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S Deshpande

Publications and source records attributed to S Deshpande.

At least 19 recordsLinked to original sources
PubMed2006

Muscle fiber orientation in muscles commonly injected with botulinum toxin: an anatomical pilot study.

The endplate zone is assumed to be at about the midpoint of a muscle fiber. This study was designed to locate the middle of the muscle fibers of commonly injected muscles, thus identifying the endplate zone of these muscles. The proximal and distal musculotendinous junctions in muscles of the upper and lower extremities were identified. Orientation of muscle fibers was determined. Measurements using common surface landmarks were used to determine the relationship of these muscles with the landmarks (e.g., biceps muscle bulk extends from the upper fourth to the lower fourth of the humerus). Figures were developed using these measurements so as to be able to extrapolate these measurements to other patients of varying sizes. Illustrations of muscle fiber orientation were done and the assumed location of motor endplate bands marked. Color illustrations will be shown. With the thought that the endplate zone is at the middle of the muscle fiber, this detailed study of muscle fibers helps identify assumed location of motor endplates of specific muscles, thereby improving technique and efficacy of botulinum toxin injections.

Adult↗
PubMed2003

The use of Irradiated Allografts in Posterior Spinal Fusion for Healed Tubercular Kyphosis in Children.

Post-tubercular spinal kyphosis in children is not only cosmetically unacceptable but functionally disabling as well, as with the progression of the deformity there is a very significant risk of late onset paraplegia. We present our preliminary results in a prospective study of 12 cases of healed post-tubercular kyphosis in children treated with isolated posterior spinal fusion using irradiated allografts and autogenous cancellous grafts.The study included 12 patients of healed post-tubercular kyphosis documented by clinical, radiological and haematological criteria, with >2 spine at risk signs radiologically. The mean age was 7 years. In situ posterior spinal fusion with irradiated allografts and autogenous cancellous bone graft without any instrumentation was done for all the patients. The total follow-up is 5 years (mean 2.8 years).Eight patients (66%) showed a correction of the kyphosis, 3 patients (25%) were static and only 1 patient showed worsening of the deformity. Eleven patients had sound fusion and 1 patient had good fusion but a pseudoarthrosis at the lower vertebral level.Good posterior fusion was achieved because of the judicious use of morcellised, irradiated cancellous allografts with autogenous cancellous grafts. The proposed mechanism of correction is selective anterior column growth vis-à-vis posterior fused mass leading to gradual self-correction and remodelling.Conclusion. In situ posterior spinal fusion with irradiated allografts is a simple, safe, easily reproducible, less morbid surgical procedure with good results which may alter the long term disability of the patients.

Journal Article↗
PubMed2003

Role of modified Widal test in the diagnosis of enteric fever.

OBJECTIVES: To evaluate the diagnostic specificity of modified Widal for recent infection in comparison with conventional Widal test. METHOD: Modified widal test was simultaneously done along with conventional Widal test in serum samples obtained from 50 bacteriologically positive cases of Salmonella typhi infection as well as 50 healthy individuals. RESULTS: A four-fold difference in the titres was noticed in the 50 sera of the test group and no charge in the titres of the control group. The early rising O antibodies which are predominantly IgM in nature. These are due to recent infection and are inactivated by 2-mercaptoethanol. On the other hand H is a mixture of IgG and IgM hence IgM portion gets inactivated giving rise to fall in titre. By inactivating IgM antibodies in modified Widal test, the agglutination would be brought about only by specific IgG while in the conventional Widal test agglutination is due to specific IgG and IgM. The difference in the titres indicates specific IgM class of antibodies which is the hallmark of recent infection. CONCLUSION: If conventional Widal test and modified Widal test are simultaneously done, one can be definite about the diagnosis of enteric fever.

Antibodies, Bacterial↗
PubMed2001

Bystander activation involving T lymphocytes in herpetic stromal keratitis.

Herpes simplex virus infection of mouse corneas can lead to the development of an immunopathological lesion, termed herpetic stromal keratitis (HSK). Such lesions also occur in TCR-transgenic mice backcrossed to SCID (TgSCID) that are unable to mount detectable HSV-specific immune responses. The present study demonstrates that lesion expression in such mice depends on continuous viral replication, whereas in immunocompetent mice, lesions occurred even if virus replication was terminated at 4 days after infection. The continuous replication in TgSCID mice was considered necessary to produce an activating stimulus to CD4(+) T cells that invade the cornea. Lesions in TgSCID were resistant to control by cyclosporin A, but were inhibited by treatment with rapamycin. This result was interpreted to indicate that T cell activation involved a non-TCR-mediated cytokine-driven bystander mechanism. Bystander activation was also shown to play a role in HSK lesions in immunocompetent mice. Accordingly, in immunocompetent DO11.10 mice, lesions were dominated by KJ1.26(+) OVA-specific CD4(+) T cells that were unreactive with HSV. In addition, KJ1.26(+) HSV nonimmune cells parked in ocularly infected BALB/c mice were demonstrable in HSK lesions. These results provide insight for the choice of new strategies to manage HSK, an important cause of human blindness.

Adoptive Transfer↗
PubMed2001

Lymphotoxin alpha-/- mice develop functionally impaired CD8+ T cell responses and fail to contain virus infection of the central nervous system.

Recent observations have indicated that viral persistence and tumor spreading could occur because of effector function-defective CD8(+) T cells. Although chronic exposure to Ag, lack of CD4 help, and epitope dominance are suggested to interfere with CTL differentiation, mechanisms underlying the defective effector function remain obscure. We demonstrate in this report that lymphotoxin alpha-deficient mice develop CD8(+) T cells at normal frequencies when infected with HSV or immunized with OVA Ag but show impaired cytotoxic and cytokine-mediated effector functions resulting in enhanced susceptibility to HSV-induced encephalitis. Although these cells display near normal levels of perforin and Fas ligand, they remain largely at a naive state as judged by high expression of CD62 ligand and failure to up-regulate activation or memory markers. In particular, these CD8(+) T cells revealed inadequate expression of the IL-12 receptor, thus establishing a link between CTL differentiation and LTalpha possibly through regulation of IL-12 receptor. Viruses and tumors could evade immunity by targeting the same pathway.

Amino Acid Sequence↗
PubMed2001

Electroanatomically guided catheter ablation of ventricular tachycardias causing multiple defibrillator shocks.

With conventional techniques, RF catheter ablation is difficult in patients with unstable VT or with multiple VTs. The feasibility of RF catheter ablation guided by three-dimensional electroanatomic mapping technique in patients whose implanted ICD continued to deliver multiple shocks due to VT despite use of antiarrhythmic medications was assessed in 19 patients (15 men, 4 women; mean age [+/- SD] 70+/-7 years). All had a prior history of MI and subsequently had received an ICD due to VT. During the 12-week preablation period, these patients received 31+/-15 shocks (range 4-62 shocks) due to refractory monomorphic VTs. An electroanatomic mapping technique using the CARTO system was performed to delineate scar tissue. RF catheter ablation was then performed at appropriate sites identified by pace mapping and by substrate mapping. Seventeen patients were on amiodarone at the time of ablation. Twenty-seven VTs were documented clinically, and 45 were induced during electrophysiological evaluation. Of the 45 tachycardias induced, 38 VTs were targeted for ablation. Catheter ablation was performed during sinus rhythm in 31 episodes and during VT in 7 episodes. During a mean follow-up of 26+/-8 weeks (range 18-48 weeks), 13 (66%) patients had no recurrence of VT (P < 0.0001) and antiarrhythmic drugs were discontinued or the number of medications reduced in 17 patients (P < 0.0001). Electroanatomic mapping is helpful in identifying sites for catheter ablation in highly symptomatic patients with refractory VT associated with myocardial scarring.

Aged↗
PubMed2001

Ventricular fibrillation sensing and detection by implantable defibrillators: is one better than the others? A prospective, comparative study.

INTRODUCTION: We prospectively compared the performance of the sensing and detection systems of three leading defibrillator manufacturers: Medtronic, Guidant, and Ventritex. METHODS AND RESULTS: Ventricular fibrillation signal was digitally recorded during defibrillator implantation and subsequently played back sequentially to a Medtronic Micro Jewel II 7223Cx, a Guidant MINI II 1762, and a Ventritex Cadet V-115C. The devices were programmed for single-zone detection, at nominal settings. Rate cutoff was set at 320 msec (185/min for the MINI). We analyzed 253 episodes from 47 patients. Median undersensing was 0%, 2.1%, and 5.3% for the Jewel, MINI, and Cadet, respectively (P < 0.001 for each paired comparison). Detection time was 4.1 +/- 1.6 seconds, 3.4 +/- 1.6 seconds, and 4.3 +/- 2.2 seconds for the Jewel, MINI, and Cadet, respectively (P < 0.001 between MINI-Jewel and MINI-Cadet; P < 0.01 between Jewel-Cadet). Delayed detection (detection time longer than the mean of all observations + 2 SD) occurred in 3 (1.2%), 7 (2.8%), and 18 (7.1%) episodes for the Jewel, MINI, and Cadet, respectively. Performance for all devices was worse when the short-separation integrated bipolar lead was used and when the episode followed a failed high-energy shock. CONCLUSION: Statistically significant differences were seen in sensing and detection performance among the devices and device/lead combinations during ventricular fibrillation. These differences are related to specific features of the respective devices and should be taken into account during clinical practice, as well as in future device development.

Adult↗
PubMed2001

Association studies of cytosolic phospholipase A2 polymorphisms and schizophrenia among two independent family-based samples.

An association between the cytosolic phospholipase A2 locus (cPLA2) and schizophrenia has been reported using two polymorphic DNA markers. In an attempt to replicate these results, two independent family-based samples were ascertained from the United States and India (86 and 159 families, respectively). No significant associations were detected in either sample.

Base Sequence↗
PubMed2001

Contribution of vascular endothelial growth factor in the neovascularization process during the pathogenesis of herpetic stromal keratitis.

This report analyzes the role of vascular endothelial growth factor (VEGF)-induced angiogenesis in the immunoinflammatory lesion stromal keratitis induced by ocular infection with herpes simplex virus (HSV). Our results show that infection with replication-competent, but not mutant, viruses results in the expression of VEGF mRNA and protein in the cornea. This a rapid event, with VEGF mRNA detectable by 12 h postinfection (p.i.) and proteins detectable by 24 h p.i. VEGF production occurred both in the virus-infected corneal epithelium and in the underlying stroma, in which viral antigens were undetectable. In the stroma, VEGF was produced by inflammatory cells; these initially were predominantly polymorphonuclear leukocytes (PMN), but at later time points both PMN and macrophage-like cells were VEGF producers. In the epithelium, the major site of VEGF-expressing cells in early infection, the infected cells themselves were usually negative for VEGF. Similarly, in vitro infection studies indicated that the cells which produced VEGF were not those which expressed virus. Attesting to the possible role of VEGF-induced angiogenesis in the pathogenesis of herpetic stromal keratitis were experiments showing that VEGF inhibition with mFlt(1-3)-immunoglobulin G diminished angiogenesis and the severity of lesions after HSV infection. These observations are the first to evaluate VEGF-induced angiogenesis in the pathogenesis of stromal keratitis. Our results indicate that the control of angiogenesis represents a useful adjunct to therapy of herpetic ocular disease, an important cause of human blindness.

Animals↗
PubMed2000

Localization of soluble major histocompatibility class II-peptide complexes on T cell surface.

Affinity purified major histocompatibility (MHC)-peptide complexes are heterodimeric cell surface glycoproteins and are known to recognize antigen-specific CD4(+) T cell receptors (TCRs). In general, the affinity of MHC-peptide complexes to TCRs are considered very low with a K(D) of 5 x 10(-5) M and, therefore, stabilization of these complexes on T cell surface was not reported earlier. This could be due to (1) incomplete occupancy of MHC molecules with antigenic peptides, (2) variability of the binding constant of peptides to MHC molecules, (3) presence of endogenously bound peptides in MHC preparations, or (4) a combination of these. Using well-characterized HLA-DR2 complex loaded with a high affinity immunodominant epitope analog from human myelin basic protein (MBP), which shows release of gamma-IFN by specific stimulation of transformed human T cell clone (SS8T). The present report demonstrates a method for the localization of bound MHC class II-peptide complexes on T cell surface by backscatter electron imaging using in-lens Field Emission Scanning Electron Microscopy (FESEM). The localization is specific to the complex recognized by the TCR on MHC class II (DR2) and MBP peptide restricted human T cells.

CD4-Positive T-Lymphocytes↗
PubMed2000

Nonhydrolyzable diubiquitin analogues are inhibitors of ubiquitin conjugation and deconjugation.

A series of nonhydrolyzable ubiquitin dimer analogues has been synthesized and evaluated as inhibitors of ubiquitin-dependent processes. Dimer analogues were synthesized by cross-linking ubiquitin containing a terminal cysteine (G76C) to ubiquitin containing cysteine at position 11 ((76-11)Ub(2)), 29 ((76-29)Ub(2)), 48 ((76-48)Ub(2)), or 63 ((76-63)Ub(2)). A head-to-head dimer of cysteine G76C ((76-76)Ub(2)) served as a control. These analogues are mimics of the different chain linkages observed in natural polyubiquitin chains. All analogues showed weak inhibition toward the catalytic domain of UCH-L3 and a UBP pseudogene. In the absence of ubiquitin, isopeptidase T was inhibited only by the dimer linked through residue 29. In the presence of 0.5 microM ubiquitin, isopeptidase T was inhibited by several of the dimer analogues, with the (76-29)Ub(2) dimer exhibiting a K(i) of 1.8 nM. However, USP14, the human homologue of yeast Ubp6, was not inhibited at the concentrations tested. Some analogues of ubiquitin dimer also acted as selective inhibitors of conjugation and deconjugation of ubiquitin catalyzed by reticulocyte fraction II. (76-76)Ub(2) and (76-11)Ub(2) did not inhibit the conjugation of ubiquitin, while (76-29)Ub(2), (76-48)Ub(2), and (76-63)Ub(2) were potent inhibitors of conjugation. This specificity is consistent with the known ability of cells to form K29-, K48-, and K63-linked polyubiquitin chains. While (76-11)Ub(2), (76-29)Ub(2), and (76-63)Ub(2) inhibited release of ubiquitin from a pool of total conjugates, (76-48)Ub(2) and (76-76)Ub(2) showed no significant inhibition. Isopeptidase T was shown to specifically disassemble two conjugates (assumed to be di- and triubiquitin with masses of 26 and 17 kDa) formed in the reticulocyte lysate system. This activity was inhibited differentially by all dimer analogues. The inhibitor selectivity for deconjugation of the 26 and 17 kDa conjugates was similar to that observed for isopeptidase T. The observations suggest that these two conjugated proteins of the reticulocyte lysate are specific substrates for isopeptidase T in lysates.

Carbon-Nitrogen Lyases↗
PubMed2000

NADPH oxidase activation increases the sensitivity of intracellular Ca2+ stores to inositol 1,4,5-trisphosphate in human endothelial cells.

Many stimuli that activate the vascular NADPH oxidase generate reactive oxygen species and increase intracellular Ca(2+), but whether NADPH oxidase activation directly affects Ca(2+) signaling is unknown. NADPH stimulated the production of superoxide anion and H(2)O(2) in human aortic endothelial cells that was inhibited by the NADPH oxidase inhibitor diphenyleneiodonium and was significantly attenuated in cells transiently expressing a dominant negative allele of the small GTP-binding protein Rac1, which is required for oxidase activity. In permeabilized Mag-indo 1-loaded cells, NADPH and H(2)O(2) each decreased the threshold concentration of inositol 1,4,5-trisphosphate (InsP(3)) required to release intracellularly stored Ca(2+) and shifted the InsP(3)-Ca(2+) release dose-response curve to the left. Concentrations of H(2)O(2) as low as 3 microm increased the sensitivity of intracellular Ca(2+) stores to InsP(3) and decreased the InsP(3) EC(50) from 423.2 +/- 54.9 to 276.9 +/- 14. 4 nm. The effect of NADPH on InsP(3)-stimulated Ca(2+) release was blocked by catalase and by diphenyleneiodonium and was not observed in cells lacking functional Rac1 protein. Thus, NADPH oxidase-derived H(2)O(2) increases the sensitivity of intracellular Ca(2+) stores to InsP(3) in human endothelial cells. Since Ca(2+)-dependent signaling pathways are critical to normal endothelial function, this effect may be of great importance in endothelial signal transduction.

Calcium↗
PubMed2000

Chemokines in autoimmune diseases.

Autoimmune diseases like multiple sclerosis (MS) and insulin-dependent diabetes (IDD) are believed to be mediated by pathogenic CD4+ autoreactive T cells which mediate selective destruction of specific host cells. Interrupting the trafficking of such T cells from host circulation to the sites of pathology, such as the central nervous system in the case of MS and the pancreas in the case of IDD, potentially offers a novel opportunity for therapeutic intervention in these diseases. The following summarizes our evolving thoughts on the role of the chemokine network in MS and IDD, and focuses on the chemokine receptor CXCR3 as a potential target for impeding T-cell-mediated destruction in these disease settings.

Autoimmune Diseases↗
PubMed2000

Electroanatomic mapping to identify breakthrough sites in recurrent typical human flutter.

The accuracy of conventional techniques in localizing previous radiofrequency (RF) ablation sites and thus breakthrough sites of recurrent atrial flutter is somewhat limited. We investigated the role of electroanatomic mapping for identifying breakthrough sites or "gaps" at the tricuspid annulus and inferior vena cava (IVC)/eustachian ridge isthmus to help RF ablation in patients with recurrent typical flutter. Twelve patients (8 men, 4 women, age 63 +/- 10 years) with recurrent typical atrial flutter were included in the study. An electroanatomic mapping system (CARTO) was used to create a voltage map and activation and propagation patterns in the right atrium. Detailed voltage, activation, and propagation mapping of the tricuspid annulus and IVC/eustachian ridge isthmus allowed precise identification of gaps in all 12 patients at the tricuspid annulus (eight sites), IVC ridges (two sites), mid-isthmus region (one site), and tricuspid annulus and IVC ridges (one site). Radiofrequency energy directed at these sites eliminated atrial flutter in all 12 patients, confirmed by noninducibility of atrial flutter and demonstration of conduction block during atrial pacing on either side of the lesion lines. During a mean follow-up of 14.8 +/- 3.5 months (range 8-19 months), paroxysmal atrial flutter recurred in only one patient and was subsequently treated with amiodarone, although this had been ineffective prior to ablation. Electroanatomic mapping can precisely identify gaps in the lesion line responsible for breakthrough of recurrent typical atrial flutter at the tricuspid annulus and at the IVC/eustachian ridge isthmus. These sites can be targeted with RF ablation with a high degree of success.

Atrial Flutter↗
PubMed2000

RSV prevention.

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Antibodies, Monoclonal↗