Super-sized Cisplatin molecule effective against cancer while being less toxic

Using chemistry and nanotechnology, researchers at Harvard and Brigham and Women’s Hospital designed a super-sized Cisplatin molecule able to deliver toxic platinum atoms to tumors while proving nontoxic to kidneys.  The research was conducted on laboratory animals.
Cisplatin is a powerful anti-cancer drug used in first-line chemotherapy but with limited use because of its toxicity. The team designed a polymer what would bind to Cisplatin, making it wrap itself into a 100 nanometers ball, too large to enter the kidneys, lungs, liver and spleen.  Once the molecule reached the tumor it falls apart dumping its toxic load on the cancerous tissue.
The new compound has been found to be effective against lung and breast cancers and outperformed Cisplatin in a transgenic ovarian cancer model that mimics the disease in humans


source: http://www.healthyfeeds.com

Minocycline could be a cheap and safe treatment for stroke

Minocycline, an old anti-inflammatory drug, could be a safe and cheap treatment for stroke, with no adverse effects if the dose is between 200 and 700 milligrams. According to researchers from the Medical College of Georgia and the University of Georgia the drug is easy to administer and can be given with tPA.
Minocycline “is an old drug that has been studied extensively in healthy young people,” said Dr. Susan C. Fagan, professor of pharmacy at UGA, assistant dean for the MCG program of the UGA College of Pharmacy and the study’s first author. “Now that we know it’s also safe in a predominantly older stroke population, we can look more closely to identify the dose necessary to give us the pharmacologic effect we need.”
The early-stage clinical trial funded by the National Institutes of Health, opens the door to a much larger clinical trial assessing the antibiotic’s efficacy. The researchers are pursuing federal funding for a 2,000-patient international trial.

source: http://www.healthyfeeds.com

Insulin Tablets with better heat resistance 08/03/2010

More than 200 Million people are victims of Diabetes in the world.
Insulin is the most commonly drug which is used against diabetes.The most common problems with the insulin are that it should be kept at cool place(4 Centigrade) and can only be administered by injection.

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But now,a chemist "Miss. Wynn Le-rope" with her fellows,has found the solution for both problems,according to which Insulin can be kept at room temperature and can also be administered in the form of tablet dosage form.
Wynn Le-rope says,"I made a new chemical formula for insulin which can resist against heat up-to room temperature.(25 Centigrade) and soon it will also available in Tablet form."
The present form of insulin need to keep at  4 Centigrade for long term use after which the chemical formula of insulin start to be changed and ultimately denatured.Due to this reason it is very difficult to handle the insulin for long term use.
"I am also working on tablet dosage form of insulin and have succeeded in initial trials.In short period,diabetic patient will get relief from the pain of injection",she further said.

 

source:

http://www.epharmacygold.com/12/post/2010/08/insulin-tablets-and-with-better-heat-resistance.html

Army’s Vaccine Plan: Inject Troops With Gas-Propelled, Electro-Charged DNA Read More http://www.wired.com/dangerroom/2010/08/armys-vaccine-plan-inject-troops-with-gas-propelled-electro-charged-dna

The Army’s got a one-two punch to perfect vaccinations and offer scientists the ability to quickly develop inoculations that stave off new dangers. First, they’ll shoot troops up using a “gene gun,” that’s filled with DNA-based vaccines. Then they’ll follow it up with “short electrical pulses to the delivery site.”
The Pentagon’s still after a comprehensive way to inoculate troops and civilians against existing illnesses, rapidly respond to emerging threats, and even predict pathogenic mutations before they happen. To that end, the military’s already funding a handful of projects, from plant-based vaccine production to genetic signatures for ultra-early diagnosis.
In a small business solicitation released last week, the Army put out a call for “Multiagent Synthetic DNA Vaccines Delivered by Noninvasive Electroporation.” The program would start by transforming conventional development methods, like standard egg-based vaccines.
The old-school methods are slow, don’t allow for readily combined vaccines, and can pose sterility risks. DNA-based vaccines, on the other hand, would be quick to engineer and offer reliable immunity — provided the DNA can enter host cells to trigger the production of immunity proteins.
Right now, DNA-based vaccines are injected into muscles, meaning a genetically engineered plasmid is delivered to “intracellular spaces,” and “is not efficiently taken up by the host cells.” So the Army would instead like to shoot people. Seriously.

In its solicitation, the Army says it wants DNA vaccines that are painted onto microscopic beads, then “deposited into skin cells by gas propulsion.” And since that method can only inject a small dose of DNA, they want researchers to combine the approach with intramuscular electroporation, which “involves injecting the DNA then quickly applying short electrical pulses.” The electric charge creates pores in cell membranes, making it easier for DNA to enter targeted cells.
Sounds great, except that current approaches to intramuscular electroporation are invasive, and, obviously, they hurt. One study in rats also noted the “possibility of low and transient tissue damage induced by electroporation.” The Army wants a gadget that doesn’t rely on jamming needles and electrical pulses into muscle, and instead are after “injection and noninvasive electroporation [that] can be performed using a single integrated device.”
DNA-based vaccines are also still in their infancy: in 2005, the first-ever DNA vaccine for horses was approved, but human trials have yet to generate stellar results. And speaking of invasive: the Army’s delivery method of choice, gene guns, use helium gas to blast DNA into cells and often require surgically exposed muscle tissue to get the job done.
In other words, the Army’s asking for a non-invasive way to do what’s not yet possible, even using surgical methods. If researchers do come up with a device that meets the lofty criteria, though, it’d be just what the Pentagon’s looking for:  a reliable way to engineer and deliver combination vaccines — not to mention a quick way to fight back against “unknown, emerging, or genetically engineered pathogens.”

Read More http://www.wired.com/dangerroom/2010/08/armys-vaccine-plan-inject-troops-with-gas-propelled-electro-charged-dna/#ixzz0vfAkFTWN

Diabetes : Dapagliflozin Clinical Trial Results Indicate Improvement In Key Glycemic Measures In Treatment-Naïve Type 2 Diabetes Patients

30 Mar 2009  

Findings published in Diabetes Care from a 12-week, Phase IIb dose-ranging study showed that dapagliflozin, a novel, selective, sodium glucose co-transporter2 (SGLT2) inhibitor, produced clinically meaningful reductions across all key glycemic measures studied [glycosylated hemoglobin level (HbA1c), fasting plasma glucose (FPG), and postprandial plasma glucose (PPG)] in treatment-naïve type 2 diabetes patients, compared to placebo. The study findings also showed that patients receiving dapagliflozin experienced greater reductions in body weight compared to patients on placebo. Adverse events across dapagliflozin and metformin doses were reported at a similar rate, which was somewhat higher than placebo.

Dapagliflozin is an investigational SGLT2 inhibitor currently in Phase III trials under joint development by Bristol-Myers Squibb Company (NYSE: BMY) and AstraZeneca (NYSE: AZN) as a once-daily therapy for the treatment of type 2 diabetes. SGLT2 inhibitors act by inhibiting the reabsorption of glucose in the kidney, thereby reducing the return of filtered glucose to the circulation.

"These data suggest that dapagliflozin, the first SGLT2 to be studied in Phase III clinical trials, may reduce important glycemic measures and facilitate weight loss in patients with type 2 diabetes," said Elisabeth Svanberg, M.D., Ph.D., vice president, Development Lead, Bristol-Myers Squibb. "We look forward to further studies of dapagliflozin to fully understand its potential in the treatment of people with type 2 diabetes," said William Mezzanotte, M.D., M.P.H., vice president, Global Products, AstraZeneca.

About the Study

This Phase IIb study, presented at the 2008 American Diabetes Association annual meeting, was designed to assess the efficacy and safety of dapagliflozin across a wide range of doses. The data represent findings from a prospective, randomized, double-blind, placebo-controlled, parallel-group study of 389 individuals with type 2 diabetes (ages 18-79) who were treatment-naïve and whose HbA1c was greater than or equal to 7 percent and less than or equal to 10 percent. After a two-week lead-in phase that included diet, exercise and placebo, individuals were randomized to one of seven separate treatment arms: dapagliflozin 2.5 mg (n=59), 5 mg (n=58), 10 mg (n=47), 20 mg (n=59), 50 mg (n=56), metformin extended release 750 mg force-titrated at Week 2 to 1500 mg (n=56) or placebo (n=54), once daily for 12 weeks. Metformin was included as a positive control benchmark; no statistical comparison was made to the metformin arm.

The primary endpoint of the study compared mean HbA1c change from baseline for each dapagliflozin group versus placebo. The secondary endpoints included FPG change from baseline as compared to placebo, dose-dependent trends in glycemic efficacy, the proportion of individuals achieving the American Diabetes Association recommended HbA1c target of less than 7 percent and the change in 24-hour urinary glucose-to-creatinine ratio.

Study Results

After 12 weeks, individuals receiving dapagliflozin demonstrated a significant adjusted mean decrease in HbA1c from baseline of -0.71 percent for dapagliflozin 2.5 mg, -0.72 percent for dapagliflozin 5 mg, -0.85 percent for dapagliflozin 10 mg, -0.55 percent for dapagliflozin 20 mg and -0.90 percent for dapagliflozin 50 mg, compared to -0.18 percent for placebo (p-value at the 2.5, 5, 10 and 50 mg dose levels less than 0.001; p-value at the 20 mg dose level equal to 0.007). The adjusted mean decrease for metformin was -0.73 percent. No log-linear dose response relationship was demonstrated (P trend = 0.41).

Dapagliflozin also demonstrated a clinically meaningful adjusted mean decrease in FPG from baseline of -16 mg/dL for dapagliflozin 2.5 mg, -19 mg/dL for dapagliflozin 5 mg, -21 mg/dL for dapagliflozin 10 mg, -24 mg/dL for dapagliflozin 20 mg and -31 mg/dL for dapagliflozin 50 mg, compared to -6 mg/dL for placebo (p-value at the 2.5 mg dose level equal to 0.03; p-value at the 5 mg dose level equal to 0.005; p-value at the 10 mg dose level equal to 0.002; p-value at the 20 mg and 50 mg dose levels less than or equal to 0.001). The adjusted mean decrease for metformin was -18 mg/dL.

The percentage of individuals treated with dapagliflozin that achieved HbA1c of less than 7 percent after the 12 week treatment period was 46 percent for dapagliflozin 2.5 mg, 40 percent for dapagliflozin 5 mg, 52 percent for dapagliflozin 10 mg, 46 percent for dapagliflozin 20 mg and 59 percent for dapagliflozin 50 mg, compared to 32 percent for placebo and 54 percent for metformin. The 50 mg result was the only statistically significant result, with a p-value equal to 0.01.

Over 12 weeks, the incidence of adverse events was 59 percent for dapagliflozin 2.5 mg, 60 percent for dapagliflozin 5 mg, 68 percent for dapagliflozin 10 mg, 68 percent for dapagliflozin 20 mg and 63 percent for dapagliflozin 50 mg; the incidence of events was 54 percent for placebo and 68 percent for metformin. The percentages of the most commonly reported (greater than or equal to 10 percent in any group) adverse events for dapagliflozin 2.5 mg, 5 mg, 10 mg, 20 mg, and 50 mg doses and placebo and metformin, respectively, were: urinary tract infection [5, 9, 11, 7, 7, 6, 7], nausea [5, 7, 6, 3, 5, 6, 11], headache [7, 5, 4, 5, 2, 11, 4], and diarrhea [2, 2, 2, 7, 2, 7, 13].

The rate of reported hypoglycemic events was 7 percent for dapagliflozin 2.5 mg, 10 percent for dapagliflozin 5 mg, 6 percent for dapagliflozin 10 mg, 7 percent for dapagliflozin 20 mg and 7 percent for dapagliflozin 50 mg; the incidence of reported hypoglycemic events was 4 percent for placebo and 9 percent for metformin. There was no occurrence of confirmed hypoglycemia (symptoms of hypoglycemia with a fingerstick glucose less than or equal to 50 mg/dL).

Effects of Dapagliflozin on Weight Loss

The Phase IIb study also evaluated the potential impact of dapagliflozin-induced glucosuria on weight loss in people with type 2 diabetes, compared to placebo. These findings included data measuring changes in total body weight and body mass index over the 12-week study period.

Overall, greater percent decreases in total body weight occurred in the dapagliflozin treatment groups: -2.7 percent for dapagliflozin 2.5 mg, -2.5 percent for dapagliflozin 5 mg, -2.7 percent for dapagliflozin 10 mg, -3.4 percent for dapagliflozin 20 mg and -3.4 percent for dapagliflozin 50 mg compared to -1.2 percent for placebo and -1.7 percent for metformin.

About Type 2 Diabetes

Diabetes (diabetes mellitus) is a chronic disease in which the body does not produce or properly use insulin. Insulin is a hormone that is needed to convert sugar, starches (carbohydrates) and other nutrients into glucose, which is used as energy needed for daily life. The cause of diabetes continues to be investigated, and both genetic and environmental factors such as obesity and lack of exercise appear to play a role. Diabetes is associated with long-term complications that affect almost every part of the body. The disease may lead to blindness, heart and blood vessel disease, stroke, kidney failure, amputations, and nerve damage.

There are two primary underlying causes associated with type 2 diabetes: the body does not produce enough insulin (insulin deficiency), and the cells ignore the insulin (insulin resistance). Symptoms of type 2 diabetes develop gradually, and their onset is not as sudden as in type 1 diabetes. Symptoms may include fatigue, frequent urination, increased thirst and hunger, weight loss, blurred vision, and slow healing of wounds or sores. Some people, however, have no symptoms.

The kidneys play a key role in the overall regulation of blood glucose levels in the body. Normally, in healthy individuals, the kidneys filter a large volume of glucose and actively reabsorb virtually all of it. In patients with type 2 diabetes that have hyperglycemia, a greater amount of glucose is filtered and reabsorbed by the kidneys despite the fact that this perpetuates the hyperglycemia.

Over time, the factors that contribute to sustained hyperglycemia lead to glucotoxicity, which worsens insulin resistance and contributes to dysfunction in the beta cells of the pancreas. In this way, hyperglycemia appears to perpetuate a vicious cycle of deleterious effects that exacerbate type 2 diabetes.

Type 2 diabetes is most often associated with older age, obesity, family history of diabetes, previous history of gestational diabetes, physical inactivity and certain ethnicities. People with type 2 diabetes often are characterized with: insulin resistance, abdominal obesity, a sedentary lifestyle, having low HDL-C ("good") cholesterol levels and high triglyceride levels and hypertension.

About SGLT2 Inhibitors

The kidney continuously filters glucose through the glomerulus; however, nearly all of this glucose is reabsorbed in a separate part of the kidney called the proximal tubule. A protein called SGLT2 is responsible for the majority of glucose reabsorption and helps the body retain glucose for it's energy requirements. Inhibiting the activity of SGLT2 helps limit the amount of glucose that is reabsorbed and retained in the body, thereby leading to the excretion of glucose in the urine.

Bristol-Myers Squibb and AstraZeneca Partnership

Bristol-Myers Squibb and AstraZeneca entered into collaboration in January 2007 to enable the companies to research, develop and commercialize two investigational drugs for type 2 diabetes - saxagliptin and dapagliflozin. The Bristol-Myers Squibb/AstraZeneca Diabetes collaboration is dedicated to global patient care, improving patient outcomes and creating a new vision for the treatment of type 2 diabetes.

About Bristol-Myers Squibb

Bristol-Myers Squibb is a global biopharmaceutical company whose mission is to extend and enhance human life. For more information visit http://www.bms.com.

About AstraZeneca

AstraZeneca is a major international healthcare business engaged in the research, development, manufacturing and marketing of meaningful prescription medicines and supplier for healthcare services. AstraZeneca is one of the world's leading pharmaceutical companies with healthcare sales of US$ 31.6 billion and is a leader in gastrointestinal, cardiovascular, neuroscience, respiratory, oncology and infectious disease medicines. For more information about AstraZeneca, please visit: http://www.astrazeneca.com.

Source
AstraZeneca

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Article URL: http://www.medicalnewstoday.com/articles/144154.php

New cochlear implant improves the quality of sound while doing less damage to the ear

A new cochlear implant developed in the Biosystems Interface Laboratory at the Georgia Institute of Technology improves the quality of sound several times more than the conventional cochlear implants.

The new device called the thin film array uses a thinner wire on which are paired 12 electrodes. The thinner wire does less damage to the ear and could preserve residual hearing more than standard cochlear implants, while the higher number of electrodes improves the quality of sound. Dr. Kenneth Iverson, one of the researchers who worked on the device, said: “For the patient, it would be like the difference between hearing a Bach concerto played by a music box versus a quartet.”
Researchers presented their findings about the new device at the 11^th International Conference on Cochlear Implants and Other Auditory Implantable Technology in Stockholm, Sweden June 30 – July 3/2010


Source:
healthyfeeds.com

Glutathione :Short discription

Glutathione

Description
Glutathione is produced in the human liver and plays a key role in intermediary metabolism, immune response and health, though many of its mechanisms and much of its behavior await further medical understanding. It is also known as gamma-Glutamylcysteineglycine and GHS. It is a small protein composed of three amino acids, cysteine, glutamic acid and glyceine. Glutatione is found in two forms, a monomerthat is a single molecule of the protein, and a dimmer that is two of the single molecules joined together. The monomer is sometimes called reduced glutathione, while the dimmer is also called oxidized glutathione. The monomer is the active form of glutathione. Oxidized glutathione is broken down to the single molecule by an enzyme called glutathione reductase.
Glutathione, in purified extracted form, is a white powder that is soluble in water and in alcohol. It is found naturally in many fruits, vegetables, and meats. However, absorption rates of glutathione from food sources in the human gastrointestinal tract are low.
 
General use
Glutathione was first isolated in yeast in 1929. Its metabolism in the body was described in 1984, and its role in cancer treatment dates from 1984.
Glutathione is a major antioxidant highly active in human lungs and many other organ systems and tissues. It has many reported uses. It has a critical role in protecting cells from oxidative stress and maintaining the immune system. Higher blood levels of glutathione have been associated with better health in elderly people, but the exact association between glutathione and the aging process has not been determined.
Among the uses that have been reported for glutathione are:
•    treatment of poisoning, particularly heavy metal poisons
•    treatment of idiopathic pulmonary firbosis
•    increasing the effectiveness and reducing the toxicity of cis-platinum, a chemo drug used to treat breast cancer
•    treating Parkinson's disease
•    lowering blood pressure in patients with diabetes
•    increasing male sperm counts in humans and animals
•    treatment of liver cancer
•    treatment of sickle cell anemia
Claims made about glutathione have included that it will increase energy, improve concentration, slow aging, and protect the skin.
The importance of glutathione is generally recognized, although its specific functions and appropriate clinical use remain under study. Similarly, because ingested glutathione has little or no effect on intracellular glutathione levels, there are questions regarding the optimal method for raising the intracellular levels.
In addition to ongoing studies of the role of glutathione in cancer and cancer therapy, there are currently clinical trials of glutathione in Amyotrophic lateral sclerosis (ALS). The U. S. National Cancer Institute has included glutathione in a study to determine whether nutritional factors could inhibit development of some types of cancer.
European researchers, with support from the Cystic Fibrosis Foundation, are examining the potential uses of inhaled glutathione in cystic fibrosis. Some physicians also use inhaled glutathione in treating airway restriction and asthma. Other studies are investigating whether administration of alpha-lipoic acid, a material that can elevate intracellular glutathione, may be beneficial in restoring the immune system in AIDS patients.
 
Preparations
Although glutathione is marketed as a nutritional supplement, it does not appear that glutathione supplements actually increase the levels of glutathione inside cells. In human studies, oral doses of glutathione had little effect in raising blood levels. Further, glutathione is so widely distributed in common foods that supplements are not normally required. Supplements of vitamin C are more effective at increasing intracellular glutathione than taking oral glutathione supplements. Oral supplements of whey protein and of alpha-lipoic acid appear to help restore intracellular levels of glutathione.
Glutathione is available as capsules of 50, 100, and 250 milligrams. It is also included in many multivitamin and multi-nutrient formulations.
 
Precautions
At this time, the only established precautions are sensitivity to any of the inactive ingredients in the preparations of glutathione or the products used to stimulate glutathione levels. This is a discussion of glutathione, not C and whey. There is some new literature that suggests supplementing it may be helpful to some cancer patients, but detrimental to others.
 
Side effects
There are no established side effects to glutathione or to the substances used to elevate glutathione levels.
 
Training & certification
Glutathione has been classified as an orphan drug for treatment of AIDS. For this purpose, medical licensure is required. Glutathione has been given intravenously for amelioration of the side effects of cisplatin therapy. Specific training is required to order, prepare, start, and monitor intravenous therapy. No specific training is required to use glutathione or the compounds which have been reported to raise glutathione levels for other purposes.

BOOKS
Pressman, A. H. Glutathione: the Ultimate Antioxidant. New York: St. Martin's Press, 1997.
Rozzorno J. E., J. T. Murray, eds. Textbook of Natural Medicine, 2nd ed. Edinborough, Scotland: Churchill Livingston, 1999.
PERIODICALS
Carlo, M. D. Jr, and R. F. Loeser. "Increased oxidative stress with aging reduces chondrocyte survival: correlation with intracellular glutathione levels." Arthritis Rheum (December 2003): 3419–30.
Hamilton D., and G. Batist. "Glutathione analogues in cancer treatment." Curr Oncol Rep (March 2004): 116–22.
Wessner, B., E. M. Strasser, A. Spittler, and E. Roth. "Effect of single and combined supply of glutamine, glycine, N-acetylcysteine, and R, S-alpha-lipoic acid on glutathione content of myelomonocytic cells." Clin Nutr (December 2003): 515–22.
Witschi A., S. Reddy, B. Stofer, and B. H. Lauterburg. "The systemic availability of oral glutathione." Eur J Clin Pharmacol
Wu, G., Y. Z. Fang, S. Yang, J. R. Lupton, and N. D. Turner. "Glutathione metabolism and its implications for health." J Nutr (March 2004): 489–92.
Zenger, F., S. Russmann, E. Junker, C. Wuthrich, M. H. Bui, and B. H. Lauterburg. "Decreased glutathione in patients with anorexia nervosa. Risk factor for toxic liver injury?" Eur J Clin Nutr. (February 2004): 238–43.
ORGANIZATIONS
ALS Therapy Development Foundation. 215 First Street, Cambridge Mass. 02142.
Cystic Fibrosis Foundation. 6931 Arlington Road, Bethesda MD 20814.
NCCAM Clearinghouse. P.O. Box 7923 Gaithersburg, MD 20898.
Samuel Uretsky, Pharm.D