Dec. 26, 2012 — Drinking to ring in the New Year may leave many suffering with the dreaded hangover. According to a 2009 study in the Journal of Food Science, published by the Institute of Food Technologists (IFT), the amino acids and minerals found in asparagus extract may alleviate alcohol hangover and protect liver cells against toxins.

Researchers at the Institute of Medical Science and Jeju National University in Korea analyzed the components of young asparagus shoots and leaves to compare their biochemical effects on human and rat liver cells. “The amino acid and mineral contents were found to be much higher in the leaves than the shoots,” says lead researcher B.Y. Kim.

Chronic alcohol use causes oxidative stress on the liver as well as unpleasant physical effects associated with a hangover. “Cellular toxicities were significantly alleviated in response to treatment with the extracts of asparagus leaves and shoots,” says Kim. “These results provide evidence of how the biological functions of asparagus can help alleviate alcohol hangover and protect liver cells.”

Asparagus officinalis is a common vegetable that is widely consumed worldwide and has long been used as an herbal medicine due to its anticancer effects. It also has antifungal, anti-inflammatory and diuretic properties.

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The above story is reprinted from materials provided by Institute of Food Technologists (IFT), via Newswise.

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Journal Reference:

1. B.-Y. Kim, Z.-G. Cui, S.-R. Lee, S.-J. Kim, H.-K. Kang, Y.-K. Lee, D.-B. Park. Effects of Asparagus officinalis Extracts on Liver Cell Toxicity and Ethanol Metabolism. Journal of Food Science, 2009; 74 (7): H204 DOI: 10.1111/j.1750-3841.2009.01263.x

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Dec. 23, 2012 — The mysterious inner workings of Chang Shan — a Chinese herbal medicine used for thousands of years to treat fevers associated with malaria — have been uncovered thanks to a high-resolution structure solved at The Scripps Research Institute (TSRI).

Described in the journal Nature this week, the structure shows in atomic detail how a two-headed compound derived from the active ingredient in Chang Shan works. Scientists have known that this compound, called halofuginone (a derivative of the febrifugine), can suppress parts of the immune system — but nobody knew exactly how.

The new structure shows that, like a wrench in the works, halofuginone jams the gears of a molecular machine that carries out “aminoacylation,” a crucial biological process that allows organisms to synthesize the proteins they need to live. Chang Shan, also known as Dichroa febrifuga Lour, probably helps with malarial fevers because traces of a halofuginone-like chemical in the herb interfere with this same process in malaria parasites, killing them in an infected person’s bloodstream.

“Our new results solved a mystery that has puzzled people about the mechanism of action of a medicine that has been used to treat fever from a malaria infection going back probably 2,000 years or more,” said Paul Schimmel, PhD, the Ernest and Jean Hahn Professor and Chair of Molecular Biology and Chemistry and member of The Skaggs Institute for Chemical Biology at TSRI. Schimmel led the research with TSRI postdoctoral fellow Huihao Zhou, PhD.

Halofuginone has been in clinical trials for cancer, but the high-resolution picture of the molecule suggests it has a modularity that would make it useful as a template to create new drugs for numerous other diseases.

The Process of Aminoacylation and its Importance to Life

Aminoacylation is a crucial step in the synthesis of proteins, the end products of gene expression. When genes are expressed, their DNA sequence is first read and transcribed into RNA, a similar molecule. The RNA is then translated into proteins, which are chemically very different from DNA and RNA but are composed of chains of amino acid molecules strung together in the order called for in the DNA.

Necessary for this translation process are a set of molecules known as transfer RNAs (tRNAs), which shuttle amino acids to the growing protein chain where they are added like pearls on a string. But before the tRNAs can move the pearls in place, they must first grab hold of them.

Aminoacylation is the biological process whereby the amino acid’s pearls are attached to these tRNA shuttles. A class of enzymes known as aminoacyl-tRNA synthetases is responsible for attaching the amino acids to the tRNAs, and Schimmel and his colleagues have been examining the molecular details of this process for years. Their work has given scientists insight into everything from early evolution to possible targets for future drug development.

Over time what has emerged as the picture of this process basically involves three molecular players: a tRNA, an amino acid and the aminoacyl-tRNA synthetase enzyme that brings them together. A fourth molecule called ATP is a microscopic form of fuel that gets consumed in the process.

The new work shows that halofuginone gets its potency by interfering with the tRNA synthetase enzyme that attaches the amino acid proline to the appropriate tRNA. It does this by blocking the active site of the enzyme where both the tRNA and the amino acid come together, with each half of the halofuginone blocking one side or the other.

Interestingly, said Schimmel, ATP is also needed for the halofuginone to bind. Nothing like that has ever been seen in biochemistry before.

“This is a remarkable example where a substrate of an enzyme (ATP) captures an inhibitor of the same enzyme, so that you have an enzyme-substrate-inhibitor complex,” said Schimmel.

The article, “ATP-Directed Capture of Bioactive Herbal-Based Medicine on Human tRNA Synthetase,” by Huihao Zhou, Litao Sun, Xiang-Lei Yang and Paul Schimmel was published in the journal Nature on Dec. 23, 2012.

This work was supported by the National Institutes of Health through grants #GM15539, #23562 and #88278 and by a fellowship from the National Foundation for Cancer Research.

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The above story is reprinted from materials provided by The Scripps Research Institute.

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Journal Reference:

1. Huihao Zhou, Litao Sun, Xiang-Lei Yang, Paul Schimmel. ATP-directed capture of bioactive herbal-based medicine on human tRNA synthetase. Nature, 2012; DOI: 10.1038/nature11774

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Dec. 8, 2012 — Research identifying genetic factors that affect survival of patients with blood cancers and evaluating the effectiveness of modified treatment strategies to improve outcomes while reducing toxicity will be presented December 8 at the 54th Annual Meeting of the American Society of Hematology (ASH).

While the cancer research community has seen many significant therapeutic advances over the last decade, only recently have investigators identified how patients’ individual genetic makeup influences their short- and long-term response to therapy, demonstrating that while the disease may respond positively to therapy, the patient may not. Current studies take these insights a step further, examining specific patient subpopulations to determine their risk for negative outcomes and whether early preventive interventions or treatment adjustments may help avoid treatment-related toxicity.

“Data presented today offer important insights into how and why patients respond to blood cancer treatment,” said William G. Woods, MD, moderator of the press conference, Pediatric Hematology/Oncology Director, and the Daniel P. Amos Children’s Chair of the Aflac Cancer Center and Blood Disorders Service at Children’s Healthcare of Atlanta. “Findings from these studies help further support the notion of one day personalizing cancer treatment to the individual, rather than to the disease, to improve survival and reduce toxicity.”

WT1 SNP rs16754 Genotype Predicts Treatment Related Mortality (TRM) in African-American and Asian Pediatric AML Patients: A Report From the Children’s Oncology Group

New research suggests that the presence of a specific genetic marker, known as WT1 SNP rs16754, may be associated with reduced toxicity from chemotherapy in African-American and Asian children with acute myeloid leukemia (AML).

AML, the second most common form of leukemia in children, is a blood cancer in which the bone marrow makes a large number of abnormal white blood cells that crowd out other healthy blood cells over time, leading to infection, anemia, or excessive bleeding. Although 60 to 70 percent of children with AML achieve long-term remission after treatment with multi-agent chemotherapy, the treatment-related mortality (TRM) associated with this intensive treatment regimen remains a major concern for this patient population. Recently, researchers have developed models that use sophisticated genome sequencing techniques to better understand how patients’ genetic makeup may influence their risk of TRM.

The WT1 gene, a tumor suppressor that regulates cell growth, can be subject to “loss-of-function” mutations that lead to the development of AML. Unlike genetic mutations, single-nucleotide polymorphisms (SNPs, naturally occurring variations in the DNA that determine an individual’s unique genetic makeup) are not typically thought to play a role in leukemia development or treatment response. However, researchers recently discovered that the presence of SNP rs16754 in the WT1 gene is correlated with improved outcomes in pediatric patients with AML. Based on the fact that the frequency of SNP rs16754 varies by race, researchers assessed the effect of this SNP on outcomes in specific ethnic patient groups.

To determine if the presence of SNP rs16754 affected survival, remission, relapse risk, and TRM in pediatric AML patients of different ethnicities, a team of investigators analyzed the DNA of 492 children with AML enrolled in the CCG-2961 protocol, a Phase III Children’s Cancer Group trial. The intensive treatment regimen delivered to patients during CCG-2961 allowed researchers to study the effects of ethnicity on patient outcome, while minimizing non-biological influences such as access to care or oral medication compliance. Of the 492 patients, 138 (28%) had the SNP rs16754 (SNP+). After stratifying the patients by ethnicity, the investigators found that the presence of SNP rs16754 varied by race, with 53 percent of Asians, 34 percent of Hispanics, 25 percent of Caucasians, and 21 percent of African Americans carrying the genetic variation. The SNP+ patients had higher five-year overall survival rates than those without the variation (SNP-) (61% vs. 44%). Within each racial subgroup, the five-year overall survival rate was higher in the SNP+ patients.

Although survival improvements in leukemia clinical trials are often attributed to increased remission rates or decreased relapse, remission and relapse rates did not differ significantly between SNP+ and SNP- patients in this study. The investigators examined whether the SNP had any association with TRM and found that TRM rates did not differ by SNP rs16754 genotype when all ethnicities were considered together. However, TRM rates in SNP+ African-American and Asian patients, when taken together, were significantly lower than in SNP- patients of those two ethnicities. African-American and Asian patients without SNP rs16754 had significantly higher rates of treatment-related toxic death compared to SNP+ patients (African-American: 25% vs. 0%; Asian: 43% vs. 0%). These results suggest that the protective effect of the presence of SNP rs16754 in reducing chemotherapy-related toxicity in pediatric AML patients is more pronounced in those of African-American and Asian descent.

“Identifying the patient-specific factors that can affect responses to treatment in different patients with the same disease brings us closer to our goal of designing personalized treatments that provide the most therapeutic benefit with the least amount of toxicity to these children,” said Phoenix Ho, MD, lead author and Attending Physician at Seattle Children’s Hospital in the Division of Pediatric Hematology/Oncology at the University of Washington School of Medicine and Research Associate at the Fred Hutchinson Cancer Research Center in Seattle. “Our analysis was conducted on a trial completed in 2002, and treatment protocols for pediatric AML have evolved since that time. Our next step is to validate our findings by studying this same association in contemporary trials. We are also designing studies to uncover the mechanism behind the association between the SNP and reduced toxicity, with the hope of translating these findings into improved treatments for pediatric AML.”

Genetic Susceptibility to Anthracycline-Related Congestive Heart Failure (CHF) in Survivors of Hematopoietic Cell Transplantation (HCT)

Researchers have identified specific genetic factors that are associated with heart failure in patients who have undergone hematopoietic stem cell transplantation (HCT) for blood cancer.

The transplantation of blood-forming stem cells from the bone marrow, circulating blood, or umbilical cord blood is the primary treatment option for many patients with blood cancer who relapse after receiving standard front-line therapies. During the transplant, healthy stem cells replace damaged cells that caused the illness, effectively curing patients of their disease. Advances in transplant strategies have led to a growing number of long-term survivors of HCT. However, this growing population of survivors is at risk for developing life-threatening complications such as congestive heart failure, due in large part to their exposure to pre-HCT treatments with a class of chemotherapy drugs called anthracyclines. Transplant survivors tend to develop heart failure earlier than the general population, and the overall survival rate following diagnosis is less than 50 percent.

By analyzing transplant patient demographics such as age and gender, treatment strategy (i.e., pre-HCT chemotherapy and chest radiation), and presence of cardiovascular risk factors such as high blood pressure, diabetes, and high cholesterol, researchers have been able to create a clinical profile to determine which patients are likely to develop heart failure after transplant. However, this current profile is limiting, as it fails to accurately explain the wide variability in the risk of heart failure between individual patients. Importantly, it does not account for how individuals’ genetic makeup can exacerbate their risk of developing heart failure.

Seeking additional insight into how genetics can influence the risk for developing heart failure later in life, researchers conducted a case-control study to identify the genetic pathways that may make certain transplant survivors more sensitive to the toxicities of pre-transplant chemotherapy and subsequently increase their risk of heart failure. In this study, the investigators evaluated specific genes responsible for the breakdown of anthracyclines into toxic byproducts (CBR1, CBR3, NQO1, MRP1, and MRP2), defense from oxidative stress, a condition that causes damage to healthy heart cells (NCF4, RAC2, CYBA, SOD), iron overload (HFE), and blood pressure and heart rate regulation (AGT, AGTR1, ACE and ADRB1, ADRB2) in 77 patients with leukemia, lymphoma, and myeloma who underwent a transplant at City of Hope between 1988 and 2007 and later developed congestive heart failure. Investigators matched the survivors with 178 controls (transplant survivors who did not experience heart failure).

After comparing the genetic makeup of the transplant survivors who developed heart failure to their controls, researchers found that patients who had variations in the MRP2, RAC2, and HFE genes had up to a three-fold higher risk of developing heart failure after transplant; these genes are responsible for key proteins that regulate the metabolism of anthracyclines and defense against oxidative stress. Females with two or more genetic variations were at the highest risk of developing the conditions when compared to males with one or none of these variations. The discovery of these genetic variations supplements previously identified clinical variables known to affect a transplant survivor’s heart health.

“Following this study we now have a much better profile of those transplant survivors who are likely to develop heart failure,” said Saro Armenian, DO, MPH, lead author and Assistant Professor in the Division of Outcomes Research and Medical Director of the Pediatric Survivorship Clinic in the Childhood Cancer Survivorship Program at City of Hope in Duarte, Calif. “Armed with these insights, we can now create better screening measures and perhaps even tailor intervention strategies based on a patients’ genetic makeup, minimizing long-term transplant-related toxicity and making a tremendous difference in the long-term health of these patients.”

Dr. Armenian will present this study in an oral presentation on Monday, December 10, at 2:45 p.m. EST at the Georgia World Congress Center in Room C108-C109, Level 1, Building C.

Daunorubicin or Not During the Induction Treatment of Childhood Standard-Risk B-Cell Precursor Acute Lymphoblastic Leukemia (SR-BCP-ALL): The Randomized Fralle 2000-A Protocol

New data demonstrate that omitting the chemotherapy drug daunorubicin from an initial treatment regimen for children with standard-risk acute lymphocytic leukemia (ALL) does not reduce survival outcomes, suggesting that these children may be able to achieve positive outcomes without having to endure a treatment associated with both short- and long-term toxicities.

ALL, the most common form of leukemia in children, is a fast-growing cancer of the white blood cells in which the bone marrow makes a large number of abnormal white blood cells that are unable to develop and fight infection. Important developments over the past 20 years have led to seminal insights about ALL in children, and today nearly 90 percent of children diagnosed with standard-risk ALL are cured. Some treatment regimens for standard-risk ALL include initial infusions of daunorubicin, a type of anthracycline. While effective, continual use of this therapy is associated with potential long-term heart damage, leading researchers to assess whether eliminating or reducing the dosage of daunorubicin during the initial one-month induction therapy period might provide the same level of efficacy as the standard treatment protocol with reduced long-term risk.

In order to assess the efficacy of ALL treatment without daunorubicin during induction therapy, a team of researchers from 20 centers across France and one center in Belgium initiated a multicenter Phase III clinical trial in which 1,128 pediatric patients with standard-risk B-cell ALL were randomized into two treatment arms. Arm A included 560 patients who received a standard dose of daunorubicin during induction therapy, while Arm B included 568 patients who did not receive initial therapy with daunorubicin. Both groups received doxorubicin during delayed intensification (last treatment phase before reaching maintenance) and a standard protocol of 24-month maintenance therapy from December 2000 to June 2010, during which five-year event-free survival (EFS) and overall survival (OS) were assessed.

For those patients treated with daunorubicin, the five-year EFS rate was 92.9 percent, compared to 93.3 percent in the non-daunorubicin arm. Overall survival rates were 97.2 percent and 98.2 percent in the daunorubicin and non-daunorubicin arms, respectively. Measurements of minimal residual disease, in which a small number of leukemic cells remain during treatment, were also equivalent in the two study arms. These results demonstrate similar efficacy rates of treatment strategies for standard-risk ALL that do or do not include induction treatment with daunorubicin.

“Our study data have the potential to benefit children with ALL in two important ways,” said Andre Baruchel, MD, lead author and Head of the Department of Pediatric Hematology at the Robert Debré University Hospital (Assistance Publique Hôpitaux de Paris) in Paris. “First, we now have strong evidence that reducing the amount of chemotherapy initially administered to these children, who constitute the majority of ALL patients, does not negatively affect their immediate outcome. Perhaps more importantly, we know and anticipate that removing harmful chemotherapy from their treatment can help minimize their risk of experiencing heart damage later in life.”

ATRA and Arsenic Trioxide (ATO) Versus ATRA and Idarubicin (AIDA) for Newly Diagnosed, Non High-Risk Acute Promyelocytic Leukemia (APL): Results of the Phase III, Prospective, Randomized, Intergroup APL0406 Study by the Italian-German Cooperative Groups Gimema-SAL-AMLSG

New research demonstrates the efficacy of the first curative treatment for acute promyelocytic leukemia (APL) that does not include chemotherapy, marking an important step toward front-line use of targeted therapies for acute leukemia.

APL is an uncommon, yet aggressive, subtype of acute myeloid leukemia (AML) in which there are too many immature white blood cells in the bone marrow, leading to a shortage of normal white and red blood cells and platelets in the blood, which is associated with clotting defects that can cause serious bleeding. Without prompt diagnosis and treatment, APL can be fatal in a matter of hours or days.

Early treatment regimens for APL relied heavily on anthracycline-based chemotherapy with daunorubicin or idarubicin. In the early 1990s, research supported the addition of a non-chemotherapeutic agent, all-trans-retinoic acid (ATRA, a vitamin A derivative developed from ancient Chinese herbal medicine), to standard regimens. ATRA causes cancer cells to develop fully into mature blood cells, which progress through full differentiation and eventually die (unlike leukemia cells that are unable to fully mature). The combination regimen of chemotherapy and ATRA dramatically improved the survival outlook for those with APL and made the disease curable in up to 80 percent of patients. More recently, another natural compound, arsenic trioxide (ATO), was integrated into APL treatment, showing higher efficacy and better tolerability when compared with conventional chemotherapy. Today, as investigators continue to report the success of targeted cancer therapies (best exemplified by imatinib for chronic myeloid leukemia), researchers have questioned whether traditional toxic chemotherapy is still necessary to achieve high cure rates for patients with APL.

To investigate whether a combination of ATO+ATRA could provide the same therapeutic benefit as conventional treatment including chemotherapy, researchers from the Italian-German cooperative teams Gruppo Italiano Malattie EMatologiche dell’Adulto (GIMEMA), Study Alliance Leukemia (SAL) group, and German-Austrian AML Study Group (AMSLG) designed a multicenter, international Phase III trial in which 162 patients with standard-risk APL were divided into two treatment arms. Patients in Arm A received a regimen of ATO+ATRA, while patients in Arm B received the standard ATRA+idarubicin (AIDA) treatment regimen. The primary study objective was event-free survival (EFS) at two years, with secondary objectives including overall survival (OS), disease-free survival (DFS), cumulative incidence of relapse (CIR) rates, molecular response, and safety.

Results suggest that the targeted ATO+ATRA therapy strategy might offer similar efficacy to the chemotherapy-based regimen. In the 154 patients who were evaluable for response, complete remission was achieved in all patients (100%) in the ATO+ATRA arm and 95 percent in the AIDA arm. EFS was observed in 97 percent in the ATO+ATRA arm, with one death and two relapses, compared to 86.7 percent in the AIDA arm, in which seven deaths and four relapses were observed. Overall survival, DFS, and CIR rates were 98.7 percent, 97 percent, and 1.6 percent, respectively, in the ATO+ATRA arm, versus 91.1 percent, 91.6 percent, and 4.3 percent, respectively, in the AIDA arm. Additionally, fewer side effects (fever, low neutrophil and platelet counts) were observed in the ATO+ATRA arm.

“This is one of the first times that we can report the success of a treatment strategy for an acute leukemia that relies solely on targeted molecular therapy,” said Francesco Lo-Coco, MD, lead author and Chairman of the APL subcommittee of the Italian GIMEMA group and Professor of Hematology at University Tor Vergata in Rome, Italy. “Our results are an important step toward the further utilization of targeted therapies for other types of leukemia, as we begin to focus on improving the overall treatment experience for patients by offering new strategies that deliver the same efficacy as traditional options with considerably lower toxicity.”

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ScienceDaily (Oct. 5, 2012) — When comes to minor complaints, chronic conditions and even fatal illnesses, people sometimes turn to ginseng and other herbal remedies.

A team of scientists from The Hong Kong Polytechnic University (PolyU) has been working on a new approach to drug development involving chemistry, biotechnology, mathematics, computer power and 5000-year ancient practices in Chinese medicine. The groundbreaking regime for herbal study and testing called quantitative-pattern-activity-relationship (“QPAR” in short) verifies the quality and health benefits of traditional herbs. While Western pharmacology focuses on purified chemical compounds such as Vitamin C, Prof. Chau Foo Tim from the Department of Applied Biology and Chemical Technology and Dr Daniel Sze from the Department of Health Technology and Informatics studied the impact from a mix of compounds, a unique property in herbs.

“Information-rich pattern called chromatographic fingerprint were used to prove the authenticity of a medicinal plant. Our research team has further utilized the ‘big data’ three dimensional (3D) fingerprints to give a good presentation of active ingredients and bioactivities that allow scientists to excavate any healing power from a mix of compounds,” said Prof. Chau.

To further bridge the gap between Chinese and Western medicines, Prof. Chau and Dr Sze have been working on a completely new drug classification and rating standard to establish a scientific link between traditional herbs and various diseases. The new QPAR standard for the first time links medicinal properties to cells, genes and proteins that trigger or contribute to a disease. For example, the magic fungus Ganoderma (靈芝) could be investigated for its ability to improve immunity by stimulating Dendritic Cells and therefore cell-mediated immune responses in our body.

“This is an innovative framework that quantifies the effect of traditional herbs would have on human health and common diseases on a sound scientific basis. QPAR can be used to verify how well Ganoderma can boost immunity and give a rating,” said Dr Sze.

The research is still at an early stage but if successful, scientists will only have to do laboratory tests and crunch on computers to build databases, and get an accurate projection of active ingredients, efficacy and toxicity for preliminary herbal study in the future.

Another breakthrough is that QPAR uses mathematical methods to make predictions and the sophisticated algorithms tapped into 5000-year ancient system of Chinese medicine which was based on the flow and balance of positive (yang) and negative (yin) energies in the body. “We believed that blending the Chinese understanding of diseases into the western medicines would yield an approach more successful in unlocking the full potential of Chinese herbs,” Dr Sze continued.

Dr Albert B. Wong, the founding president of the Modernised Chinese Medicine Association who was also a member of Hong Kong SAR Government’s Panel on Promoting Testing and Certification Services in Chinese Medicine Trade, shared his views on this novel technique. “Health benefits of herbal remedies are widely known but not yet proven. People don’t want to waste money or gamble on unproven treatments and then miss the chance of beating the diseases. New innovations are needed to bring transparency and credibility into herbal medicine.”

Dr Wong also believed that this innovation would drive the evolution of herbal trade. “Herbs can be grown, hand-picked or collected. The quality of active ingredients and medicinal effects also varies with region, altitude, growing techniques and processing methods. QPAR provides a scientific way to quickly verify the authenticity and active ingredients by different sources, making herbal trade fairer and more transparent. Drug companies would better control the prices and quality of raw herbs and also enforce standardisation and consistence across products. From the consumers’ point of view, it is worth to spend the money on products that can give exactly what they want for their health benefits.”

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ScienceDaily (Sep. 21, 2012) — Taking Gingko biloba supplements does not improve memory, attention or problem solving in healthy individuals, according to researchers from the University of Hertfordshire.

The paper, published in Human Psychopharmacology: Clinical and Experimental, is the first meta-analytic review examining the effects of Gingko biloba on healthy people across all age groups. The researchers led by Professor Keith Laws found zero impact on the cognitive functions whatever the age of the people, the dose taken or the length of time of taking Gingko biloba supplements.

Gingko biloba, the oldest tree living species, has been used extensively in traditional Chinese herbal medicine for thousands of years.  Today, it is one of the most widely used plant-based products available without prescription in Europe and North America, where is it marketed as a dietary supplement to treat blood disorders and, more specifically, to enhance memory both for healthy individuals and also for those trying to ward off Alzheimer’s Disease.

Keith Laws, Professor of psychology, said: “Gingko biloba has been widely used for a number of years to reduce the mental decline associated with aging.  But more recently it has been marketed as a memory enhancing supplement for healthy individuals – and it is crucial to establish the validity for such claims.

“Our findings show that taking Gingko biloba supplements at any age to boost memory have no impact at all – and may be a waste of time and money.”

The paper, “Is Gingko biloba a cognitive enhancer in healthy individuals? A meta-analysis”, examines the published research of thirteen randomised control trials of over 1000 healthy individuals across all ages. 

Other recently published studies have also shown that there is no evidence to support taking Gingko biloba supplements to protect against developing Alzheimer’s Disease.

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The above story is reprinted from materials provided by University of Hertfordshire, via AlphaGalileo.

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Journal Reference:

1. Keith R Laws, Hilary Sweetnam, Tejinder K Kondel. Is Ginkgo biloba a cognitive enhancer in healthy individuals? A meta-analysis. Human Psychopharmacology: Clinical and Experimental, 2012; DOI: 10.1002/hup.2259

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (Feb. 12, 2012) — For roughly two thousand years, Chinese herbalists have treated Malaria using a root extract, commonly known as Chang Shan, from a type of hydrangea that grows in Tibet and Nepal. More recent studies suggest that halofuginone, a compound derived from this extract’s bioactive ingredient, could be used to treat many autoimmune disorders as well. Now, researchers from the Harvard School of Dental Medicine have discovered the molecular secrets behind this herbal extract’s power.

It turns out that halofuginone (HF) triggers a stress-response pathway that blocks the development of a harmful class of immune cells, called Th17 cells, which have been implicated in many autoimmune disorders.

“HF prevents the autoimmune response without dampening immunity altogether,” said Malcolm Whitman, a professor of developmental biology at Harvard School of Dental Medicine and senior author on the new study. “This compound could inspire novel therapeutic approaches to a variety of autoimmune disorders.”

“This study is an exciting example of how solving the molecular mechanism of traditional herbal medicine can lead both to new insights into physiological regulation and to novel approaches to the treatment of disease,” said Tracy Keller, an instructor in Whitman’s lab and the first author on the paper.

This study, which involved an interdisciplinary team of researchers at Massachusetts General Hospital and elsewhere, will be published online February 12 in Nature Chemical Biology.

Prior research had shown that HF reduced scarring in tissue, scleroderma (a tightening of the skin), multiple sclerosis, scar formation and even cancer progression. “We thought HF must work on a signaling pathway that had many downstream effects,” said Keller.

In 2009, Keller and colleagues reported that HF protects against harmful Th17 immune cells without affecting other beneficial immune cells. Recognized only since 2006, Th17 cells are “bad actors,” implicated in many autoimmune diseases such as inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis and psoriasis. The researchers found that minute doses of HF reduced multiple sclerosis in a mouse model. As such, it was one of a new arsenal of drugs that selectively inhibits autoimmune pathology without suppressing the immune system globally. Further analysis showed that HF was somehow turning on genes involved in a newly discovered pathway called the amino acid response pathway, or AAR.

Scientists have only recently appreciated the role of the nutrient sensing-AAR pathway in immune regulation and metabolic signaling. There is also evidence that it extends lifespan and delays age-related inflammatory diseases in animal studies on caloric restriction. A conservationist of sorts, AAR lets cells know when they need to preserve resources. For example, when a cell senses a limited supply of amino acids for building proteins, AAR will block signals that promote inflammation because inflamed tissues require lots of protein.

“Think about how during a power outage we conserve what little juice we have left on our devices, foregoing chats in favor of emergency calls,” said Whitman. “Cells use similar logic.”

For the current study, the researchers investigated how HF activates the AAR pathway, looking at the most basic process that cells use to translate a gene’s DNA code into the amino acid chain that makes up a protein.

The researchers were able to home in on a single amino acid, called proline, and discovered that HF targeted and inhibited a particular enzyme (tRNA synthetase EPRS) responsible for incorporating proline into proteins that normally contain it. When this occurred, the AAR response kicked in and produced the therapeutic effects of HF-treatment.

Providing supplemental proline reversed the effects of HF on Th17 cell differentiation, while adding back other amino acids did not, establishing the specificity of HF for proline incorporation. Added proline also reversed other therapeutic effects of HF, inhibiting its effectiveness against the malaria parasite as well as certain cellular processes linked to tissue scarring. Again, supplementation with other amino acids had no such effect. Such mounting evidence clearly demonstrated that HF acts specifically to restrict proline.

The researchers think that HF treatment mimics cellular proline deprivation, which activates the AAR response and subsequently impacts immune regulation. Researchers do not yet fully understand the role that amino acid limitation plays in disease response or why restricting proline inhibits Th17 cell production.

Nevertheless, “AAR pathway is clearly an interesting drug target, and halofuginone, in addition to its potential therapeutic uses, is a powerful tool for studying the AAR pathway,” said Whitman.

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The above story is reprinted from materials provided by Harvard Medical School. The original article was written by Cathryn Delude.

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Journal Reference:

1. Tracy L Keller, Davide Zocco, Mark S Sundrud, Margaret Hendrick, Maja Edenius, Jinah Yum, Yeon-Jin Kim, Hak-Kyo Lee, Joseph F Cortese, Dyann F Wirth, John David Dignam, Anjana Rao, Chang-Yeol Yeo, Ralph Mazitschek, Malcolm Whitman. Halofuginone and other febrifugine derivatives inhibit prolyl-tRNA synthetase. Nature Chemical Biology, 2012; DOI: 10.1038/nchembio.790

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (Nov. 23, 2011) — A pioneering system which uses a plant’s DNA to identify and authenticate a species has been developed in Leicester. Experts from De Montfort University (DMU) have developed a method which can detect the use of illegal or counterfeit plants in medicine and could also be used to boost conservation by identifying and monitoring the exploitation of endangered plant species.

Currently, species are identified by measuring levels of chemical compounds in plants but the same level of compounds may be present in a number of different species.

DNA identification relies upon the genetic individuality of the species which is unique and therefore is much more accurate. The system, which is also faster and cheaper than the current means of identification, can detect the presence of the plant species expected in a product as well as detect any adulterant material, therefore showing if the plant medicine being tested is what it is supposed to be.

Scientists working on the new method at DMU are currently focused on the authentication of plants used in complementary and alternative medicines. These medicines have been increasing in popularity in Europe and America in recent years, with 35% of adults in the UK having used them.

The system has already proved successful with St. John’s Wort, one of the most highly used medicinal plants in Europe and America, used to treat depression, anxiety and sleep disorders. It is also currently being tested on Black Cohosh, one of the highest selling medicinal plants, used to combat menopausal symptoms, menstrual cramps, arthritis, muscle pain and indigestion.

Over the past decade Black Cohosh has been linked to a small number of cases of liver damage and other significant health issues but on inspection it has been suggested that the adverse reactions may have resulted from a substitute plant being used instead of the genuine one.

The potential harm that could result from adulteration of plant medicines is the driving force behind the UK Medicines and Healthcare Products Regulatory Agency’s implementation of the EU Traditional Herbal Medicines Directive.

This requires suppliers to register their products before they sell them — a very time consuming and expensive process. The use of this DNA system could reduce the timescale and provide a simpler method to demonstrate compliance with the regulators.

Adrian Slater, Professor of Biomolecular Technology at DMU, is leading the research. He said: “The development of this test could revolutionise the way information is collected on different species and will allow for better accuracy when plants are identified and authenticated.

“This could have huge implications for the billion pound medicinal plant business as until the development of DNA testing you couldn’t be sure that what you were being sold was the genuine product. It could also greatly improve plant conservation and help to identify and monitor endangered plant populations.” The £50,000 research project is being funded by the East Midlands Healthcare and Bioscience iNet. It is hoped that the system will be available for use in 2015.

The research is being conducted in DMU’s Faculty of Health and Life Sciences. Other research highlights within the faculty include the development of an artificial pancreas, a test which can determine the amount of medication in the blood by a single spot of blood and a tool which can help in the early detection of skin cancer.

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The above story is reprinted from materials provided by De Montfort University.

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (July 11, 2011) — An extract of the poisonous shrub Jatropha curcas acts as a strong painkiller and may have a mode of action different from conventional analgesics, such as morphine and other pharmaceuticals. Details of tests are reported in the current issue of the International Journal of Biomedical Engineering and Technology.

Omeh Yusuf and Ezeja Maxwell of the Micheal Okpara University of Agriculture in Umudike, Nigeria, explain how J. curcas, also known as the “physic nut” is a perennial shrub that grows to 5 meters in height and belongs to the Euphobiaceace family. It is native to Central America but grows widely in other tropical and subtropical countries of Africa and Asia. The plant’s fruit is combined with the stem bark of Cochlospermum planchonii in Nigerian medicine for treating diabetes mellitus and is also used traditionally as a painkiller. Other medicinal activities have been reported. The plant’s seeds have been used for making soap, candles, detergents, lubricants and dyes and the seed oil is used in biodiesel.

The researchers extracted what they believed to be the physiologically active components of the leaves of J. curcas using methanol as solvent. They compared the effects of this extract at 100, 200 and 400 milligrams per kilogram of body mass, against 400 mg/kg of acetylsalicylic acid (aspirin) in standard laboratory animal tests for assessing the strength of painkillers.

They found that 100 mg/kg was an inadequate dose, however, 200 and 400 mg/kg doses produced analgesia comparable to aspirin, affirming the use of the plant for pain relief in traditional medicine. The team suspect that the extract may be acting through both peripheral and central pain mechanisms. Yusuf and Maxwell are now carrying out more work on isolating and characterizing the active ingredient in the extract and in determining the precise mode of action.

The search for novel analgesic drugs that have a different side-effect profile and lack the tolerance and addiction problems associated with morphine and other opiates is an important avenue of research in drug discovery science. Very few leads from traditional and herbal medicine are successful in generating a new product, but it should be remembered that aspirin and morphine themselves were both originally derived from natural sources.

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Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Inderscience Publishers, via EurekAlert!, a service of AAAS.

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Journal Reference:

1. Omeh S. Yusuf, Ezeja I. Maxwell. The evaluation of the analgesic activity of the methanolic leaf extract of Jatropha curcas (Linn) in experimental animals. International Journal of Biomedical Engineering and Technology, 2011 – Vol. 6, No.2 pp. 200 – 207 DOI: 10.1504/IJBET.2011.041124

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (July 11, 2011) — An extract of the poisonous shrub Jatropha curcas acts as a strong painkiller and may have a mode of action different from conventional analgesics, such as morphine and other pharmaceuticals. Details of tests are reported in the current issue of the International Journal of Biomedical Engineering and Technology.

Omeh Yusuf and Ezeja Maxwell of the Micheal Okpara University of Agriculture in Umudike, Nigeria, explain how J. curcas, also known as the “physic nut” is a perennial shrub that grows to 5 meters in height and belongs to the Euphobiaceace family. It is native to Central America but grows widely in other tropical and subtropical countries of Africa and Asia. The plant’s fruit is combined with the stem bark of Cochlospermum planchonii in Nigerian medicine for treating diabetes mellitus and is also used traditionally as a painkiller. Other medicinal activities have been reported. The plant’s seeds have been used for making soap, candles, detergents, lubricants and dyes and the seed oil is used in biodiesel.

The researchers extracted what they believed to be the physiologically active components of the leaves of J. curcas using methanol as solvent. They compared the effects of this extract at 100, 200 and 400 milligrams per kilogram of body mass, against 400 mg/kg of acetylsalicylic acid (aspirin) in standard laboratory animal tests for assessing the strength of painkillers.

They found that 100 mg/kg was an inadequate dose, however, 200 and 400 mg/kg doses produced analgesia comparable to aspirin, affirming the use of the plant for pain relief in traditional medicine. The team suspect that the extract may be acting through both peripheral and central pain mechanisms. Yusuf and Maxwell are now carrying out more work on isolating and characterizing the active ingredient in the extract and in determining the precise mode of action.

The search for novel analgesic drugs that have a different side-effect profile and lack the tolerance and addiction problems associated with morphine and other opiates is an important avenue of research in drug discovery science. Very few leads from traditional and herbal medicine are successful in generating a new product, but it should be remembered that aspirin and morphine themselves were both originally derived from natural sources.

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Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Inderscience Publishers, via EurekAlert!, a service of AAAS.

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Journal Reference:

1. Omeh S. Yusuf, Ezeja I. Maxwell. The evaluation of the analgesic activity of the methanolic leaf extract of Jatropha curcas (Linn) in experimental animals. International Journal of Biomedical Engineering and Technology, 2011 – Vol. 6, No.2 pp. 200 – 207 DOI: 10.1504/IJBET.2011.041124

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

ScienceDaily (June 30, 2011) — Researchers from Boston University School of Medicine (BUSM) using a traditional Korean medicine, SO-CHEONG-RYONG-TANG (SCRT) that has long been used for the treatment of allergic diseases in Asia, found that SCRT treatment alleviates asthma-like pulmonary inflammation via suppression of specific chemokines or proteins. These findings appear online in the Annals of Allergy, Asthma & Immunology.

Asthma is a unique form of chronic respiratory disease characterized by reversible airway obstruction and pulmonary inflammation. It represents one of the most common chronic inflammatory diseases affecting an estimated 300 million people worldwide with an expected increase to 400 million by 2025. The sharply rising prevalence and incidence of asthma causes global concern both in the developed as well as in developing countries.

“In order to elucidate the mechanism of how SCRT modulates the allergic response, we evaluated the immunomodulatory effects of SCRT in a murine model of asthma induced by a house dust extract containing cockroach allergens and endotoxin,” explained Jiyoun Kim, PhD, a research assistant professor of pathology and laboratory medicine at BUSM. “In this study multiple aspects of pulmonary inflammation were examined including the production of inflammatory mediators and the pulmonary recruitment of inflammatory cells,” he added.

The researchers found SCRT treatment significantly reduced airway hyper-reactivity as measured by both whole body plethysmography and direct measurement of airway resistance. The researchers report that the immune response of pulmonary inflammation was significantly inhibited by SCRT treatment as demonstrated by reduced plasma IgE antibody levels and improved lung histology. SCRT significantly reduced the number of neutrophils in the bronchoalveolar (BAL) fluid and also significantly reduced the BAL levels of CXC chemokines both expressed as part of the immune response, providing a potential mechanism for the reduced inflammation.

This study was supported by grants from the National Institutes of Health and the Oriental Medicine R&D Project of the Ministry of Health & Welfare of the Republic of Korea.

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Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Boston University Medical Center.

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Journal Reference:

1. Jiyoun Kim, Sudha Natarajan, Hyunsu Bae, Sung-Ki Jung, William Cruikshank, Daniel G. Remick. Herbal medicine treatment reduces inflammation in a murine model of cockroach allergen–induced asthma. Annals of Allergy, Asthma & Immunology, 2011; DOI: 10.1016/j.anai.2011.05.001

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.