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Biomedical subjects

V K Singh

Publications and source records attributed to V K Singh.

At least 19 recordsLinked to original sources
PubMed1992

Immunoblot detection of antibodies to myelin basic protein in Alzheimer's disease patients.

Based on a suspected pathological relationship of autoimmunity in Alzheimer's disease (AD), antibodies to myelin basic protein (MBP) were investigated in the sera of AD patients, healthy controls and disease controls. As detected by the protein-immunoblotting technique at a screening serum dilution of 1:400, sera from 16 of 18 (89%) AD patients were positive for antibodies to MBP. In contrast, sera from only 7 of 90 controls (healthy adults and elderlies, Parkinson's disease patients, mentally-retarded children and Down's syndrome patients) showed a positive reaction. This approximately 11-times higher incidence of antibodies to MBP in AD patients was statistically significant (P < or = 0.0001) and may indicate an autoimmune process in the pathophysiology of the disease.

Adult↗
PubMed1992

Possible association of the extended MHC haplotype B44-SC30-DR4 with autism.

We previously reported that the complement C4B null allele appears to be associated with infantile autism. Since the C4B null allele is known to be part of the extended or ancestral haplotype [B44-SC30-DR4], we investigated the incidence of [B44-SC30-DR4] in 21 autistic children and their parents. This extended haplotype was increased by almost six-fold in the autistic subjects as compared with healthy controls. Moreover, the total number of extended haplotypes expressed on chromosomes of autistic subjects was significantly increased as compared with those expressed on chromosomes of healthy subjects. We conclude that a gene related to, or included in, the extended major histocompatibility complex may be associated with autism.

Adolescent↗
PubMed1992

Stimulation of interleukin-6 production by corticotropin-releasing factor.

Based on the immune-modulating properties of corticotropin-releasing factor (CRF), the effect of this peptide for interleukin-6 (IL-6) production was investigated. Using human peripheral blood mononuclear cells (MNC), the amount of bioactive IL-6 produced was significantly (P less than or equal to 0.05) increased by CRF (10(-10) to 10(-7) M range). However, the IL-6 production of lipopolysaccharide-treated MNC cultures was not modified. At concentrations of greater than or equal to 10 nM, CRF and two analogous peptides (Tyr-CRF and alpha-helical CRF) elicited 16- to 21-fold stimulation of IL-6 production by MNC. Purified monocytes, but not purified lymphocytes, were the cells that responded to CRF action exhibiting nearly 19-fold stimulation at 100 nM concentration. The CRF-induced production of IL-6 cytokine by peripheral blood MNC may suggest a messenger role for this neurohormone in the feedback control of neuroendocrine-immune circuitry.

Adult↗
PubMed1992

Suppression of experimental autoimmune uveitis in rats by the oral administration of the uveitopathogenic S-antigen fragment or a cross-reactive homologous peptide.

The oral administration of S-antigen fragment (a synthetic peptide designated as peptide M and known to be uveitopathogenic for rat, guinea pig, and monkey) to Lewis rats prior to challenge with an emulsion of peptide M and CFA resulted in either a total or partial suppression of experimental autoimmune uveitis (EAU), a T cell-mediated autoimmune disease studied as a model for human uveitis and experimental autoimmune pinealitis (EPA). Both the clinical and histopathologic manifestations of the disease were suppressed in a dose-dependent manner. Pinealitis associated with EAU was also suppressed by the oral administration of peptide M. Additionally, ingestion of a fragment of baker's yeast (Saccharomyces cerevisiae) histone H3, which has five consecutive amino acids identical to peptide M and which has been found to be uveitopathogenic in Lewis rats, induced tolerance to either peptide M or synthetic histone H3 peptide. In addition, the proliferative response to peptide M was inhibited in peptide M-fed rats. The suppression of EAU and in vitro lymphocyte proliferative responses to peptide M were observed to be antigen specific, since oral feeding of a control protein (BSA) exerted no suppressive effect. Furthermore, the T cells isolated from the spleen and lymph nodes of animals rendered tolerant by oral administration of peptide M can transfer protection against EAU adoptively. These results demonstrate that the oral administration of an autoantigen or its homologous peptide initiates an antigen-specific cellular mechanism which may ameliorate EAU.

Administration, Oral↗
PubMed1992

Neurogenic bladder in acquired immune deficiency syndrome (AIDS).

This is the first report of incidence of neurogenic bladder in patients with acquired immune deficiency syndrome (AIDS) and emphasizes that it is a significant cause of various voiding dysfunctions in these patients. Neurologic disease occurs in about one third of patients with AIDS. Both central and peripheral nervous systems may be involved. Urodynamic evaluation is necessary for assessment and management of neurogenic voiding disorders in this group of patients.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Molecular mimicry: uveitis induced in Macaca fascicularis by microbial protein having sequence homology with retinal S-antigen.

S-antigen (S-Ag), a well characterized 45-kDa protein in the photoreceptor cells, induces predominantly T-cell-mediated autoimmune uveitis when injected into experimental animals. Recently, we have shown that native histone H3 protein derived from yeast (Saccharomyces cerevisiae), or a synthetic peptide that is homologous with S-Ag peptide M in having six consecutive amino acids, induces experimental autoimmune uveitis (EAU) similar to that induced by native S-Ag in the Lewis rat. In this study, monkeys (Macaca fascicularis) immunized with histone H3 peptide developed a strong cellular immune response to this peptide as well as to peptide M. However, no significant inflammation or hypervascularization was observed in the retina or the iris during the experimental period, when they were examined clinically with an inverted ophthalmoscope. Histopathological examination showed that all monkeys injected with histone H3 peptide or with native histone H3 lost a large number of photoreceptor rod cells and developed neovascularization in the outer nuclear cell layer of the retina. These histopathological findings in the monkey retina closely resemble those seen in human patients with some types of uveitis. The possible involvement of microbial proteins having sequence homology with normal retinal proteins in the pathogenicity of human uveitis is discussed.

Amino Acid Sequence↗
PubMed1991

Concealed rhythms by double ventricular parasystole.

Electrocardiograms taken from 11 patients in sinus rhythm with ventricular ectopic rhythms from two different foci were analyzed to find the number of sinus beats, S, between the ectopic rhythms (S values). Three out of 11 patients had the S values typical for concealed ectopic rhythms. One of them had concealed bigeminy of 2n-1 form that occasionally shifted to 2n form. Following the shift, S values of 2n-1 form were always achieved by the occurrence of double ventricular ectopic rhythms in succession. Concealed trigeminy of 3n and 3n-2 form was seen in the other two patients. Double ventricular ectopic rhythms had bizarre abnormal QRS complexes of two different morphologies and were inscribed in opposite directions. Ectopic rhythms in each case had parasystolic characteristics. These observations suggest bifocal automaticity as a mechanism for bidirectional ventricular tachycardia.

Cardiac Complexes, Premature↗
PubMed1991

Post-prostatectomy incontinence. A urodynamic and fluoroscopic point of view.

Sixty-three male patients suffering from post-prostatectomy incontinence were studied by urodynamics and fluoroscopy. In almost half the patients (49%) the sole cause of incontinence was detrusor instability. Incontinence due to damage of the sphincter mechanism was present in less than half of the patients (47%). However, almost half of these patients (53%) had concomitant detrusor instability. Only a small number of patients (4%) had incontinence due to other causes. It appears that post-prostatectomy incontinence is not always due to a surgical misadventure. Many older patients may have preexisting neurologic disorders (e.g., Parkinson disease, diabetic autonomic neuropathy, alcoholic neuropathy, and various spinal cord disorders) which can profoundly affect the outcome of prostatic surgery. Detrusor instability should be considered when evaluating post-prostatectomy incontinence.

Adult↗
PubMed1991

Modulation of natural killer cell-mediated lysis by corticotropin-releasing neurohormone.

Existence of a reciprocal neuroendocrine-immune relationship led us to study an immunomodulatory role for the corticotropin-releasing factor (CRF) which is a low molecular weight peptide neurohormone of the neuroendocrine system. In the present study, the CRF-induced modulation of natural killer (NK) cell-mediated lysis (CML) was investigated. The pretreatment for 16-18 h of human peripheral blood mononuclear cells (MNC) with CRF in nanomolar concentrations caused a statistically significant increase in the CML function of NK cells as measured against K562 target cells in the 4-h 51Cr-release assay. The maximum stimulation occurred at a final concentration of 1 nM CRF despite some variability from one blood donor to another. The depletion of monocytes from MNC abolished the stimulatory effect of CRF but the effect was reconstituted by the supplementation of monocyte-derived interleukin-1 (IL-1), suggesting the involvement of IL-1 in the stimulation of NK cell-mediated lysis. Additionally, the CRF-induced stimulatory effect was inhibited by specific antibodies to IL-1 (anti-IL-1) or beta-endorphin (anti-beta E), indirectly suggesting that IL-1 and beta E may act as the mediators of stimulation by CRF of NK cell function. Based on these in vitro studies, we hypothesize that the CRF modulates NK cell-mediated lysis via initial stimulation of monocytes to produce IL-1 triggering the release by B cells of beta E for the stimulation of NK cell function.

Cells, Cultured↗
PubMed1991

Changes of soluble interleukin-2, interleukin-2 receptor, T8 antigen, and interleukin-1 in the serum of autistic children.

Immune abnormalities in autistic children led us to study for indirect evidence of immune activation as measured by the serum analysis of soluble interleukin-2 (sIL-2), interleukin-2 receptor (sIL-2R), T8 antigen (sT8), and interleukin-1 (sIL-1). The serum concentration of these soluble antigens was quantitated by enzyme-linked immunosorbent assays. The concentration of sIL-2 and sT8, but not of sIL-2R and sIL-1, antigens was significantly (P less than 0.05) increased in the sera of autistic children over that in the control healthy children or children with mental retardation (non-Down's syndrome). This finding indirectly indicates that the activation of a subpopulation of T cells occurs in some children with autism.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1991

Circulating immune complexes in pre-eclampsia.

Serum samples from 20 non-pregnant women, 30 women with normal pregnancy and 50 women with pregnancy associated with pre-eclampsia were tested for circulating immune complexes using the polyethyleneglycol precipitation method. A highly significant positive correlation was found between circulating immune complexes and severe pre-eclampsia (BP greater than 140/90 mm Hg, albuminuria greater than 0.25 g/l). In contrast to this the difference in immune complex levels between non-pregnant subject, normal pregnancy cases and patients with mild pre-eclampsia was not statistically significant. A significant positive correlation was found between the level of circulating immune complexes and the severity of albuminuria. These findings suggest that circulating immune complexes, though not seeming to play an aetiological role in pre-eclampsia may very well be involved in its pathogenesis.

Antigen-Antibody Complex↗
PubMed1990

Molecular mimicry between a uveitopathogenic site of S-antigen and viral peptides. Induction of experimental autoimmune uveitis in Lewis rats.

S-Antigen (S-Ag) is a well characterized 45,000 m.w. photoreceptor cell protein. When injected into susceptible animal species, including primates, it induces an experimental autoimmune uveitis, a predominantly T cell-mediated autoimmune disease of the retina and uveal tract of the eye, and of the pineal gland. In this study we found an amino acid sequence homology between a uveitopathogenic site of S-Ag, several viral proteins and one additional nonviral protein. An experimental autoimmune uveitis and pinealitis was induced in Lewis rats with these different synthetic peptides, corresponding to the amino sequence of hepatitis B virus DNA polymerase, gag-pol polyprotein of Baboon endogenous virus and gag-pol polyprotein of AKV murine leukemia virus and potato proteinase inhibitor IIa, which contain three or more consecutive amino acids identical to peptide M in S-Ag. Lymph node cells from rats immunized with either peptide M or the different synthetic peptides showed a significant degree of cross-reaction. Mononuclear cells from monkeys (Macaca fascicularis) immunized with peptide M also showed significant proliferation when incubated with either peptide M or synthetic peptides as measured by in vitro lymphocyte mitogenesis assay using [3H]TdR. Based on our findings we conclude that a viral infection may sensitize the mononuclear cells that can cross-react with self proteins by a mechanism termed molecular mimicry. Tissue injury from the resultant autoantigenic event can take place in the absence of the infectious virus that initiated the immune response.

Amino Acid Sequence↗