Researchers studying multiple sclerosis (MS) have long been looking for the specific molecules in the body that cause lesions in myelin, the fatty, insulating cells that sheathe the nerves. Nearly a decade ago, a group at Mayo Clinic found a new enzyme, called Kallikrein 6, that is present in abundance in MS lesions and blood samples and is associated with inflammation and demyelination in other neurodegenerative diseases. In a study the same group found that an antibody that neutralises Kallikrein 6 is capable of staving off MS in mice.
‘We were able to slow the course of disease through early chronic stages, both in the brain and spinal cord,’ says lead author Isobel Scarisbrick, Ph.D., of the Mayo Clinic Department of Physical Medicine and Rehabilitation.
Researchers looked at mice representing a viral model of MS. The model is based on the theory that infection with viral infection early in life results in an eventual abnormal immune response in the brain and spinal cord. One week after being infected with a virus, the mice showed elevated levels of Kallikrein 6 enzyme in the brain and spinal cord. However, when researchers treated mice to produce an antibody capable of blocking and neutralising the enzyme, they saw a decrease in diseases effecting the brain and spinal cord, including demyelination. The Kallikrein 6 neutralising antibody had reduced inflammatory white blood cells and slowed the depletion of myelin basic protein, a key component of the myelin sheath.
The findings in the MS model have implications for other conditions affecting the brain and spinal cord. The group has previously shown that the Kallikrein 6 enzyme, produced by immune cells, is elevated in spinal cord injury, while other studies have shown it to be elevated in animal models of stroke and patients with post-polio syndrome.
‘These findings suggest Kallikrein 6 plays a role in the inflammatory and demyelinating processes that accompany many types of neurological conditions,’ says Dr. Scarisbrick. ‘In the early chronic stages of some neurological diseases, Kallikrein 6 may represent a good molecule to target with drugs capable of neutralizing its effects.’ Mayo Clinic

A study of almost 3,800 pregnancies has provided the most accurate and direct evidence to date that malaria infection reduces early foetal growth. Low birth weight is the most important risk factor for neonatal mortality in developing countries. The research highlights the importance of preventing malaria in pregnancy.
According to the World Malaria Report 2011, malaria killed an estimated 655,000 people in 2010. The disease is one of the most common parasitic infections to affect pregnancy. Previous studies have suggested that infection with both P. falciparum and P. vivax malaria during pregnancy reduces birth weight whether or not maternal symptoms are present. However, these studies have been hampered by difficulties in estimating gestational age accurately and diagnosing malaria infection in early pregnancy.
Now researchers at the Shoklo Malaria Research Unit on the border of Thailand and Myanmar, part of the Wellcome Trust-Mahidol University-Oxford University Tropical Medicine Research Programme, have used ultrasound scans to provide the first direct evidence of the effect of malaria on foetal growth in pregnancy. Antenatal ultrasound, which is essential for dating pregnancy accurately, is becoming more widely available in developing countries. The technology also allows the diameter of the foetus’s head to be measured. For infections that occur in early pregnancy, the researchers believe that the size of the head may be the most appropriate indicator of growth restriction.
The ultrasound scans revealed that the diameter of the average foetus’s head was significantly smaller when malaria infection occurred in the first half of pregnancy when compared to pregnancies unaffected by malaria. On average, at the mid-pregnancy ultrasound scan the foetuses’ heads were 2% smaller when affected by malaria. Even a single infection of treated P. falciparum or P. vivax malaria was associated with reduced foetal head diameter, irrespective of whether the woman had shown symptoms or not.
However, although a single early detected and well-treated malaria episode had an effect on foetal head size at mid-trimester, this was not seen at delivery, suggesting that early treatment with effective drugs may allow for growth to recover later in pregnancy.
Strategies to prevent malaria in pregnancy have focused on the second half of pregnancy, when most of the foetal weight gain takes place, but this works suggests that focus should be on the first trimester too. Pregnant woman need to be educated about the risks of malaria in pregnancy and where possible in areas of high risk, offered preventative medication from early pregnancy onwards.

Developed in Canada and conducted by researchers from the University of Ottawa Heart Institute, in partnership with Spartan Bioscience, the world’s first bedside genetic test has received acknowledgment by The Lancet. The article entitled ‘Point-of-care genetic testing for personalisation of antiplatelet treatment (RAPID GENE): a prospective, randomised, proof-of-concept trial’ reports on the use of a simple cheek swab test, the Spartan RX CYP2C19, performed by nurses at the patient’s bedside. This revolutionary technology allows patients with the genetic variant CYP2C19*2 to be rapidly identified. Cardiac stent patients with this variant are at risk of reacting poorly to standard anti-platelet therapy with Plavix (clopidogrel).
The study demonstrated that tailored drug treatment therapy made possible by genetic testing successfully protected all of the patients with the at-risk genetic variant from subsequent adverse events, while 30 per cent of patients treated with standard therapy did not receive adequate protection. The test is a significant step towards the realisation of personalised medicine.

Scientists from the University of Liverpool’s School of Environmental Sciences are working with computer modelling specialists from C-MMACS in India to predict areas of the country that are at most risk of malaria outbreaks, following changes in monsoon rainfall. The number of heavy rainfall events in India has increased over the past 50 years, but research has tended to focus on the impact this has on agriculture rather than the vector-borne diseases, such as malaria and Japanese encephalitis. The model could help inform early intervention methods to prevent the spread of malaria at key points in the seasonal monsoon cycle, reducing the economic and health impacts of the disease. It is already known that an anomalous season of heavy rainfall, when heat and humidity are high, allows mosquitoes to thrive and spread infection to humans. In order to prepare health services and prevent epidemics there is need for a way of predicting when these events are likely to occur in areas that are not accustomed to annual outbreaks of malaria. C-MMACS is rapidly developing its computer modelling capabilities using technology that can address the impacts of climate variability on agriculture and water systems. This knowledge, together with the Liverpool models of vector-borne diseases, will help develop systems to predict when changes in the monsoonal rain may occur and which areas are most likely to see an increase in malaria.

Fibroid uterine tumours affect an estimated 15 million women in the United States, causing irregular bleeding, anaemia, pain, and infertility. Despite the high prevalence of the tumours, which occur in 60 percent of women by age 45, the molecular cause has been unknown.
New Northwestern Medicine pre-clinical research has for the first time identified the molecular trigger of the tumour — a single stem cell that develops a mutation, starts to grow uncontrollably and activates other cells to join its frenzied expansion.
‘It loses its way and goes wild,’ said Serdar Bulun, MD, the chair of obstetrics and gynaecology at Northwestern University Feinberg School of Medicine and Northwestern Memorial Hospital. ‘No one knew how these came about before. The stem cells make up only 1.5 percent of the cells in the tumour, yet they are the essential drivers of its growth.’
The stem cell initiating the tumour carries a mutation called MED12. Recently, mutations in the MED12 gene have been reported in the majority of uterine fibroid tissues. Once the mutation kicks off the abnormal expansion, the tumours grow in response to steroid hormones, particularly progesterone.
For the study, researchers examined the behaviour of human fibroid stem cells when grafted into a mouse, a novel model initiated by Northwestern scientist Takeshi Kurita, PhD, a research associate professor of obstetrics and gynaecology. The most important characteristic of fibroid stem cells is their ability to generate tumours. Tumours originating from the fibroid stem cell population grew 10 times larger compared to tumours initiated with the main cell population, suggesting a key role of these tumour stem cells is to initiate and sustain tumour growth.
‘Understanding how this mutation directs the tumor growth gives us a new direction to develop therapies,’ said Bulun, also the George H. Gardner Professor of Clinical Gynecology. University Feinberg School of Medicine