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At least 289 records · Page 16Linked to original sources
PubMed2001

New-generation proton pump inhibitors: overcoming the limitations of early-generation agents.

Proton pump inhibitors (PPIs) are now generally considered the drugs of choice for treatment of patients with serious or refractory acid-related diseases. However, despite some popular notions to the contrary, these agents are not equivalent in their pharmacokinetic, pharmacodynamic and efficacy profiles. When the two newest PPIs, rabeprazole and esomeprazole, are compared with the older drugs in this class (omeprazole, lansoprazole and pantoprazole), the newer PPIs offer several key advantages over older agents, particularly in terms of the management of gastro-oesophageal reflux disease. Rabeprazole and esomeprazole achieve more rapid and profound inhibition of acid secretion than do older agents, and they sustain this suppression to provide acid control and symptom relief over 24 h. The balanced hepatic metabolism of rabeprazole, involving both cytochrome P450 (CYP)-mediated reactions in the liver and nonenzymatic reactions, appears to confer an advantage over older PPIs in that genetic polymorphisms for CYP 2C19 do not significantly influence rabeprazole clearance and, potentially, clinical efficacy. The metabolism of esomeprazole also involves CYP 2C19, but the pharmacokinetic effects of genetic differences in the expression of this enzyme are not known. However, esomeprazole is also intended to minimize pharmacological variability. Unlike esomeprazole, the use of rabeprazole is not complicated by clinically significant drug-drug interactions of the type that have been reported for omeprazole and the wide range of medications metabolized by CYP 2C19.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1975

Trypsin-activated complex of human factor B with cobra venom factor (CVF), cleaving C3 and C5 and generating a lytic factor for unsensitized guinea pig erythrocytes. I. Generation of the activated complex.

A complex formed between cobra venom factor (CVF) and isolated human factor B (B) was found to be converted by trypsin to a stable enzyme, CVF-B which cleaved the third component (C3) and the fifth component (C5) of human complement. The formation of CVF-B by trypsin required divalent cations, whereas the formation of the lytic factor from human serum occurred even in the presence of EDTA. CVF-B purified by gel filtration could initiate the hemolysis of unsensitized guinea pig erythrocytes when incubated with human complement components C5 to C9 in 0.01 M EDTA buffer. C3 was not required for the lysis of guinea pig erythrocytes initiated by CVF-B because of the beta1C precipitation line formed between human serum and anti-beta1C antibody did not inhibit the hemolysis by CVF-B in agarose gel. Treatment of beta1C and beta1F globulins in whole human serum with CVF-B in the presence of 0.01 M EDTA converted them to components with higher mobilities on immunoelectrophoresis.

ABO Blood-Group System↗
PubMed1977

The generation of memory cells. I. The role of C3 in the generation of B memory cells.

Adult thymectomized, repopulated mice were chronically depleted of circulating C3 by treatment with cobra venom factor after primary immunization with dinitrophenylated haemocyanin (DNP-KLH). This treatment totally abrogated the development of B-cell memory in such mice, as assayed by a co-operative lymphocyte transfer. The failure of memory development appeared to involve impaired precursor proliferation following priming. It was further shown that the localization of DNP-KLH in splenic lymphoid follicles is both antibody and C3-dependent; thymus-deprived mice make sufficient antibody to DNP-KLH to effect follicular localization of the antigen. On the basis of these and earlier observations we suggest that the development of B-memory cells involves the formation of antigen-antibody-C3 complexes on dendritic cells in lymphoid follicles. C3 may serve to stabilize the antigen bridge between dendritic cells and virgin precursors. In complete contrast, C3 depletion had little effect on the functional expression of primed B cells, thus suggesting that only the early stages of B-cell triggering are C3 dependent.

Animals↗