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Biomedical subjects

B Singh

Publications and source records attributed to B Singh.

At least 361 records · Page 20Linked to original sources
PubMed1997

Schwartz-Jampel syndrome: evidence of central nervous system dysfunction.

We report four patients with Schwartz-Jampel syndrome showing evidence of central conduction impairment documented by somatosensory evoked potentials. Median nerve somatosensory evoked potential showed normal latencies to Erb's point and N13 in all patients. Interpeak latencies between N13 and N19 were prolonged in five nerves, with complete block in three nerves. Posterior tibial nerve somatosensory evoked potentials were performed in three patients. Peripheral latencies were normal in all patients. Interpeak latencies between lumbar and cervical potentials were prolonged in two patients, with conduction delay between cervical and cortical potentials in five of the six nerves tested. Visually evoked potentials, brainstem auditory evoked potentials, electromyography, and nerve conduction velocity studies were normal in all patients. Parents' median nerve and posterior tibial nerve somatosensory evoked potentials were normal.

Brain↗
PubMed1997

Early haemodialysis in acute tubular necrosis.

The study was conducted in 35 cases of acute tubular necrosis of varied aetiology. Cases were divided in 2 groups, Group A--17 cases treated conservatively and Group B--18 cases managed by early haemodialysis. Criteria for early haemodialysis were blood urea < 120 mg% and serum creatinine < 7 mg%. Before starting therapy both the groups had comparable biochemical and renal parameters (p > 0.05). Overall mortality was lower in Group B as compared to Group A (22.2% Vs 29.4). Complication events such as uraemic encephalopathy, pulmonary oedema, haematemesis and malena, thrombophlebitis and vomiting were significantly lower in Group B (p < 0.05). Hospital stay was also significantly lower (p < 0.05) in Group B (18 +/- 2.5 days Vs 28 +/- 3 days), this can reduce the cost of treatment also.

Humans↗
PubMed1997

Right hepatic artery pseudoaneurysm after laparoscopic cholecystectomy.

A case of pseudoaneurysm of the right hepatic artery after laparoscopic cholecystectomy is reported. The patient presented with recurrent episodes of massive upper gastrointestinal bleeding. Diagnosed on selective angiography, the patient was treated with ligation of the right hepatic artery at laparotomy.

Aneurysm↗
PubMed1997

Laparoscopic diagnosis of gallbladder agenesis.

We describe the case of a 32-year-old patient with gallbladder agenesis encountered at laparoscopy. Diagnostic confirmation was made by endoscopic retrograde cholangiopancreatography and computerized scanning. Formal laparotomy was avoided. A review of the literature is presented.

Adult↗
PubMed1997

Daughter diverticula from Meckel's diverticulum.

Daughter diverticula arising from the body of Meckel's diverticulum are rare. We detected such an occurrence in a 35-year-old man at appendectomy. These are probably primary and not pulsion or traction diverticula, as they do not have a muscle wall.

Adult↗
PubMed1997

Ileal amoebiasis.

Whilst colonic amoebiasis and its complications are well-documented, ileal amoebiasis has not been described in the literature. We report the cases of two patients with ileal amoebiasis and outline their management and outcome. It is important that surgeons working in areas endemic for amoebiasis be mindful of this entity.

Adult↗
PubMed1997

Modulation of insulin-dependent diabetes mellitus (IDDM) in NOD mice by autoreactive T cells.

Insulin-dependent diabetes mellitus (IDDM) is a T-cell-mediated autoimmune disease characterized by the destruction of insulin-producing beta cells in the islet of Langerhans. Islet autoantigen-specific T cells play a major role in the pathogenesis of the disease. Susceptibility loci for autoimmune diabetes such as the major histocompatability complex (MHC) may function by producing different repertoires of T cells, which could gain autoreactivity following activation, resulting in autoimmune disease. However, all the T cells infiltrating the islets are not destructive. A number of autoreactive T-cell lines capable of preventing development of IDDM have been isolated. Most of these cell lines are reactive to self I-Ag7. Presence of these regulatory T cells along with the effector cells in nonobese diabetic (NOD) mice suggests that IDDM may be a result of the imbalance of these two types of cells. Modulation of the immune response by inducing autoreactive regulatory T cells could be a way of treating autoimmune disorders.

Animals↗
PubMed1996

Cloning and characterization of cDNA for adenosine kinase from mammalian (Chinese hamster, mouse, human and rat) species. High frequency mutants of Chinese hamster ovary cells involve structural alterations in the gene.

The enzyme adenosine kinase constitutes the major purine nucleoside phosphorylating activity in mammalian cells. In view of its central role in adenosine metabolism, which is an important physiological regulator, an understanding of the primary structure of adenosine kinase is of much interest. Using microsequence information from peptides derived from purified Syrian hamster liver enzyme, we have succeeded in isolating full length cDNA clones encoding adenosine kinase from Chinese hamster ovary cells and mouse 3T3 cells. The open reading frames in these clones consist of 334 and 335 amino acids and encode proteins of molecular masses 37364 Da and 37489 Da, respectively. In addition, the coding and upstream sequences for adenosine kinase from human (HeLa cells) and rat liver have also been cloned and sequenced. Transfection of an adenosine-kinase-deficient mutant (selected for resistance to the adenosine analog toyocamycin) of Chinese hamster ovary cells with a plasmid containing the cloned adenosine kinase cDNA, leads to regaining of adenosine kinase activity in the transformed cell. The adenosine kinase transformants also simultaneously lost their toyocamycin resistance and became similarly sensitive to the analog as the parental wild-type Chinese hamster ovary cells. The cloned adenosine kinase cDNA was also used to examine structural changes in mutants affected in adenosine kinase. In Chinese hamster ovary cells, one type of mutant that lacks adenosine kinase activity and displays high degree of resistance to various adenosine analogs, is obtained at an unusually high spontaneous frequency (10(-4)-10(-3)). Results of Southern and northern-blot analysis provide evidence that this group of mutants involves gross structural alterations affecting the adenosine kinase gene. Such structural alterations are not observed in another type of mutant which exhibits increased resistance only to C-adenosine analogs. Sequence similarity searches indicate that several of the bacterial and yeast sugar kinases (ribokinase, fructokinase and inosine-guanosine kinase) exhibit limited but significant similarity to the mammalian adenosine kinase. The sequence similarity data support the possibility that adenosine kinase shares a common evolutionary ancestor with these protein sequences.

Adenosine Kinase↗
PubMed1996

Quantitative thresholds of MHC class II I-E expressed on hemopoietically derived antigen-presenting cells in transgenic NOD/Lt mice determine level of diabetes resistance and indicate mechanism of protection.

Two homozygous lines of transgenic NOD/Lt mice expressing MHC class II I-E molecules at quantitatively different levels were utilized to study mechanisms of I-E-mediated diabetes prevention. In line 12, I-E expression on APC at levels comparable with that in BALB/cByJ controls conferred only partial diabetes resistance. In line 5, greater than normal I-E levels on APC correlated with nearly complete resistance. Levels of endogenously encoded I-Ag7 correlated inversely with transgene-induced I-E expression. T cell transfer experiments into NOD/severe combined immunodeficient mice demonstrated the presence of pathogenic T cells in I-E+ donors, and that continuous expression of I-E on hemopoietically derived APC was required to block their pathogenic function. T cells from transgenic and nontransgenic NOD/Lt mice primed in vivo against the beta cell autoantigen 65-kDa isoform of glutamic acid decarboxylase (GAD65) and two peptides derived from this protein proliferated when restimulated in vitro. However, reverse-transcription PCR and ELISA measurements of cytokine mRNA and protein levels showed that the GAD65-reactive T cells from both line 5 and line 12 mice produced higher levels of IL-4 and lower levels of IFN-gamma than similar T cells from standard NOD/Lt mice. Thus, the inverse relationship between I-E and I-Ag7 expression was associated with qualitative differences in T cell responses to putative beta cell autoantigens. Collectively, these data indicate quantitative increases in I-E expression on APC may block insulin-dependent diabetes mellitus by altering the balance of cytokines produced by beta cell autoreactive T cells.

Amino Acid Sequence↗
PubMed1996

Modulation of antigen presentation and class II expression by a class II-associated invariant chain peptide.

During the process of MHC class II assembly, the class II-associated invariant chain peptide (CLIP) remains bound within the peptide binding groove until its subsequent removal, which is mediated by H-2 M. We have defined the functional role of CLIP, through saturation of the endosomal compartment with exogenous CLIP-(85-101), resulting in reduced class II MHC on the surface of APCs and an impeded T cell response. Conversely, incubation of the same cells with immunogenic peptides or proteins resulted in an up-regulation of surface class II MHC. T cells from CLIP- plus Ag-immunized mice showed a marked decrease in Ag-specific response over that in mice primed with Ag alone. A B cell hybridoma, TA3 (H-2d,k) incubated with CLIP in vitro showed dramatically reduced MHC class II I-A surface expression. APCs derived from CLIP-immunized mice exhibited down-regulation of surface class II MHC, but not of CD45 (B220). Electrophoretic studies showed that the addition of exogenous CLIP resulted in a relative decrease in SDS-stable MHC class II heterodimers in TA3 cells. Studies with FITC-CLIP and FITC-OVA-(323-339) peptides demonstrated that exogenously added CLIP peptide does not bind to surface class II molecules via the endogenous route, whereas OVA peptide does. This suggests that exogenously added CLIP acts intracellularly, perhaps in the compartment where H-2 M intersects with class II molecules. These findings demonstrate the functional role of CLIP to regulate MHC class II-mediated Ag presentation in CD4+ T cell responses.

Amino Acid Sequence↗
PubMed1996

Regulation of intracellular level of Na+, K+ and glycerol in Saccharomyces cerevisiae under osmotic stress.

The intracellular level of Na+ and K+ ofS. cerevisiae strain AB1375 revealed that under KCl as well as sorbitol stress, the cationic level was comparable to the level under no stress conditions. On the other hand, there was a sharp drop in the intracellular K+ content and increase in the Na+ content on addition of NaCl to the medium. However, the total cationic level was close to that under control conditions. In addition to changes in the cationic level, an enhanced production and accumulation of glycerol were also observed under osmotic stress. A regulatory mechanism co-ordinating the intracellular concentration of glycerol as well as Na+, K+ content under osmotic stress conditions has been proposed.

Glycerol↗
PubMed1996

[Reproducibility of computer-assisted mouth occlusion pressure measurements].

BACKGROUND: The measurement of mouth occlusion pressure is an easy method to assess respiratory drive and muscle function. Lately there is a variety of computer assisted programmes, but their precision is discussed controversially. In this study we analysed the repeatability of measurements of mouth occlusion pressures performed by a computer assisted measurement unit. PATIENTS AND METHODS: We examined maximal inspiratory mouth occlusion pressure (PI(max)), mouth occlusion pressure 100 ms after onset of inspiration (PO.1) and PI(max) after 100 ms (PO.1(max)) of 32 patients with COPD. Subjects were divided into group A (normal blood gas pressures) and group B (hypercapnia due to alveolar hypoventilation). Controls (K) consisted of 22 healthy men. Criteria for repeatability were analysis of variance, intraindividual standard deviation of the mean and the variation coefficient of 5 consecutive measurements. RESULTS: Controls produced the highest values for PI(max) and the lowest ones for PO, 1. Intraindividual standard deviation was small as well as the variation coefficient; we found no statistically significant differences. Compared with controls in group A PI(max) values were markedly reduced with elevated PO.1 values. Intraindividual standard deviation and variation coefficient were low, differences not significant. We observed similar results for group B, variance analysis showed no significant differences, deviation around the mean was small. CONCLUSION: Our data suggest a high repeatability of measurements of mouth occlusion pressures. Especially patients with severe COPD and alveolar hyperventilation are able to produce valid and reliable test results.

Adult↗
PubMed1996

Further characterization of the c-mos transcript and its cell cycle specific expression in NIH3T3 cells.

The mouse c-mos proto-oncogene is primarily expressed in germ cells. Our previous studies demonstrated c-mos RNA expression in mouse somatic cells, with the highest level present in the G2 phase of the cell cycle (Tsui et al., 1993). We have identified the transcription start site of this G2 specific c-mos transcript to be located about 1580 bp upstream from the open reading frame based on RT-PCR and RNase protection experiments. Upstream sequences containing this transcription start site directed highest expression of the luciferase reporter gene in M phase of the cell cycle. These results suggest that c-mos transcripts are produced in G2 phase and that c-Mos protein albeit at extremely low levels would accumulate in M phase.

3T3 Cells↗
PubMed1996

Native, but not genetically inactivated, pertussis toxin protects mice against experimental allergic encephalomyelitis.

Treatment of SJL mice with 400 ng Bordetella pertussis toxin (PT) either in saline or emulsified in incomplete Freund's adjuvant protected the mice against experimental autoimmune encephalomyelitis (EAE) induced 28 days later by a synthetic peptide of myelin proteolipid protein (PLP139-151) in complete Freund's adjuvant. However, treatment with a genetically inactivated pertussis toxin in which the catalytic and NAD-binding sites of the ADP-ribosyltransferase subunit were modified by site-directed mutagenesis was without effect. In vitro, lymphocyte proliferation was considerably enhanced by both the native and the inactivated toxin, at concentrations of 0.1-1 microgram/ml. However, strong inhibition of proliferation was also observed with the native toxin only, at concentrations that were two to three orders of magnitude lower than that required for the mitogenic effect (0.1-1 ng/ml). The inhibition of proliferation was detectable in the case of high-background proliferation, after stimulation with antigen (PLP139-151) or purified protein derivative of Mycobacterium tuberculosis), or with anti-CD3 monoclonal antibody, but not after stimulation with concanavalin A or phorbol esters and Ca2+ ionophore. These results suggest that the inhibitory effect of PT operates by interfering selectively with a T cell receptor-dependent signaling pathway. The biological significance of the in vitro inhibitory effect of PT was demonstrated by a considerable decrease and/or delay in the ability of lymphocytes grown with PLP139-151 and low concentrations of PT to transfer EAE to naive recipients.

Allosteric Site↗