Recent advances in calcium transport by the kidney.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Kumar.
Explore the source record for details and available documents.
An indirect immunofluorescent technique for rapid diagnosis of patients of Japanese encephalitis (JE) was developed by demonstrating the viral antigen in CSF cells. The CSF samples of 31 consecutive patients admitted with acute viral encephalitis during 1987 were studied. In 15 patients the diagnosis of JE virus infection was made on the same day. Classical techniques for virus detection and antibody serology were also conducted in these patients. The indirect immunofluorescence for JE virus antigen detection in CSF cells proved to be a rapid and simple procedure for making a quick diagnosis of infection.
A greater dependence on transsarcolemmal Ca2+ flux and immaturity of Ca2+ sequestration capacity may potentiate Ca2(+)-mediated reperfusion injury in the newborn myocardium. The effect of serum ionized Ca2+ concentration on left ventricular systolic and diastolic function after ischemia was studied in 5-7-day-old piglets undergoing a 90-minute period of cold-blood cardioplegic arrest. In the control group, Ca2+ was maintained at 1.2 mM (Group A [n = 6]). The cardioplegic solution and bypass perfusate were modified to achieve a low Ca2+ concentration, 0.25 mM, in Group B (n = 6). Left ventricular pressure-volume loops were acquired by using high-fidelity pressure-sensor-tipped and volume-conductance catheters. Ventricular function was assessed from the slope of end-systolic (Ees) and end-diastolic (k) pressure-volume relations during transient caval occlusion. Both groups showed a significant reduction in Ees after ischemia (p less than 0.05). Intergroup comparison of Ees after ischemia demonstrated a better recovery of the systolic function in the low Ca2+ group, 64 +/- 7% versus 49 +/- 6% in the normal Ca2+ group (p = 0.05). There was a significant increase in chamber stiffness index in group A (k, 0.48 +/- 0.06 to 0.65 +/- 0.05 ml-1, p less than 0.01) versus no significant change in group B. This study shows 1) the feasibility of acquiring continuous pressure-volume data in neonatal hearts by using a conductance catheter system, and 2) better preservation of systolic function and diastolic compliance in normal newborn myocardium by low Ca2+ concentration in the peri-ischemic period.
This communication reports the clinical features of 92 children with Japanese encephalitis diagnosed on the basis of viral isolation from brain or cerebrospinal fluid and/or a 4-fold or higher rise in antibody titre in paired sera by haemagglutination inhibition (HI) test, followed by detection of specific IgM HI antibody. More than a third of the patients (38%) were from urban areas. A high incidence of fever (94.5%), coma (100%) and convulsions (84.7%) was seen. Focal neurological deficit was found in 29.3 per cent of patients and pleocytosis in the cerebrospinal fluid in 32.3 per cent. An extrapyramidal syndrome developed in 21.3 per cent patients during the convalescent stage. Thirty four (36.9%) patients died while in hospital. Mortality was significantly related to a short prodromal stage, deep coma, abnormalities in tone and breathing and decerebrate posturing. Japanese encephalitis represents a severe disease in children with a high early mortality.
Renal osteodystrophy is a complex disorder which can be divided into five distinct bone histologic subtypes: mild bone disease, hyperparathyroid bone disease, mixed bone disease, osteomalacia, and low-turnover bone disease. Hyperparathyroidism develops in renal failure due to two principal abnormalities: 1,25(OH)2D3 deficiency and hyperphosphatemia. Treatment of these problems is important in order to prevent hyperparathyroidism. Most cases of osteomalacia, mixed bone disease, and low-turnover bone disease are influenced by aluminum status and parathyroid hormone. Aluminum-associated bone disease can be treated with termination of aluminum exposure and/or deferoxamine therapy. Numerous diagnostic pitfalls exist in the evaluation of renal osteodystrophy, and the bone biopsy is extremely important to avoid these problems and plan proper therapy.
The purpose of this review is to highlight reasons why increased attention should be paid to the prevention and treatment of psychiatric disorders at childbirth. The two main psychiatric disorders that are associated with childbirth--postnatal depression and postpartum psychosis--are reviewed, together with a discussion of the maternity blues. An overview of each condition is presented, identifying incidence rates, clinical manifestations, and appropriate treatment approaches. Recommendations are made for coordination and development of services as a means to achieve prevention and treatment of postpartum psychiatric disorders.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Esch. coli strains manifesting localised (17), diffuse (8) or aggregative (17) phenotypes of adherence to HEp-2 cells were tested for their ability to adhere to human enterocytes isolated from duodenal biopsies of adult volunteers to obtain further evidence of their enteropathogenecity. Esch. coli strains H10407+; CFAI+ and LT+ STp+ STh+, F 294 B; a localised adherent strain positive with entero-adherent factor probe reported previously to attach to small intestinal enterocytes and F 582 C; LT- STp+ STh+ were the positive controls: H10407P (CFAI- mutant of H10407+) and K12 served as negative control strains. Adherence of variable degree was seen with 35.3 per cent of enteroaggregative Esch. coli (EAggEc) and with 58.8 per cent of enteroadherent Esch. coli localised (EAEC-L); EAEC-diffuse (EAEC-D) did not adhere to the human enterocytes. The possibility that EAgg EC and diffuse phenotypes may adhere better to lower small intestine or the large intestine, needs to be investigated.
Explore the source record for details and available documents.
Immunologic status of 43 children, 13 with bronchiolitis and 30 with bronchial asthma was studied, and compared with 10 infants and 16 healthy children of respective control groups. Humoral immunity was assessed by absolute eosinophil count and B cell count (EAC rosette method) and cellular immunity by T cell count (E rosette method) and DNCB skin test. B cell subset of lymphocytes were raised in both the study groups but associated significant eosinophilia was seen only in bronchial asthma. The study demonstrated significantly lower mean T cell count and depressed DNCB reactivity in children of bronchial asthma. Children with bronchiolitis too had significantly lower mean T cell count. Thus both humoral and cellular immunity were altered in children with bronchial asthma and bronchiolitis.
A sandwich ELISA for quantitation of tetanus toxin was devised using commercially available horse antitetanus antiserum and its HRP-conjugate. With commercial toxoid as a standard the assay had a lower sensitivity of 100 ng/ml and was linear up to 100 micrograms/ml. In terms of Lf equivalents the ELISA assay was linear from 0.02 to 20 Lf/ml. The Lf activity in 20 preparations of tetanus toxin as determined by ELISA was comparable to the activity measured by conventional flocculation tests (r = 0.987).
Adenosine deaminase was estimated in ascitic fluids of 49 patients with ascites (19 tuberculous, 20 cirrhotic, and 10 malignant). The adenosine deaminase concentration in tuberculous ascitic fluid was 98.8 +/- 20.1 U/L (mean +/- SD), which was significantly more than that noted in cirrhotic (14 +/- 10.6 U/L) or malignant (14.6 +/- 6.7 U/L) ascitic fluids (p less than 0.001 for each). At a cut-off value of greater than 33 U/L, the sensitivity, specificity, positive and negative predictive value, and the overall diagnostic accuracy for diagnosing tuberculous ascites were 100%, 96.6%, 95%, 100%, and 98%, respectively. We conclude that estimation of adenosine deaminase in ascitic fluid is an easy and reliable method for diagnosing tuberculous ascites.
Interferons are regulatory secretory proteins that have a variety of biological activities, including antiproliferative actions against tumor cell lines and tumors in vivo. Among the several interferon-inducible genes, modulation of 2'-5'-oligoadenylate synthetase expression has been the focus of considerable attention because of its implication in growth regulation. In the studies presented here, we report growth inhibition of A431 cells by gamma-interferon and provide new evidence to support the possible involvement of 2'-5'-oligoadenylate synthetase. We observed that the antiproliferative effect of gamma-interferon on cultures of A431 cells was accompanied by prolongation of G0-G1 phase and profound morphological changes, which were progressively prominent from day 4 onward. The levels of 2'-5'-oligoadenylate synthetase enzyme activity and mRNA were significantly elevated following gamma-interferon treatment and correlated well with the kinetics of growth-inhibitory effects. There were differential induction and expression of different isoenzyme forms of 2'-5'-oligoadenylate synthetase: the Mr 100,000 and Mr 40,000 proteins were induced maximally to varying degree by day 4, with subsequent decline; in contrast, the Mr 67,000 protein was induced late and remained high up to day 9 after gamma-interferon treatment. In accord with these observations, fractionation of enzymatic activity also revealed differences in the enzyme activities of 2'-5'-oligoadenylate synthetase forms from control and treated cells. Therefore, these observations demonstrate the existence of possible differential regulation of 2'-5'-oligoadenylate synthetase isoenzymes and strengthen the concept that growth inhibition of cells may be mediated via induction of 2'-5'-oligoadenylate synthetase.
Zinc ions in the micromolar range exhibited a strong inhibitory activity toward platelet activating factor (PAF)-induced human washed platelet activation, if added prior to this lipid chemical mediator. The concentration of Zn2+ required for 50% inhibition of aggregation (IC50) was inversely proportional to the concentration of PAF present. The IC50 values (in microM) for Zn2+ were 8.8 +/- 3.9, 27 +/- 5.8, and 34 +/- 1.7 against 2, 5, and 10 nM PAF, respectively (n = 3-6). Zn2+ exhibited comparable inhibitory effects on [3H]serotonin secretion and the IC50 values (in microM) were 10 +/- 1.2, 18 +/- 3.5, and 35 +/- 0.0 against 2, 5, and 10 nM PAF, respectively (n = 3). Under the same experimental conditions, aggregation and serotonin secretion induced by ADP (5 microM), arachidonic acid (3.3 microM), or thrombin (0.05 U/ml) were not inhibited. Introduction of Zn2+ within 0-2 min after PAF addition not only blocked further platelet aggregation and [3H]serotonin secretion but also caused reversal of aggregation. Analysis of [3H]PAF binding to platelets showed that Zn2+ as well as unlabeled PAF prevented the specific binding of [3H]PAF. The inhibition of [3H]PAF specific binding was proportional to the concentration of Zn2+ and the IC50 value was 18 +/- 2 microM against 1 nM [3H]PAF (n = 3). Other cations, such as Cd2+, Cu2+, and La3+, were ineffective as inhibitors of PAF at concentrations where Zn2+ showed its maximal effects. However, Cd2+ and Cu2+ at high concentrations exhibited a significant inhibition of the aggregation induced by 10 nM PAF with IC50 values being five- and sevenfold higher, respectively, than the IC50 for Zn2+, and with the IC50 values for inhibition of binding of 1 nM [3H]PAF being 5 and 19 times higher, respectively, than the IC50 for Zn2+. The specific inhibition of PAF-induced platelet activation and PAF binding to platelets suggested strongly that Zn2+ interacted with the functional receptor site of PAF or at a contiguous site.
A major unanswered question in central nervous system physiology concerns the mechanism by which cerebrospinal fluid (CSF) Ca2+ homeostasis is maintained in the face of hypo- or hypercalcemia. To address this question, we sought and found a protein of Mr approximately 140,000 in choroid plexus plasma membranes that forms a phosphorylated intermediate with characteristics of a plasma membrane Ca2+-pump. A choroid plexus plasma membrane protein of this molecular weight also bound to a monoclonal antibody prepared against the human erythrocyte plasma membrane Ca2+-Mg2+ ATPase Ca2+-pump. When this monoclonal antibody was used for immunohistochemical localization, the plasma membrane Ca2+-pump was found primarily in the CSF-facing membranes of choroid plexus cells from rats, cats, and man. The localization of a plasma membrane Ca2+-pump in the CSF-facing membranes of the choroid plexus suggests that the choroid plexus, by mechanisms including this pump, may regulate CSF Ca2+ concentrations.
Purified rat pancreas protein kinase C (PKC) is activated by unsaturated free fatty acids (oleic and arachidonic). The ethyl esters of these fatty acids are ineffective as enzyme activators. However, when the ethyl esters are added in combination with a free fatty acid, there is significant enhancement of enzyme activation. Nearly optimal PKC activation was obtained when non-activating ethyl oleate or ethyl arachidonate was added to sub-optimally activating concentrations of oleic or arachidonic acids. In addition to the ethyl esters, 1-monooleylglycerol also had a potentiating effect on PKC activation by oleic acid. However, the degree of activation observed in the presence of a free fatty acid and an acyl ester of the fatty acid quantitatively never surpassed that produced by sn-1,2-dioleylglycerol. Our findings indicate that significant PKC activation can be achieved by presenting the enzyme with an environment which we believe approximates the structural characteristics of the endogenous activator, sn-1,2-diacylglycerol.
The intestinal brush-border membrane contains a high concentration of calmodulin bound to a 105,000 dalton (105 kDa) protein. Binding of radioiodinated calmodulin to this protein does not require calcium but is inhibited by trifluoperazine and excess unlabelled calmodulin. Recent evidence suggests that the 105 kDa protein in conjunction with calmodulin may be involved in the regulation of calcium transport across the brush-border membrane. In this report, we evaluated the binding of the 105 kDa protein to other radioiodinated calcium-binding proteins including the vitamin D-dependent intestinal calcium-binding protein. We observed that troponin C and S100 beta protein both bound strongly to the 105 kDa protein. The binding of S100 beta was inhibited by EGTA, but was little affected by trifluoperazine and excess unlabelled S100 beta, whereas that of troponin C was inhibited by trifluoperazine and excess unlabelled troponin C, but was little affected by EGTA. Both troponin C and S100 beta bound to a large number of proteins to which calmodulin did not bind. The vitamin D-dependent calcium-binding protein (calbindin) from chick intestine and rat kidney also bound to the 105 kDa protein, albeit more weakly than troponin C, S100 beta and calmodulin. The binding of the calbindins was increased by EGTA and was little affected by trifluoperazine and excess unlabelled calbindin. Parvalbumin, rat osteocalcin, and alpha-lactalbumin showed little binding to any brush-border membrane protein. Our results indicate that the 105 kDa calmodulin-binding protein of the intestinal brush border can bind to a variety of calcium-binding proteins all of which contain homologous regions thought to be the calcium-binding sites. Only the binding of troponin C resembles the binding of calmodulin, however, in being inhibited by trifluoperazine and excess unlabelled ligand. The functional significance of these observations in terms of regulating calcium transport across the brush-border membrane remains to be established.