О хронических "мигренозниках"

Статья о страдающих хроническими и спорадическими мигренями, на http://www.eurekalert.org/pub_releases/2010-02/bmj-cms021610.php

Chronic migraineurs sicker, poorer and more depressed than episodic migraineurs

Sociodemographic and comorbidity profiles of chronic migraine and episodic migraine sufferers

Chronic migraine sufferers tend to be in poorer general health, less well off, and more depressed than those with episodic migraine, reveals research published ahead of print in the Journal of Neurology Neurosurgery and Psychiatry.

The findings are based on almost 12,000 adults with episodic - a severe headache on up to 14 days of the month - or chronic migraine - headache on 15 or more days of the month.

All participants were already part of the American Migraine Prevalence and Prevention (AMPP) study, a long term US population based study of 24,000 headache sufferers, which has included regular surveys since 2004.

The research team analysed data collected in the 2005 survey on socioeconomic circumstances and other health problems.

The results showed that those with chronic migraine had significantly lower levels of household income, were less likely to be working full time, and were almost twice as likely to have a job related disability than their peers with episodic migraine.

They were twice as likely to be depressed, anxious, and experiencing chronic pain. And they were significantly more likely to have other serious health problems.

These included asthma, bronchitis, and chronic obstructive pulmonary disease (COPD), high blood pressure, diabetes, high cholesterol and obesity. They were also around 40% more likely to have heart disease and angina and 70% more likely to have had a stroke.

The authors point out that chronic migraine "can be an especially disabling and burdensome condition."

Previous research indicates that chronic migraineurs have a relatively high level of sick leave, reduced productivity, and poorer quality of family life than episodic migraineurs.

It also suggests that few are diagnosed correctly and that only around one in three are treated appropriately.

The differences unearthed between the two groups in the present study might reflect differences in biological risk factors and provide valuable clues as to how episodic migraine progresses to chronic migraine, suggest the authors

Три новых статьи об эффектах наркотических веществ

http://scienceblogs.com/drugmonkey/2010/02/synthetic_marijuana_k2_spice_j.php - о синтетической марихуане
http://www.scientificblogging.com/news_articles/does_recreational_drug_use_damage_memory - о проблемах с памятью у употребляющих психотропные вещества
http://scienceblogs.com/drugmonkey/2010/02/as_many_dependent_on_cannabis.php - о связи курения марихуаны и употребления героина

Отличный пост о повреждениях ДНК и стволовых клетках

Две мои любимейшие темы в одном чудесном посте. Автор - Ed Yong
All of our cells are staffed by armies of executioners. They are usually restrained but when unleashed, they can set off a fatal chain reaction that kills the cell. This suicide squad does away with billions of cells every day. It helps to balance the production of new cells with the loss of old ones, to sculpt growing tissues and to destroy potential cancer cells.

But a new study suggests that the executioners aren't always lethal. In fact, they're essential for life. Through the unorthodox method of damaging our DNA, they can actually activate important genes. This technique for switching genes on is new to science but it's apparently vital for allowing some types of stem cell to produce new types of tissue.
Stem cells are bundles of untapped potential, with the ability to produce hundreds of specialist cells across the body. This process is called differentiation. Its details vary depending on which type of cell is being produced, but scientists have recently found that some aspects are apparently common to all tissues, be they muscle, blood or bone. Surprisingly, one of these is the recruitment of executioner proteins - caspases.
Caspases cut up other proteins and in doing so, some of them produce yet more caspases. The result is a growing army of death, hacking and slashing its way through the cell. But one of these killers - caspase-3 - is a necessary part of differentiation. Get rid of it and, suddenly, stem cells can't produce their specialised daughters. Now, thanks to Brian Larsen from the Sprott Centre for Stem Cell Research, we know why.
Caspase-3 activates a protein called CAD (or caspase-activated DNase in full) by slicing apart other proteins holding it at bay. Once released, CAD lives up to its villainous acronym. It pairs up with an identical twin to create a molecule that looks and acts like a pair of scissors. The pair can cut DNA, cleaving the famous double helix in two. These sorts of cuts are normally very bad news for a cell. If they aren't repaired quickly and accurately, the consequences can include death or cancer.
But Larsen has found that stem cells deliberately break their own DNA by recruiting caspase-3 and CAD. This act of self-harm switches on important genes that are needed for differentiation; without it, the generalist cells can't specialise. This is an entirely new way of activating genes and it appears to be both important and widespread.
Larsen studied stem-like cells called myoblasts, which give rise to various types of muscle cells. As the myoblasts differentiated, Larsen watched for signs of shattered DNA using a clever test called the 'comet assay'. The technique involves puncturing a cell and placing it in an electric field. The field drives DNA through the punctured cell but only if it has already been broken into small pieces. If it has, it appears as a streak outside the cell, rather like the tail of a comet.
Sure enough, the comet test revealed that differentiating cells suffer from significant amounts of damaged DNA. Thankfully, the injuries are only temporary and the cells soon marshal their repairmen to fix the breaks.
The myoblasts need these breaks to produce muscle fibres and to create the breaks, they rely on caspase-3 and its ability to activate CAD. Larsen managed to block the development of muscle fibres by dousing myoblasts with chemicals that neutralise caspase-3. The same thing happened if he used cells with mutant versions of CAD, which couldn't be activated. In both cases, the cells failed to show any signs of broken DNA.
CAD targets a gene called p21 that's absolutely necessary for the development of muscle and plenty of other tissues. Larsen found that CAD cuts p21's 'promoter', a stretch of DNA lying next to the gene that's responsible for switching it on. Somehow, these cuts activate the gene. It's still not clear how this works, but Larsen has some ideas. The cuts could change how the surrounding DNA is packaged, exposing the p21 gene and making it easier to 'read'. Alternatively, the cuts could remove chemical 'marks' attached to the DNA that would otherwise silence it.
Damaging your own DNA may seem like a rather extreme tactic for a cell to take but it's not unheard of as a deliberate ploy. Whenever we face new infections, our body generates antibodies by breaking the DNA of special genes, stitching them back together in new combinations. That's a very controlled process, but so is the damage that leads to differentiation. It's a careful surgical strike, rather than a shock and awe campaign.
During differentiation, Larsen found that DNA breaks are actually few and far between. They appear to be carefully orchestrated so that the entire genome doesn't become a shattered mess. This precision is even more remarkable when you consider that CAD cuts DNA indiscriminately, with little care for specific sequences. Larsen thinks that CAD is constrained by the way the DNA is packaged, so that only places that are meant to be cut are exposed for slicing and dicing. Only further experiments will tell if he is right.

Reference: Larsen et al. 2010. Caspase 3/caspase-activated DNase promote cell differentiation by inducing DNA strand breaks. http://dx.doi.org/10.1073/pnas.0913089107

Статья с http://scienceblogs.com/notrocketscience/2010/02/our_cells_produce_new_tissues_by_recruiting_executioners_to.php


Суицидальная нетрадиционность...

Оказывается, самоидентификация геев, лесбиянок и бисексуалов увеличивает риск суицида. Читаем на http://www.eurekalert.org/pub_releases/2010-02/jgh-yws020510.php
Mental health professionals have long-known that gay, lesbian and bisexual (GLB) teens face significantly elevated risks of mental health problems, including suicidal thoughts and suicidal attempts. However, a group of McGill University researchers in Montreal has now come to the conclusion that self-identity is the crucial risk-factor, rather than actual sexual behaviours. Their results were published in February in the Journal of the American Academy of Child & Adolescent Psychiatry.
The researchers administered a detailed, anonymous questionnaire to nearly 1,900 students in 14 Montreal-area high schools, and found that those teens who self-identified as gay, lesbian or bisexual, or who were unsure of their sexual identity, were indeed at higher risk for suicidal ideation and attempts. However, teens who had same-sex attractions or sexual experiences – but thought of themselves as heterosexual – were at no greater risk than the population at large. Perhaps surprisingly, but consistent with previous studies, the majority of teens with same-sex sexual attraction or experience considered themselves to be heterosexual.
"This is the first study that has separated sexual identity from sexual attractions and behaviours in looking at risk for poor mental health outcomes," said corresponding author Dr. Brett Thombs, of the Lady Davis Institute for Medical Research (LDI) at the Jewish General Hospital.
"It's important to realize that a large proportion of people who have sex with or are attracted to people of the same sex do not identify themselves as gay, lesbian or bisexual. They consider themselves heterosexual." added co-author Dr. Richard Montoro of the McGill University Health Centre (MUHC). "Those students were not at all at risk of worse mental health outcomes."
"The main message is that it's the interface between individuals and society that causes students who identify as gay, lesbian, or bisexual the most distress," said study first author Yue Zhao, a McGill University graduate student working with Dr. Thombs.. "Sexual orientation has three different components. The first is identity, which is dependent on the society in which one lives; the second is attraction or fantasy; and the third is behaviour. Previous studies have not addressed which of those components may explain why GLB youth are at risk."
"What this all means is that clinicians need to look not just at individuals and their sexuality, they really need to assess the environment they are coming from and how they see themselves within it," said study co-author Dr. Karine Igartua. Igartua and Montoro are co-directors of the McGill University Sexual Identity Centre (MUSIC), the first gay and lesbian mental health centre in Canada.
"Our findings also clearly suggest that further study of the link between anti-gay sentiment and suicidality need to be undertaken," added Thombs.


Новости о ферментах репарации ДНК

Читаем на http://www.biologynews.net/archives/2010/01/28/researchers_find_new_way_to_study_how_enzymes_repair_dna_damage.html
Researchers at Ohio State University have found a new way to study how enzymes move as they repair DNA sun damage -- and that discovery could one day lead to new therapies for healing sunburned skin.
Ultraviolet (UV) light damages skin by causing chemical bonds to form in the wrong places along the DNA molecules in our cells. Normally, other, even smaller molecules called photolyases heal the damage. Sunburn happens when the DNA is too damaged to repair, and cells die.
Photolyases have always been hard to study, in part because they work in tiny fractions of a second. In this week's online edition of the Proceedings of the National Academy of Sciences, Ohio State physicist and chemist Dongping Zhong and his colleagues describe how they used ultra-fast pulses of laser light to spy on a photolyase while it was healing a strand of DNA.
This is the first time that anyone has observed this enzyme motion without first attaching a fluorescent molecule to the photolyase, which disturbs its movements. They were able to see the enzyme's motion to help the healing process as it happens in nature.
"Now that we have accurately mapped the motions of a photolyase at the site of DNA repair, we can much better understand DNA repair at the atomic scale, and we can reveal the entire repair process with unprecedented detail," said Zhong, the Robert Smith Associate Professor of Physics, and associate professor in the departments of chemistry and biochemistry at Ohio State.
Such small motions are very hard to study. Typically, researchers deal with the problem by attaching tiny bits of fluorescent molecules to the enzymes they are trying to study. But adding an extra molecule to an enzyme such as photolyase could change how it moves.
"Once you tag it, you can't be sure that the motions you detect are the true motions of the molecule as it would normally function," Zhong explained.
So instead of using tags, he and his team took laser "snapshots" of a single photolyase in action in the laboratory. They mapped the shape and position of the photolyase molecule as it broke up the harmful chemical bonds in DNA caused by UV light. The whole reaction lasted only a few billionths of a second.
In nature, DNA avoids damage by converting UV rays into heat. Sunscreen lotions protect us by reflecting sunlight away from the skin, and also by dissipating UV as heat.
Sunburn happens when the DNA absorbs the UV energy instead of converting it to heat. This is due in part to the random position of the DNA molecule within our cells when the UV hits it. When the UV energy is absorbed, it triggers chemical reactions that form lesions -- errant chemical bonds -- along the DNA strand.
If photolyases are unable to completely repair the lesions, the DNA can't replicate properly. Badly damaged cells simply die — that's what gives sunburn its sting. Scientists also believe that chronic sun damage creates mutations that lead to diseases such as skin cancer.
The work in Zhong's lab is fundamental to the understanding of how those molecules interact. Other researchers could use this information to design drugs to heal sun damage.
"Of course, the ultimate goal of studying DNA repair is to help design artificial systems to mimic it," he said.

Source : Ohio State University