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Air Quality (The Hindustan Times: 20171109
http://paper.hindustantimes.com/epaper/viewer.aspx
Choke is on Delhi, air worsens
EMERGENCY MEASURES L-G orders civic agencies to hike parking, ban trucks, stop
construction activities as AQI hits record high; odd-even could be back if trend continues
The toxic air in the National Capital Region worsened on Wednesday, forcing the
administration to sound the alarm and announce tougher emergency measures in an attempt
to reverse the trend.
SUNIL GHOSH/HT PHOTO
n A child wears a protective mask in Noida on Wednesday.
As the average daily air quality index (AQI) hit a season-high 478, the lieutenant governor of
Delhi banned the entry of trucks inside city limits, halted all construction activities, and
ordered civic bodies to enforce a fourfold hike in parking fees. Schools will remain shut till
Sunday.
In a high-level meeting attended by members of the Supreme Court-appointed pollution
control panel (EPCA) and chief minister Arvind Kejriwal, L-G Anil Baijal asked the Delhi
government to prepare for oddeven road rationing if the situation worsened.
Though the scheme, which allows only odd- and even-numbered vehicles to operate on
alternate days, was to be implemented if the AQI breached the “severe+” mark of 500, the
EPCA and the Central Pollution Control Board (CPCB) urged the L-G to treat the current
condition grave enough to roll out the measure.
“The CPCB task force has advised EPCA that given the prevailing air pollution emergency in
the city, there is a need to take actions which are listed in the severe-plus category,” the body
said in a statement.
DAILY NEWS BULLETINLEADING HEALTH, POPULATION AND FAMILY WELFARE STORIES OF THE DayThursday 20171109
A final decision will be taken on Thursday evening, according to EPCA member Sunita
Narain.
With visibility falling to an alarming 50 metres in some parts, pile-ups were reported at
multiple locations. On the Yamuna Expressway, over 20 vehicles collided and around 22
people suffered minor injuries on Wednesday morning.
For the second day in a row, operations at the Delhi airport were hampered and there were
delays of up to two hours. See page 14
Breathing is injurious to health
Delhi pollution: Breathing is injurious to health (The Indian express: 20171109)
http://indianexpress.com/article/cities/delhi/delhi-pollution-breathing-is-injurious-to-health-
4928873/
MoEF secretary C K Mishra wrote to the chief secretaries of Delhi, Rajasthan, Uttar Pradesh
and Haryana — all the states EPCA had written to a day earlier — asking them to follow the
steps required to control air pollution.
As Delhi’s air inched towards the unbreathable, a slew of announcements and urgent requests
followed: a timer on the Central Pollution Control Board (CPCB) website to monitor Delhi’s
smog, twice daily, the Ministry of Environment and Forests (MoEF) reaching out to states
asking them to take preventive measures as “topmost priority”, and the Delhi government
announcing ban on construction and barring entry of trucks in the city. Other key measures
announced include increasing parking fee four times, and shutting schools till Sunday.
The day’s average air quality index was 478, indicating “severe” levels of pollution —
perilously close to the maximum of 500, after which “emergency” is declared. But with MeT
department officials predicting no change in weather soon, and government officials fearing
further increase in pollution, Delhi Chief Minister Arvind Kejriwal termed the situation as an
“emergency”.
“The CPCB’s task force is meeting on a daily basis and will put out health warnings if the
PM levels cross emergency levels,” said CPCB’s A Sudhakar.
Smog Canopies Delhi On Wednesday Morning
MoEF secretary C K Mishra wrote to the chief secretaries of Delhi, Rajasthan, Uttar Pradesh
and Haryana — all the states EPCA had written to a day earlier — asking them to follow the
steps required to control air pollution. “These steps are critical to prevent any further
deterioration… I would urge that the directions given by EPCA be implemented in letter and
spirit,” Mishra wrote.
After a meeting with the L-G Anil Baijal, Kejriwal and other officials too announced a slew
of measures, including stopping the entry of trucks to Delhi, barring essential commodities,
stopping civil construction and increasing parking fees, including at Metro stations, four
times.
Orders were also issued to begin preparations for the odd-and-even scheme. Transport
Minister Kailash Gahlot said, “We will enforce odd-even scheme if air quality turns severe
plus. I have also directed DTC to procure 500 buses to augment public transport.” The Delhi
government also announced that all schools will remain closed till Sunday and issued a health
advisory.
For all the latest Delhi News, download Indian Express App
Smog
Smog rises to emergency levels: How the haze can harm (The Indian
express: 20171109)
http://indianexpress.com/article/explained/delhi-air-pollution-smog-health-tips-schools-shut-
stubble-burning-haryana-punjab-4928852/
As smog raises pollution towards emergency levels, Indian Express explains where it came
from, why it tends to linger in Delhi, and the ways in which it can impact health.
What is the thick haze that has enveloped Delhi and surrounding areas since Monday night?
It is smog. Smog occurs in a location that is far away from the actual source of pollution, and
is a result of various factors: geography of the place, sunlight, calmness of winds, post-
harvest crop burning, firing of brick kilns, pollution emitted by vehicles and industrial
activity. The processes that lead to smog usually take place after the hazardous pollutants
have drifted away in the wind. In Delhi, there are two winds — one carrying pollutants from
stubble burning in Punjab and the other bringing in moisture from Uttar Pradesh — that are
colliding above the national capital. This, combined with the near-still wind conditions near
the ground level, have effectively trapped the pollutants, leading to the smog.
How is smog different from fog?
Fog in just condensed water vapour close to the ground. When water vapour saturates the air,
the vapour starts to condense back into a liquid, as water droplets. These droplets, suspended
in the air, appear as the thick haze that is known as fog. This results in low visibility. On the
other hand, when pollution is high, nitrogen oxides and dust particles interact with sunlight to
form ground-level ozone, leading to the building up of haze. This is smog, a result of a
photochemical reaction of sunlight with pollutants that have been released into the
atmosphere.
Also Read | Delhi pollution: Toxic smog suffocates national capital; schools shut,
construction halted
What are these pollutants?
WHO classifies particulate matter — the major components being “sulphate, nitrates,
ammonia, sodium chloride, black carbon, mineral dust and water” — into two broad types,
PM10 and PM2.5, with the numbers indicating the diameter of the particles in microns. In
Delhi, the ground-level ozone and PM 2.5 play the most significant role in formation of
smog.
Chronic exposure to both PM10 and PM2.5 can lead to the “risk of developing cardiovascular
and respiratory diseases, as well as of lung cancer”, says WHO. Both can penetrate and lodge
deep inside the lungs; PM2.5 can “cross into the blood, causing damage in many organ
systems,” says WHO.
Smog Causes Series Of Accidents Near Dhankaur
How serious is this smog?
On Tuesday, Delhi’s air inched towards an “emergency scale”, with the Central Pollution
Control Board recording the average air quality at 487 (it dropped to 448 on Wednesday)
with an upper limit of 500. The Indian Medical Association, which has termed it a “medical
emergency”, says that this air can be equated to smoking 50 cigarettes a day.
See Pics | Delhi smog: City wakes up in ‘gas chamber’ for second day in a row
How harmful is it?
The direct impact of smog is on the lungs and the heart. Higher levels of nitrogen dioxide
precipitate asthma; higher levels of sulphur dioxide precipitate chronic bronchitis.
Particulate matter, Delhi’s main concern, can damage the lungs and worsen asthma due to
inflammation of the air tract. PM2.5, which can enter the lungs and also the lung lining,
carries long-term risks including lung cancer, reduced lung function, skin diseases and
reduction in life expectancy.
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Growth minus development
Widening gender gap, rising malnutrition and hunger call for policy
intervention. (The Indian express: 20171109)
http://indianexpress.com/article/opinion/columns/global-hunger-index-india-ranking-child-
mortality-national-health-mission-malnutrition-food-security-gender-disparity-4928750/
In rapid-fire, the country was recently hit by three global rankings. The first was the ease of
doing business and India improved its global rank, according to the Brettenwoods experts.
Now this is happiness. As an economist I believe the turnaround to the higher growth path
will come if we do a bit of pump priming and then private investment will be sucked in.
While some sarkari economists agree with me, this is still not the dominant view. So
improving the ease of doing business is obviously good news. Of the three rankings this was
the only one the chambers of commerce and corporate honchos went ga ga over. The
Purchasing Managers’ Index improved. This was somewhat effervescent, since even in the
past an improved PMI has always not led to better outcomes, but the sentiment was
understandable.
The second was bad news. The gender disparity gap has gone up in India and its already poor
ranking worsened. Women hold up half the sky, the UN poster says. Women are half the
country: Somewhat less in India because of the shameful sex ratio, but still a large number. If
growth is not just corporate GDP but human welfare, then this is worrisome. I mean the
world over women are liberating themselves, and in civilised India we think so too, and want
it to be more so. But it is not so. The statistics used are pretty robust and so even Indian
economists who never agree on anything will find it difficult to quibble on this gap.
Women and the girl child also star in the next global ranking. That’s the malnutrition and
hunger index. The absolute numbers are frightening. Forty per cent of the world’s hungry and
malnourished children are in India. Now poverty and hunger cut offs are always controversial
and can make a marginal difference — poverty more so and malnutrition less as it’s based on
biological measurements. Having defined a poverty line in the seventies of the last century,
which I have wanted revised but which kept on resurfacing like a rabbit out of a hat, I am not
surprised at the debate. But there was a sensible suggestion in these columns. Uma Lele
(‘Feeding India’, IE, November 3), who has a lot of global experience in these matters, in a
mature tone admonished us for being clever on a substantial issue where marginal changes
were not the big issue but the big problem whichever way you looked at it was. This needed
remedying and when you do so the information base improves. Nothing works more than
questions from senior policymakers to improve the statistical base of a decision.
I am impressed by the argument that for hunger use anthropomorphic rather than survey-
based calorie norms because biometric measures give you the physical reality as it were
rather than expenditure converted to food and then to calories. Strangely, there is a
connection between the worsening gender disparity and the hunger numbers. Weak mothers
will give birth to weak children. The baby will not get enough nourishment in the womb.
Again, in the early years of childhood, the limits to which he or she will grow are being set. It
is not that life is a matter of precise paths. But the boundaries in which outcomes will work
out are set in early years.
A couple of decades ago, I had to make some tax-free money to fund my daughter’s second
year in college in the US and decided in the vacations to work on food security UN
consultancies. In Egypt, I discovered that in the desert provinces of Upper Egypt — actually
Lower Egypt if you are in Cairo or Alexandria, but they look at everything from the
perspective of the Nile — malnutrition in women was high. When I was presenting my
results a top official, a retired general, went at me and said they are alright, my soldiers come
from there. I had to tell him that weak and anaemic mothers will never give birth to strong
soldiers.
So let’s get this straight. Even if your concern is not like mine on human welfare, but security
in the narrowest military sense of the term, let’s get rid of the problem of hunger rather than
be smart on statistics to wish it all away. The link between the gender gap and malnutrition is
much too obvious to ignore. So let’s get back to the three rankings of last week: Ease of
doing business is good while gender gap and hunger are not so. Policy-wise let’s travel from
growth to development.
The writer, a former Union minister, is chancellor, Central University of Gujarat.
Smoking (The Asian Age: 20171109)
http://onlineepaper.asianage.com/articledetailpage.aspx?id=9360102
Masks, Purifiers (The Asian Age: 20171109)
http://onlineepaper.asianage.com/articledetailpage.aspx?id=9360368
Gene therapy
How gene therapy saved a little boy's life (Medical News Today: 20171109)
https://www.medicalnewstoday.com/articles/320018.php
When a rare genetic condition destroyed nearly 80 percent of a 7-year-old's skin, doctors
were sure he would die. But the stars aligned and an experimental gene therapy treatment
saved his life.
Modern medicine is amazing. We can transplant hearts and even faces, as well as treat
countless diseases. However, when it comes to genetic conditions, we have yet to arrive in
the 21st century.
Epidermolysis bullosa (EB) — which is sometimes referred to as butterfly disease — is one
such genetic condition. It is caused by several different mutations in proteins that hold the
two layers of the skin, the epidermis and dermis, together.
Junctional EB (JEB) affects around 5 percent of individuals with EB and is caused by
mutations in proteins that sit at the junction between the skin layers.
Dr. Leena Bruckner-Tuderman — from the Department of Dermatology in the University
Medical Center at the University of Freiburg and the EB Center Freiburg, both in Germany
— explained to me that people with JEB are in constant pain, and that "[...] minor mechanical
stress or friction can cause the [skin] layers to separate and to form blisters and wounds."
"Frequent medical treatments and hospital visits are necessary," she added, "but no cure
exists for JEB."
This is the story of how an experimental gene therapy saved a little boy's life, giving hope to
the hundreds of thousands of families affected by EB worldwide.
'We were sure that he would die'
Dr. Tobias Rothoeft — who works in the Department of Neonatology and Pediatric Intensive
Care of University Children's Hospital at Ruhr University Bochum in Germany — explained
in a press briefing how he came to care for the young boy.
He is a co-lead author of the study, which describes the treatment and which is published
today in the journal Nature.
"We got this kid transferred in summer 2015 from another tertiary care hospital [...],"
explained Dr. Rothoeft. "He was admitted there because he had developed an infection in
which he rapidly lost nearly two thirds of his body surface area. When he was admitted to our
burns center, he was in a septic state [...] so we had a lot of trouble in the first days keeping
this kid alive."
After trying several different treatments — including a skin graft from the boy's father — the
medical team were left with few options.
"After nearly 2 months, we were absolutely sure that we could [do] nothing for this kid and
that he would die."
Dr. Tobias Rothoeft
But the boy's parents asked if anything else could be done.
"We studied the literature again and approached Dr. De Luca and his team and he promised
us he could give us enough skin to heal this kid," Dr. Rothoeft explained.
This was to be the pivotal moment.
Growing skin
Dr. Michele De Luca — a professor of biochemistry and director of the Centre for
Regenerative Medicine "Stefano Ferrari" at the University of Modena and Reggio Emilia in
Italy — has spent a lifetime developing therapies for skin and eye conditions.
While Dr. Rothoeft and his colleagues were doing their best to keep the boy alive, Dr. De
Luca and his team were busy preparing the cells in their laboratories in Modena.
Are stem cells and regenerative medicine living up to their promises?
Are stem cells and regenerative medicine living up to their promises?
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Growing keratinocytes, or cells from the epithelium, is relatively straightforward. This is
based on a technique that was developed in the 1970s and still in use today for the treatment
of severe burn injuries.
The big difference in this case was that the team had to correct the genetic mutation that
causes JEB. Dr. De Luca has been working on a technique to achieve this feat for nearly 20
years. To fix the genetic defect, the researchers used a virus to insert a normal copy of the
faulty gene into the cells.
In fact, they treated two people with JEB with genetically modified keratinocytes — and the
results were published in 2006 and 2016.
This case was to be their biggest challenge yet; never before had they attempted to repair
such a large area of skin.
Three operations later...
By the time the boy went into his first operation, he had lost nearly 80 percent of his skin.
The surgical team applied genetically modified skin grafts to his arms and legs.
Afterward, he was kept in an artificial coma for 12 days in order to keep the grafts immobile
and allow the cells to attach.
The procedure was a success and the patient showed the first signs of improvement.
For co-lead study author Dr. Tobias Hirsch — from the Department of Plastic Surgery in the
Burn Centre of BG University Hospital Bergmannsheil at Ruhr Bochum University — the
seemingly infinite supply of cells that Dr. De Luca was able to grow was a clear advantage.
"So you can have double the whole body surface or even more. So that's a fantastic option for
me as a surgeon to treat this child, because we can get as [many] cells as we need to cover all
open areas on the child."
Dr. Tobias Hirsch
A second and third operation followed to cover his back, buttocks, and parts of his shoulders,
hands, and chest in genetically modified grafts.
Finally, the team could stop his pain medication. After spending nearly 8 months in the
intensive care unit, the little boy was allowed to go home.
Playing soccer
Fast-forward 21 months, and "the kid is doing quite well," according to Dr. Rothoeft. "The
skin is of good quality, [...] it's perfectly smooth and it's quite stable. If he gets any bruises
like small kids [...] have, they just heal as normal skin heals."
"He still has some blisters in non-transplanted areas," Dr. Rothoeft added. "He never had any
blisters where we transplanted him."
Children with EB often can't take part in activities that put them at risk of harming their skin.
But not our young patient; he's happily playing soccer with his siblings and friends.
Dr. Rothoeft explained that because the little boy can take part in activities that other children
with EB would never do, he does get some blisters. But he did say that "the problem with the
blisters is restricted on 2 or 3 percent of his body surface area now in areas which we did not
transplant."
Overall, however, the patient's quality of life has improved tremendously, Drs. Hirsch and
Rothoeft agreed.
"The change is from being on morphine the whole day to no drugs at all at the moment."
Dr. Tobias Rothoeft
A breakthrough for gene therapy
For the field of gene therapy, this is clearly a success story. What the team was also able to
show with this work is that it only takes a small number of stem cells to regrow skin.
Dr. De Luca speculates that based on their data, these stem cells exist in the skin for our
entire lifetime, which is a topic that scientists have been arguing about for years.
"From a biological point of view, [...] we think this epidermis will stay forever. [...] The big
message is that once you've regenerated the epidermis with stem cells, [the cells] behave as
they are supposed to."
Dr. Michele De Luca
However, the significance of this finding goes beyond the basic science of how our skin
works; it also gives researchers such as Dr. De Luca the necessary information to grow just
the right mix of cells in the laboratory for a stem cell therapy.
So, what does this breakthrough mean for others with EB? "Here," urges Dr. De Luca, "we
should be very, very cautious."
Clinical trials ongoing
The mutations that cause other forms of EB may be more difficult to fix. "We might have
problems that we did not encounter in JEB," Dr. De Luca explained. "But this is only going
to be discovered after the phase I/II clinical trials, which we are doing right now."
The results of a clinical trial involving four people living with dystrophic EB highlight this
issue. The mutation in question here affects type VII collagen, which is a protein essential to
the structural integrity of the skin.
Although the team saw an initial improvement in wound healing, the effect started to taper
off after 1 year. The study authors speculate that this may due to limited numbers of stem
cells available from these people, as their skin is very damaged due to the disease.
In an editorial published in the journal Molecular Therapy, Prof. Bruckner-Tuderman
comments that the study "underscores the challenges of designing effective molecular
therapies for genetic diseases."
But the results published in Nature today leave Prof. Bruckner-Tuderman, who was not
involved in the study, hopeful.
"The development of experimental therapies like [this] one [...] gives hope that evidence-
based curative treatments will at some point become possible and clinical reality for many
patients with JEB and other forms of EB."
Prof. Leena Bruckner-Tuderman
This treatment is a significant breakthrough not only for JEB, but for skin science, gene
therapy, and regenerative medicine alike. But most importantly, it saved a life.
Cellular stress
Cellular stress 'resets lifespan profoundly'(Medical News Today: 20171109)
https://www.medicalnewstoday.com/articles/320009.php
Surprising results from a recent study show that stressing a cell can reverse signs of cellular
aging. The findings might open doors to more successful ways to slow the aging process.
Although the desire to stave off aging has a whiff of vanity about it, it's not all about reducing
wrinkles and covering gray hair; getting older comes with a range of diseases that grow
steadily more prevalent as our population ages.
Those interested in senescence are keen to understand the molecular pathways involved in
aging in the hope that associated disease processes will also be unlocked.
Molecular bioscientists from Northwestern University in Evanston, IL, recently gained a new
and surprising insight into cellular aging. Their findings are published this week in the
journal Cell Reports.
This new study focused on the transparent nematode Caenorhabditis elegans. This species is
often used as a model for human aging and disease; its cellular properties and biochemical
environment are similar to our own.
Aging worms give fresh clues
Despite the fact that life in the wild rarely allows an organism to survive into old age, all
animals age when given the chance. Events and processes that happen as an animal ages are
shared across species.
For instance, as C. elegans ages, the way that it handles proteins in the cell, or proteostasis, is
compromised. For a cell to function properly, proteins must be built, folded, and degraded at
the correct rates. The machinery responsible for this becomes progressively less accurate as
time goes on, resulting in misshapen and faulty proteins building up in the cytoplasm.
Similarly, in humans, misfolded proteins accumulate as part of some neurodegenerative
conditions, such as Huntington's, Parkinson's, and Alzheimer's disease.
The researchers behind the new study, which was headed up by senior study author Prof.
Richard I. Morimoto, put the cells' mitochondria — or the so-called powerhouses of the cell
— under mild duress.
What they found came as a surprise: under these conditions, mitochondria sent out signals to
the protein machinery, preventing it from failing. This, in turn, reduced the buildup of badly
packed proteins.
'It's like magic'
These surprising findings fly in the face of the previously held notion that stressing
mitochondria has negative effects, as Prof. Morimoto explains. He says, "This has not been
seen before."
"People have always known that prolonged mitochondrial stress can be deleterious," he
explains. "But we discovered that when you stress mitochondria just a little, the
mitochondrial stress signal is actually interpreted by the cell and animal as a survival
strategy. It makes the animals completely stress-resistant and doubles their lifespan. It's like
magic."
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These unexpected findings offer a new and intriguing lens with which to view the aging
process in humans; they may provide a key to how the process might be slowed.
"Our goal is not trying to find ways to make people live longer but rather to increase health at
the cellular and molecular levels so that a person's span of good health matches their
lifespan."
Prof. Richard I. Morimoto
Building on previous research
The new study's findings are based on earlier work carried out by Prof. Morimoto and
Johnathan Labbadia, a former postdoctoral fellow in Prof. Morimoto's laboratory who now
works at University College London in the United Kingdom.
In a previous study, they found that in C. elegans, deficits in proteostasis begin at
reproductive maturity. The decline is sparked by inhibitory signals from the germline cells
that prevent tissues from producing protective responses to stress. In C. elegans, this occurs
8–12 hours after the onset of adulthood, but the animal will normally live for another 3 week.
Knowing when C. elegans would begin the decline, in the current study, they used 2-day-old
animals. They hoped to be able to identify the genes and pathways involved that produce the
molecular failure.
Prof. Morimoto and his team screened approximately 22,000 genes on the hunt for those
responsible for the decline. They honed in on a set of genes called the mitochondrial electron
transport chain (ETC), which seemed to be important. "Mild downregulation of ETC activity"
resulted in healthier animals, as did small doses of xenobiotics and exposure to pathogens.
As Prof. Morimoto explains, "I never would have guessed this — a low stress signal resets
the organismal lifespan profoundly. What we are learning is that some of these stress signals
are interpreted by the organism as a way to reset itself and to live longer. When mitochondria
function optimally, the cells and tissue are robust."
Designing a way to implement these findings in a form that will be useful for humans is a
long way off. However, the study sheds new and unexpected light on the still mysterious
process of aging. Simply adding new avenues to follow is a result in itself.
Sleep disturbance
Sleep disturbance in diabetic women can prove to be deadly (New Kerala:
20171109)
https://www.newkerala.com/news/fullnews-286586.html
Women suffering from diabetes, need to give a look!
Sleep disturbance in female diabetes patients can give way to elevated blood sugar levels,
neuropathic pain and fatigue, a recent study has suggested.
In a study, conducted on 90 women with type 2 diabetes, these life threatening conditions
were found even after controlling factors such as age, diabetes duration, depressive
symptoms, and distress.
Senior author at Chicago College of Nursing Dr. Cynthia Fritschi said, "Sleep disturbance in
patients with diabetes is common and may negatively affect blood glucose".
The findings suggest that a comprehensive sleep evaluation for diabetes patients should also
include tests on symptoms such as neuropathic pain and fatigue.
"A thorough sleep assessment, especially in female adults, must include a symptom
assessment. To do otherwise limits our ability to treat sleep disturbance effectively in this
population", Dr. Cynthia added.
This study first appeared in the Journal of Advanced Nursing.
HIV patients
HIV patients at high risk of heart, kidney disease (New Kerala: 20171109)
https://www.newkerala.com/news/fullnews-286491.html
: HIV patients are at greater risk for a heart attack or stroke and are also at risk for chronic
kidney disease and vice versa, according to a study.
More than 1400 people in the study being treated for HIV had been diagnosed with chronic
kidney disease, and more than 900 had experienced a cardiovascular disease event.
Almost 11% of these patients had experienced both chronic kidney disease and
cardiovascular disease, with many of these events occurring just one year apart.
Professor Boyd, an infectious diseases expert with the Adelaide Medical School, University
of Adelaide, led an international team to investigate additional diseases associated with HIV
infection and its treatment.
Drawing on data from the international D:A:D (Data collection on Adverse events of Anti-
HIV Drugs) study, Professor Boyd and colleagues assessed the risks of cardiovascular
disease and chronic kidney disease in people with HIV infection. They found elevated risks
of each disease occurring simultaneously.
"Our research found that people with HIV at high risk of cardiovascular disease had a
corresponding 5.63-fold increase in risk of chronic kidney disease -- a finding not consistent
with the general community," Professor Boyd says.
"This study adds to the international body of research that shows we need to pay close
attention to the broader, general healthcare of people living with HIV.
"It's wonderful that anti-HIV medication has been able to save the lives of so many with HIV;
what we need to do now is to help people with HIV realise the full potential of their much-
extended life expectancy.
"Despite much effort over the past decade to focus attention on reducing cardiovascular risk
in HIV-positive people, there has been a lack of attention to the management of this disease
in people living with HIV. Unfortunately, this has implications for other diseases, and the
interaction between diseases creates substantial risks for future life-threatening events," he
says.
Professor Boyd says the research shows that the risks for cardiovascular and chronic kidney
disease in people with HIV should be assessed together.
"We strongly urge both people with HIV and their doctors to be aware of these risks, and to
treat them as a combined healthcare issue, not separately," he says.
"Primary prevention and effective management of these diseases, prioritising interventions
that have been repeatedly shown in the general community, will convey the same if not
greater benefits for the population of HIV-positive people."
"This approach should be incorporated in to the development of guidelines and defining
future research priorities for HIV-positive people," he says.
The research is published in the journal PLOS Medicine.
High-protein diet
How high-protein diet can prevent, treat obesity (New Kerala: 20171109)
https://www.newkerala.com/news/fullnews-286259.html
High protein diet contains an amino acid called phenylalanine that, according to a latest
research, is a new hunger suppressant.
The study shows how phenylalanine reduces food intake by affecting the gut and the brain,
and suggests that it may be used to prevent or treat obesity.
Although high protein diets have been shown to be satisfying and to promote weight loss,
they can be hard to maintain and may lead to other health problems in the long-term.
Phenylalanine is an amino acid produced in the gut when protein is digested and has
previously been shown to affect the release of gut hormones that reduce appetite in rodents.
However, it was unclear exactly how the amino acid was causing this release and whether
other systems were involved in phenylalanine's appetite supressing effects.
To investigate the effects of phenylalanine on appetite and gut hormone release, Professor
Kevin Murphy and colleagues at Imperial College London, examined the effect of the amino
acid on food intake and brain activity in areas known to be involved in appetite regulation.
Mice were given phenylalanine, either orally or rectally, to assess the effects on different
parts of the gut.
Food intake was monitored at regular intervals over 24 hours and the amount of activity in
brain areas associated with appetite regulation was also assessed. Both oral and rectal
phenylalanine reduced food intake of the mice and increased activation in a brain area known
to be involved in regulating appetite.
After rectal administration, even an amount of phenylalanine 10 times lower than would be
eaten daily on a high protein diet, resulted in reduced food intake and activated the appetite
regulating centres in the brain.
These data suggest that phenylalanine may reduce appetite through different pathways in the
upper and lower gut. Although unknown whether phenylalanine has the same effects on
human appetite, this research indicates that the amino acid may have an important role in
regulating food intake that could be used to treat obesity.
Mariana Norton, the PhD student who conducted the study, comments, "Understanding how
food is detected in the gut may help to identify ways of treating or preventing obesity. The
next step is to establish whether phenylalanine can drive similar appetite reducing effects in
humans."
Norton further states, "Diets high in protein are known to encourage weight loss but adhering
to them can be difficult. Identifying the mechanisms that sense the protein may allow us to
use drugs or functional foods to hijack appetite regulation, and treat obesity."
The findings were presented at the Society for Endocrinology annual conference in
Harrogate.
Environmental Health (Dainik Gagaran: 20171109)
http://epaper.jagran.com/ePaperArticle/09-nov-2017-edition-National-page_9-8853-13449-
262.html
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ȡ[ ȧपरवाह ¡ ȣ ¡ ȣȲहै। सभी को अपनी ] æ ȡj Ȳऔर आनंद ȧĤȡǔÜ ȧ ͬ Ȳ ȡतो है,
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जहर घुल रहा होता है, ¡ ȣȲ ȯ ɉ Ʌमौजूद Ǘͧ Ǚͪ - ͧ ğ ȧ तथा Ǘê Ȣɉके मरने से मदृा
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का ͧ ȡ न हो तो \ Û ` ×ȡ Ʌ [ ȡ से 50 ĤǓ \ ͬ तक ȧ Ǚͪƨ हो सकती है। ȡ ȣ
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` ×Û हो गई है। ȡçĚȣ राजधानी Ʌमंगलवार को वायु Ǖ × ȡसूचकांक 500 के पैमाने पर 448
अकं के साथ गंभीर è पर मापा गया। अभी तो Ǒ[ ɉ ȧ Ǖǽ] ¡ ȣहुई है तब ये हालात ¡ ɇ, अगर
अब भी ठोस कदम ¡ ȣȲउठाए गए तो आने वाले समय Ʌǔè Ǔ \ ͬ भयावह हो सकती है। ¡ ȡ ȡȲͩ
Ǒã ȣसरकार ने हालात को देखते हुए Ǔ ȡ[ ȡ Ⱦपर एक ¡ Ý ȯतक का ĤǓ Ȳ लगा Ǒ ȡ है।
Ȫ ɉ को ȯĚȪ व ȡ[ Ǔ ɉ से सफर करने ȧ सलाह ȣ जा ¡ ȣ है।1^Ȳͫ ȯͫ
f Ȫͧ f लगातार चतेावनी ȡȣकर रहा है। उसके ] Ē ¡ पर ¡ ȣèǗ ɉको बंद करने का Ǔ [
ͧ ȡगया है, ȡͩ Í ɉ ȧसेहत खराब न होने पाए। Ȳè ȡके Ǔ ȯ डॉ के.के. \ Ē ȡ ने Ȫ ɉ
से अपील ȧ है ͩ वे सुबह और शाम को न ¡ Ʌया घर से कम से कम बाहर Ǔ Ʌ@घने धुधं को
देखते हुए 19 नवंबर से Ǒã ȣ Ʌआयोिजत होने वाले हाफ मैराथन दौड़ को भी Ƨ करने का Ǔ [
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ǕĤȢ Ȫ[ ȧ ͧ ȡǐ पर बने ȡ[ ĤǗ Ĥȡͬ ने Ǒã ȣऔर आसपास के ȡÏ ɉको
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Ĥ Ǘͪ कर Ǒ ȡहै। ¡ ȡ ȡȲͩ Ǒã ȣ ȧआबोहवा Ʌजहर एक Ǔ ͧ Ĥ Đͩ ȡके तहत रोजाना घूल
रहा था, ȯͩ ȡ ȣजलाने, ȹके आगमन और ȣȡ ȣपर \ Ǔ Ȳǒğ पटाखेबाजी ने हालात को
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ȡ[ ȧपरवाह ¡ ȣ ¡ ȣȲहै। सभी को अपनी ] æ ȡj Ȳऔर आनंद ȧĤȡǔÜ ȧ ͬ Ȳ ȡतो है,
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Ʌपंजाब, ¡ ǐ ȡ ȡ, ȡ è ȡ और ǔæ Ȣ` × Ĥȯ Ʌͩ ȡ ɉɮȡȡधान ȧफसल ȧकटाई
के बाद उसके \ ȯɉ(ȡ ȣ) को जलाने का ͧ ͧ ȡ ǕǾ हो जाता है। नई फसल ȧ ã बुआई
करने के È Ʌͩ ȡ ȡ ȣको अपने ȯ ɉ Ʌ¡ ȣजला देते ¡ ɇ@यह Đ साल दर साल ɉ ¡ ȣ
चलता रहता है। हमारे ͩ ȡ इस बात से अजंान रहते ¡ ɇͩ इस आग से, एक ओर जहां ȡ[ Ʌ
जहर घुल रहा होता है, ¡ ȣȲ ȯ ɉ Ʌमौजूद Ǘͧ Ǚͪ - ͧ ğ ȧ तथा Ǘê Ȣɉके मरने से मदृा
ȧ ` [ ȡ घटती है, िजससे अनाज ` ×ȡ भी Ĥ ȡͪ होता है। \ ȯǐ ȧ Ǚͪ Ȱ£ ȡǓ ɉ के
अनुसार भारत Ʌ\ Û ` ×ȡ Ʌकमी का एक बड़ा कारण वायु ĤǗ है। Ǒ भारत वायु ĤǗ
का ͧ ȡ न हो तो \ Û ` ×ȡ Ʌ [ ȡ से 50 ĤǓ \ ͬ तक ȧ Ǚͪƨ हो सकती है। ȡ ȣ
जलाने से वायुमंडल Ʌ ȡ[ ȡ_ h È ȡ̂ , ȡ[ Ȫ Ȫh È ȡ̂ और ͧ ȯ ] Ǒ ͪȰ ȣ Ȱ ɉ ȧ
ȡğ बहुत \ ͬ बढ़ जाती है। ȡ ȣका बहुतायत Ʌजलाया जाना, Ǒã ȣव आसपास के ¢ ȯğɉ Ʌ
ĤǗ बढ़ने ȧ Ĥ Ǖ वजह बन गई है।1 ͪæ मौसम संगठन ȧ Ē Ȣ हाउस Ǖ ȯǑ के
Ǖ ȡǒ ,2016 Ʌवायुमंडल Ʌिजस Ý ȡ से वायु Ʌ ȡ[ डाई-h È ȡ̂ जमा हुई है, उसने ͪ ȯ
आठ लाख साल का ǐ Ȩ[तोड़ Ǒ ȡहै। 1(लेखक बनारस Ǒ¡ Ȳ Ǘͪæ ͪɮ ȡ Ʌ\ Ú ¡ ɇ)
Food and Nutrition (Dainik Gagaran: 20171109)
http://epaper.jagran.com/ePaperArticle/09-nov-2017-edition-National-page_14-8898-16399-
262.html
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