18 October 2013

CureTech Ltd.Israel: PIDILIZUMAB (CT-011)

The company’s products are antibodies and peptide-therapeutics designed to modulate the immune response allowing it to exert its anti-cancer activity in an effective manner. Our lead product, pidilizumab (CT-011), is a humanized monoclonal antibody that interacts with PD-1, a B7 receptor-family-associated protein, and exhibits efficient anti-cancer immune response against a wide variety of mouse and human tumors. A Phase II program has been initiated including 3 sponsored studies: the first, a Phase II clinical trial in patients with diffuse large B cell lymphoma has been completed. Enrolment to 2 additional Phase II studies in patients with metastatic colorectal cancer and metastatic melanoma has been completed. In addition to these 3 studies, several investigator-initiated studies in different indications including follicular lymphoma, multiple myeloma, AML, renal cell carcinoma, pancreatic cancer and prostate cancer are ongoing.

17 October 2013

CONN SYNDROME: Patient info.on adrenalectomy in Dutch.

http://www.nijsmellinghe.nl/1177/kijkoperatie-om-de-bijnier-te-verwijderen http://www.jeroenboschziekenhuis.nl/website/patientenfolders/URO/URO-063%20Laparoscopische%20verwijdering%20van%20de%20bijnier.pdf http://www.umcn.nl/Informatiefolders/4892-Laparoscopische_retroper-i.pdf http://www.erasmusmc.nl/cs-patientenzorg/2419534/2419537/214086/21416521/6088874-02_07aiOperatieaand1.pdf http://www.uza.be/behandeling/bijnierresectie http://www.nvacp.nl/page/Medisch/Aandoeningen/Bijnieren

11 October 2013

USA "GARD": HEREDITARY ANGIOEDEMA

Who first described hereditary angioedema? Hereditary angioedema (HAE) was first described as a “syndrome” by Quincke in 1882 and was later detected in 1888 by William Osler to have a hereditary nature.[1] 1. Webb, M. et al. 2000. Management of children with hereditary angioedema: a report of two cases. Available at: http://www.aapd.org/assets/1/25/Webb-22-02.pdf. Accessed on October 11, 2013. The US Hereditary Angioedema Association Seven Waterfront Plaza 500 Ala Moana Blvd., Suite 400 Honolulu, HI 96813 Toll free: (866) 798-5598 Web site: http://www.haea.org/ Tamandra Carter Information Specialist The Genetic and Rare Diseases (GARD) Information Center is funded by two parts of the National Institutes of Health (NIH): the National Center for Advancing Translational Sciences Office of Rare Diseases Research (NCATS-ORDR) and the National Human Genome Research Institute (NHGRI). The GARD Information Center provides the public with access to current, reliable, and easy to understand information about rare or genetic diseases in English or Spanish. Information Specialists are available by phone Monday through Friday, 12:00 p.m. to 6:00 p.m. Eastern time (excluding Federal holidays). PO Box 8126 Gaithersburg, MD 20898-8126 Toll-free: 1-888-205-2311 Telephone: 301-251-4925 TTY: 1-888-205-3223 Fax: 301-251-4911 E-mail: GARDinfo@nih.gov Web site: http://rarediseases.info.nih.gov/GARD

08 October 2013

DAILY MAIL : WORLD LITERACY

at the same level, whereas countries like Korea are showing huge improvement between generations Picture of Britain: This graph shows how the UK compared to other industrial nations when it came to numeracy Interesting: Countries like Japan, Netherlands and Sweden were the top performing in terms of literacy, even though children start school often years later than British youngsters Read more: http://www.dailymail.co.uk/news/article-2449481/Education-crisis-Up-8-5MILLION-numeracy-level-10-year-old.html#ixzz2hBd5fqRR

SCIENCE: NOBEL PRIZE FOR MEDICINE

Three researchers who studied how cells shuttle around essential molecules in tiny intracellular sacs have won this year’s Nobel Prize in physiology or medicine. James Rothman of Yale University; Randy Schekman of the University of California, Berkeley; and Thomas Südhof of Stanford University earned the award "for their discoveries of machinery regulating vesicle traffic, a major transport system in our cells," according to the announcement from the Nobel Assembly at Karolinska Institute in Stockholm. The three researchers independently unraveled basic cellular mechanisms several decades ago—in Schekman's case, almost 40 years ago. Although mistakes in cellular transport systems can cause a variety of diseases—including diabetes and neurological and immunological disorders—their work has not yet led to any new drugs or therapies, but it has helped others develop diagnostic tests. Schekman, who's also an investigator at the Howard Hughes Medical Institute (HHMI), a former editor of the Proceedings of the National Academy of Sciences, and the current editor-in-chief of the open access journal eLife, studied intracellular transport in yeast cells in the 1970s. He identified cells whose transport machinery didn't function properly, causing the vesicles to pile up in the cell, and identified the mutated genes responsible for those problems—a discovery that helped understand how intracellular traffic works under normal circumstances. Rothman, who has been at Yale since 2008, is honored for work he did on vesicular transport in mammalian cells while at Stanford University, Princeton University, and the Memorial Sloan-Kettering Cancer Center in the 1980s and 1990s. Rothman showed how a protein complex enables vesicles to dock and fuse with their target membranes, a process in which proteins on the sacs and their targets bind to each other like the two sides of a zipper. (Each half of the zipper complex has to match the other precisely, allowing the cell to direct compounds exactly where they need to do.) The mechanism is used both inside a cell and when a vesicle arrives at a cell from the outside to deliver its contents. Südhof was born in Germany and came to the University of Texas Southwestern Medical Center in Dallas in 1982 to work in the lab of Michael Brown and Joseph Goldstein, who both won a Nobel in 1985. Südhof receives his share of this year's prize for transport studies as well—in his case, of how neurotransmitters, an all-important class of chemical messengers, are transported between neighboring nerve cells. In the 1990s, Südhof—now also an HHMI investigator, like Schekman—identified proteins that respond to an influx of calcium into the neuron, allowing other, nearby proteins to bind to vesicles containing neurotransmitters and let their content flow into the nerve cell. His work helped explain how nervous systems can achieve their amazing speed and temporal precision.

07 October 2013

06 October 2013

ProMed: MYCO. LEPRAE

(prevalence Leprosy in India increasing) Infect Genet Evol. 2012 Jan;12(1):121-6. doi: 10.1016/j.meegid.2011.10.023. Epub 2011 Nov 11. Dynamics of Mycobacterium leprae transmission in environmental context: deciphering the role of environment as a potential reservoir. Turankar RP, Lavania M, Singh M, Siva Sai KS, Jadhav RS. Source Stanley Browne Laboratory, TLM Community Hospital, Nand Nagari, Delhi 110093, India. Abstract Leprosy is a disease caused by Mycobacterium leprae. Various modes of transmission have been suggested for this disease. Transmission and risk of the infection is perhaps related to presence of the infectious cases and is controlled by environmental factors. Evidence suggests that humidity may favor survival of M. leprae in the environment. Several reports show that non-human sources like 'naturally' infected armadillos or monkeys could act as reservoir for M. leprae. Inanimate objects or fomites like articles used by infectious patients may theoretically spread infection. However, it is only through detailed knowledge of the biodiversity and ecology that the importance of this mode of transmission can be fully assessed. Our study focuses here to decipher the role of environment in the transmission of the disease. Two hundred and seven soil samples were collected from a village in endemic area where active cases also resided at the time of sample collection. Slit skin smears were collected from 13 multibacillary (MB) leprosy patients and 12 household contacts of the patients suspected to be hidden cases. DNA and RNA of M. leprae were extracted and amplified using M. leprae specific primers. Seventy-one soil samples showed presence of M. leprae DNA whereas 16S rRNA could be detected in twenty-eight of these samples. Samples, both from the environment and the patients, exhibited the same genotype when tested by single nucleotide polymorphism (SNP) typing. Genotype of M. leprae found in the soil and the patients residing in the same area could help in understanding the transmission link in leprosy. Copyright © 2011 Elsevier B.V. All rights reserved. (Comment: check for enlarged supratrochleal lymph node. Also Ulnar & Great auricular nerve thickening)