International conference on traditional medicine calls for common South-East Asian agenda

The international conference on traditional medicine for South East Asian Countries opened on Tuesday with a call to carve a common regional agenda from education to practice, from regulatory aspects research.
“Harmonized approaches based on best acceptable models existing in the region or other parts of the world could be instrumental in steering unified development of traditional medicine education, practice, regulation and progress toward mutual recognition of systems, qualifications, pharmacopoeias and other related aspects. Time has come to take up a common regional agenda for traditional medicine,” said Union Health Minister Ghulam Nabi Azad, while inaugurating the two-day conference here on Tuesday.
The Minister pointed out that the South-East Asian (SEA) countries had a rich heritage of several systems of Traditional Medicine. “They have vast resources of medicinal plants and huge repositories of knowledge. Different systems of traditional medicine have been used in the South-East Asia Region (SEAR) countries for centuries. Due to this long history, the role of Traditional Medicine and its practitioners have been recognized by the governments in this region,” he said.
Addressing the inaugural session, Dr Samlee Plianbang Chang, regional director General of WHO outlined the steps to be taken for promoting the traditional medicine in SEARO countries. The conference is being organised jointly by the AYUSH Department of the Health Ministry and the WHO.
AYUSH secretary Anil Kumar arrated the huge infrastructure of AYUSH developed by Govt. of India in the country and initiatives taken by the Department in quality of AYUSH drugs and practices. He appreciated the strengths of TM in prevention and control of non communicable diseases (NCDs) and recommended for strengthening these systems by solid research.
Health Ministers from Sri Lanka and Bangladesh, senior officials from different countries in the region, heads of research councils and senior practitioners of the traditional medicines were taking part in the conference.
Source:Pharmabiz

Silibinin, found in milk thistle, protects against UV-induced skin cancer

A pair of University of Colorado Cancer Center studies published this month show that the milk thistle extract, silibinin, kills skin cells mutated by UVA radiation and protects against damage by UVB radiation – thus protecting against UV-induced skin cancer and photo-aging.“When you have a cell affected by UV radiation, you either want to repair it or kill it so that it cannot go on to cause cancer. We show that silibinin does both,” says Rajesh Agarwal, PhD, co-program leader of Cancer Prevention and Control  at the CU Cancer Center and professor at the Skaggs School of Pharmacy and Pharmaceutical Sciences.The first study, published in the journal Photochemistry and Photobiology worked with human skin cells subjected to UVA radiation, which makes up about 95 percent of the sun’s radiation that reaches Earth. The Agarwal Lab treated these UVA-affected cells with silibinin. With silibinin, the rate at which these damaged cells died increased dramatically.“When you take human skin cells – keratinocytes – and treat them with silibinin, nothing happens. It’s not toxic. But when you damage these cells with UVA radiation, treatment with silibinin kills the cells,” Agarwal says, thus removing the mutated cells that can cause skin cancer and photo-aging.Specifically, the study shows that pretreatment with silibinin resulted in higher release of reactive oxygen species (ROS) within the UVA-exposed cells, leading to higher rates of cell death.The second study, published this month by the same authors in the journal Molecular Carcinogenesis shows that instead of beneficially killing cells damaged by UVA radiation, treatment with silibinin protects human skill cells from damage by UVB radiation, which makes up about 5 percent of the sun’s radiation reaching Earth.Again, remember Agarwal’s suggestion that the prevention of UV-induced skin cancer can happen in two ways: by protecting against DNA damage or by killing cells with damaged DNA. With UVA, silibinin kills; with UVB, it protects, in this case by increasing cells’ expression of the protein interleukin-12, which works to quickly repair damaged cells.“It has been 20 years of work with this compound, silibinin,” Agarwal says. “We first noticed its effectiveness in treating both skin and solid cancers, and we now have a much more complete picture of the mechanisms that allow this compound to work.”Agarwal and colleagues continue to test the effectiveness of silibinin in cancer prevention and treatment in cell lines and mouse models, and are working toward human trials of silibinin-based therapeutics.

Source:UCCC

SOME OMEGA-3 OILS BETTER THAN OTHERS FOR PROTECTION AGAINST LIVER DISEASE

Research at Oregon State University has found that one particular omega-3 fatty acid has a powerful effect in preventing liver inflammation and fibrosis – common problems that are steadily rising along with the number of Americans who are overweight.The American Liver Foundation has estimated that about 25 percent of the nation’s population, and 75 percent of those who are obese, have nonalcoholic fatty liver disease. This early-stage health condition can sometimes progress to more serious, even fatal diseases, including nonalcoholic steatohepatitis, or NASH, as well as cirrhosis and liver cancer.The study, published online in the Journal of Nutrition, was one of the first to directly compare the effects of two of the omega-3 fatty acids often cited for their nutritional value, DHA and EPA.In research with laboratory animals, it found that EPA had comparatively little effect on preventing the fibrosis, or scarring, that’s associated with NASH. However, DHA supplementation reduced the proteins involved in liver fibrosis by more than 65 percent.“A reduction of that magnitude in the actual scarring and damage to the liver is very important,” said Donald Jump, a principal investigator with the Linus Pauling Institute at OSU and a professor in the College of Public Health and Human Sciences.“Many clinical trials are being done with omega-3 fatty acids related to liver disease,” Jump said. “Our studies may represent the first to specifically compare the capacity of EPA versus DHA to prevent NASH. It appears that DHA, which can also be converted to EPA in the human body, is one of the most valuable for this purpose.”The issues have taken center stage as the weight of Americans continues to rise, with a related increase in the incidence of fatty liver disease and liver damage.NASH is a progressive form of liver disease that is associated with chronic inflammation and oxidative stress, resulting from excess fat storage in the liver. Chronic inflammation can eventually lead to fibrosis, cirrhosis, or even liver cancer. While management of lifestyle, including weight loss and exercise, is one approach to control the onset and progression of fatty liver disease, other approaches are needed to prevent and treat it.About 30-40 percent of people with nonalcoholic fatty liver disease progress to NASH, which in turn can result in cirrhosis, a major risk factor for liver cancer. While this research studied the prevention of fatty liver disease, Jump said, ongoing studies are examining the capacity of DHA to be used in NASH therapy.The levels of omega-3 oils needed vary with the health concern, officials say.“Omega-3 fatty acids are typically recommended for the prevention of cardiovascular disease,” Jump said. “Recommended intake levels of omega-3 fatty acids in humans for disease prevention are around 200-500 milligrams of combined DHA and EPA per day.”Levels used in therapy to lower blood triglycerides, also a risk factor for cardiovascular disease, are higher, about 2-4 grams of combined EPA and DHA per day. The OSU studies with mice used DHA at levels comparable to the triglyceride therapies.“DHA was more effective than EPA at attenuating inflammation, oxidative stress, fibrosis and hepatic damage,” the researchers wrote in their conclusion. “Based on these results, DHA may be a more attractive dietary supplement than EPA for the prevention and potential treatment of NASH in obese humans.”This work was the result of a four-year study supported by the USDA National Institute of Food and Agriculture, as well as the National Institutes of Health. Co-authors on the paper included Christopher M. Depner and Kenneth A. Philbrick, both graduate students in the Nutrition Graduate Program at OSU. 

Source:OSU

Exercise Cuts Prostate Cancer Risk in Caucasians

Among Caucasian men who do have prostate cancer, exercise was found to reduce the risk of the disease, finds study published in CANCER. Unfortunately, the benefits do not seem to apply to African-American men.Previous research has linked exercise to a reduced risk of developing prostate cancer. Studies have also revealed that African-American men have an increased risk of developing prostate cancer and of dying from the disease compared with Caucasians. It is not clear if exercise as a function of race plays any role in these disparities. 
To investigate, Lionel L. Bañez, MD, of the Durham Veterans Affairs Medical Center, and his colleagues asked 307 men (164 white; 143 black) undergoing a prostate biopsy to complete a survey that assessed their exercise amounts per week. The exercise categories included sedentary, mildly active, moderately active, and highly active. Among Caucasians, men who were moderately or highly active were 53% less likely to have biopsy results indicating that they had prostate cancer compared with men who were sedentary or mildly active. There was no association between exercise amount and prostate cancer among black men. 
The investigators also looked to see if exercise influenced the grade of tumors that were detected in men who did develop prostate cancer. Among men with cancer, those who exercised had a 13% reduced risk of having high grade disease, meaning that their cancer cells looked particularly abnormal under a microscope and were likely to quickly grow and spread. When this relationship was further explored as a function of race, it remained significant in Caucasians but not in African Americans. 
"These findings that African-American men may not benefit from exercise the way Caucasian men do could be a contributor to why African- American race is a risk factor for prostate cancer and aggressive prostate cancer. Further studies are needed to investigate the mechanism behind this racial disparity in deriving cancer-related benefits from exercise which disfavors African-American men," said Dr. Bañez.
 Source: Durham Veterans Affairs Medical Center

Scientists Discover Cause of Memory Decline in Elderly

The scientists found in mice that significantly more neurons are generated in the brains of older animals if a signaling molecule called Dickkopf-1 is turned off. 
In tests for spatial orientation and memory, mice in advanced adult age whose Dickkopf gene had been silenced reached an equal mental performance as young animals. 
The hippocampus - a structure of the brain whose shape resembles that of a seahorse - is also called the "gateway" to memory. This is where information is stored and retrieved. Its performance relies on new neurons being continually formed in the hippocampus over the entire lifetime. 
"However, in old age, production of new neurons dramatically decreases. This is considered to be among the causes of declining memory and learning ability", Prof. Dr. Ana Martin-Villalba, a neuroscientist, explains. 
Martin-Villalba, who heads a research department at the German Cancer Research Center (DKFZ), and her team are trying to find the molecular causes for this decrease in new neuron production (neurogenesis). 
Neural stem cells in the hippocampus are responsible for continuous supply of new neurons. Specific molecules in the immediate environment of these stem cells determine their fate: They may remain dormant, renew themselves, or differentiate into one of two types of specialized brain cells, astrocytes or neurons. One of these factors is the Wnt signaling molecule, which promotes the formation of young neurons. However, its molecular counterpart, called Dickkopf-1, can prevent this. 
"We find considerably more Dickkopf-1 protein in the brains of older mice than in those of young animals. We therefore suspected this signaling molecule to be responsible for the fact that hardly any young neurons are generated any more in old age," the scientists said. 
They tested their assumption in mice whose Dickkopf-1 gene is permanently silenced. 
Martin-Villalba's team discovered that stem cells in the hippocampus of Dickkopf knockout mice renew themselves more often and generate significantly more young neurons. 
The difference was particularly obvious in two-year old mice: In the knockout mice of this age, the researchers counted 80 percent more young neurons than in control animals of the same age. Moreover, the newly formed cells in the adult Dickkopf-1 mutant mice matured into potent neurons with multiple branches. In contrast, neurons in control animals of the same age were found to be more rudimentary already. 
The DKFZ researchers used standardized tests to study how the mice orient themselves in a maze. While in the control animals, the younger ones (3 months) performed much better in orienting themselves than the older ones (18 months), the Dickkopf-1-deficient mice showed no age-related decline in spatial orientation capabilities. Older Dickkopf-1 mutant mice also outperformed normal animals in tests determining spatial memory. 
"Our result proves that Dickkopf-1 promotes age-related decline of specific cognitive abilities," said Ana Martin-Villalba. 
"Although we had expected silencing of Dickkopf-1 to improve spatial orientation and memory of adult mice, we were surprised and impressed that animals in advanced adult age actually reach the performance levels of young animals," she added. 
These results give rise to the question whether the function of Dickkopf-1 may be turned off using drugs. 
Antibodies blocking the Dickkopf protein are already being tested in clinical trials for treating a completely different condition.
Source-ANI