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Saturday, 25 January 2020

Weight loss and health improvements with Mediterranean, fasting & Paleo diets

Image result for Weight loss and health improvements with Mediterranean, fasting and Paleo diets

Weight loss and health improvements with Mediterranean, fasting & Paleo diets


There were some weight loss and health benefits for overweight adults who followed the Mediterranean, Intermittent Fasting and Paleo diets, though adherence to the diets dropped off considerably during the one-year study, new University of Otago research shows.
Intermittent fasting -- whereby participants limit their energy intake to about 25 per cent of their usual diet (500kcal for women and 600kcal for men) on two self-selected days per week, led to slightly more weight loss than the other diets. The Mediterranean diet also improved blood sugar levels.
Co-lead author Dr Melyssa Roy, a Research Fellow in the Department of Medicine, says the amount of weight loss was modest -- on average two to four kilograms for the 250 participants, but for those choosing the fasting or Mediterranean diets, clinically significant improvements in blood pressure were also seen.
The aim of the research was to examine how effective all three diets were in a "real world" setting, where participants self-selected which diet they wished to follow, without any ongoing support from a dietitian.
Dr Roy says the evidence shows that for some people the Mediterranean, fasting or paleo (Paleolithic) diets can be "healthful, beneficial ways to eat."
"This work supports the idea that there isn't a single 'right' diet -- there are a range of options that may suit different people and be effective. In this study, people were given dietary guidelines at the start and then continued with their diets in the real world while living normally. About half of the participants were still following their diets after a year and had experienced improvements in markers of health.
"Like the Mediterranean diet, intermittent fasting and paleo diets can also be valid healthy eating approaches -- the best diet is the one that includes healthy foods and suits the individual."
The Mediterranean diet encouraged consumption of fruit, vegetables, whole-grain breads and cereals, legumes, nuts, seeds and olive oil with moderate amounts of fish, chicken, eggs and diary and red meat once a week or less.
The paleo diet consists of mostly less-processed foods with an emphasis on eating fruit and vegetables, animal proteins, nuts, coconut products and extra-virgin olive oil. While "original" Paleo diets strictly exclude all legumes, dairy and grains, this study used a modified version including some dairy as well as up to one serving daily of legumes and grain-based food.
Co-lead author Dr Michelle Jospe, a Postdoctoral Fellow in the Department of Medicine, says the results showed people found the Mediterranean diet to be the easiest to adhere to.
"Our participants could follow the diet's guidelines more closely than the fasting and paleo diets and were more likely to stay with it after the year, as our retention rates showed."
Most of the 250 participants (54 per cent) chose the fasting diet, while 27 per cent chose the Mediterranean and 18 per cent the paleo. After 12 months, the Mediterranean diet had the best retention rate with 57 per cent of participants continuing, with 54 per cent still fasting and 35 per cent still on the paleo diet.
After 12 months, the average weight loss was 4.0kg for those choosing the fasting diet, 2.8kg on the Mediterranean diet and 1.8kg on the paleo diet.
Reduced systolic blood pressure was observed among those participating in the fasting and Mediterranean diets, together with reduced blood sugar levels in the Mediterranean diet.
Dr Jospe explains participants who said they were still following their diet at 12 months lost even more weight, showing the importance of choosing a diet that is sustainable.
She believes the results of this study are relevant to the thousands of people following self-chosen diets with little supervision and indicates more realistic outcomes.

Story Source:
Materials provided by University of OtagoNote: Content may be edited for style and length.

Friday, 24 January 2020

Researchers regrow damaged nerves with polymer and protein

Image result for University of Pittsburgh School of Medicine researchers have created a biodegradable nerve guide -- a polymer tube -- filled with growth-promoting protein that can regenerate long sections of damaged nerves, without the need for transplanting stem cells or a donor nerve. So far, the technology has been tested in monkeys, and the results of those experiments appeared today in Science Translational Medicine. "We're the first to show a nerve guide without any cells was able to bridge a large, 2-inch gap between the nerve stump and its target muscle," said senior author Kacey Marra, Ph.D., professor of plastic surgery at Pitt and core faculty at the McGowan Institute for Regenerative Medicine. "Our guide was comparable to, and in some ways better than, a nerve graft." Half of wounded American soldiers return home with injuries to their arms and legs, which aren't well protected by body armor, often resulting in damaged nerves and disability. Among civilians, car crashes, machinery accidents, cancer treatment, diabetes and even birth trauma can cause significant nerve damage, affecting more than 20 million Americans. Peripheral nerves can regrow up to a third of an inch on their own, but if the damaged section is longer than that, the nerve can't find its target. Often, the disoriented nerve gets knotted into a painful ball called a neuroma. The most common treatment for longer segments of nerve damage is to remove a skinny sensory nerve at the back of the leg -- which causes numbness in the leg and other complications, but has the least chance of being missed -- chop it into thirds, bundle the pieces together and then sew them to the end of the damaged motor nerve, usually in the arm. But only about 40 to 60% of the motor function typically returns. "It's like you're replacing a piece of linguini with a bundle of angel hair pasta," Marra said. "It just doesn't work as well." Marra's nerve guide returned about 80% of fine motor control in the thumbs of four monkeys, each with a 2-inch nerve gap in the forearm. The guide is made of the same material as dissolvable sutures and peppered with a growth-promoting protein -- the same one delivered to the brain in a recent Parkinson's trial -- which releases slowly over the course of months. The experiment had two controls: an empty polymer tube and a nerve graft. Since monkeys' legs are relatively short, the usual clinical procedure of removing and dicing a leg nerve wouldn't work. So, the scientists removed a 2-inch segment of nerve from the forearm, flipped it around and sewed it into place, replacing linguini with linguini, and setting a high bar for the nerve guide to match. Functional recovery was just as good with Marra's guide as it was with this best-case-scenario graft, and the guide outperformed the graft when it came to restoring nerve conduction and replenishing Schwann cells -- the insulating layer around nerves that boosts electrical signals and supports regeneration. In both scenarios, it took a year for the nerve to regrow. The empty guide performed significantly worse all around. With these promising results in monkeys, Marra wants to bring her nerve guide to human patients. She's working with the Food and Drug Administration (FDA) on a first-in-human clinical trial and spinning out a startup company, AxoMax Technologies Inc. "There are no hollow tubes on the market that are approved by the FDA for nerve gaps greater than an inch. Once you get past that, no off-the-shelf tube has been shown to work," Marra said. "That's what's amazing here." Story Source: Materials provided by University of Pittsburgh. Note: Content may be edited for style and length.
Researchers regrow damaged nerves with polymer and protein
University of Pittsburgh School of Medicine researchers have created a biodegradable nerve guide -- a polymer tube -- filled with growth-promoting protein that can regenerate long sections of damaged nerves, without the need for transplanting stem cells or a donor nerve.
So far, the technology has been tested in monkeys, and the results of those experiments appeared today in Science Translational Medicine.
"We're the first to show a nerve guide without any cells was able to bridge a large, 2-inch gap between the nerve stump and its target muscle," said senior author Kacey Marra, Ph.D., professor of plastic surgery at Pitt and core faculty at the McGowan Institute for Regenerative Medicine. "Our guide was comparable to, and in some ways better than, a nerve graft."
Half of wounded American soldiers return home with injuries to their arms and legs, which aren't well protected by body armor, often resulting in damaged nerves and disability. Among civilians, car crashes, machinery accidents, cancer treatment, diabetes and even birth trauma can cause significant nerve damage, affecting more than 20 million Americans.
Peripheral nerves can regrow up to a third of an inch on their own, but if the damaged section is longer than that, the nerve can't find its target. Often, the disoriented nerve gets knotted into a painful ball called a neuroma.
The most common treatment for longer segments of nerve damage is to remove a skinny sensory nerve at the back of the leg -- which causes numbness in the leg and other complications, but has the least chance of being missed -- chop it into thirds, bundle the pieces together and then sew them to the end of the damaged motor nerve, usually in the arm. But only about 40 to 60% of the motor function typically returns.
"It's like you're replacing a piece of linguini with a bundle of angel hair pasta," Marra said. "It just doesn't work as well."
Marra's nerve guide returned about 80% of fine motor control in the thumbs of four monkeys, each with a 2-inch nerve gap in the forearm.
The guide is made of the same material as dissolvable sutures and peppered with a growth-promoting protein -- the same one delivered to the brain in a recent Parkinson's trial -- which releases slowly over the course of months.
The experiment had two controls: an empty polymer tube and a nerve graft. Since monkeys' legs are relatively short, the usual clinical procedure of removing and dicing a leg nerve wouldn't work. So, the scientists removed a 2-inch segment of nerve from the forearm, flipped it around and sewed it into place, replacing linguini with linguini, and setting a high bar for the nerve guide to match.
Functional recovery was just as good with Marra's guide as it was with this best-case-scenario graft, and the guide outperformed the graft when it came to restoring nerve conduction and replenishing Schwann cells -- the insulating layer around nerves that boosts electrical signals and supports regeneration. In both scenarios, it took a year for the nerve to regrow. The empty guide performed significantly worse all around.
With these promising results in monkeys, Marra wants to bring her nerve guide to human patients. She's working with the Food and Drug Administration (FDA) on a first-in-human clinical trial and spinning out a startup company, AxoMax Technologies Inc.
"There are no hollow tubes on the market that are approved by the FDA for nerve gaps greater than an inch. Once you get past that, no off-the-shelf tube has been shown to work," Marra said. "That's what's amazing here."

Story Source:
Materials provided by University of PittsburghNote: Content may be edited for style and length.

Beauty sleep could be real, say body clock biologists

Woman waking up from bed (stock image). | Credit: (c) volha_r / stock.adobe.com
Woman waking up from bed (stock image).

Biologists from The University of Manchester have explained for the first time why having a good night's sleep really could prepare us for the rigours of the day ahead.
The study in mice and published in Nature Cell Biology, shows how the body clock mechanism boosts our ability to maintain our bodies when we are most active.
And because we know the body clock is less precise as we age, the discovery, argues lead author Professor Karl Kadler, may one day help unlock some of the mysteries of aging.
The discovery throws fascinating light on the body's extracellular matrix -which provides structural and biochemical support to cells in the form of connective tissue such as bone, skin, tendon and cartilage.
Over half our body weight is matrix, and half of this is collagen -- and scientists have long understood it is fully formed by the time we reach the age of 17.
But now the researchers have discovered there are two types of fibrils -- the rope-like structures of collagen that are woven by the cells to form tissues.
Thicker fibrils measuring about 200 nanometres in diameter -- a million million times smaller than a pinhead -- are permanent and stay with us throughout our lives, unchanged from the age of 17.
But thinner fibrils measuring 50 nanometres, they find, are sacrificial, breaking as we subject the body to the rigours of the day but replenishing when we rest at night.
The collagen was observed by mass spectrometry and the mouse fibrils were observed using state of the art volumetric electron microscopy -- funded by the Wellcome Trust -- every 4 hours over 2 days.
When the body clock genes where knocked out in mice, the thin and thick fibrils were amalgamated randomly.
"Collagen provides the body with structure and is our most abundant protein, ensuring the integrity, elasticity and strength of the body's connective tissue," said Professor Kadler
"It's intuitive to think our matrix should be worn down by wear and tear, but it isn't and now we know why: our body clock makes an element which is sacrificial and can be replenished, protecting the permanent parts of the matrix.
He added: "So if you imagine the bricks in the walls of a room as the permanent part, the paint on the walls could be seen as the sacrificial part which needs to be replenished every so often.
"And just like you need to oil a car and keep its radiator topped up with water, these thin fibrils help maintain the body's matrix."
"Knowing this could have implications on understanding our biology at its most fundamental level. It might, for example, give us some deeper insight into how wounds heal, or how we age.

Story Source:
Materials provided by University of ManchesterNote: Content may be edited for style and length.

Scientists breach brain barriers to attack tumors

Illustration of human brain and tumor (stock image). | Credit: (c) Sebastian Kaulitzki / stock.adobe.com
Illustration of human brain and tumor (stock image).

The brain is a sort of fortress, equipped with barriers designed to keep out dangerous pathogens. But protection comes at a cost: These barriers interfere with the immune system when faced with dire threats such glioblastoma, a deadly brain tumor for which there are few effective treatments.
Yale researchers have found a novel way to circumvent the brain's natural defenses when they're counterproductive by slipping immune system rescuers through the fortresses' drainage system, they report Jan. 15 in the journal Nature.
"People had thought there was very little the immune system could do to combat brain tumors," said senior corresponding author Akiko Iwasaki. "There has been no way for glioblastoma patients to benefit from immunotherapy."
Iwasaki is the Waldemar Von Zedtwitz Professor of Immunobiology and professor of molecular, cellular, and developmental biology and an investigator for the Howard Hughes Medical Institute.
While the brain itself has no direct way for disposing of cellular waste, tiny vessels lining the interior of the skull collect tissue waste and dispose of it through the body's lymphatic system, which filters toxins and waste from the body. It is this disposal system that researchers exploited in the new study.
These vessels form shortly after birth, spurred in part by the gene known as vascular endothelial growth factor C, or VEGF-C.
Yale's Jean-Leon Thomas, associate professor of neurology at Yale and senior co-corresponding author of the paper, wondered whether VEGF-C might increase immune response if lymphatic drainage was increased. And lead author Eric Song, a student working in Iwasaki's lab, wanted to see if VEGF-C could specifically be used to increase the immune system's surveillance of glioblastoma tumors. Together, the team investigated whether introducing VEGF-C through this drainage system would specifically target brain tumors.
The team introduced VEGF C into the cerebrospinal fluid of mice with glioblastoma and observed an increased level of T cell response to tumors in the brain. When combined with immune system checkpoint inhibitors commonly used in immunotherapy, the VEGF-C treatment significantly extended survival of the mice. In other words, the introduction of VEGF-C, in conjunction with cancer immunotherapy drugs, was apparently sufficient to target brain tumors.
"These results are remarkable," Iwasaki said. "We would like to bring this treatment to glioblastoma patients. The prognosis with current therapies of surgery and chemotherapy is still so bleak."
The study was primarily funded by the Howard Hughes Medical Institute and the National Institutes of Health.
Other Yale authors are Tianyang Mao, Huiping Dong, Ligia Simoes,Braga Boisserand, and Marcus Bosenberg. Salli Antila and Kari Alitalo of the University of Helsinki are also authors.

Story Source:
Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.

Mosquitoes engineered to repel dengue virus

Aedes aegypti mosquito (stock image). | Credit: (c) tacio philip / stock.adobe.com
Aedes aegypti mosquito (stock image).

An international team of scientists has synthetically engineered mosquitoes that halt the transmission of the dengue virus.
Led by biologists at the University of California San Diego, the research team describes details of the achievement in Aedes aegypti mosquitoes, the insects that spread dengue in humans, on January 16 in the journal PLOS Pathogens.
Researchers in UC San Diego Associate Professor Omar Akbari's lab worked with colleagues at Vanderbilt University Medical Center in identifying a broad spectrum human antibody for dengue suppression. The development marks the first engineered approach in mosquitoes that targets the four known types of dengue, improving upon previous designs that addressed single strains.
They then designed the antibody "cargo" to be synthetically expressed in female A. aegypti mosquitoes, which spread the dengue virus.
"Once the female mosquito takes in blood, the antibody is activated and expressed -- that's the trigger," said Akbari, of the Division of Biological Sciences and a member of the Tata Institute for Genetics and Society. "The antibody is able to hinder the replication of the virus and prevent its dissemination throughout the mosquito, which then prevents its transmission to humans. It's a powerful approach."
Akbari said the engineered mosquitoes could easily be paired with a dissemination system, such as a gene drive based on CRISPR/CAS-9 technology, capable of spreading the antibody throughout wild disease-transmitting mosquito populations.
"It is fascinating that we now can transfer genes from the human immune system to confer immunity to mosquitoes. This work opens up a whole new field of biotechnology possibilities to interrupt mosquito-borne diseases of man," said coauthor James Crowe, Jr., M.D., director of the Vanderbilt Vaccine Center at Vanderbilt University Medical Center in Nashville, Tenn.
According to the World Health Organization, dengue virus threatens millions of people in tropical and sub-tropical climates. Severe dengue is a leading cause of serious illness and death among children in many Asian and Latin American countries. The Pan American Health Organization recently reported the highest number of dengue cases ever recorded in the Americas. Infecting those with compromised immune systems, dengue victims suffer flu-like symptoms, including severe fevers and rashes. Serious cases can include life-threatening bleeding. Currently no specific treatment exists and thus prevention and control depend on measures that stop the spread of the virus.
"This development means that in the foreseeable future there may be viable genetic approaches to controlling dengue virus in the field, which could limit human suffering and mortality," said Akbari, whose lab is now in the early stages of testing methods to simultaneously neutralize mosquitoes against dengue and a suite of other viruses such as Zika, yellow fever and chikungunya.
"Mosquitoes have been given the bad rap of being the deadliest killers on the planet because they are the messengers that transmit diseases like malaria, dengue, chikungunya, Zika and yellow fever that collectively put 6.5 billion people at risk globally," said Suresh Subramani, professor emeritus of molecular biology at UC San Diego and global director of the Tata Institute for Genetics and Society (TIGS). "Until recently, the world has focused on shooting (killing) this messenger. Work from the Akbari lab and at TIGS is aimed at disarming the mosquito instead by preventing it from transmitting diseases, without killing the messenger. This paper shows that it is possible to immunize mosquitoes and prevent their ability to transmit dengue virus, and potentially other mosquito-borne pathogens."
Coauthors of the research include: UC San Diego graduate student Stephanie Gamez; Anna Buchman and Ming Li of the Section of Cell and Developmental Biology, Division of Biological Sciences, UC San Diego; Igor Antoshechkin of the California Institute of Technology, Shin-Hang Lee, Shin-Wei Wang and Chun-Hong Chen of the National Health Research Institutes (Taiwan); and Melissa Klein, Jean-Bernard Duchemin and Prasad Paradkar of CSIRO Health and Biosecurity.

Story Source:
Materials provided by University of California - San Diego. Original written by Mario Aguilera. Note: Content may be edited for style and length.

Dozens of non-oncology drugs can kill cancer cells

Cancer treatment concept (stock image). | Credit: (c) tashatuvango / stock.adobe.com
Cancer treatment concept (stock image).

Drugs for diabetes, inflammation, alcoholism -- and even for treating arthritis in dogs -- can also kill cancer cells in the lab, according to a study by scientists at the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute. The researchers systematically analyzed thousands of already developed drug compounds and found nearly 50 that have previously unrecognized anti-cancer activity. The surprising findings, which also revealed novel drug mechanisms and targets, suggest a possible way to accelerate the development of new cancer drugs or repurpose existing drugs to treat cancer.
"We thought we'd be lucky if we found even a single compound with anti-cancer properties, but we were surprised to find so many," said Todd Golub, chief scientific officer and director of the Cancer Program at the Broad, Charles A. Dana Investigator in Human Cancer Genetics at Dana-Farber, and professor of pediatrics at Harvard Medical School.
The new work appears in the journal Nature Cancer. It is the largest study yet to employ the Broad's Drug Repurposing Hub, a collection that currently comprises more than 6,000 existing drugs and compounds that are either FDA-approved or have been proven safe in clinical trials (at the time of the study, the Hub contained 4,518 drugs). The study also marks the first time researchers screened the entire collection of mostly non-cancer drugs for their anti-cancer capabilities.
Historically, scientists have stumbled upon new uses for a few existing medicines, such as the discovery of aspirin's cardiovascular benefits. "We created the repurposing hub to enable researchers to make these kinds of serendipitous discoveries in a more deliberate way," said study first author Steven Corsello, an oncologist at Dana-Farber, a member of the Golub lab, and founder of the Drug Repurposing Hub.
The researchers tested all the compounds in the Drug Repurposing Hub on 578 human cancer cell lines from the Broad's Cancer Cell Line Encyclopedia (CCLE). Using a molecular barcoding method known as PRISM, which was developed in the Golub lab, the researchers tagged each cell line with a DNA barcode, allowing them to pool several cell lines together in each dish and more quickly conduct a larger experiment. The team then exposed each pool of barcoded cells to a single compound from the repurposing library, and measured the survival rate of the cancer cells.
They found nearly 50 non-cancer drugs -- including those initially developed to lower cholesterol or reduce inflammation -- that killed some cancer cells while leaving others alone.
Some of the compounds killed cancer cells in unexpected ways. "Most existing cancer drugs work by blocking proteins, but we're finding that compounds can act through other mechanisms," said Corsello. Some of the four-dozen drugs he and his colleagues identified appear to act not by inhibiting a protein but by activating a protein or stabilizing a protein-protein interaction. For example, the team found that nearly a dozen non-oncology drugs killed cancer cells that express a protein called PDE3A by stabilizing the interaction between PDE3A and another protein called SLFN12 -- a previously unknown mechanism for some of these drugs.
These unexpected drug mechanisms were easier to find using the study's cell-based approach, which measures cell survival, than through traditional non-cell-based high-throughput screening methods, Corsello said.
Most of the non-oncology drugs that killed cancer cells in the study did so by interacting with a previously unrecognized molecular target. For example, the anti-inflammatory drug tepoxalin, originally developed for use in people but approved for treating osteoarthritis in dogs, killed cancer cells by hitting an unknown target in cells that overexpress the protein MDR1, which commonly drives resistance to chemotherapy drugs.
The researchers were also able to predict whether certain drugs could kill each cell line by looking at the cell line's genomic features, such as mutations and methylation levels, which were included in the CCLE database. This suggests that these features could one day be used as biomarkers to identify patients who will most likely benefit from certain drugs. For example, the alcohol dependence drug disulfiram (Antabuse) killed cell lines carrying mutations that cause depletion of metallothionein proteins. Compounds containing vanadium, originally developed to treat diabetes, killed cancer cells that expressed the sulfate transporter SLC26A2.
"The genomic features gave us some initial hypotheses about how the drugs could be acting, which we can then take back to study in the lab," said Corsello. "Our understanding of how these drugs kill cancer cells gives us a starting point for developing new therapies."
The researchers hope to study the repurposing library compounds in more cancer cell lines and to grow the hub to include even more compounds that have been tested in humans. The team will also continue to analyze the trove of data from this study, which have been shared openly (https://depmap.org) with the scientific community, to better understand what's driving the compounds' selective activity.
"This is a great initial dataset, but certainly there will be a great benefit to expanding this approach in the future," said Corsello.
This collaboration involved the Broad's Center for the Development of Therapeutics, the PRISM team, the Cancer Data Sciences team, and the labs of Todd Golub and Matthew Meyerson. The work was funded in part by SIGMA (Carlos Slim Foundation, Slim Initiative in Genomic Medicine for the Americas), the National Institutes of Health, and an anonymous donor.

Story Source:
Materials provided by Broad Institute of MIT and Harvard. Original written by Leah Eisenstadt. Note: Content may be edited for style and length.

Tuesday, 21 January 2020

Is the Universe Expanding at an Accelerated Rate?

Is the Universe Expanding at an Accelerated Rate?

A new study challenges the cosmological model and suggests that the universe is not expanding at an accelerated rate.
The standard model of cosmology assumes that the universe is isotropic with no preferred direction and no preferred frame of reference; that is, we are not special and our position in the universe is not from a privileged vantage point. Within this framework, observational data led us to the conclusion that 70% of the universe is expanding at an accelerated rate, and this accelerating force is due to an unknown form of energy known as ‘dark energy’. This so-called ‘dark energy’ is now thought to be due to quantum fluctuations of the vacuum energy.
However, a new study by a team of European scientists explored these ideas further. They wanted to see what would happen when they measure the deceleration parameter – the measurement of cosmic acceleration – from our own ‘special’ frame of reference.
The expansion of the universe is measured in terms of the Hubble constant, which is currently measured by two different methods. One method looks at the early universe through the observation of the Cosmic Microwave Background (CMB) and the other method looks at the local universe through the light emitted by galaxies, Cepheid variables and/or Type 1a supernovae. It was the latter method that led to the conclusion that the universe was expanding at an accelerating rate, resulting in astrophysicists Adam Reiss, Brian Paul Schmidt and Saul Perlmutter receiving the 2011 Nobel Prize in Physics.
However, in each case, the measurements are taken in the framework of the cosmological model which assumes that the universe is isotropic and homogeneous. This assumption is contradicted by the inhomogeneous distribution of galaxies and the lack of correlations on large angular scales, with the only confirmation coming from studies of the early universe through observed temperature fluctuations in the CMB radiation. It has therefore been suggested that this isotropic and homogeneous universe only exists at the larger scales, although this has yet to be confirmed.
The team therefore decided to see what happens when they remove this assumption from their analysis and measure the expansion in our own ‘heliocentric’ frame of reference.
“In the absence of any evidence of convergence to the CMB rest frame, this assumption is unjustified since it is very possible that the observed bulk flow stretches out to much larger scales.”
– Jacques Colin, Roya Mohayaee, Mohammed Rameez and Subir Sarkar
Utilising the latest extended sample size of supernovae data from the Joint Lightcurve Analysis catalogue, they were able to extract the redshifts for 740 Type 1a supernovae. To convert from a heliocentric frame of reference to a CMB frame of reference, the observed redshifts are generally corrected for ‘peculiar’ velocities – that is, velocities relative to a standard frame of rest. Therefore, to obtain the redshifts in our local frame of reference – the heliocentric frame – these corrections had to be undone.
Intriguingly, their results showed that the acceleration is a relatively local effect with a significant dipole component directed along the direction we are moving with respect to the CMB. This dipole component, in alignment with the CMB dipole moment, rejects the assumption of isotropy. It could therefore be that the cosmic acceleration inferred from supernovae observations is not due to dark energy and instead due to us being tilted observers located in a bulk flow.

RSF in perspective

Everything in the universe – including the universe itself – is in a continuous dance of expansion, contraction and rotation. This is true from the smallest system, to fundamental particles, to stars and galaxies, and right up to the universe itself. Depending on our perspective, the different systems will appear as coherent systems within systems or as areas of apparent randomness. So, although the universe is expanding, it could appear to be accelerating or decelerating depending on the scale of the observation and the vantage point of the observer.

Social Media Marketing

Image result for social media
Social media marketing is the use of social media platforms to connect with
your audience to build your brand, increase sales, and drive website traffic.
This involves publishing great content on your social media profiles, listening
to and engaging your followers, analyzing your results, and running social
media advertisements.
The major social media platforms (at the moment) are Facebook, Instagram,
Twitter, LinkedIn, Pinterest, YouTube, and Snapchat.
There are also a range of social media management tools that help businesses
to get the most out of the social media platforms listed above. For example,
Buffer is a platform of social media management tools, which can help you
achieve success with your social media marketing. Whether you want to build
a brand or grow your business, we want to help you succeed.

A Quick Overview of Social Media Marketing

Social media marketing first started with publishing. Businesses were
sharing their content on social media to generate traffic to their websites
and, hopefully, sales. But social media has matured far beyond being
just a place to broadcast content.
Nowadays, businesses use social media in a myriad of different ways.
For example, a business that is concerned about what people are saying
about its brand would monitor social media conversations and response
to relevant mentions (social media listening and engagement). A business
that wants to understand how it’s performing on social media would analyze
its reach, engagement, and sales on social media with an analytics tool
(social media analytics). A business that wants to reach a specific set of
audience at scale would run highly-targeted social media ads (social media advertising).
As a whole, these are often also known as social media management.

The three Core Pillars of Social Media Marketing

1. Strategy

Before you dive right in and publish something on social media, let’s take
a step back and look at the bigger picture. The first step is to think about
your social media strategy.
What are your goals? How can social media help you achieve your 
business goals? Some businesses use social media for increasing their
brand awareness, others use it for driving website traffic and sales. Social
media can also help you generate engagement around your brand, create
a community, and serve as a customer support channel for your customers.
Which social media platforms do you want to focus on? The
major social media platforms, mentioned above, are Facebook, Instagram,
Twitter, LinkedIn, Pinterest, YouTube, and Snapchat. There are also smaller
and up-and-coming platforms, such as Tumblr, Tik Tok, and Anchor, and
social messaging platforms, such as Messenger, WhatsApp, and WeChat.
When starting out, it’s better to pick a few platforms that you think your target
audience is on than to be on all platforms.
What type of content do you want to share? What type of content
will attract your target audience best? Is it images, videos, or links? Is it
educational or entertaining content? A good place to start is to create a
marketing persona, which will help you answer these questions. And this
doesn’t have to be fixed forever; you can always change your strategy
according to how your social media posts perform.
To help you create a great social media strategy, here are our long-form,
step-by-step guides on creating a social media strategy and social media 
marketing plan.

2. Planning and Publishing

Social media marketing for small businesses usually starts with having a
 consistent presence on social media. Close to three billion people
(3,000,000,000!) use social media. By being present on social media
platforms, you give your brand an opportunity to be discovered by your
future customers.
Publishing to social media is as simple as sharing a blog post, an image,
or a video on a social media platform. It’s just like how you would share on
your personal Facebook profile. But you will want to plan your content ahead
of time instead of creating and publishing content spontaneously. Also, to
ensure that you are maximizing your reach on social media, you need to
publish great content that your audience likes, at the right timing and frequency.
There are now a variety of social media scheduling tools, such as Buffer 
Publish, that can help you publish your content automatically at your preferred
time. This saves you time and allows you to reach your audience when they are
most likely to engage with your content.
3. Listening and Engagement
As your business and social media following grow, conversations about your
brand will also increase. People will comment on your social media posts, tag
you in their social media posts, or message you directly.
People might even talk about your brand on social media without letting you
know. So you will want to monitor social media conversations about your
brand. If it’s a positive comment, you get a chance to surprise and delight
them. Otherwise, you can offer support and correct a situation before it gets
worse.
You can manually check all your notifications across all the social media
platforms but this isn’t efficient and you won’t see posts that didn’t tag your
business’s social media profile. You can instead use a social media listening 
and engagement tool, such as Buffer Reply, that aggregates all your social
media mentions and messages, including posts that didn’t tag your business’s
social media profile.

Sunday, 19 January 2020

Molecular switch for repairing central nervous system disorders

Neurons illustration (stock image). | Credit: (c) whitehoune / stock.adobe.com
Neurons illustration (stock image).

A molecular switch has the ability to turn on a substance in animals that repairs neurological damage in disorders such as multiple sclerosis (MS), Mayo Clinic researchers discovered. The early research in animal models could advance an already approved Food and Drug Administration therapy and also could lead to new strategies for treating diseases of the central nervous system.
Research by Isobel Scarisbrick, Ph.D., published in the Journal of Neuroscience finds that by genetically switching off a receptor activated by blood proteins, named Protease Activated Receptor 1 (PAR1), the body switches on regeneration of myelin, a fatty substance that coats and protects nerves.
"Myelin regeneration holds tremendous potential to improve function. We showed when we block the PAR1 receptor, neurological healing is much better and happens more quickly. In many cases, the nervous system does have a good capacity for innate repair," says Dr. Scarisbrick, principal investigator and senior author. "This sets the stage for development of new clinically relevant myelin regeneration strategies."
Myelin, Thrombin and the Nervous System
Myelin acts like a wire insulator that protects electrical signals sent through the nervous system. Demyelination, or injury to the myelin, slows electrical signals between brain cells, resulting in loss of sensory and motor function. Sometimes the damage is permanent. Demyelination is found in disorders such as MS, Alzheimer's disease, Huntington's disease, schizophrenia and spinal cord injury.
Thrombin is a protein in blood that aids in healing. However, too much thrombin triggers the PAR1 receptor found on the surface of cells, and this blocks myelin production. Oligodendrocyte progenitor cells capable of myelin regeneration are often found at sites of myelin injury, including demyelinating injuries in multiple sclerosis.
"These oligodendroglia fail to differentiate into mature myelin regenerating cells for reasons that remain poorly understood," says Dr. Scarisbrick. "Our research identifies PAR1 as a molecular switch of myelin regeneration. In this study, we demonstrate that blocking the function of the PAR1, also referred to as the thrombin receptor, promotes myelin regeneration in two unique experimental models of demyelinating disease."
The Research
The research focused on two mouse models. One was an acute model of myelin injury and the other studied chronic demyelination, each modeling unique features of myelin loss present in MS, Alzheimer's disease and other neurological disorders. Researchers genetically blocked PAR1 to block the action of excess thrombin.
The research not only discovered a new molecular switch that turns on myelin regeneration, but also discovered a new interaction between the PAR1 receptor and a very powerful growth system called brain derived neurotropic factor (BDNF). BDNF is like a fertilizer for brain cells that keeps them healthy, functioning and growing.
Significantly, the researchers found that a current Food and Drug Administration-approved drug that inhibits the PAR1 receptor also showed ability to improve myelin production in cells tested in the laboratory.
"It is important to say that we have not and are not advocating that patients take this inhibitor at this time," says Dr. Scarisbrick. "We have not used the drug in animals yet, and it is not ready to put in patients for the purpose of myelin repair. Using cell culture systems, we are showing that this has the potential to improve myelin regeneration."
Additional research is needed to verify and advance the findings toward clinical practice.
The study was made possible by a grant from the National Multiple Sclerosis Society with support from the Mayo Clinic Rehabilitation Medicine Research Center, the Center for Multiple Sclerosis and Autoimmune Neurology and the Mayo Clinic Center for Regenerative Medicine.

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Materials provided by Mayo Clinic. Original written by Susan Buckles. Note: Content may be edited for style and length.

Scientists breach brain barriers to attack tumors

Illustration of human brain and tumor (stock image). | Credit: (c) Sebastian Kaulitzki / stock.adobe.com
Illustration of human brain and tumor (stock image).

The brain is a sort of fortress, equipped with barriers designed to keep out dangerous pathogens. But protection comes at a cost: These barriers interfere with the immune system when faced with dire threats such glioblastoma, a deadly brain tumor for which there are few effective treatments.
Yale researchers have found a novel way to circumvent the brain's natural defenses when they're counterproductive by slipping immune system rescuers through the fortresses' drainage system, they report Jan. 15 in the journal Nature.
"People had thought there was very little the immune system could do to combat brain tumors," said senior corresponding author Akiko Iwasaki. "There has been no way for glioblastoma patients to benefit from immunotherapy."
Iwasaki is the Waldemar Von Zedtwitz Professor of Immunobiology and professor of molecular, cellular, and developmental biology and an investigator for the Howard Hughes Medical Institute.
While the brain itself has no direct way for disposing of cellular waste, tiny vessels lining the interior of the skull collect tissue waste and dispose of it through the body's lymphatic system, which filters toxins and waste from the body. It is this disposal system that researchers exploited in the new study.
These vessels form shortly after birth, spurred in part by the gene known as vascular endothelial growth factor C, or VEGF-C.
Yale's Jean-Leon Thomas, associate professor of neurology at Yale and senior co-corresponding author of the paper, wondered whether VEGF-C might increase immune response if lymphatic drainage was increased. And lead author Eric Song, a student working in Iwasaki's lab, wanted to see if VEGF-C could specifically be used to increase the immune system's surveillance of glioblastoma tumors. Together, the team investigated whether introducing VEGF-C through this drainage system would specifically target brain tumors.
The team introduced VEGF C into the cerebrospinal fluid of mice with glioblastoma and observed an increased level of T cell response to tumors in the brain. When combined with immune system checkpoint inhibitors commonly used in immunotherapy, the VEGF-C treatment significantly extended survival of the mice. In other words, the introduction of VEGF-C, in conjunction with cancer immunotherapy drugs, was apparently sufficient to target brain tumors.
"These results are remarkable," Iwasaki said. "We would like to bring this treatment to glioblastoma patients. The prognosis with current therapies of surgery and chemotherapy is still so bleak."
The study was primarily funded by the Howard Hughes Medical Institute and the National Institutes of Health.
Other Yale authors are Tianyang Mao, Huiping Dong, Ligia Simoes,Braga Boisserand, and Marcus Bosenberg. Salli Antila and Kari Alitalo of the University of Helsinki are also authors.

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Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.