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At least 613 records · Page 34Linked to original sources
PubMed1991

High intracellular pH in CFPAC: a pancreas cell line from a patient with cystic fibrosis is lowered by retrovirus-mediated CFTR gene transfer.

Expression of CFTR from a retroviral vector in CFPAC, a pancreatic adenocarcinoma cell line derived from a patient with Cystic Fibrosis, causes a decrease in the average intracellular pH (pHi) in these transduced clones (PLJ-CFTR), as compared to CFPAC or CFPAC transduced with control virus (PLJ clones). Whereas the average pHi calculated based on results obtained in two PLJ-CFTR clones, PLJ-CFTR-20 (n = 2) and PLJ-CFTR-6 (n = 5), was 7.46 +/- 0.07, the average pHi calculated from results obtained in CFPAC (n = 13), PLJ-6 (n = 11) and PLJ-10 (n = 3) was pH 7.83 +/- 0.11. This finding suggests that CFTR may be involved, directly or indirectly, in the regulation of pHi in the pancreas.

Benzoates↗
PubMed2001

Changes in the exocrine pancreas secondary to altered small intestinal function in the CF mouse.

The exocrine pancreas of the cystic fibrosis (CF) mouse (cftr(m1UNC)) is only mildly affected compared with the human disease, providing a useful model to study alterations in exocrine function. The CF mouse pancreas has approximately 50% of normal amylase levels and approximately 200% normal Muclin levels, the major sulfated glycoprotein of the pancreas. Protein biosynthetic rates and mRNA levels for amylase were not altered in CF compared with normal mice, and increases in Muclin biosynthesis and mRNA paralleled the increased protein content. Stimulated pancreatic amylase secretion in vitro and in vivo tended to be increased in CF mice but was not statistically significant compared with normal mice. We show for the first time that the CF mouse duodenum is abnormally acidic (normal intestinal pH = 6.47 +/- 0.05; CF intestinal pH = 6.15 +/- 0.07) and hypothesize that this may result in increased signaling to the exocrine pancreas. There were significant increases in CF intestinal mRNA levels for secretin (310% of normal, P < 0.001) and vasoactive intestinal peptide (148% of normal, P < 0.05). Furthermore, CF pancreatic cAMP levels were 147% of normal (P < 0.01). These data suggest that the CF pancreas may be chronically stimulated by cAMP-mediated signals, which in turn may exacerbate protein plugging in the acinar/ductal lumen, believed to be the primary cause of destruction of the pancreas in CF.

Amylases↗
PubMed1976

Quantitative evaluation of serum pancreatic isoamylases in cystic fibrosis.

The amylase in sera of 20 patients with cystic fibrosis of the pancreas (CFP), 17 of whom had pancreatic insufficiency (PI), and of 34 normal control subjects was separated into its pancreatic and salivary components and quantitated. Electrophoretic separation was achieved on polyacrylamide disc gels with subsequent sectioning of the gel columns. The amylase content in international units per liter (IU/L.) was obtained for each section by the insoluble blue starch substrate method. The mean total serum amylase of the CFP patients with PI was significantly lower than the control group. A highly significant decrease was found when the pancreatic isoamylase was considered alone. The salivary isoamylase level remained essentially the same. Three patients with CFP but without PI demonstrated higher than normal pancreatic amylase values in the serum. These patients may be in an early stage of a progressive involvement of the pancreas in which there is an increased release of amylase. This method of electrophoretic separation and quantitation of the serum amylase is sensitive and efficient and allows the simultaneous processing of multiple specimens. The results obtained agree with previously published ratios of serum isoamylases. Our method should be valuable in the study of other diseases of the exocrine pancreas and salivary glands.

Adolescent↗
PubMed1967

Sodium transport: inhibitory factor in sweat of patients with cystic fibrosis.

A factor inhibitory to sodium transport exists in the sweat of patients with cystic fibrosis of the pancreas. When the duct system of the rat parotid was perfused with sweat from patients, marked inhibition of sodium reabsorption was observed. Perfusion with sweat from normal subjects caused no change in sodium reabsorption. The factor thus demonstrated may be responsible for the increased sodium concentrations in the sweat of patients with cystic fibrosis.

Absorption↗
PubMed1961

The ultrastructure and histophysiology of human eccrine sweat glands.

The electron microscopy of human eccrine sweat glands has been studied before and after stimulation by pilocarpine iontophoresis. The identity of the dark and clear cells in the secretory segment as defined by Montagna et al. (23) was determined by studying serial sections, thin for electron microscopy and thick for light microscopy. Cells with numerous apical secretory vacuoles are termed mucoid (dark) cells, since these vacuoles stain positively for acid mucopolysaccharide. Clear cells are intimately associated with intercellular canaliculi. The "cuticular border" of surface cells of the duct is a condensation of tonofilaments and granules. Numerous mitochondria are concentrated in basal cells of the duct. The presence of mucoid cells in the secretory segment may bear on the interpretation of the pathologic findings in the disease cystic fibrosis of the pancreas, and suggests that this disease may be due to a basic disorder of mucopolysaccharide production. The possible roles of the various cellular components in the elaboration of sweat are discussed.

Cell Membrane↗