U.S. Dist. Judge Full Of Hate Richard J. Leon said NO cheaper prices

cheaper prices are against the Constitution

yes indeedy

http://www.washingtonpost.com/wp-dyn/content/article/2005/12/22/AR2005122202018.html

Prescription Drug Plan in D.C. Barred

A federal judge ruled yesterday that a District law designed to reduce the price of prescription drugs is unconstitutional and blocked its implementation.

U.S. District Judge Richard J. Leon said the law, passed this fall, violates constitutional protections of interstate commerce and goes against the will of Congress.
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actually Leon is protecting a law made by pharmaceutical companies

fuck D.C.

constitution, or so it would seem.....

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=16317694&itool=pubmed_Abstract

Just off the presses.... portal vein hypertension, biliary cirrhosis. For the record, my brother was put on this by his doc for hypertension. It is known as "L-Arginine" a simple, non-toxic protein. Google it.


A role for asymmetric dimethylarginine in the pathophysiology of portal hypertension in rats with biliary cirrhosis.

Laleman W, Omasta A, Van de Casteele M, Zeegers M, Vander Elst I, Van Landeghem L, Severi T, van Pelt J, Roskams T, Fevery J, Nevens F.

Laboratories of Hepatology, University Hospital Gasthuisberg, Leuven, Belgium.

Reduced intrahepatic endothelial nitric oxide synthase (eNOS) activity contributes to the pathogenesis of portal hypertension (PHT) associated with cirrhosis. We evaluated whether asymmetric dimethylarginine (ADMA), a putative endogenous NOS inhibitor, may be involved in PHT associated with cirrhosis. Two rat models of cirrhosis (thioacetamide -induced and bile duct excision -induced, n = 10 each), one rat model of PHT without cirrhosis (partial portal vein-ligated , n = 10), and sham-operated control rats (n = 10) were studied. We assessed hepatic NOS activity, eNOS protein expression, plasma ADMA levels, and intrahepatic endothelial function. To evaluate intrahepatic endothelial function, concentration-effect curves of acetylcholine were determined in situ in perfused normal rat livers and livers of rats with TAA- or BDE-induced cirrhosis (n = 10) that had been preincubated with either vehicle or ADMA; in addition, measurements of nitrite/nitrate (NOx) and ADMA were made in perfusates. Both models of cirrhosis exhibited decreased hepatic NOS activity. In rats with TAA-induced cirrhosis, this decrease was associated with reduced hepatic eNOS protein levels and immunoreactivity. Rats with BDE-induced cirrhosis had eNOS protein levels comparable to those in control rats but exhibited significantly higher plasma ADMA levels than those in all other groups. In normal perfused liver, ADMA induced impaired endothelium-dependent vasorelaxation and reduced NOx perfusate levels, phenomena that were mimicked by N(G)-nitro-L-arginine-methyl ester. In contrast to perfused livers with cirrhosis induced by TAA, impaired endothelial cell-mediated relaxation in perfused livers with cirrhosis induced by BDE was exacerbated by ADMA and was associated with a decreased rate of removal of ADMA (34.3% +/- 6.0% vs. 70.9% +/- 3.2%). In conclusion, in rats with TAA-induced cirrhosis, decreased eNOS enzyme levels seem to be responsible for impaired NOS activity; in rats with biliary cirrhosis, an endogenous NOS inhibitor, ADMA, may mediate decreased NOS activity.

PMID: 16317694

How does that follow?

****ing Republican ***holes. Ripping off the sick.

:puke:

:grr: