FOOTHILL RANCH, CA--(Marketwire - November 15, 2010) - Medical Marijuana Inc (PINKSHEETS: MJNA) applauds Arizona voters for approving Proposition 203, which legalizes marijuana for medical use. MJNA Chairman Bruce Perlowin stated, "Arizonans who benefit from the medical efficacy of marijuana can now obtain legal and safe marijuana with a recommendation from their doctor to alleviate their suffering."
The Arizona measure will allow patients with diseases including cancer, HIV/AIDS, Hepatitis C and any other "chronic or debilitating" disease that meets guidelines to buy 2½ ounces of marijuana every two weeks or grow plants. Also proposed are 120 state-regulated clinics to dispense marijuana. Those living more than 25 miles from a clinic will be allowed to grow 12 plants for their own medicine. Medical marijuana cards and recommendations for patients from other states will be honored in Arizona, though those patients will not be allowed purchase to marijuana in the dispensaries.. continue reading .
Over at NATAP the coverage continues on the AASLD meeting. 36 versus 48 weeks of treatment with peginterferon alfa-2a plus ribavirin for genotype 1/4 patients with undetectable HCV RNA at week 8: Final results of a randomized multicenter study
Genotype 1b vs 1a and Peg/Rbv Lead-In -
HIV and Hepatitis : Higher Doses May Overcome Poor Response to Interferon in Hepatitis C Patients with Unfavorable IL28B Gene Pattern
Are IL28B Gene Variations Associated with Outcomes in People with Hepatitis B?
HCV Advocate has updated: Basics: Getting Benefits Under Social Security with HCV (Hepatitis C)
A new website has been launched by StemCells, Inc. Press Release: In addition to showcasing StemCells' people, science and technologies, the new website provides users with easier access to key online content associated with the Company's scientific achievements and therapeutic product development programs targeting the central nervous system and the liver.
From the website :"The Promise of Cell Therapy Cell-based therapy using liver stem or progenitor cells has the potential to offer a better alternative for treating a broad range of liver diseases. A cell-based therapeutic could provide or support liver function in patients with liver disease and would have numerous advantages over whole organ transplantation. "
Because of recent interest in Stem Cell research, a note of caution; not all websites or information is legitimate. This site however is and has been launched for your protection. International Society for Stem Cell Research (ISSCR) It provides information about stem cell biology as well as questions to ask clinics offering these often-experimental treatments.
Videos worth watching : A National Strategy for Viral Hepatitis Control: AASLD 2010 Dr. Gish summarizes key points from the President's Choice lecture on viral hepatitis presented by HHS Assistant Secretary for Health, Dr. Howard Koh.
Medscape Gastroenterology, November 2010
A New Era of Hepatitis C Therapy: AASLD 2010 From this year's "Liver Meeting," Dr. Younossi reports on advancements in personalized medicine for hepatitis C infection.
Medscape Gastroenterology, November 2010
Best Video Of The Month: Leon Schiff LectureGenetics and Personalized Medicine for the Treatment of Hepatitis C. and President's Choice Lecture - Viral Hepatitis: Confronting a Silent Epidemic
Listen to Dr. Koh's Presentation
JCI online early table of contents: Nov. 15, 2010
EDITOR'S PICK:
At-TRIB(1)-uting a gene a new function in the liver
Specific, relatively uncommon variations at a region of human chromosome 8 have recently been linked to fat (lipid) levels in the blood that decrease an individual's risk of atherosclerosis (a disease of the major arterial blood vessels that is a main cause of heart attack and stroke). The only currently described gene in this region of chromosome 8 is TRIB1, but it has not been previously linked in any way to regulation of lipid levels. Now, a team of researchers, led by Jan Breslow, at The Rockefeller University, New York, and Daniel Rader, at the University of Pennsylvania School of Medicine, Philadelphia, has identified in mice a role for this gene in regulating lipid production by the liver. Specifically, overexpression of Trib1 in the liver decreased levels of lipids such as cholesterol in the blood, while lack of Trib1 increased levels of the same lipids. These data suggest that TRIB1 is the gene responsible for the associations between chromosome 8 and lipid levels in the blood.
TITLE: Trib1 is a lipid- and myocardial infarction–associated gene that regulates hepatic lipogenesis and VLDL production in mice
AUTHOR CONTACT: Jan L. Breslow The Rockefeller University, New York, New York, USA. Phone: 212.327.7700; Fax: 212.327.7165; E-mail: breslow@rockefeller.edu.
Daniel J. Rader University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Phone: 215.573.4176; Fax: 215.573.8606; E-mail: rader@mail.med.upenn.edu.
View this article at: http://www.jci.org/articles/view/44213?key=9213f656566ab4e5d75a
VIROLOGY: The proteins PD-1 and Tim-3: double trouble for hepatitis C virus immune cells
In a large proportion of patients who become infected with hepatitis C virus (HCV), the virus evades the anti-viral immune response to establish a persistent infection. In these individuals, the function of HCV-specific immune cells known as CTLs is impaired as a result of inhibitory signals emanating from proteins such as Tim-3 and PD-1 on their surface. A team of researchers, led by Hugo Rosen, at the University of Colorado Denver, Aurora, has now generated data that suggest that blocking the inhibitory proteins Tim-3 and PD-1 might provide a new approach to treating individuals with a persistent HCV infection.
The team determined that expression of PD-1 and Tim-3 on HCV-specific CTLs was characteristic of individuals acutely infected with HCV who were more likely to develop persistent HCV infection. Importantly, blockade of either PD-1 or Tim-3 enhanced the in vitro proliferation of HCV-specific CTLs, while blockade of Tim-3 increased the ability of these cells to kill cells expressing HCV proteins. The authors therefore conclude that coexpression of PD-1 and Tim-3 on HCV-specific CTLs is associated with the development of persistent HCV infection and suggest that simultaneous blockade of PD-1 and Tim-3 might be therapeutically useful.
TITLE: Tim-3 expression on PD-1+ HCV-specific human CTLs is associated with viral persistence, and its blockade restores hepatocyte-directed in vitro cytotoxicity
AUTHOR CONTACT: Hugo R. Rosen University of Colorado Denver, Aurora, Colorado, USA. Phone: 303.724.1858; Fax: 303.724.1891; E-mail: Hugo.Rosen@ucdenver.edu.
View this article at: http://www.jci.org/articles/view/43127?key=b248ddb642397e4495f7
PHYSIOLOGY: Patients explain exactly why we need the chemical element selenium
The trace element selenium is essential for cellular function. This is predominantly because it must be incorporated into some proteins, in the form of selenocysteine, for them to function. A multiprotein complex that includes the protein SECISBP2 is responsible for incorporating selenocysteine into proteins. A team of researchers, led by Krishna Chatterjee, at the University of Cambridge, United Kingdom, has now identified two individuals with distinct mutations in their two SECISBP2 genes and characterized their clinical defects. These individuals had reduced levels of most of the 25 known human selenoproteins and this led to a complex multisystem disorder that included, but was not limited to, a lack of sperm, muscle wasting, increased sensitivity to UV light, and impaired thyroid function. This analysis has provided new insight into the diverse biological processes in which selenoproteins are involved.
TITLE: Mutations in the selenocysteine insertion sequence–binding protein 2 gene lead to a multisystem selenoprotein deficiency disorder in humans
AUTHOR CONTACT: V. Krishna K. Chatterjee University of Cambridge, Addenbrooke's Hospital, Cambridge, United Kingdom. Phone: 44.1223.336842; Fax: 44.1223.330598; E-mail: kkc1@mole.bio.cam.ac.uk.
View this article at: http://www.jci.org/articles/view/43653?key=c5d65a1724a465493437
TUMOR IMMUNOLOGY: Genetic modification: the secret to a long-lived antitumor immune response
One anticancer approach many researchers are seeking to develop is the transfer into patients of immune cells known as T cells that have been manipulated such that they attack and destroy the patient's tumor. Although this approach has proven beneficial in some individuals, in most, the antitumor immune response has not been long-lived enough to be of benefit. However, a team of researchers, led by Christopher Touloukian, at Indiana University School of Medicine, Indianapolis, has developed an approach that led to long-lived antitumor immune responses by CD4+ T cells in a mouse model of melanoma skin cancer. They hope that it might be possible to one day translate this approach for clinical benefit.
TITLE: Transplantation of mouse HSCs genetically modified to express a CD4-restricted TCR results in long-term immunity that destroys tumors and initiates spontaneous autoimmunity
AUTHOR CONTACT: Christopher E. Touloukian Indiana University School of Medicine, Indianapolis, Indiana, USA. Phone: 317.278.9945; Fax: 317.274.7592; E-mail: ctoulouk@iupui.edu.
View this article at: http://www.jci.org/articles/view/43274?key=7bf052002ef6fdaf85a4
METABOLIC DISEASE: Uncovering new way to stop fat accumulation in mice
The most common cause of liver dysfunction in the United States is a condition known as nonalcoholic fatty liver disease (NAFLD). A form of NAFLD known as hepatic steatosis is associated with obesity and type 2 diabetes. It arises as a result of increased generation and accumulation of lipids (fats) in the liver. Renaud Dentin and colleagues, at Institut Cochin, France, have now provided new insight into the mechanisms underlying hepatic steatosis in mice. Specifically, they find a role for the proteins p300 and SIK2 in regulating lipid production in the liver. Taken together, all the data lead the authors to suggest that SIK2 activators and specific p300 inhibitors might provide new approaches to treating hepatic steatosis in individuals with obesity and type 2 diabetes.
TITLE: Salt-inducible kinase 2 links transcriptional coactivator p300 phosphorylation to the prevention of ChREBP-dependent hepatic steatosis in mice
AUTHOR CONTACT: Renaud Dentin Institut Cochin, Université Paris Descartes, CNRS, UMR 8104, INSERM, U1016, Paris, France. Phone: 33.1.53.73.27.20; Fax: 33.1.53.73.27.03; Email: renaud.dentin@inserm.fr.
View this article at: http://www.jci.org/articles/view/41624?key=5a93c7622e5586b36422
AUTOIMMUNITY: Attacking the symptoms of SLE
Systemic lupus erythematosus (SLE) is a relatively common autoimmune disorder, i.e., a disorder caused by a person's immune system turning on that person's body and inflicting tissue damage. The disease can affect the skin, joints, kidneys, and other organs. There is no cure for SLE, although there are good treatments to combat many of the symptoms. A team of researchers, led by Liliana Schaefer, at the Institut für Allgemeine Pharmakologie und Toxikologie/ZAFES, Germany, has now identified, through work in mice, a potential new target for treating the symptoms of SLE
One marker of disease activity in individuals with SLE is CXCL13, which is a protein that attracts immune cells known as B cells. The team has now identified a mechanism by which CXCL13 is induced in a mouse model of SLE. Specifically, increased levels of the molecule biglycan interacted with proteins known as TLR2/4 to trigger production of CXCL13. Importantly, biglycan deficiency was associated with reduced disease. Further, as levels of biglycan were elevated in patients with SLE, the authors suggest that targeting biglycan-TLR2/4 interactions might provide a new approach to treating the symptoms of SLE.
TITLE: The proteoglycan biglycan regulates expression of the B cell chemoattractant CXCL13 and aggravates murine lupus nephritis
AUTHOR CONTACT: Liliana Schaefer Institut für Allgemeine Pharmakologie und Toxikologie/ZAFES, Frankfurt am Main, Germany. Phone: 49.69.6301.7899; Fax: 49.69.6301.83027; E-mail: Schaefer@med.uni-frankfurt.de.
View this article at: http://www.jci.org/articles/view/42213?key=052d725fc21fdefd1cba
METABOLISM: How the hormone glucagon tips the balance to increase blood glucose levels
A team of researchers, led by Alan Cherrington, at Vanderbilt University Medical Center, Nashville, has provided new insight into the mechanisms by which blood levels of glucose — one of the main sources of energy for the cells in our body — are regulated.
Given the importance of glucose as a source of energy for cells, maintaining adequate levels of glucose in the blood is extremely important. The opposing effects of the hormones insulin and glucagon are key to this: insulin induces liver, muscle, and fat cells to take up glucose from the blood and store it, while glucagon induces the liver to release stored glucose into the blood. In the study, Cherrington and colleagues show in dogs that although insulin potently inhibits the effects of glucagon when blood glucose levels are normal, glucagon overcomes the inhibitory effects of insulin when blood glucose levels are low. Further analysis provided insight into the mechanisms underlying this critical regulatory process.
TITLE: Insulin-induced hypoglycemia increases hepatic sensitivity to glucagon in dogs
AUTHOR CONTACT: Alan D. Cherrington Vanderbilt University Medical Center, Nashville, Tennessee, USA. Phone: 615.322.7013; Fax: 615.343.0490; E-mail: alan.cherrington@vanderbilt.edu.
View this article at: http://www.jci.org/articles/view/40919?key=68178aa990f04879e640
Additional news will be posted on the blog later today.
Enjoy the day folks
Tina
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