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Biomedical subjects

D Goyal

Publications and source records attributed to D Goyal.

10 recordsLinked to original sources
PubMed2006

Lung and blood mononuclear cell responses of tuberculosis patients to mycobacterial proteins.

The differences in specificity of human lung and peripheral lymphocytes for mycobacterial antigens (Ag) need to be evaluated in order to identify vaccine candidates against pulmonary tuberculosis (TB). Therefore, the present study examined the response to low molecular weight secretory proteins of Mycobacterium tuberculosis in bronchoalveolar lavage (BAL) and peripheral blood mononuclear cells (PBMCs) from minimal pulmonary TB and non-TB patients. Ag85A, Ag85B, culture filtrate protein (CFP)-31, CFP-22.5, CFP-21, M. tuberculosis protein-64 and an as yet uncharacterised 19 kDa protein were found to be predominantly recognised by BAL cells of TB patients on the basis of lymphocyte proliferation and significant interferon-gamma release. However, recognition of CFP-8, 6-kDa early secreted antigenic target, CFP-10, CFP-14.5, M. tuberculosis secretory protein-17 and five other as yet uncharacterised low molecular weight polypeptides was found to be high on the basis of lymphocyte proliferation at the level of PBMCs. Furthermore, BAL macrophages, and not blood monocytes, were found to produce nitric oxide (NO) in response to mycobacterial Ags. Among polypeptides predominantly recognised by BAL lymphocytes, only Ag85A and Ag85B were found to induce both NO and interleukin-12 (p40) by alveolar macrophages. In conclusion, the present results indicate heterogeneity in antigen recognition by bronchoalveolar lavage cells and peripheral mononuclear blood cells of minimal tuberculosis patients, and also suggest the utility of antigen 85 complex polypeptides for the development of a future mucosal antituberculous vaccine.

Antigens, Bacterial↗
PubMed2001

Transnasal access for sampling a skull base lesion.

SUMMARY: Transnasal needle access for sampling was used in two patients with posterior nasopharyngeal lesions. The procedure was performed under CT guidance. This new technique is simple and appears suitable for selected cases. The two cases and the details of the procedure are described.

Adult↗
PubMed2000

A classification system for characterization of physical and non-physical work factors.

A comprehensive evaluation of work-related performance factors is a prerequisite to developing integrated and long-term solutions to workplace performance improvement. This paper describes a work-factor classification system that categorizes the entire domain of workplace factors impacting performance. A questionnaire-based instrument was developed to implement this classification system in industry. Fifty jobs were evaluated in 4 different service and manufacturing companies using the proposed questionnaire-based instrument. The reliability coefficients obtained from the analyzed jobs were considered good (0.589 to 0.862). In general, the physical work factors resulted in higher reliability coefficients (0.847 to 0.862) than non-physical work factors (0.589 to 0.768).

Energy Metabolism↗
PubMed2000

Japanese encephalitis with movement disorder and atypical magnetic resonance imaging.

With the advent of magnetic resonance imaging, brain lesions associated with Japanese encephalitis are increasingly being recognized and correlated with movement disorder. Bilateral haemorrhagic thalamic infarcts on MRI, suggested as a characteristic finding in Japanese encephalitis were conspicuous by their absence in this case report of Japanese encephalitis.

Adolescent↗
PubMed1998

Low dose poly I:C prevents diabetes in the diabetes prone BB rat.

Poly I:C, an inducer of IFN-alpha and other cytokines, has been used to study the development of diabetes in both the BioBreeding (BB) diabetes prone rat and non-obese diabetic (NOD) mouse animal models of insulin-dependent diabetes mellitus (IDDM). Surprisingly, poly I:C accelerates the disease in the BB rat while inhibiting it in the NOD mouse. Since cytokines can have dose related opposing effects on immune responses, we hypothesized that the paradoxical effect of polyinosinic polycytidylic acid (poly I:C) on diabetes in the two animal models is dose related. Accordingly, we compared the incidence of diabetes and degree of insulitis in diabetes prone BB rats administered saline and poly I:C at doses (0.05 microg/g body weight and 0.1 microg/g body weight) up to 100-fold lower than doses (poly-5 microg/g) previously found to accelerate diabetes. In addition, the non-specific suppressor activity of mononuclear splenocytes from BB rats administered low dose (poly-0.05 microg/g body weight), high dose (poly-5 microg/g body weight), and saline were compared. The development of diabetes was inhibited in rats treated with each dose of poly I:C. The degree of insulitis in poly-I:C treated animals was also less severe. The total white blood cell count and proportion of RT6+ T-cells and each T-cell subset were unaltered by poly I:C. When compared to splenocytes of control animals, splenocytes from poly I:C (0.05 microg/g body weight) treated rats suppressed responder cell proliferation to concanavalin A and alloantigen. However, spleen cells from high dose poly-I:C did not suppress responder cell proliferation to alloantigen. In adoptive transfer studies, the administration of spleen cells from poly-0.05 treated rats decreased the development of diabetes in recipient BB rats. In vitro studies also demonstrated that poly-I:C inhibits the proliferative response of BB rat spleen cells to concanavalin A. The administration of poly-0.05, but not poly-5.0, decreased TNF-alpha mRNA and IL-10 mRNA content in spleen cells. We conclude that poly I:C, at a dose 100 times lower than that required to accelerate diabetes prevents the development of diabetes in BB rates by interfering with the development of insulitis. The induction of suppressor cell activity induced by low dose poly-I:C in vivo and the inhibition of T-cell responses by poly-I:C in vitro suggests that the diabetes sparing activity of poly I:C is mediated by augmented immunoregulatory cell activity. Further studies with poly I:C may be important in increasing our understanding of the pathogenesis of IDDM and provide a means to prevent it.

Animals↗
PubMed1998

The B-subunit of cholera toxin induces immunoregulatory cells and prevents diabetes in the NOD mouse.

The B-subunit of the cholera toxin molecule (CT-B) has T-cell immunomodulatory properties. Because the pathogenesis of diabetes in the nonobese diabetic (NOD) mouse model of IDDM is thought to be a T-cell-mediated process due to an imbalance of immunoregulatory and anti-islet effector cells, we examined the effect of CT-B administration on the development of diabetes in the NOD mouse and assessed whether this potential diabetes-sparing effect of CT-B is mediated by changes in immunoregulatory and/or anti-islet cytotoxic effector cell activity. The administration of either intravenous or intraperitoneal CT-B decreased the development of diabetes with no apparent drug toxicity. At 6 months of age, only 18% of CT-B vs. 75% of saline-treated animals had diabetes. Histopathological examination revealed less islet atrophy in CT-B-treated animals. The in vitro proliferative responses of mononuclear splenocytes and thymocytes to concanavalin A and lipolysaccharide and the proportion of B-cells and T-cell subsets were not altered by CT-B treatment. CT-B administration did not inhibit the primary immunization of mice to tetanus toxoid. The development of diabetes in irradiated NOD mice was slower in the animals injected with spleen cells (SC) from CT-B-treated than from saline-treated NOD mice, suggesting that CT-B decreases anti-islet effector cell activity. The injection of SC from CT-B-treated mice inhibited the adoptive transfer of diabetes by SC from diabetic mice into irradiated NOD mice, documenting that CT-B administration induces regulatory cell activity. In conclusion, CT-B administration prevents the development of diabetes in NOD mice by inhibiting the immune destruction of islets. This islet-sparing activity appears mediated, at least in part, by the induction of regulatory cells and, in turn, suppression of anti-islet effector cells, which is not associated with generalized immunosuppression or T- or B-cell depletion.

Adoptive Transfer↗
PubMed1996

A cryptic plasmid pBL1 from Brevibacterium lactofermentum causes growth inhibition and filamentation in Escherichia coli.

A shuttle vector composed of pBL1, a 4.46-kb cryptic plasmid from coryneform bacterium Brevibacterium lactofermentum, and Escherichia coli vector pHSG298 was found to inhibit growth and cause cell filamentation in E coli. After construction of several deletions of pBL1, a 1.23-kb AccI-HindIII fragment was found responsible. DNA sequence analysis showed that this fragment contained a 726-bp-long open reading frame (ORF3), encoding a protein with 242 amino acid residues. Corresponding to ORF3, a 28-kDa protein was detected in an in vitro protein synthesis system. ORF3 was dispensable for the stable maintenance of pBL1 in coryneform bacteria.

Brevibacterium↗