Alexey Adamov, the painter. Painting: Landscape, genre, sea (marine).

About the artist

About Alexei Adamov it is not easy to tell all because a true artist is always in search. It is well-known search that assumes a difficult or even intricate road in life. After all, life is not a bed of roses and no roses without thorns. Naturally, you can disagree with the painter’s point of view, but an instinct prompts us to agree — we feel unable to be indifferent to Adamov’s painting. It contains the charm and fascination of contemplating the beauty of nature. And it sets us thinking. First of all, it sets thinking about eternity and momentariness of human existence, about the joy of life and sadness of wasting away. It is impossible to simulate all these emotions. It is possible only to come nearer to them little by little, enriching one’s divine gift of aesthetic vision.


Alexei Adamov is a person of indomitable energy. After his first personal exhibition of paintings in Taganrog in the building of Chekhov Library in 1997, Adamov became a well-known painter: his exhibition at the Don Artistic Fund in 2001, in Prague in the years of 2001-2002, in 2003 his pictures were exhibited in Paris and in Moscow Exhibition Hall of the Union of Artists. Adamov’s works of art constantly take part in opening days and exhibitions in various galleries of Moscow and of Europe. On August 13, 2004 was held his exhibition at the Moscow Exhibition Hall of the Union of Artists. This fact is undoubtedly proof of his innate genius and great acknowledgement of his creative personality.


You know Art is Beauty and it is a sign of kindness, too. We hope this eternal value won’t be depleted by the generous artist.


Ms.Ludmila Milukova

Boston College Chemists use nanowires to power photosynthesis

In this study, Boston College chemists use nanowires to power photosynthesis - collecting sunlight energy that powers reactions capable of synthesizing basic compounds of two popular pain-killing, and anti-inflammatory drugs.

NIST silicon nanowires. A nanowire is a wire of dimensions the size of a nanometer (a billionth of a meter). Alternatively, nanowires can be defined as structures that have a lateral size constrained to tens of nanometers or less and an unconstrained longitudinal size. (Photo: Softpedia)

Harnessing the power of the sun has inspired scientists and engineers to look for ways to turn sunlight into clean energy to heat houses, fuel factories and power devices. While a majority of this research focuses on energy production, some researchers are looking at the potential uses of these novel solar technologies in other areas.

Boston College Assistant Professor of Chemistry Dunwei Wang’s work with silicon nanowires and his related construct, Nanonets, has shown these stable, tiny wire-like structures can be used in processes ranging from energy collection to hydrogen-generating water-splitting.

Teaming up with fellow Boston College Assistant Professor of Chemistry Kian L. Tan, the researchers have taken aim at a role for nanowires in photosynthesis.

Their work has produced a process that closely resembles photosynthesis, employing silicon nanowires to collect light energy to power reactions capable of synthesizing the basic compounds of two popular pain-killing, anti-inflammatory drugs, they report in the current edition of Angewandte Chemie, the journal of the German Chemical Society.

The reaction sequence offers an approach that differs from earlier attempts to sequester carbon dioxide with sunlight and solves the vexing problem of carbon’s low selectivity, which so far has limited earlier methods to the production of fuels. Tan and Wang report their process offers the selectivity required to produce complex organic intermediaries capable of developing pharmaceuticals and high-value chemicals.

The process succeeds in taming stubborn carbon, which structurally resists most efforts to harness it for a single chemical product. Typically, refined forms of carbon molecules must first be produced to produce the necessary results.

“If we can start to use carbon dioxide and light to power reactions in organic chemistry, there’s a huge benefit to that. It allows you to bypass the middle man of fossil fuels by using light to drive the chemical reaction,” said Tan. “The key is the interaction of two fields – materials and synthetic chemistry. Separately, these fields may not have accomplished this on their own. But together, we combined our knowledge to make it work.”

During photosynthesis, plants capture sunlight and use this solar energy and carbon dioxide to fuel chemical reactions.

Tan and Wang used silicon nanowires as a photocathode, exploiting the wire’s efficient means of converting solar energy to electrical energy. Electrons released from the atoms in the nanowires are then transferred to organic molecules to trigger chemical reactions.

In this case, the researchers used aromatic ketones, which when struck by electrons become active and attack and bind carbon dioxide. Further steps produced an acid that allowed the team to create the precursors to ibuprofen and naproxen with high selectivity and high yield, the team reports.

Tan and Wang were joined in the research by Research Assistant Guangbi Yuan, PhD ’12, graduate student Rui Liu, doctoral student Candice L. Joe, and former doctoral student Thomas E. Lightburn, PhD ’11.

Tan said it is no accident that the process so closely resembles natural photosynthesis, as chemists are constantly drawing inspiration from nature in their work.

“Researchers in my field are always drawing inspiration from nature,” said Tan. “You take the basic lessons and you try to do it in an artificial way. In this work, we’re trying to learn lessons from nature, although we can’t copy nature directly.”

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For more info, contact: 

Ed Hayward
ed.hayward@bc.edu
617-552-4826 

Boston College 

Why chronic pain is all in your head (Neuroscience)

First study to show early brain changes predict which patients develop chronic pain

When people have similar injuries, why do some end up with chronic pain while others recover and are pain free? The first longitudinal brain imaging study to track participants with a new back injury has found the chronic pain is all in their heads –- quite literally.

A new Northwestern Medicine study shows for the first time that chronic pain develops the more two sections of the brain — related to emotional and motivational behavior — talk to each other. The more they communicate, the greater the chance a patient will develop chronic pain.

Chronic pain is one of the most expensive health care conditions in the U. S. yet there still is not a scientifically validated therapy for this condition.

The finding provides a new direction for developing therapies to treat intractable pain, which affects 30 to 40 million adults in the United States.

Researchers were able to predict, with 85 percent accuracy at the beginning of the study, which participants would go on to develop chronic pain based on the level of interaction between the frontal cortex and the nucleus accumbens.

The study is published in the journal Nature Neuroscience.

“For the first time we can explain why people who may have the exact same initial pain either go on to recover or develop chronic pain,” said A. Vania Apakarian, senior author of the paper and professor of physiology at Northwestern University Feinberg School of Medicine.

“The injury by itself is not enough to explain the ongoing pain. It has to do with the injury combined with the state of the brain. This finding is the culmination of 10 years of our research.”

The more emotionally the brain reacts to the initial injury, the more likely the pain will persist after the injury has healed. “It may be that these sections of the brain are more excited to begin with in certain individuals, or there may be genetic and environmental influences that predispose these brain regions to interact at an excitable level,” Apkarian said.

The nucleus accumbens is an important center for teaching the rest of the brain how to evaluate and react to the outside world, Apkarian noted, and this brain region may use the pain signal to teach the rest of the brain to develop chronic pain.

“Now we hope to develop new therapies for treatment based on this finding,” Apkarian added.

Chronic pain participants in the study also lost gray matter density, which is likely linked to fewer synaptic connections or neuronal and glial shrinkage, Apkarian said. Brain synapses are essential for communication between neurons.

“Chronic pain is one of the most expensive health care conditions in the U. S. yet there still is not a scientifically validated therapy for this condition,” Apkarian said. Chronic pain costs an estimated $600 billion a year, according to a 2011 National Academy of Sciences report. Back pain is the most prevalent chronic pain condition.

A total of 40 participants who had an episode of back pain that lasted four to 16 weeks — but with no prior history of back pain — were studied. All subjects were diagnosed with back pain by a clinician. Brain scans were conducted on each participant at study entry and for three more visits during one year.

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Other Northwestern authors on the paper include lead author Marwan N. Baliki, Bogdan Petre, Souraya Torbey, Kristina M. Herrmann, Lejian Huang and Thomas J. Schnitzer.

The study was funded by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health grant NS35115.

Scientists identify gene linked to facial, skull and cognitive impairment

A gene whose mutation results in malformed faces and skulls as well as mental retardation has been found by scientists. Credit: Phil Jones

A gene whose mutation results in malformed faces and skulls as well as mental retardation has been found by scientists.

They looked at patients with Potocki-Shaffer syndrome, a rare disorder that can result in significant abnormalities such as a small head and chin and intellectual disability, and found the gene PHF21A was mutated, said Dr. Hyung-Goo Kim, molecular geneticist at the Medical College of Georgia at Georgia Health Sciences University.

The scientists confirmed PHF21A's role by suppressing it in zebrafish, which developed head and brain abnormalities similar to those in patients. "With less PHF21A, brain cells died, so this gene must play a big role in neuron survival," said Kim, lead and corresponding author of the study published in The American Journal of Human Genetics. They reconfirmed the role by giving the gene back to the malformed fish – studied for their adeptness at regeneration – which then became essentially normal. They also documented the gene's presence in the craniofacial area of normal mice.

While giving the normal gene unfortunately can't cure patients as it does zebrafish, the scientists believe the finding will eventually enable genetic screening and possibly early intervention during fetal development, including therapy to increase PHF21A levels, Kim said. It also provides a compass for learning more about face, skull and brain formation.

The scientists zeroed in on the gene by using a distinctive chromosomal break found in patients with Potocki-Shaffer syndrome as a starting point. Chromosomes – packages of DNA and protein – aren't supposed to break, and when they do, it can damage genes in the vicinity.

"We call this breakpoint mapping and the breakpoint is where the trouble is," said Dr. Lawrence C. Layman, study co-author and Chief of the MCG Section of Reproductive Endocrinology, Infertility and Genetics. Damaged genes may no longer function optimally; in PHF21A's case it's about half the norm.

"When you see the chromosome translocation, you don't know which gene is disrupted," Layman said. "You use the break as a focus then use a bunch of molecular techniques to zoom in on the gene." Causes of chromosomal breaks are essentially unknown but likely are environmental and/or genetic, Kim said.

Little was known about PHF21A other than its role in determining how tightly DNA is wound in a package with proteins called histones. How tightly DNA is wound determines whether proteins called transcription factors have the access needed to regulate gene expression, which is important, for example, when a gene needs to be expressed only at a specific time or tissue. PHF21A is believed to primarily work by suppressing other genes, for example, ensuring that genes that should be expressed only in brain cells don't show up in other cell types, Kim said.

Next steps include using PHF21A as a sort of geographic positioning system to identify other "depressor" genes it regulates then screening patients to look for mutations in those genes as well. "We want to find other people with different genes causing the same problem," Layman said, and they suspect the genes PHF21A interacts with or regulates are the most likely suspects. It's too early to know what percentage of Potocki-Shaffer syndrome patients have the PHF21A mutation, Kim noted. "Now that we know the causative gene, we can sequence the gene in more patients and see if they have a mutation," Layman said.

They also want to look at less-severe forms of mental deficiency, including autism, for potentially milder mutations of PHF21A. More than a dozen of the 25,000 human genes are known to cause craniofacial defects and mental retardation, which often occur together, Kim said.

Provided by Georgia Health Sciences University

"Scientists identify gene linked to facial, skull and cognitive impairment." July 5th, 2012. http://medicalxpress.com/news/2012-07-scientists-gene-linked-facial-skull.html

Posted by
Robert Karl Stonjek