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joi, 15 decembrie 2011

Caffeine Study Shows Sport Performance Increase

Main Category: Sports Medicine / Fitness
Also Included In: Nutrition / Diet
Article Date: 15 Dec 2011 - 2:00 PST

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Caffeine combined with carbohydrate could be used to help athletes perform better on the field, according to new research by a sport nutrition expert.

Mayur Ranchordas, a senior lecturer and performance nutritionist at Sheffield Hallam University, carried out studies on footballers using caffeine and carbohydrates combined in a drink. Along with improvements in endurance caused by ingesting carbohydrate, the athletes' skill level improved after taking caffeine and carbohydrate together.

Mayur said: "There is already plenty of research that shows that caffeine and carbohydrate improve endurance, but this study shows that there is also a positive effect on skill and performance.

"We carried out three different soccer-specific match simulations of 90 minutes each two 45 minute sessions that tested agility, dribbling, heading and kicking accuracy. The test was designed to mimic a football game where the participants had to carry out multiple repeated sprints, dribble the ball around cones and shoot accurately.

"We found that the combination of carbohydrate and caffeine allowed players to sustain higher work intensity for the sprints, as well as improving shooting accuracy and dribbling during simulated soccer activity.

"These findings suggest that, for athletes competing in team sports where endurance and skill are important factors, ingesting a carbohydrate and caffeine drink, as opposed to just a carbohydrate drink, may significantly enhance performance. Our findings suggest that soccer players should choose a carbohydrate caffeine drink over a carbohydrate drink to consume before kick off and at half-time."

Article adapted by Medical News Today from original press release. Source: Sheffield Hallam University
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marți, 13 decembrie 2011

Childhood Cancer Survivors' Exposure To Chemotherapy, Radiation Does Not Increase Risk Of Birth Defects In Their Children

Main Category: Pediatrics / Children's Health
Also Included In: Cancer / Oncology
Article Date: 13 Dec 2011 - 1:00 PST

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A large, retrospective study shows that children of childhood cancer survivors who received prior treatment involving radiation to testes or ovaries and/or chemotherapy with alkylating agents do not have an increased risk for birth defects compared to children of survivors who did not have such cancer treatment. The findings provide reassurance that increased risks of birth defects are unlikely for cancer survivors who are concerned about the potential effects of their treatment on their children, and can help guide family planning choices.

"We hope this study will become part of the arsenal of information used by the physicians of childhood cancer survivors if reproductive worries arise," said lead author Lisa Signorello, Sc.D., associate professor of medicine at Vanderbilt University in Nashville, TN, and senior epidemiologist at the International Epidemiology Institute in Rockville, MD.

"Childhood cancer survivors face real reproductive concerns, including unknowns related to the effects of therapy. But, hopefully this study will provide some reassurance that their children are unlikely to be at increased risk for genetic defects stemming from their earlier treatment."

According to Signorello, childhood cancer patients frequently receive aggressive, though life-saving, radiation and chemotherapy treatments that can affect their ability to have children. For girls, radiation to the pelvis and the resulting damage to the uterus has been associated with a risk for pregnancy outcomes such as miscarriage and preterm birth, and effects on the ovaries can lead to infertility. Radiotherapy and chemotherapy with alkylating agents (e.g., busulphan, cyclophosphamide and dacarbazine) are DNA-damaging treatments, affecting both cancer and healthy cells. Studies to date have not adequately addressed the question of whether genetic damage from a parent's treatment could be passed down to their offspring. Genetic-based birth defects are rare in the general population (about 3 percent), and while previous research results indicated little or no increased risk for birth defects among the offspring of cancer survivors, such studies were relatively small in size and lacked detailed information about radiation and chemotherapy treatments, such as specific radiation doses to the testes and ovaries.

In the current study, investigators used information from the Childhood Cancer Survivor Study, a large retrospective study of treatment and outcomes in more than 20,000 childhood cancer survivors diagnosed between 1970 and 1986. Signorello and her colleagues examined data from 4,699 children of 1,128 men and 1,627 women who were 5-year childhood cancer survivors. The survivors reported their children's health problems through questionnaires, and investigators also examined medical records from survivors and their children, focusing on survivors' history of radiation to the testes or ovaries and chemotherapy with alkylating agents.

Of the survivors, 63 percent (1,736) had received radiation for their cancer as children, and 44 percent of men (496) and 50 percent of women (810) had received chemotherapy with alkylating agents. Overall, 2.7 percent (129) of the survivors' children had at least one birth defect, such as Down syndrome, achondroplasia or cleft lip. Researchers found that 3 percent of children of mothers exposed to radiation or treated with alkylating chemotherapy agents had a genetic birth defect, compared to 3.5 percent of children of mothers who were cancer survivors but did not have such exposures. Only 1.9 percent of children of male cancer survivors who received these DNA-damaging treatments had such birth defects, compared to 1.7 percent of children of male survivors who did not have this type of chemotherapy or radiation. The researchers concluded that children of cancer survivors were not at higher risk for birth defects stemming from parents' exposure to chemotherapy and/or radiation.

The researchers also noted that a strength of their study is the comparison they made to the children of other cancer survivors and not to the children of people randomly sampled from the general population. Signorello said that comparing cancer survivors to individuals in the general population can be difficult because the latter may not be as thorough in reporting health problems of their children, and the children of cancer survivors may be under heightened clinical surveillance and may appear to have higher rates of birth defects as a result. The investigators did, however, find that the overall prevalence of birth defects among the cancer survivors' children was very similar to what has been reported in the general population.

The study is among the largest to examine birth defects in children of childhood cancer survivors, and among the first to evaluate birth defects using medical records to validate both the children's health problems and the parents' radiation and chemotherapy exposures.

"The possibility of birth defects in offspring has been a lingering concern among cancer survivors because it's hard to address," Signorello said. "We know these are rare outcomes, and a large study group was needed to address these questions. It took years to validate the parents' self-reported outcomes, and to assemble and use the medical records of radiation and chemotherapy treatment exposures to allow us to quantify their exposure doses. These are the strongest results to date, adding greater certainty to other studies examining this common concern among survivors of childhood cancer."

The researchers would like to continue to sequence the DNA of families of childhood cancer survivors (survivors and their children) to see if there is any evidence of radiation- or chemical-induced genetic damage, even if the children did not have birth defects. They would also like to combine data from all U.S. and international studies on this topic in order to provide even larger, more definitive results.

"As the proportion of childhood cancer survivors within our population grows, it is clear that a very large number of former patients will be impacted by the results of this study. Cancer survivors and newly diagnosed patients worry about the effect that chemotherapy and radiation therapy may have on their future children. While we as oncologists have felt the risk of congenital abnormalities to be low, we now have concrete data from a very large number of children to support us in our conversations with survivors and newly diagnosed patients. These results will reassure survivors that their previous cancer therapy does not appear to result in an increased risk of birth defects in their future offspring."

Article adapted by Medical News Today from original press release. Source: American Society of Clinical Oncology
Visit our pediatrics / children's health section for the latest news on this subject. American Society of Clinical Oncology Please use one of the following formats to cite this article in your essay, paper or report:

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American Society of Clinical Oncology. "Childhood Cancer Survivors' Exposure To Chemotherapy, Radiation Does Not Increase Risk Of Birth Defects In Their Children." Medical News Today. MediLexicon, Intl., 13 Dec. 2011. Web.
13 Dec. 2011. APA
American Society of Clinical Oncology. (2011, December 13). "Childhood Cancer Survivors' Exposure To Chemotherapy, Radiation Does Not Increase Risk Of Birth Defects In Their Children." Medical News Today. Retrieved from
http://www.medicalnewstoday.com/releases/239068.php.

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joi, 8 decembrie 2011

Promising Multiple Sclerosis Treatment Targets Immune Cells To Increase Neuroprotection

Main Category: Multiple Sclerosis
Article Date: 08 Dec 2011 - 0:00 PST

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Laquinimod is an orally available synthetic compound that has been successfully evaluated in phase II/III clinical studies for the treatment of relapsing-remitting multiple sclerosis (RRMS). The mechanism of action of laquinimod has not been fully elucidated, but a study published in the January 2012 issue of The American Journal of Pathology suggests that laquinimod triggers immune cells within the central nervous system to produce and release brain-derived neurotrophic factor (BDNF), contributing to the repair or survival of neurons and thus limiting brain damage.

"Our data are indicative of a direct and sustained effect of laquinimod on the up-regulation of bioactive BDNF in patients with RRMS. Additionally, we demonstrate that laquinimod targets monocytes and skews the phagocyte population towards a regulatory phenotype, which in turn mediates immune modulation in vivo," explained Jan Thöne, MD, of the Department of Neurology at St. Josef-Hospital Bochum and Ruhr-University Bochum, Germany.

Neurotrophins, such as BDNF, are essential for the development and maintenance of neurons and axons in the central nervous system. Although BDNF is mainly produced by neurons, several types of immune cells also secrete BDNF, suggesting a role in neuroprotection.

To elucidate the mechanism of action of laquinimod, and to explore its potential neuroprotective capacity, the researchers evaluated levels of BDNF in the serum of RRMS patients treated with laquinimod in phase II clinical trials. A significant and robust BDNF increase occurred in 76% of the laquinimod-treated patients, with up to an 11-fold increase in BDNF serum levels observed in individual patients. BDNF elevation in individual patients was independent of relapse rate, and there was no correlation between BDNF levels and age, gender, or baseline disability. Yet, the source of serum BDNF subsequent to treatment remained questionable.

Experiments with animal models corroborated the findings in human patients. Experimental autoimmune encephalomyelitis (EAE; a model of MS) was induced in mice with a conditional BDNF deficiency in immune cells (LLF mice) and in wild-type (WT) control mice. Treatment with laquinimod resulted in a significant reduction in EAE incidence and disease severity in the WT mice. The effect of laquinimod was significantly reduced in the LLF-mice.

Further studies showed that WT mice treated with a suboptimal dose of laquinimod demonstrated a significant reduction in the inflammatory area and level of demyelination. These mice also displayed a reduction of macrophage infiltration and a significant preservation of axonal densities in comparison with laquinimod-treated LLF mice and controls. The data suggest a BDNF-dependent mechanism of action for laquinimod in autoimmune demyelination.

To investigate whether laquinimod-treated monocytes mediate immune modulation in vivo, laquinimod-stimulated monocytes were injected into WT mice at an early EAE disease stage. The mice showed less severe disease course than controls. Transfer of laquinimod-treated cells derived from LLF mice into WT mice with ongoing EAE did not influence disease course. The cells also secrete significantly less IL-10, an immunomodulatory cytokine that is associated with the generation of regulatory monocytes.

"Consistent with immunomodulatory properties, laquinimod skewed monocytes towards a regulatory phenotype and also acted via modulation of BDNF, which may contribute to neuroprotection in MS patients," said Dr. Thöne. "To date, selective targeting of monocytes has not been described for any other MS pipeline drug, highlighting an innovative mechanism of action of laquinimod."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our multiple sclerosis section for the latest news on this subject. The article is "Modulation of Autoimmune Demyelination by Laquinimod via Induction of Brain Derived Neurotrophic Factor," by J. Thöne, G. Ellrichmann, S. Seubert, I. Peruga, D-H. Lee, R. Conrad, L. Hayardeny, G. Comi, S. Wiese, R.A. Linker, R. Gold (doi: 10.1016/j.ajpath.2011.09.037). It will appear in The American Journal of Pathology, Volume 10, Issue 1 (January 2012) published by Elsevier.
Elsevier Health Sciences Please use one of the following formats to cite this article in your essay, paper or report:

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