Crystalloid lysozyme inclusions in Paneth cells of vitamin A-deficient rats.
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Biomedical subjects
Publications and source records attributed to M J Koch.
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An outbreak of infectious kerato-conjunctivitis is described in a dairy herd during the (winter)stable period. Moraxella was isolated from lacrimation fluid from three animals. The development of the infection was possibly precipitated by a vaccination with modified live IBR virus, adenovirus type 3 and parainfluenza virus type 3. Presumably, climatological-stable conditions play an important role in the clinical manifestation of the infection.
The effect of vitamin A-deficiency on jejunal Paneth cells in rats was investigated. Crystalloid particles were observed in secretion granules of Paneth cells from 6 out of 8 rats with vitamin A-deficiency. The particles were similar to those found in Paneth cells under other experimental conditions. Using an immuno-electron-microscopic technique we demonstrated a clear lysozyme immunoreactivity of these particles. In 2 vitamin A-deficient rats tubular structures have been detected in addition to the crystalloid particles. Crystalloid particles or tubular structures were not detectable in a control group of 8 vitamin A-supplemented rats. The morphological alterations of Paneth cells may be correlated to an impaired local immunity of the intestine during vitamin A-deficiency.
The transport and metabolic properties of dehydroascorbic acid have been evaluated in the small intestine of one ascorbic acid-dependent animal species (guinea pig) and one ascorbic acid-synthesizing animal species (rat). Loops of guinea pig jejunum in vitro brought about net transepithelial absorption of L-[14C]dehydroascorbic acid with most of the absorbed substrate appearing in the reduced form (ascorbic acid). Saturation of brush-border transport occurs at a lower concentration than saturation of the enzymatic reduction. Rat intestine did not bring about net transepithelial transport. The intestines of both guinea pigs and rats took up substantial dehydroascorbic acid from the serosal bathing solution, with the majority appearing in the mucosa as ascorbic acid. It is proposed that in guinea pig intestinal mucosa, dehydroascorbic acid reductase has a nutritional role in extracting the vitamin from chyme and reducing it for subsequent use in the body. The intestines of both guinea pig and rat appear to take up dehydroascorbic acid across the basolateral surface and reduce it, thus maintaining a substantial endogenous level of ascorbic acid in the mucosa. The transport and metabolic properties described might play an important role as a protective antioxidant mechanism in intestinal mucosa.
Quantitation of ascorbate at concentrations normally found in biological samples and foods has previously been shown to be possible by HPLC analysis. Prefilled amine columns from three manufacturers were presently used to evaluate their potential for separating low concentrations of [14C]ascorbic acid from its degradation products, [14C]dehydroascorbic acid and [14C]diketogulonic acid. A successful separation was achieved on some columns with as little as 200 cpm (30 pmol) of total ascorbate injected. On other columns, injection of 30-500 pmol of ascorbate resulted in as much as 80% of [14C]ascorbic acid eluting with an unpredictable retention time. In these instances the inclusion of nonlabeled ascorbic acid (0.5 mg/ml) to the sample resulted in most of the [14C]ascorbic acid activity eluting at the expected retention time of ascorbic acid. The inclusion of ascorbic acid in samples injected onto the column also resulted in a more discrete peak in the elution of dehydroascorbic acid, and more complete recovery of the total [14C]activity (ascorbic acid, dehydroascorbic acid, and diketogulonic acid) injected onto the column.
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The unidirectional influx of folic acid across the mucosal border of hamster duodenum and rat jejunum was determined. Influx follows saturation kinetics, is sodium-dependent, and is inhibited by methotrexate and is sodium-dependent, and is inhbited by methotrexate and folinic acid in the mucosal bathing solution. In hamster duodenum, the maximal influx is 1.2 nmol/(cm2.h), and the folic acid concentration required to give a half maximal influx (Km) is 7.2 micron.. At mucosal folic acid concentration of 1.5 micron, influx is reduced at least 65% by removal of sodium from the bathing solution. The influx process is significantly inhibited by cyanide and 2,4-dinitrophenol. The possibility was evaluated that the acidic microclimate at the brush border regulates the rate of folic acid transport and that inhibition of transmural transport by sodium-free media, ouabain, and methotrexate is brought about indirectly by an increase in pH of the microclimate. The data favor the alternative concept of a sodium-dependent carrier mechanism for entry of folic acid into the cells. The information presented is consistent with active transport of folic acid by a sodium-gradient mechanism, but additional information will be necessary to substantiate such a model.
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The electrical potential profile of rabbit ileum was investigated in vitro with the microelectrode technique. The transmural electrical potential difference (PD), designated psims, was immediately reduced by 60% upon cooling the tissue from 37 to 7 degrees C; the PD across the mucosal membrane (transmucosal PD, psimc) was simultaneously reduced by 37%. These electrical changes could not be attributed to alternations in either transmembrane ion concentration gradients or total tissue conductance. The psimc and psims may have substantial values even after the concentration gradients of Na and K across the cell membane are eliminated, provided that active transport mechanisms are still operative. Conversely, in the presence of approximately normal transmembrane ion concentration gradients, but when active transport mechanisms have been inhibited. psimc is reduced by 45% and psims is zero. These observations are consistent with a model of electrolyte transport in which psims and the normal transmembrane cation concentration gradients are established by rheogenic active transport of Na out of the cell. The psimc is generated both by rheogenic active Na transport and by cation concentration gradients which exist across the cell membrane. The Koefoed-Johnsen and Ussing model (Acta Physiol. Scand., 1958, vol. 42, p. 298) of electrolyte transport by epithelial cells does not adequately describe the electrical properties of ileum.
Descending rabbit colon, stripped of muscularis externa, absorbs Na and Cl under short-circuit conditions and exhibits a residual ion flux, consistent with HCO3 secretion, whose magnitude is approximately equal to the rate of active Cl absorption. Net K transport was not observed under short-circuit conditions. The results of ion replacement studies and of treatment with ouabain or amiloride suggest that the short-circuit current ISC is determined solely by the rate of active Na transport and that the net movements of Cl and HCO3 are mediated by a Na-independent, electrically-neutral, anion exchange process. Cyclic AMP stimulates an electrogenic Cl secretion, abolishes HCO3 secretion but does not affect the rate of Na absorption under short-circuit conditions. Studies of the effect of transepithelial potential difference on the serosa-to-mucosa fluxes Jism of Na, K and Cl suggest that JNasm,JIsm and one-third of JCl-sm may be attributed to ionic diffusion. The permeabilities of the passive conductance pathway(s) are such that Pk:PNa:PCl= 1.0:0.07:0.11. Electrolyte transport by in vitro rabbit colon closely resembles that reported from in vivo studies of mammalian colon and thus may serve as a useful model for the further study of colonic ion transport mechanisms.
A case-control epidemiologic study of childhood polymyositis is presented. Parents of 42 cases of childhood polymyositis were interviewed along with parents of controls matched for sex and age. Extensive review of past medical history, animal exposure history, residential and family history, and immunization history failed to reveal any significant differences between the two groups. The only suggestive difference was exposure to bacteriologically confirmed streptococcal diseases in 20 cases as compared to 13 controls.
A case is described of presumed quinidine hepatotoxicity, characterized by the development of fever, abnormal serum transaminase values, which improved after cessation of the drug but recurred after a challenge dose, and centrizonal hepatocellular necrosis detected on liver biopsy. Morphological changes on electron microscopy, consistent with a drug reaction, are also described. Pertinent features of previous case reports are analyzed, and the histological findings by light microscopy of the present and past cases are discussed. It is suggested that the development of unexplained fever within 1 month of quinidine administration should lead to consideration of possible hepatotoxicity.
The neurologic status of 2,000 veterans who had had surgery for peptic ulcer between 1952 and 1957 was evaluated. In 1970, a total of 156 of these men were examined, 97 of whom had procedures that disrupted the normal continuity of the upper gastrointestinal tract. Twenty-one had neurologic disorders, including 17 patients with peripheral neuropathies. Procedures bypassing the ampulla of Vater were performed in 15 of these. The only detected factor associated with neurologic manifestations was weight loss since surgery. A mortality study of the total population revealed 865 patients had died by the end of 1973. There were seven deaths attributed to neurologic causes, one in a patient with amyotrophic lateral sclerosis and one in another with spinal paralysis. All seven were among the 70% of the deceased who had had surgery that disrupted the continuity of the upper gastrointestinal tract. Thus, we conclude that the type of surgery influenced the likelihood of neurologic complications, but at least for motor neuron disease, the increased risk was not appreciable.
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