























Artificial Blood Is Patient-
Ready
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 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 cells that are fit to go in a persons body, project leader Marc
Turner, medical director at SNBTS, told Forbes. Before now, we havent 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-marrow-
like environment for a month. Blood cells are then extracted from the cell culture. If the
technique can be scaled up to industrial 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 supply.
Although similar research has been 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 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 disorder called thalassaemia, in
which the body makes unusually low levels of hemoglobina 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 Science today (May 8). The results suggest that the
production of new neuronsneurogenesisprompted by the exercise wiped out the mices
memories. They might also explain why human infants, whose brains exhibit abundant
neurogenesis, do not have long-term memories.
In general, hippocampal neurogenesis has been thought to be the basis for memory and
theyre suggesting that its the basis for amnesia, saidThomas Insel, director of the
National Institute of Mental Health. Thats 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 that? Sheena Josselyn and her husband Paul
Frankland, who are both neuroscientists at the University of Toronto, pondered precisely
that question after noticing that their two-year-old 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 hippocampusa brain region involved in learning and memory. Hippocampal neurons
are produced rapidly during infancy, but neuronal generation in the region slows to a trickle
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 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 shocksand
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 freezea fear response. But if the mice 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 memorya finding that seems at odds with Josselyn and
Franklands. However, said Ren 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 informationthat 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 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 running clears your
mind, said Josselyn, and in a sense I would say thats true. But clearing ones mind is not
necessarily detrimental, she added. For instance, I dont want to remember where I parked
my car two weeks ago because thats going to interfere with me remembering where I
parked it today. . . . We think that neurogenesis and forgetting is an important part of
healthy memory. We dont 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 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 umanongmagkonsulta 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 pinangingitlugan 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.