Thu, May 27 01:59 PM
Toronto, May 27 (IANS) Scientists have discovered a protein switch that will help kill deadly water-based pathogens like E. coli and make for safer drinking water.
Zongchao Jia, a professor of biochemistry at Queen's University, and post-doctoral student Jimin Zheng, discovered exactly how the AceK protein acts as a switch in some bacteria to bypass the energy-producing cycle.
This bypassing allows dangerous bacteria like E. coli and salmonella to go into a survival mode and adapt to low-nutrient environments, such as water.
The unique feature of this discovery is that the switching on and off take place in the same location of the protein. Normally, these two opposing activities would happen in two different 'active sites'.
'From a protein function point of view, this is unique and has never been discovered anywhere else,' says Jia.
The discovery opens the door for scientists to identify a molecule that can keep the bypass switch from turning on so bacteria will die in water.
As a result, drinking water would be cleaner and the incident of water bacterial contamination could be reduced.
'While other organisms cannot survive without nutrients, the bypass controlled by AceK allows the bacteria to live and cause health problems,' says Jia.
Conversely, discovering a molecule to keep the bypass switch turned on could produce a supply of the bacteria which biotechnology companies use to produce compounds such as insulin.
Instead of using glucose in the fermenting process, companies could use less nutritional and cheaper acetate.
The cost difference would be tremendous and the process would produce less carbon dioxide making the process much more environmentally friendly, said a Queen's release.
'So we haven't found a cure to stop diseases like E. coli water contamination, but we've provided a template for people to design a molecule that will disable its ability to survive in water,' says Jia.
'It's like we have discovered how a lock works and now all we need is to design a key,' concluded Jia.
These findings have been published in Nature.
Thursday, May 27, 2010
FDA: Rare Cases of Liver Injury Reported with Use of Xenical, Alli
Thursday, 27 May 2010
The U.S. Food and Drug AdministrationThe U.S. Food and Drug Administration advised consumers and health care professionals about potential rare occurrences of severe liver injury in patients taking the weight-loss medication orlistat, marketed as Xenical and Alli.
The FDA has approved a revised label for the prescription drug Xenical. The agency is working with the manufacturer of Alli on label revisions to reflect this rare occurrence.
Both Xenical and Alli are medications contain the same active ingredient, orlistat. Xenical, available only by prescription, contains 120 milligrams of orlistat. Alli, sold over-the-counter without a prescription, contains 60 mg of orlistat. An estimated 40 million people worldwide have taken either Xenical or Alli.
The FDA's safety information and labeling changes are based on a review of cases of severe liver injury reported in individuals taking orlistat. The agency has identified 13 cases of severe liver injury, 12 of which were reports from outside of the United States. The only U.S. report of severe liver injury involved Alli. At this time, a cause-and-effect relationship of severe liver injury with orlistat use has not been established.
People who take Xenical or Alli should be aware that liver injury with orlistat - while rare - has been reported. Those taking the drug also should be aware of the signs and symptoms of liver injury, which include itching, yellow eyes or skin, dark urine, loss of appetite, or light-colored stools.
The U.S. Food and Drug AdministrationThe U.S. Food and Drug Administration advised consumers and health care professionals about potential rare occurrences of severe liver injury in patients taking the weight-loss medication orlistat, marketed as Xenical and Alli.
The FDA has approved a revised label for the prescription drug Xenical. The agency is working with the manufacturer of Alli on label revisions to reflect this rare occurrence.
Both Xenical and Alli are medications contain the same active ingredient, orlistat. Xenical, available only by prescription, contains 120 milligrams of orlistat. Alli, sold over-the-counter without a prescription, contains 60 mg of orlistat. An estimated 40 million people worldwide have taken either Xenical or Alli.
The FDA's safety information and labeling changes are based on a review of cases of severe liver injury reported in individuals taking orlistat. The agency has identified 13 cases of severe liver injury, 12 of which were reports from outside of the United States. The only U.S. report of severe liver injury involved Alli. At this time, a cause-and-effect relationship of severe liver injury with orlistat use has not been established.
People who take Xenical or Alli should be aware that liver injury with orlistat - while rare - has been reported. Those taking the drug also should be aware of the signs and symptoms of liver injury, which include itching, yellow eyes or skin, dark urine, loss of appetite, or light-colored stools.
Tuesday, May 25, 2010
List of top M.Pharm Colleges in India
| Degree / Course | College / Institute | State | Eligibility | Course Duration |
| Pharmacy-M Pharm | Goa College of Pharmacy, Panaji 403001 | Goa | B.Pharm. | 2 year |
| Pharmacy-M Pharm | AL-Ameen College of Pharmacy, Hosur Road Near Lalbagh, Main Gate, Bangalore 560027 | Karnataka | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Bombay College of Pharmacy Kalina, Santacruz, Mumbai 400098 | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | University College of Pharmaceutical Science, Warangal 506009 | Andhra Pradesh | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Principal K. M. Kundnani, College of Pharmacy, Plot 47, Worli, Seaface, Mumbai 400025 | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Kanak Manjari Institute of Pharmaceutical Sciences, Chhend, Sector - 20, Rourkela | Orissa | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Nagpur University Department of Pharmaceutical Sciences, Nagpur 440010 | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | NDM VP Samaj College of Pharmacy, Shivajinagar, Gangapur Road, Nasik 422002 | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Department of Pharmaceutical Sciences, J.V.D. College of Engineering, Visakhapatnam 530003 | Tamil Nadu | B.Pharm. | 2 year |
| Pharmacy-M Pharm | College of Pharmacy, Pravaranagar A/P Loni 413736, Distt. Ahmednagar | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | College of Pharmacy, Sri Rama Krishna Institute of Pharamedical Sciences, 395, Sarojini Naidu Road, Coimbatore 641044 | Tamil Nadu | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Lallubhai Motilal College of Pharmacy, Navrangpura, Ahmedabad 380009 | Gujarat | B.Pharm. | 2 year |
| Pharmacy-M Pharm | CU Shah Coll of Pharmacy, Vidya Vihar Santacruz (W), Mumbai | Maharashtra | B.Pharm. | 2 year |
| Pharmacy-M Pharm | College of Pharmaceutical Sciences, Kasturba Medical College, Manipal 576119 | Karnataka | B.Pharm. | 2 year |
| Pharmacy-M Pharm | University Institute of Pharmaceutical Technology, Annamalai University, Annamalainagar 608002 | Tamil Nadu | B.Pharm. | 2 year |
| Pharmacy-M Pharm | JSS College of Pharmacy Rocklands, Elkhill Rd., Ootacamund 643001 | Tamil Nadu | B.Pharm. | 2 year |
| Pharmacy-M Pharm | CL Baid Metha College of Pharmacy, Jyoti Nagar, Tharapakkam, Madras 600096 | Tamil Nadu | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Government College of Pharmacy, Lalbagh Road, Bangalore 560027 | Karnataka | B.Pharm. | 2 year |
| Pharmacy-M Pharm | Dr. Harisingh Gour Vishwavidyalaya, Deptt. of Pharmaceutical Science, Sagar 470003 | Madhya Pradesh | B.Pharm. | 2 year |
New Twist on Potential Malaria Drug Target Acts by Trapping Parasites in Cells
Friday, 21 May 2010
Harvard School of Public Health (HSPH) researchers and colleagues seeking to block invasion of healthy red blood cells by malaria parasites have instead succeeded in locking the parasites within infected blood cells, potentially containing the disease. The findings reveal an essential step in the biology of the most common and severe malaria parasite, Plasmodium falciparum, and offer a new drug target for fighting one of the world's most common and dangerous infections.
Malaria sickens up to one half billion people every year and kills up to one million, mostly children in sub-Saharan Africa. The high fevers, shaking chills, flu-like symptoms, and anemia can be fatal unless treated quickly. Malaria has grown resistant to a long list of drugs, and vaccines are still in experimental stages.
Working with the malaria parasite and human blood in test tubes and lab dishes, the research team identified a single fast-acting protein in the parasite that enables it and several dozen of its offspring to escape from a human red blood cell in preparation for quick invasion of many more healthy blood cells. Eliminating that protein traps the parasites in the cell.
After an infected mosquito bites a person, malaria parasites move into the liver, where they silently mature and multiply within weeks. Malaria parasites make people sick weeks or months later when they enter red blood cells and begin an exponential expansion. In a single cell, a parasite produces up to 32 offspring in about two days, which burst out to infect more red blood cells.
"This is the stage where things have to happen very fast for the parasite," said senior author Manoj Duraisingh, HSPH assistant professor of immunology and infectious diseases and senior author of the paper in the May 14 Science. "The parasite doesn't like to spend much time outside the cell. It grows and matures, and immediately following rupture, enters a new cell. It was a surprise that this protein kinase, which we thought would be involved in red blood cell invasion, turns out to be essential for the parasite getting out of the cell."
The study helps define the exit of the parasite from a blood cell as a highly choreographed process and distinguishes the egress and invasion steps, the researchers said.
"When the parasite gets out of the red blood cell, it has a matter of seconds or minutes to get into new red blood cells, or it will be cleared or killed by the human immune system," said first author Jeffrey Dvorin, a postdoctoral research fellow in the Duraisingh Lab at HSPH and a clinical fellow in pediatric infectious diseases at Children's Hospital Boston. "We found an important trigger for the parasite to exit cells that may be independent from the invasion trigger."
Even better, the protein is found in the parasite and in plants, but not in humans, which means a drug targeted to that protein may be less toxic for people. The protein belongs to a family of Plasmodium falciparum calcium-dependent protein kinases, or PfCDPK5 for short in this case. Other members of the family have been implicated in parasite egress of red blood cells, but this is the first study using a genetic technique to validate a protein critical for parasite egress of red blood cells, according to the researchers.
Many companies and labs are looking for inhibitors of parasite egress and invasion of red blood cells, but no anti-malarial drugs yet target these stages of the parasite lifecycle, Dvorin said.
The paper also demonstrates the usefulness of a new tool that can be used to evaluate additional members of the kinase family, as well as other signaling pathways that regulate key events in the blood stage of malaria infection. As of 2002, "we have a malaria genome of about 6,000 genes," said Duraisingh. "We need a means of prioritizing specific gene candidates for further drug development."
The method, first developed in a mammalian cell culture system by co-author Thomas Wandless of Stanford University, allows scientists to analyze the function of certain proteins and to identify other potential therapeutic targets in the malaria parasite, the researchers said.
As adapted for this study, Dvorin and his colleagues reverse-engineered candidate genes to make faulty proteins that would only survive in the presence of a stabilizing chemical. Without that constant protection, the protein is eliminated from the parasite.
"For 24 hours a day, 7 days a week, we grew the parasites in the presence of the stabilizing chemical," Dvorin said. "After the parasites invaded new red blood cells, we washed away the stabilizing drug. Even though the parasites seemed to develop just fine, they were unable to leave the red blood cell."
Interestingly, the team's work also produced an elusive scientific tool for their colleagues in the vaccine field: Mature invasive parasites. "One of the experiments in the paper mechanically releases the parasites, which have matured into virulent and invasive forms," Duraisingh said. "People have been trying to get viable parasites in this form for study. This is a great resource for vaccine studies."
"A Plant-Like Kinase in Plasmodium falciparum Regulates Parasite Egress From Erythrocytes," Science, May 14, 2010, J.D. Dvorin et. al.
This work was supported by Pediatric Scientist Development Program Fellowship awards, National Institutes of Health, Burroughs Wellcome Fund New Investigator in the Pathogenesis of Infectious Diseases Fellowship, the Medical Research Council UK, a Wellcome Trust Project grant, and an EU FP7 grant MALSIG.
Malaria sickens up to one half billion people every year and kills up to one million, mostly children in sub-Saharan Africa. The high fevers, shaking chills, flu-like symptoms, and anemia can be fatal unless treated quickly. Malaria has grown resistant to a long list of drugs, and vaccines are still in experimental stages.
Working with the malaria parasite and human blood in test tubes and lab dishes, the research team identified a single fast-acting protein in the parasite that enables it and several dozen of its offspring to escape from a human red blood cell in preparation for quick invasion of many more healthy blood cells. Eliminating that protein traps the parasites in the cell.
After an infected mosquito bites a person, malaria parasites move into the liver, where they silently mature and multiply within weeks. Malaria parasites make people sick weeks or months later when they enter red blood cells and begin an exponential expansion. In a single cell, a parasite produces up to 32 offspring in about two days, which burst out to infect more red blood cells.
"This is the stage where things have to happen very fast for the parasite," said senior author Manoj Duraisingh, HSPH assistant professor of immunology and infectious diseases and senior author of the paper in the May 14 Science. "The parasite doesn't like to spend much time outside the cell. It grows and matures, and immediately following rupture, enters a new cell. It was a surprise that this protein kinase, which we thought would be involved in red blood cell invasion, turns out to be essential for the parasite getting out of the cell."
The study helps define the exit of the parasite from a blood cell as a highly choreographed process and distinguishes the egress and invasion steps, the researchers said.
"When the parasite gets out of the red blood cell, it has a matter of seconds or minutes to get into new red blood cells, or it will be cleared or killed by the human immune system," said first author Jeffrey Dvorin, a postdoctoral research fellow in the Duraisingh Lab at HSPH and a clinical fellow in pediatric infectious diseases at Children's Hospital Boston. "We found an important trigger for the parasite to exit cells that may be independent from the invasion trigger."
Even better, the protein is found in the parasite and in plants, but not in humans, which means a drug targeted to that protein may be less toxic for people. The protein belongs to a family of Plasmodium falciparum calcium-dependent protein kinases, or PfCDPK5 for short in this case. Other members of the family have been implicated in parasite egress of red blood cells, but this is the first study using a genetic technique to validate a protein critical for parasite egress of red blood cells, according to the researchers.
Many companies and labs are looking for inhibitors of parasite egress and invasion of red blood cells, but no anti-malarial drugs yet target these stages of the parasite lifecycle, Dvorin said.
The paper also demonstrates the usefulness of a new tool that can be used to evaluate additional members of the kinase family, as well as other signaling pathways that regulate key events in the blood stage of malaria infection. As of 2002, "we have a malaria genome of about 6,000 genes," said Duraisingh. "We need a means of prioritizing specific gene candidates for further drug development."
The method, first developed in a mammalian cell culture system by co-author Thomas Wandless of Stanford University, allows scientists to analyze the function of certain proteins and to identify other potential therapeutic targets in the malaria parasite, the researchers said.
As adapted for this study, Dvorin and his colleagues reverse-engineered candidate genes to make faulty proteins that would only survive in the presence of a stabilizing chemical. Without that constant protection, the protein is eliminated from the parasite.
"For 24 hours a day, 7 days a week, we grew the parasites in the presence of the stabilizing chemical," Dvorin said. "After the parasites invaded new red blood cells, we washed away the stabilizing drug. Even though the parasites seemed to develop just fine, they were unable to leave the red blood cell."
Interestingly, the team's work also produced an elusive scientific tool for their colleagues in the vaccine field: Mature invasive parasites. "One of the experiments in the paper mechanically releases the parasites, which have matured into virulent and invasive forms," Duraisingh said. "People have been trying to get viable parasites in this form for study. This is a great resource for vaccine studies."
"A Plant-Like Kinase in Plasmodium falciparum Regulates Parasite Egress From Erythrocytes," Science, May 14, 2010, J.D. Dvorin et. al.
This work was supported by Pediatric Scientist Development Program Fellowship awards, National Institutes of Health, Burroughs Wellcome Fund New Investigator in the Pathogenesis of Infectious Diseases Fellowship, the Medical Research Council UK, a Wellcome Trust Project grant, and an EU FP7 grant MALSIG.
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