kidney diseases

http://kidney.niddk.nih.gov/kudiseases/pubs/hemodialysis/
http://kidney.niddk.nih.gov/kudiseases/pubs/peritoneal/
http://kidney.niddk.nih.gov/kudiseases/pubs/vascularaccess/
http://www.wisegeek.com/what-is-hemofiltration.htm
http://vasculitis.med.jhu.edu/typesof/typesof.html
http://www.unckidneycenter.org/kidneyhealthlibrary/antigbm.html

http://images.google.com/imgres?imgurl=http://www.paterson.man.ac.uk/images/carcinogenesis/carcino2.jpg&imgrefurl=http://www.paterson.man.ac.uk/carcinogenesis/dna-damage.stm&usg=__XQ90Sj4dV-IonzGkzeuO3KxMIpg=&h=289&w=530&sz=19&hl=en&start=1&um=1&tbnid=tVzyLBNOUC4FEM:&tbnh=72&tbnw=132&prev=/images%3Fq%3DO6-methylguanine%26hl%3Den%26rls%3Dcom.microsoft:*:IE-SearchBox%26rlz%3D1I7GGLJ%26sa%3DN%26um%3D1

myweb.unomaha.edu/~dstack/2250/Overheads/EWG_EDG.PDF

Selectivity, Specificity, Potency

http://www.biomedcentral.com/1472-6904/5/3

H1N1 virus

http://www.virology.ws/2009/04/30/structure-of-influenza-virus/
http://glorious.tigblog.org/post/654575

Epcam role in cancer and Anti-epcam drugs

A fusion protein immunotoxin consisting of a humanized, single-chain monoclonal antibody fragment specific for the epithelial cell adhesion molecule (EpCAM) conjugated with a truncated form of Pseudomonas exotoxin A with potential antineoplastic activity. Anti-EpCAM-Pseudomonas-exotoxin fusion protein binds to Ep-CAM-positive tumor cells, thereby delivering the Pseudomonas exotoxin A moiety specifically; the Pseudomonas exotoxin A moiety then inactivates elongation factor 2 (EF-2) through ADP ribosylation, resulting in inhibition of protein synthesis in target cells. EpCAM, a cell surface protein, is expressed by a variety of tumor cells and is frequently found in head and neck cancers. Check for active clinical trials or closed clinical trials using this agent.
http://www.cancer.gov/drugdictionary/?CdrID=485164

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WGD-4BHSXSD-R&_user=126089&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1097247906&_rerunOrigin=scholar.google&_acct=C000010279&_version=1&_urlVersion=0&_userid=126089&md5=d62a213546f48f1aab6d8502766c72a3

http://pis.to/cgtg/publications/Kanerva%20Hemminki.%20Int%20J%20Cancer%20Review%2004.pdf

http://clincancerres.aacrjournals.org/content/13/13/3899.full

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WN5-4FXNRH9-2&_user=126089&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1097266874&_rerunOrigin=scholar.google&_acct=C000010279&_version=1&_urlVersion=0&_userid=126089&md5=8f56edbd76d15d8236514b3fd12c1601

News: HPV vaccine

http://news.sky.com/skynews/Home/UK-News/Cervical-Cancer-HPV-Vaccine-Now-Available-In-Boots-Pharmacies-Across-England-And-Wales/Article/200909215379269?lpos=UK_News_Article_Related_Content_Region_8&lid=ARTICLE_15379269_Cervical_Cancer_HPV_Vaccine_Now_Available_In_Boots_Pharmacies_Across_England_And_Wales
http://news.sky.com/skynews/Home/UK-News/Cervical-Cancer-HPV-Vaccine-Now-Available-In-Boots-Pharmacies-Across-England-And-Wales/Article/200909215379269?lpos=UK_News_Article_Related_Content_Region_8&lid=ARTICLE_15379269_Cervical_Cancer_HPV_Vaccine_Now_Available_In_Boots_Pharmacies_Across_England_And_Wales

Bystander activation, molecular mimicry

cmr.asm.org/cgi/reprint/19/1/80.pdf

PBOX-15 and Fludarabine

'Fludarabine is licensed for the initial treatment of advanced B-cell chronic lymphocytic leukaemia (CLL) or after first-line treatment in patients with sufficient bone-marrow reserves; it is given by mouth, by intravenous injection, or by intravenous infusion. Fludarabine is well tolerated but it does cause myelosuppression, which may be cumulative. Immunosuppression is also common (see panel on cladribine and fludarabine below), and co-trimoxazole is used to prevent pneumocystis infection. Immune-mediated haemolytic anaemia, thrombocytopenia, and neutropenia are less common side-effects.

The Scottish Medicines Consortium has advised (October 2006) that fludarabine is accepted for restricted use for the treatment of B-cell chronic lymphocytic leukaemia (CLL) in patients with sufficient bone marrow reserves. First-line treatment should only be initiated in patients with advanced disease, Rai stages III/IV (Binet stage C), or Rai stages I/II (Binet stage A/B) where the patient has disease-related symptoms or evidence of progressive disease.

NICE guidance
Fludarabine monotherapy for the first-line treatment of chronic lymphocytic leukaemia (February 2007)

Fludarabine monotherapy, is not recommended for the first-line treatment of chronic lymphocytic leukaemia.'

BNF

http://www.pnptherapeutics.com/technology-how.html
http://www.pnptherapeutics.com/technology-how.html

PBOX-15: anti-leukaemia drug under development
http://www.freepatentsonline.com/6806267-0-large.jpg
http://www.springerlink.com/content/rq5j447430578094/fulltext.html

http://www.farmakeutikoskosmos.gr/html/page.asp?lang=1&pageID=40&recID=460

Tay-Sachs

"What is Tay-Sachs Disease?

Tay-Sachs disease is a fatal genetic lipid storage disorder in which harmful quantities of a fatty substance called ganglioside GM2 build up in tissues and nerve cells in the brain. The condition is caused by insufficient activity of an enzyme called beta-hexosaminidase A that catalyzes the biodegradation of acidic fatty materials known as gangliosides. Gangliosides are made and biodegraded rapidly in early life as the brain develops.

Infants with Tay-Sachs disease appear to develop normally for the first few months of life. Then, as nerve cells become distended with fatty material, a relentless deterioration of mental and physical abilities occurs. The child becomes blind, deaf, and unable to swallow. Muscles begin to atrophy and paralysis sets in. Other neurological symptoms include dementia, seizures, and an increased startle reflex to noise. A much rarer form of the disorder occurs in patients in their twenties and early thirties and is characterized by an unsteady gait and progressive neurological deterioration. Persons with Tay-Sachs also have "cherry-red" spots in their eyes. The incidence of Tay-Sachs is particularly high among people of Eastern European and Askhenazi Jewish descent. Patients and carriers of Tay-Sachs disease can be identified by a simple blood test that measures beta-hexosaminidase A activity. Both parents must carry the mutated gene in order to have an affected child. In these instances, there is a 25 percent chance with each pregnancy that the child will be affected with Tay-Sachs disease. Prenatal diagnosis is available if desired.


Is there any treatment?

Presently there is no treatment for Tay-Sachs disease. Anticonvulsant medicine may initially control seizures. Other supportive treatment includes proper nutrition and hydration and techniques to keep the airway open. Children may eventually need a feeding tube.

What is the prognosis?

Even with the best of care, children with Tay-Sachs disease usually die by age 4, from recurring infection."

http://www.ninds.nih.gov/disorders/taysachs/taysachs.htm