Background: The new coronavirus, severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has caused more than 210 000 deaths worldwide. However, little is known about the causes of death and the virus's pathologic features.
Although being equal in short-term efficacy and overall tolerability our results suggest a better gastrointestinal tolerability for iron sucrose. Larger trials are mandatory to prove a possible advantage of iron sucrose in short- and long-term efficacy as well as in tolerability over iron sulfate in the management of IDA in IBD.
The cholecystokinin (CCK) family of peptides and their receptors are widely distributed throughout the gastrointestinal and central nervous systems where they regulate secretion, motility, growth, anxiety, and satiety. The CCK receptors can be subdivided into at least two subtypes, CCKA and CCKB on the basis of pharmacological studies. We report here the purification of the CCKA receptor to homogeneity from rat pancreas by using ion-exchange and multiple affinity chromatographic separations. This allowed partial peptide sequencing after chemical/enzymatic ceavage and synthesis of degenerate oligonucleotide primers. These primers were used for initial cloning of the cDNA from rat pancreas by PCR. The predicted protein sequence ofthe cDNA clone contained the five partial peptide sequences obtained from the purified protein.Seven putative transmembrane domains suggest its membership in the guanine nucleotide-binding regulatory proteincoupled receptor superfamily. In vitro transcripts of the cDNA clone were functionally expressed in Xenopus oocytes and displayed the expected agonist and antagonist specificity.The cholecystokinin (CCK) family of peptides was originally isolated from the mammalian gastrointestinal tract (1) and was one of the first gastrointestinal peptides to be discovered in the brain (2). Their receptors appear throughout the gastrointestinal and nervous systems and can be pharmacologically classified into two subtypes, CCKA and CCKB (3). CCKA receptors mediate physiologic gallbladder contraction, pancreatic growth and enzyme secretion, delayed gastric emptying, relaxation of the sphincter of Oddi, and potentiation of insulin secretion (3). The CCKA type receptor also appears in the anterior pituitary, the myenteric plexus, and areas of the central nervous system (midbrain) where CCK-containing dopaminergic neurons have been implicated in the pathogenesis of schizophrenia, Parkinson disease, drug addiction, and feeding disorders (4). Experimental rat pancreatic carcinogenesis is promoted by CCK through the CCKA type receptor (5). CCK acting at peripheral CCKA receptors and at central CCKA and CCKB gastrin receptors plays a significant role in the nervous system control of appetite (6).Recently, antagonists highly selective and potent for each of the CCK receptor subtypes have been developed. The two most potent and selective antagonists are L-364,718 (7) and PD134308 (8) for CCKA and CCKB receptors, respectively.In pancreatic acinar cells, CCKA receptors are coupled to a guanine nucleotide-binding regulatory protein (G protein), which activates phospholipase C, breakdown of inositol phospholipids, mobilization of intracellular calcium, and activation of protein kinase C (3). Activation of this pathway in Xenopus oocytes by CCK receptors that have been functionally expressed in the plasma membrane after injection of either rat brain total RNA (9) or the rat pancreatic acinar carcinoma cell line, AR42J (10), mRNA (11) results in a depolarizing current due to Ca2+-dependent chloride channels o...
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