Biomedical subjects
A Gupta
Publications and source records attributed to A Gupta.
Haemostatic function in coronary artery disease (CAD).
Tests to evaluate haemostatic function bleeding time (BT), prothrombin time (PT) partial thromboplastin time with kaolin (PTTK), thrombin time (TT), platelet count, platelet function tests (platelet adhesiveness and microthrombus index) and plasma fibrinogen levels were performed in 30 patients of coronary artery disease (14 myocardial infarction, 16 angina pectoris) and 20 age and sex matched controls. There was no statistically significant difference in platelet adhesiveness and mean microthrombus index in patients and controls. The BT, PT, PTTK and TT were normal in all patients and controls. Stepwise logistic regression analysis showed that plasma fibrinogen was an independent risk factor in the production of CAD.
Trabeculectomy with mitomycin-C for postkeratoplasty glaucoma: a preliminary study.
BACKGROUND AND OBJECTIVE: To evaluate the safety and efficacy of trabeculectomy with mitomycin-C in the management of postkeratoplasty glaucoma. PATIENTS AND METHODS: Included in this study were 16 eyes of 16 patients who underwent trabeculectomy with mitomycin-C for medically uncontrolled postkeratoplasty glaucoma, each having at least 6 months of follow-up. RESULTS: The mean pretrabeculectomy intraocular pressure (IOP) with maximal medical therapy was 34.6 mm Hg (range 24-45 mm Hg). The mean IOP following trabeculectomy with mitomycin-C was 14.2 mm Hg (range 8-36 mm Hg) by the end of a mean follow-up of 14.2 months (range 8-32 months). Fourteen eyes (87.5%) had complete success, 1 eye (6.25%) had qualified success, and 1 eye (6.25%) had failure. All the patents had the same or better visual acuity, compared with the preoperative value. None of the patients had postoperative complications, such as shallow anterior chamber, epithelial defect, or hypotony. CONCLUSIONS: Trabeculectomy with mitomycin-C is a safe and effective modality in the management of medically uncontrolled postkeratoplasty glaucoma.
Nasolacrimal stimulation of aqueous tear production.
PURPOSE: Aqueous tear production decreases after anesthetizing the ocular surface. Loss of the nasolacrimal reflex is a risk factor for neurotrophic keratopathy and keratoconjunctivitis sicca. The purpose of this study was to evaluate the effect of nasal mucosal anesthesia on aqueous tear production. METHODS: Eleven healthy human volunteers with a normal ocular surface and Schirmer I tear-test scores > 10 mm participated in this study. Schirmer I values were obtained daily for 3 days to establish a normal baseline. On a separate day, the right nasal mucosa was anesthetized with aerosolized 10% lidocaine (Xylocaine). After a 10-min period to allow the anesthetic to take effect and reflex tearing to subside, the Schirmer I test was repeated. A saline nasal spray was used as a control. RESULTS: Baseline Schirmer I values for both eyes had a mean of 22.98 +/- 1.05 mm (SEM). There was no difference in Schirmer scores between the two eyes after nasal anesthesia (p > 0.6); however, when these were compared with the baseline Schirmer I values, a significant decrease in tear production was noted (p < 0.001). The mean Schirmer I value after nasal anesthesia was 15.18 +/- 1.38 mm (SEM), a 34% decrease from baseline. The difference between the baseline and the normal saline control values was not significant (p = 0.160). There was a significant difference in Schirmer test scores between the saline control and nasal anesthesia groups (p < 0.02). CONCLUSIONS: In addition to sensory neural stimulation from the ocular surface, sensory stimulation of the nasal mucosa also promotes aqueous tear production. These results may help explain the decreased tear production observed in patients who have nasal mucosal damage, disease, or denervation.
Topical ketorolac 0.5% solution for the treatment of vernal keratoconjunctivitis.
The efficacy of topical ketorolac 0.5% in treatment of vernal keratoconjunctivitis (VKC) was evaluated in a randomised double-blind prospective trial in 21 patients. Ketorolac treated eyes showed 50.7% reduction in main symptoms of itching compared to 33.3% relief in placebo treated eyes after 2 weeks of treatment (p < 0.01). Photophobia, ropy discharge, and conjunctival injection also lessened by 39.9%, 31.6%, and 39.1%, respectively, in ketorolac treated eyes compared to 23.8%, 17.3%, and 20.3% in placebo group. Transient stinging sensation was observed in 3 (14.3%) patients on ketorolac therapy. This study shows efficacy of ketorolac 0.5% solution in controlling symptoms in VKC.
Primary argon laser trabeculoplasty vs pilocarpine 2% in primary open angle glaucoma: two years follow-up study.
In a prospective study, the efficacy of argon laser trabeculoplasty (ALT) was evaluated and compared with pilocarpine 2% as primary treatment in newly diagnosed primary open angle glaucoma (POAG). Out of 38 patients with POAG included in this study, one eye each of 36 patients underwent ALT, and one eye each of 26 patients received pilocarpine 2% every 8 hours. The mean pre-treatment IOP was 25.48 +/- 4.13 mmHg in ALT group and 24.47 +/- 3.51 mmHg in the pilocarpine group. The mean post treatment IOP at 2 year follow was 18.2 +/- 2.55 mmHg in ALT group and 18.27 +/- 2.22 mmHg in the pilocarpine group. Post treatment IOP was significantly lower than pre-treatment IOP in both ALT and pilocarpine groups. The post treatment fall in IOP showed no significant difference in ALT versus pilocarpine 2% at various follow up intervals (p > 0.05). This study showed equal efficacy of ALT and pilocarpine 2% as initial therapy of POAG.
Subretinal neovascularization associated with retinochoroidal coloboma.
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Optic neuritis following snake bite.
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Grain-boundary effects on the magnetoresistance properties of perovskite manganite films.
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Hyperhomocysteinemia confers an independent increased risk of atherosclerosis in end-stage renal disease and is closely linked to plasma folate and pyridoxine concentrations.
BACKGROUND: A high level of total plasma homocysteine is a risk factor for atherosclerosis, which is an important cause of death in renal failure. We evaluated the role of this as a risk factor for vascular complications of end-stage renal disease. METHODS AND RESULTS: Total fasting plasma homocysteine and other risk factors were documented in 176 dialysis patients (97 men, 79 women; mean age, 56.3 +/- 14.8 years). Folate, vitamin B12, and pyridoxal phosphate concentrations were also determined. The prevalence of high total homocysteine values was determined by comparison with a normal reference population, and the risk of associated vascular complications was estimated by multiple logistic regression. Total homocysteine concentration was higher in patients than in the normal population (26.6 +/- 1.5 versus 10.1 +/- 1.7 mumol/L; P < .01). Abnormally high concentrations (> 95th percentile for control subjects, 16.3 mumol/L) were seen in 149 patients (85%) with end-stage renal disease (P < .001). Patients with a homocysteine concentration in the upper two quintiles (> 27.8 mumol/L) had an independent odds ratio of 2.9 (CI, 1.4 to 5.8; P = .007) of vascular complications. B vitamin levels were lower in patients with vascular complications than in those without. Vitamin B6 deficiency was more frequent in patients than in the normal reference population (18% versus 2%; P < .01). CONCLUSIONS: A high total plasma homocysteine concentration is an independent risk factor for atherosclerotic complications of end-stage renal disease. Such patients may benefit from higher doses of B vitamins than those currently recommended.
Reactive oxygen species. Enzymatic and nonenzymatic antioxidants in patients undergoing open heart surgery.
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Large magnetotunneling effect at low magnetic fields in micrometer-scale epitaxial La0.67Sr0.33MnO3 tunnel junctions.
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Magnetic-field-induced multiple electronic states in La0.5Ca0.5MnO3+ delta.
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Isolation of type II epithelial cells from rabbit fetal lungs by adherence on an IgG-coated surface.
The lung is comprised of about 40 different cell types, of which only 15% are type II cells. These are the major, if not the sole, source of synthesis and secretion of lung surfactant. To date a large number of methods have been described for the isolation of pure populations of type II cells using a wide variety of techniques, but most of these have employed differential centrifugation methods and have used adult rodents. The present study reports the isolation of type II cells from fetal rabbit lungs by the immunoglobin G plating method. Pure populations of fetal type II cells in high yield and with good viability were obtained by the procedure for the first time from rabbit fetal tissue.
Perovskite oxide superlattices: Magnetotransport and magnetic properties.
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The small RNA, DsrA, is essential for the low temperature expression of RpoS during exponential growth in Escherichia coli.
dsrA encodes a small, untranslated RNA. When over-expressed, DsrA antagonizes the H-NS-mediated silencing of numerous promoters. Cells devoid of DsrA grow normally and show little change in the expression of a number of H-NS-silenced genes. Expression of a transcriptional fusion of lacZ to dsrB, the gene next to dsrA, is significantly lower in cells carrying mutations in dsrA. All expression of beta-galactosidase from the dsrB::lacZ fusion is also dependent on the stationary phase sigma factor, RpoS. DsrA RNA was found to regulate dsrB::lacZ indirectly, by modulating RpoS synthesis. Levels of RpoS protein are substantially lower in a dsrA mutant, both in stationary and exponential phase cells. Mutations in dsrA decrease the expression of an RpoS::LacZ translational fusion, but not a transcriptional fusion, suggesting that DsrA is acting after transcription initiation. While RpoS expression is very low in exponential phase at temperatures of 30 degrees C and above, at 20 degrees C there is substantial synthesis of RpoS during exponential growth, all dependent on DsrA RNA. dsrA expression is also increased at low temperatures. These results suggest a new role for RpoS during exponential growth at low temperatures, mediated by DsrA.
Monocytes in HIV type 1-infected individuals lose expression of costimulatory B7 molecules and acquire cytotoxic activity.
Monocytes/macrophages control the function of lymphocytes through positive and negative regulation. They release immunostimulatory cytokines and initiate costimulatory signals in T cells through the expression of B7 molecules. Their negative regulatory functions include the capacity to destroy cells with which they form cellular conjugates. We show here that HIV-1 infection skews monocyte function toward negative regulation by restraining the expression of costimulatory B7 molecules and by enhancing the cytolytic monocyte function. Monocytes that express constitutively B7, a membrane component that facilitates the engagement of costimulatory signals in T cells, lose this marker after HIV-1 infection and become refractory to inducers of B7 expression. The appearance of monocytes with reduced B7 expression is associated with an increased cytolytic monocyte capacity. Monocytes from HIV-1-infected donors destroy antibody-targeted normal lymphocytes more efficiently than do normal monocytes and they destroy CD4+ T cells specifically without the exposure to an exogenous ligand. CD4-reactive HIV-1 envelope molecules, expressed on monocytes as a consequence of infection or of opsonization by antibody, may specifically target CD4+ T lymphocytes for destruction and may thereby contribute to the preferential loss of CD4 T cells in HIV-1-infected individuals.
AIDS patient monocytes target CD4 T cells for cellular conjugate formation and deletion through the membrane expression of HIV-1 envelope molecules.
The human immunodeficiency virus (HIV) causes in humans the acquired immunodeficiency syndrome (AIDS). It replicates at a high rate in lymphoid organs even before it causes clinical symptoms. It binds to CD4 cell surface markers and destroys T lymphocytes that express the receptor. The immune system replenishes CD4 T cells at a formidable rate but, unable to keep up with the losses, allows the CD4 T cell compartment to disintegrate gradually. The net loss of CD4 T cells is an indicator for disease progression. How the virus destroys CD4 T cells and whether their loss accounts for the ensuing immunodeficiency have not been fully explained. We have reported evidence, and confirm here, that HIV-infected subjects deposit on monocytes immune complexes containing the virus or its envelope molecule gp120. Armed with these immune complexes monocytes form specific cellular conjugates with CD4 T cells and kill them. The destruction of normal CD4 T cells by monocytes from AIDS patients can be blocked by soluble CD4 and by free gp120. Normal monocytes and macrophages can be armed with CD4-binding gp120, and so induced to destroy CD4 T cells, by incubating them with gp120 and gp120-specific antibody. CD4-reactive HIV-1 components have a short half-life on the phagocyte surface. Removed from the HIV-infected environment, monocytes clear their surfaces of antibody-complexed viral components within hours, which abrogates their ability to destroy CD4 T cells. Rearming the monocytes with gp120-anti-gp120 complexes restores their capacity to destroy CD4 T cells. The data imply that for uninterrupted deletion of CD4 T cells, monocytes require a continued productive HIV-1 infection of their host.