Vitamin D, best known for its role in calcium uptake and bone density has also been shown to have beneficial effects on the immune system, with some studies demonstrating a correlation between higher vitamin D intake and a lower incidence of cancer, and that adequate vitamin D levels may also decrease the risk of autoimmune diseases such as multiple sclerosis and rheumatoid arthritis. Now, a recent study, conducted by doctors across London hospitals and published in the Proceedings of the National Academy of Sciences, has shown that tuberculosis (TB) patients recovered more quickly when given both the vitamin and antibiotics. This idea is reminiscent of earlier times when TB patients, in the days before antibiotics, were prescribed sunbathing, which increases vitamin D production. This study found that recovery was almost two weeks faster when vitamin D was added to the treatment regime, with patients clearing the infection in 23 days on average, compared to 36 days for patients given antibiotics and a placebo. Vitamin D treatment will not replace antibiotics, but might well become a useful extra weapon, particularly with the increasing prevalence of drug-resistant TB. The vitamin seems to work by reducing the inflammatory response to the infection and helping the lungs to heal more quickly. If these lung cavities heal more quickly, patients are infectious for a shorter period of time and may also suffer less lung damage. Stronger evidence and trials to find the best dose and form of vitamin D will be needed before the treatment is put into widespread use.

http://www.pnas.org/

Two new studies from the Johns Hopkins Bloomberg School of Public Health and the Chronic Kidney Disease Prognosis Consortium found that the presence of chronic kidney disease itself can be a strong indicator of the risk of death and end-stage renal disease (ESRD) even in patients without hypertension or diabetes. Both hypertension and diabetes are common conditions with chronic kidney disease with hypertension being the most prevalent.
Chronic kidney disease affects 10 to 16 percent of all adults in Asia, Europe, Australia and the United States. Kidney function is measured by estimating glomerular filtration rate and kidney damage is often quantified by measuring albumin, the major protein in the urine standardised for urine concentration.
In the hypertension meta-analysis, low kidney function and high urine protein was associated with all-cause and cardiovascular mortality and ESRD in both individuals with and without hypertension. The associations of kidney function and urine protein with mortality outcomes were stronger in individuals without hypertension than in those with hypertension, whereas the kidney function and urine protein associations with ESRD did not differ by hypertensive status.
In the diabetes analysis, individuals with diabetes had a higher risk of all-cause, cardiovascular mortality and ESRD compared to those without diabetes across the range of kidney function and urine protein. Despite their higher risks, the relative risks of these outcomes by kidney function and urine protein are much the same irrespective of the presence or absence of diabetes.
‘Chronic kidney disease should be regarded as at least an equally relevant risk factor for mortality and ESRD in individuals without hypertension as it is in those with hypertension,’ said Bakhtawar K. Mahmoodi, MD, PhD, lead author of the hypertension analyses.
‘These data provide support for clinical practice guidelines which stage chronic kidney disease based on kidney function and urine protein across all causes of kidney disease. The conclusions are strengthened by the findings of leading studies and the participation of investigators from 40, countries and a detailed analysis of over 1 million participants,’ said Josef Coresh, MD, PhD, MHS, the Consortium’s principal investigator and professor in the Bloomberg School’s Department of Epidemiology. EurekAlert

Researchers in the Taub Institute at Columbia University Medical Center (CUMC) have identified a mechanism that appears to underlie the common sporadic (non-familial) form of Parkinson’s disease, the progressive movement disorder. The discovery highlights potential new therapeutic targets for Parkinson’s and could lead to a blood test for the disease. The study was based mainly on analysis of human brain tissue.
Studies of rare, familial (heritable) forms of Parkinson’s show that a protein called alpha-synuclein plays a role in the development of the disease. People who have extra copies of the alpha-synuclein gene produce excess alpha-synuclein protein, which can damage neurons. The effect is most pronounced in dopamine neurons, a population of brain cells in the substantia nigra that plays a key role in controlling normal movement and is lost in Parkinson’s. Another key feature of Parkinson’s is the presence of excess alpha-synuclein aggregates in the brain.
As the vast majority of patients with Parkinson’s do not carry rare familial mutations, a key question has been why these individuals with common sporadic Parkinson’s nonetheless acquire excess alpha-synuclein protein and lose critical dopamine neurons, leading to the disease.
Using a variety of techniques, including gene-expression analysis and gene-network mapping, the CUMC researchers discovered how common forms of alpha-synuclein contribute to sporadic Parkinson’s. ‘It turns out multiple different alpha-synuclein transcript forms are generated during the initial step in making the disease protein; our study implicates the longer transcript forms as the major culprits,’ said study leader Asa Abeliovich, MD, PhD, associate professor of pathology and cell biology and neurology at CUMC. ‘Some very common genetic variants in the alpha-synuclein gene, present in many people, are known to impact the likelihood that an individual will suffer from sporadic Parkinson’s. In our study, we show that people with ‘bad’ variants of the gene make more of the elongated alpha-synuclein transcript forms. This ultimately means that more of the disease protein is made and may accumulate in the brain.’
‘An unusual aspect of our study is that it is based largely on detailed analysis of actual patient tissue, rather than solely on animal models,’ said Dr. Abeliovich. ‘In fact, the longer forms of alpha-synuclein are human-specific, as are the disease-associated genetic variants. Animal models don’t really get Parkinson’s, which underscores the importance of including the analysis of human brain tissue.’
‘Furthermore, we found that exposure to toxins associated with Parkinson’s can increase the abundance of this longer transcript form of alpha-synuclein. Thus, this mechanism may represent a common pathway by which environmental and genetic factors impact the disease,’ said Dr. Abeliovich.
The findings suggest that drugs that reduce the accumulation of elongated alpha-synuclein transcripts in the brain might have therapeutic value in the treatment of Parkinson’s. The CUMC team is currently searching for drug candidates and has identified several possibilities.
The study also found elevated levels of the alpha-synuclein elongated transcripts in the blood of a group of patients with sporadic Parkinson’s, compared with unaffected controls. This would suggest that a test for alpha-synuclein may serve as a biomarker for the disease. ‘There is a tremendous need for a biomarker for Parkinson’s, which now can be diagnosed only on the basis of clinical symptoms. The finding is particularly intriguing, but needs to be validated in additional patient groups,’ said Dr. Abeliovich. A biomarker could also speed clinical trials by giving researchers a more timely measure of a drug’s effectiveness. Columbia University Medical Center

If you throw a ball underwater, you’ll find that the smaller it is, the faster it moves: A larger cross-section greatly increases the water’s resistance. Now, a team of MIT researchers has figured out a way to use this basic principle, on a microscopic scale, to carry out biomedical tests that could eventually lead to fast, compact and versatile medical-testing devices.
The results is based on work by graduate student Elizabeth Rapoport and assistant professor Geoffrey Beach, of MIT’s Department of Materials Science and Engineering (DMSE).
The balls used here are microscopic magnetic beads that can be ‘decorated’ with biomolecules such as antibodies that cause them to bind to specific proteins or cells; such beads are widely used in biomedical research. The key to this new work was finding a way to capture individual beads and set them oscillating by applying a variable magnetic field. The rate of their oscillation can then be measured to assess the size of the beads.
When these beads are placed in a biological sample, biomolecules attach to their surfaces, making the beads larger — a change that can then be detected through the biomolecules effect on the beads’ oscillation. This would provide a way to detect exactly how much of a target biomolecule is present in a sample, and provide a way to give a virtually instantaneous electronic readout of that information.
This new technique, for the first time, allows these beads — each about one micrometer, or millionth of a meter, in diameter — to be used for precise measurements of tiny quantities of materials. This could, for example, lead to tests for disease agents that would need just a tiny droplet of blood and could deliver results instantly, instead of requiring laboratory analysis. MIT

A current focus in global health research is to make medical tests that are not just cheap, but virtually free. One such strategy is to start with paper – one of humanity’s oldest technologies – and build a device like a home-based pregnancy test that might work for malaria, diabetes or other diseases.
A University of Washington bioengineer recently developed a way to make regular paper stick to medically interesting molecules. The work produced a chemical trick to make paper-based diagnostics using plain paper, the kind found at office supply stores around the world.
‘We wanted to go for the simplest, cheapest starting material, and give it more capability,’ said Daniel Ratner, a UW assistant professor of bioengineering and lead author of the paper
‘We also wanted to make the system as independent of the end applications as possible, something any researcher could plug into.’
Many paper-based diagnostics are made from nitrocellulose, a sticky membrane used in pregnancy tests and by medical researchers to detect proteins, DNA or antibodies in the human immune system.
Ratner hopes to replace that specialised membrane with cheap, ubiquitous paper, and to use it for any type of medical test – not just the big, biological molecules.
The UW technique uses minimal equipment or know-how. The researchers used a cheap, industrial solvent called divinyl sulfone that can be bought by the gallon and has been used for decades as an adhesive. Ratner’s group discovered they could dilute the chemical in water, carefully control the acidity, then pour it into a Ziploc bag and add a stack of paper, shake for a couple of hours, and finally rinse the paper and let it dry.
The dried paper feels smooth to the touch but is sticky to all kinds of chemicals that could be of medical interest: proteins, antibodies and DNA, for example, as well as sugars and the small-molecule drugs used to treat most medical conditions.
‘We want to develop something to not just ask a single question but ask many personal health questions,’ Ratner said. ‘‘Is there protein in the urine? Is this person diabetic? Do they have malaria or influenza?’’
To test their idea, the researchers ran the treated paper through an inkjet printer where the cartridge ink had been replaced with biomolecules, in this case a small sugar called galactose that attaches to human cells. They printed the biomolecules onto the sticky paper in an invisible pattern. Exposing that paper to fluorescent ricin, a poison that sticks to galactose, showed that the poison was present.
Now that they have proven their concept, Ratner said, they hope other groups will use the paper to develop actual diagnostic tests. University of Washington