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Biomedical subjects

S Sanyal

Publications and source records attributed to S Sanyal.

At least 73 records · Page 4Linked to original sources
PubMed1991

Autonomic function tests and clinical significance of dysautonomia in chronic liver disease.

Autonomic function in 20 patients with chronic liver diseases was assessed clinically and by various tests like Valsalva ratio, expiratory-inspiratory ratio, postural tachycardia index, atropine ratio, blood pressure response to assumption of erect posture, hand immersion in cold water, and finger wrinkling response to hand immersion in warm water. Eighty per cent of the patients showed some clinical evidence of dysautonomia. While a good correlation between various clinical complaints of dysautonomia and the extent of parasympathetic dysfunction was observed in the individual patient, a significantly greater impairment of sympathetic function tests was observed in oliguric cirrhotics as compared to their non-oliguric counterparts.

Adult↗
PubMed1990

Development and degeneration of retina in rds mutant mice: immunoassay of the rod visual pigment rhodopsin.

Development and loss of photoreceptor cells in mice, afflicted by the rds (retinal degeneration slow) gene, was analyzed by measuring the ocular visual pigment content as rhodopsin (spectroscopy) and opsin (immunoassay). With regard to the postnatal age, where opsin was just detectable, and to the initial rate of opsin synthesis, the mutants did not strongly deviate from the normal animals. The final maximal visual pigment level was, however, about half of normal for the heterozygous mutants and about 3% of normal for the homozygous mutants, both in the pigmented and in the albino strain. In the pigmented normal or heterozygous mutant the (rhod)opsin levels remain stable up to at least 1 year of age. For the corresponding albino animals this was only observed up to 9 months of age. Thereafter the level declines. In the homozygous mutants, maximal opsin levels were observed at about 3 weeks postnatal. Subsequently, this level gradually declined to about 40% in the pigmented and about 15% in the albino mutant. The results indicate that the rds gene does not directly affect the biosynthetic pathways of opsin. The physiological effect of the rds gene is aggravated by photodamage for which the albino animal is particularly susceptible.

Aging↗
PubMed1990

Gossypol-induced inhibition of glucose uptake in human ejaculated spermatozoa may be mediated by lipid peroxidation.

Gossypol, a plant-derived polyphenolic compound known to exert contraceptive actions in men, inhibits 14C-glucose uptake in vitro in human ejaculated spermatozoa. Spermatozoal glucose uptake was found to increase monotonically up to 40 min, and then decreased by 60 min, possibly because of the saturation of the transport loci in the membrane. Gossypol at the concentrations of 5 and 10 microns caused a reduction of both the linear portion of the uptake and the fall afterwards. Gossypol similarly affects both the Na-dependent and -independent glucose uptake. The kinetic parameters of glucose uptake indicate that gossypol might be interfering with the transport/carrier protein as reduction in maximum uptake velocity (Vmax) was observed without any change in the affinity constant (Km). Similarly, gossypol also produced an increase in spermatozoal lipid peroxidation as evidenced by a steep rise in thiobarbituric acid reaction products in the human sperm cells. A significant decrease in total phospholipid level and the individual classes was noted after gossypol addition. Gossypol-induced inhibition of glucose uptake may be related to the generation of lipid peroxides and consequent membrane damage.

Glucose↗
PubMed1990

Technetium-99m amino acid chelates: correlation of their physico-chemical and physiological parameters. Part I.

Ten alpha-aminocarboxylic acids were chelated with 99mTc and purified by sephadex gel chromatography. Their hepatobiliary and renal excretion patterns were determined in rats. It was observed that lipophilicity of these chelates is the only determinant in governing their hepatobiliary excretion, whereas their renal excretion is dependent on some other factors in addition to lipophilicity. Depression of renal excretion in presence of probenecid indicated an interaction of renal tubular transport enzymes with these chelates, which was explained from their hexacoordinated dioxotechnetium (V) chelate structure (II).

Amino Acids↗
PubMed1990

Cysteine, a chelating moiety for synthesis of technetium-99m radiopharmaceuticals: II. Attempt to synthesize renal tubular radiopharmaceuticals.

N-acyl glycine residue is known to interact with renal tubular transport enzymes and thereby promotes renal tubular secretion. Recently, a similar renal property was also observed with dioxotechnetium aminocarboxy chelates. Therefore, a radiopharmaceutical was designed containing both the above groups with the expectation that an efficient 99mTc labelled renal tubular agent could be developed by this process with which evaluation of various renal parameters will be possible. The synthesized compound, though secreted through the renal tubular pathway, did not show the expected efficiency. It was indicated that the renal property of the molecule was entirely due to chelated dioxotechnetium moiety and the expected effect of the acyl glycine residue was not observed in the molecule.

Animals↗
PubMed1990

Development and degeneration of retina in rds mutant mice: ultraimmunohistochemical localization of S-antigen.

In the developing photoreceptor cells of the homozygous rds mutant mice S-antigen is localized over the ciliary protrusion as in the control mice, and to a lesser extent over the inner segments, perikaryal cytoplasma and the cell terminals. As the outer segments develop in the normal retina, the discs become increasingly immunoreactive. In the rds/rds retina the outer segments fail to develop but small membrane bound vesicles, immunoreactive for S-antigen are extruded and phagocytized by the retinal pigment epithelium. In the retina of older mutant mice, as the photoreceptor cells degenerate slowly, the surviving cells continue to show persistent immunoreactivity for S-antigen in the different regions of the photoreceptor cells. In the heterozygotes the outer segments are reduced and appear abnormal, but the localization of S-antigen is similar to normal. In the receptor region of the normal retina and in the deviant membranous structures in the mutant retina the localization of S-antigen is similar to that of opsin. However, some differences in the subcellular localization of these two photoreceptor specific proteins have been observed. It is concluded that the rds gene acts subsequent to the synthesis of these proteins and possibly at the site of disc assembly.

Animals↗
PubMed1990

Postnatal development of photoreceptor-specific proteins in mice with hereditary retinal degeneration. An immunocytochemical study.

The postnatal development of immunoreactivity for photoreceptor-specific markers was studied in mice carrying the genes rd (retinal degeneration) and rds (retinal degeneration slow) in different combinations. Antibodies raised against three specific photoreceptor proteins (opsin, alpha-transducin and S-antigen) were applied on retinae from mice with the following allelic combinations at the rd and rds loci: +/+, +/+ (control); rd/rd, +/+; rds/rds, +/+; rds/+, +/+; and rd/rd, rds/rds. Immunoreactivity for each antibody appeared simultaneously in normal and mutants. Thereafter, the immunoreactivity patterns in the mutants diverged from the normal phenotype. Except for a dramatic loss of photoreceptor cells in the mutants, the main divergence from the normal development consisted of a progressive loss of the intracellular immunoreactivity compartmentalization for each protein. As degeneration progressed, the remaining photoreceptors became homogeneously labelled; one this labelling pattern was acquired, it was maintained during subsequent stages of development. It is proposed that this pattern, common for all phenotypes studied, may be due to the loss of structural and biochemical polarity of the photoreceptor cells undergoing degeneration, and that this may be an important primary or secondary aspect of the disease process.

Animals↗
PubMed1990

The eye of the blind mole rat, Spalax ehrenbergi. Rudiment with hidden function?

The rudimentary eyes of the mole rat (Spalax ehrenbergi) are located under the skin and do not respond to light stimuli. However, removal of the eyes disturbs photoperiod perception in these animals. To help clarify the possibly remaining function of the eyes in this species, the authors studied their development and ultrastructure. In the early embryos the presumptive eye regions--the epithelium, lens vesicle, and optic cup--appear initially normal. As development progresses, the iris-ciliary body complex originates prematurely from the margin of the optic cup and shows a very rapid and massive growth. This pigment-laden tissue mass remains attached to the corneal stroma, obliterates the anterior chamber, and prevents the formation of the corneal endothelium and Descemet's membrane. In the developing lens the elongation of the lens fibers leads to the formation of a rudimentary lens nucleus that becomes disorganized and vacuolated and eventually also becomes vascularized. The optic fissure fails to close, the eyes remain colobomatous, and the optic disc appears atrophic. In contrast, retinal histogenesis progresses relatively normally, resulting in structurally reduced but well-differentiated photoreceptor, neuronal, and ganglion cell layers in the adult eye. Immunohistochemically, the presence of opsin could be demonstrated in the photoreceptor cells. The latter features may indicate that these rudimentary eyes are still functioning in the complex neuroendocrine pathways mediating photoperiodicity.

Animals↗
PubMed1990

Effect of cimetidine on intestinal absorption & digestive functions in mice.

Oral administration of cimetidine, an antiulcerogenic drug, at a dose of 100 mg per kg body weight in mice, caused significant inhibition of glucose and amino acid uptake in small intestinal segments either after 2 and 24 h (single treatment) or 15 days (daily). Cimetidine also caused a significant decrease in intestinal brush border membrane associated enzymes, sucrase, lactase, maltase and alkaline phosphatase, but increases the activity of leucine aminopeptidase. Kinetic analysis indicated that cimetidine decreased the maximum of apparent initial enzyme velocity (Vmax) of disaccharidases, while substrate affinity constant (Km) was not altered, indicating the noncompetitive nature of inhibition. However, the inhibition of alkaline phosphatase was found to be of mixed type as both Km and Vmax were altered. In vitro addition of cimetidine also produced significant inhibition of enzymes, the inhibition constant (Ki) for sucrase, lactase, maltase and alkaline phosphatase being 22.8, 4.5, 11.5 and 4.8 mM, respectively. It was further observed that in vitro addition of cimetidine also decreased Vmax in case of maltase, sucrase and lactase, Km was unchanged, whereas in case of alkaline phosphatase there was a decrease in Vmax and increase in Km, as compared to the controls.

Absorption↗
PubMed1989

Gossypol inhibition of Ca++ uptake and Ca++-ATPase in human ejaculated spermatozoal plasma membrane vesicles.

Gossypol, a plant-derived polyphenolic compound known to exert contraceptive actions in men, inhibits Ca++-transport and Ca++-activated ATPase in isolated plasma membranes of ejaculated human sperm cells. It also inhibits the membrane bound Mg++- and Na+ + K+-dependent ATPases, 5'-nucleotidase and alkaline phosphatase systems. Ca++-ATPase inhibition by gossypol is non-competitive. It abolishes the discontinuity in Arrhenius expression of temperature dependence of Ca++-ATPase and increases the energy of activation. Phosphatidyl choline and Na+-deoxycholate inhibit Ca++-transport activity in the membrane vesicles. The apparent similarity of Ca++-transport inhibition by gossypol and phosphatidyl choline may indicate the possible capability of this compound to induce changes in the lipid microenvironment of the membranes, wherein the integral proteins operate. Inhibitory effect of gossypol on the plasma membrane Ca++-pump suggests that gossypol may affect sperm motility by a mechanism which is related to the structure and functions of the plasma membrane.

5'-Nucleotidase↗
PubMed1989

Histotypic differentiation of neonatal mouse retina in organ culture.

Retinae from neonatal mice were explanted in toto, with or without the retinal pigment epithelium (RPE) and adjoining mesenchymal cells, and maintained in organ culture for up to 3 weeks. The explants remained flat, rosette formation was minimal and histogenetic changes followed in the normal sequence. After 11, 14 and 21 days in vitro the three cellular layers--the outer nuclear layer including well differentiated rod and cone perikarya, the inner nuclear layer and the ganglion cell layer--with the intervening plexiform layers were comparable to those of the in vivo eyes. Electron microscopic analysis revealed that in the explants without RPE the nuclear layers developed as in vivo, but receptor outer segments (ROS) were not formed. When the RPE was present, receptor inner segments appeared normal and ROS including profuse disc structures were developed. Presence of synaptic elements was also recognized. Mesenchymal cells, when present differentiated into choroidal and scleral tissues and appeared to play a supportive role for the RPE cells. The system is described in detail and its suitability for the analysis of various cellular and metabolic factors in the development of the retina is discussed.

Animals↗
PubMed1989

Development and degeneration of retina in rds mutant mice: altered disc shedding pattern in the heterozygotes and its relation to ocular pigmentation.

In the heterozygous mutant (rds/+) mice, receptor outer segments (ROS) are irregular in form and are shed as abnormally large phagosomes. In the albino rds/+ mice, peak frequency of pigment epithelial (RPE) phagosomes is higher than normal and is recorded near the end of the light period, instead of at the time of light onset as in the normal (+/+) albino mice. In pigmented mice of both genotypes, the maximum numbers of phagosomes in the RPE remain lower than in the albinos. In pigmented +/+ mice the number of phagosomes is already high at the time of light onset. The number rises to peak after one hour and then declines slowly. The lowest frequency is reached after the end of the light period. In pigmented rds/+ mice, the number of phagosomes in the RPE is lowest at the time of light onset. The number rises rapidly to peak level within two hours, then declines and remains low until light onset. If the dark period is prolonged, phagosome frequency in the rds/+ RPE remains lower than in +/+ RPE. If the light period is prolonged, phagosome frequency in the rds/+ RPE remains at a higher level than in the +/+ RPE. This differential response to altered light regimen in the rds/+ and +/+ mice is less pronounced in the pigmented than in the albino individuals. The phagosomes in the rds/+ RPE are larger than in the +/+ RPE in all light regimens. These results show that ocular pigmentation may modify the circadian pattern of ROS disc shedding in the rds/+ retina.

Animals↗
PubMed1989

Postnatal development of photoreceptor proteins in mutant mice and Abyssinian cats with retinal degeneration.

Using immunocytochemical techniques, development of opsin, transducin alpha and S-antigen in photoreceptor cells of the mice homozygous or heterozygous for the rd or rds genes has been found to be similar to that of control animals during the first postnatal week. Even though the absolute amounts of these proteins are low (eg. opsin in the rds retina) or decrease in the postnatal period (as in the rd retina), we can demonstrate their persistence during the entire degeneration process. In fact, the content of the proteins in the photoreceptor perikarya actually appear to be higher after postnatal day 11 in all mutants studied. Thus, one of the major manifestations of the mutant retinae is a loss of polarity of the photoreceptor cells at the time of ROS degeneration without a loss in the ability to synthesize these important proteins of the visual cycle. This correlates well with the apparent defect in IRBP secretion and its intracellular accumulation in mutant photoreceptor cells as previously observed (van Veen et al. 1986). In the Abyssinian cat model for progressive retinal atrophy, the development an cellular distribution of all the proteins studied are similar in affected and control retinae until the beginning of stage 2 of the disease. At this time, outer segments begin to degenerate and immunoreactivity increases in the photoreceptor perikarya. The IRBP content of the retina declines markedly at stage 2, preceding extensive loss of photoreceptors.

Aging↗
PubMed1989

A comparative survey of synaptic changes in the rod photoreceptor terminals of rd, rds and double homozygous mutant mice.

In the developing retina of homozygous rd/rd mutant mice the time of onset of degenerative changes and the period of rapid photoreceptor cell loss overlaps the later phase of differentiation during which the maturation of the receptors and the completion of the synaptic connections take place. It remains unresolved if the retarded synaptogenesis within the photoreceptor terminals of the rod cells is a direct effect of the mutant gene or an indirect consequence of premature cell death. In the retina of homozygous rds/rds mutant mice early indication of gene expression within the photoreceptor cells is also recorded as photoreceptor outer segments fail to develop. However, during the very slow rate of degeneration, the surviving cells develop normal synaptic contacts within their terminals. Furthermore, some of the rod cells, though not the cones, go on to enlarge their synaptic structures as more and more photoreceptor cells are lost. In the retina of double homozygous mutant rd/rd;rds/rds mice the photoreceptor cells remain lacking in outer segments, as would be expected, but curiously enough, survive longer than in the rd/rd retina. Among this population of photoreceptor cells with extended life-span profiles of rod terminals are frequently encountered which contain a normal synaptic structure - one synaptic ribbon with two laterally placed processes of horizontal cells and one medially facing process of a bipolar cell. A number of these terminals also show signs of synaptic enlargement. Thus it can be concluded that some of the terminals of the rod photoreceptor cells of the double homozygous rd/rd,rds/rds mice, which survive longer than in the rd/rd mice, develop synapses that are either comparable to normal or resemble those of the rds/rds retina. These findings suggest that retarded synaptogenesis within the rod terminals of the rd/rd retina is likely to result from a pathogenic defect affecting the whole cell and is not due to a specific or exclusive action of the mutant gene on the synaptic components involved.

Animals↗
PubMed1989

Effect of antiulcerogenic drug, ranitidine, on intestinal absorption and digestive functions in mice.

Oral administration of antiulcerogenic drug ranitidine significantly inhibits glucose and amino acid uptake in small intestinal segments. It also inhibits activities of brush border membrane disaccharidases and alkaline phosphatase but increases the activity of leucine aminopeptidase. Kinetic analysis reveals noncompetitive and mixed type of inhibition for disaccharidases and alkaline phosphatase, respectively. In vitro addition of the drug to membrane preparation shows similar type of results as seen in vivo with the inhibition constant (ki) for sucrase, lactase, maltase and alkaline phosphatase as 12.5, 5, 11.5 and 19.5 mM, respectively.

Animals↗
PubMed1988

A developmental study of interphotoreceptor retinoid-binding protein (IRBP) in single and double homozygous rd and rds mutant mouse retinae.

Interphotoreceptor retinoid-binding protein (IRBP) was studied using immunochemical and immunocytochemical techniques in retinae of mice with allelic combinations at the rd and rds loci at different stages of development and degeneration. Until postnatal day 7 (P7), IRBP is located intracellularly in developing retinae of the different genotypes. Thereafter, IRBP is present mainly in the interphotoreceptor matrix. As previously noted, cell death is slowest in the heterozygous +/+,rds/+ mutant with loss increasing in order in +/+,rds/rds, rd/rd, rds/rds and rd/rd,+/+ animals. The IRBP content of the total retina also approximates this pattern, with lowest amounts by far in rd/rd, rds/rds and rd/rd,+/+ mutants (after P14). Interestingly though, IRBP loss significantly precedes visual cell loss in the rd/rd,rds/rds retina. In all the mutants, the remaining rod cells in the outer nuclear layer exhibit synthesis of intracellularly located IRBP at late stages of degeneration. In the single homozygous rd/rd,+/+ and the double homozygous rd/rd,rds/rds mutants, IRBP is present intracellularly during the entire degenerative process with somewhat less intracellular IRBP in the rd/rd,rds/rds mutant. Retinae of homozygous +/+,rds/rds and heterozygous +/+,rds/+ animals exhibit a normal distribution pattern of IRBP immunoreactivity until loss of photoreceptor cells becomes pronounced at later stages of the disease. Many of the remaining cells at this time are probably cone elements although they are structurally changed. Double labeling with IRBP and S-antigen demonstrates, in many but not all, the presence of both proteins in the same cell body. Immunocytochemistry clearly demonstrated the presence of IRBP in remaining photoreceptor cells at late stages of the disease. Thus, the biochemically measured loss of IRBP appears to be a complex process neither directly dependent on the loss of photoreceptor outer segments and reduced interphotoreceptor matrix space (e.g. there is a sustained IRBP level in rodless rds mutants) nor simply due to cell death (e.g. in the rd/rd,rds/rds mutant, IRBP loss significantly precedes cell loss). That this IRBP is mainly intracellular, however, may indicate an abnormality in secretion which, combined with other factors, induces a degenerated and less differentiated phenotype.

Animals↗
PubMed1988

Development and degeneration of retina in rds mutant mice: altered disc shedding pattern in the albino heterozygotes and its relation to light exposure.

The number of phagosomes in the retinal pigment epithelium (RPE) of normal albino mice, maintained in cyclic light, is highest at the time of onset of light. The number declines to the lowest level around the start of the dark period. If the dark period is prolonged, the pattern of shedding remains cyclic but the phagosome count is higher than normal. If the light period is prolonged the phagosome count remains low and the rise to the peak is delayed. The number of phagosomes in the RPE of albino rds/+ mice, maintained in cyclic light, peaks to higher than normal level and the peak is recorded near the end of the light period. If the dark period is prolonged the phagosome count in the RPE of rds/+ mice remains lower than in the similarly treated normal mice. The phagosome count in the RPE of rds/+ mice, exposed to a prolonged light period, remains higher than in the similarly treated normal mice. In both normal and rds/+ mice, born and reared in total darkness, the pattern of disc shedding is very different but the rds/+ mice show a relatively higher frequency of phagosomes in the RPE than the normal mice. The phagosomes in the rds/+ RPE are larger than normal. An increase in size appears to correspond with increased rate of shedding in the rds/+ mice and to a lesser extent also in normal mice. Thus, the pattern of disc shedding in the albino rds/+ mice, which is different from the normal albino mice, also shows a different reaction to changes in the environmental light.

Animals↗