Biomedical subjects
Publications and source records attributed to A G Kumar.
Oral manifestations may be the important indicators of ongoing human immunodeficiency virus (HIV) infection. Serum samples were collected from 100 patients repeatedly attending dental outpatients' department of SV Medical College and SVRR Hospital, Tirupati and tested for the presence of HIV antibodies. HIV 1 antibodies were detected in one person, the seropositivity rate being 1%.
We are now developing the means to evaluate components of this inflammatory response that may facilitate healing. A key event in the change in the inflammatory response is the development of a cytokine cascade that promotes phenotypic changes in the infiltrating leukocytes, which endow them with the ability to promote fibroblast proliferation and collagen deposition, the hallmarks of healing.
BACKGROUND: Healing after myocardial infarction is characterized by the presence of macrophages in the infarcted area. Since augmented monocyte influx has been implicated as a potential mechanism for improved healing after reperfusion, we wished to study the induction of monocyte chemoattractant protein-1 (MCP-1) during reperfusion. METHODS AND RESULTS: The cDNA for MCP-1 was cloned from a canine jugular vein endothelial cell (CJVEC) library and exhibited 78% identity with the deduced amino acid sequence of human MCP-1. Samples of myocardium were taken from control and ischemic segments after 1 hour of ischemia and various times of reperfusion; total RNA was isolated from myocardial samples and probed with a cDNA probe for canine MCP-1. Induction of MCP-1 mRNA occurred only in previously ischemic segments within the first hour of reperfusion, peaked at 3 hours, and persisted throughout the first 2 days of reperfusion. In the absence of reperfusion, no significant MCP-1 induction was seen. Both ischemic (but not preischemic) cardiac lymph and human recombinant TNF-alpha induced MCP-1 in CJVECs. MCP-1 was identified by immunostaining on infiltrating cells and venular (but not arterial) endothelium by 3 hours. In contrast, in situ hybridization showed MCP-1 mRNA to be confined to the endothelium of small veins (venules) 10 to 70 microns in diameter. CONCLUSIONS: MCP-1 mRNA is induced in the endothelium of a specific class of small veins immediately after reperfusion. MCP-1 induction is confined to the previously ischemic area that has been reperfused. We suggest a significant role for MCP-1 in monocyte trafficking in the reperfused myocardium.
Vascular cell adhesion molecule-1 (VCAM-1) is a member of the Ig superfamily that shows increased expression in a number of pathologic conditions. The role of VCAM-1 in human disease remains undefined and murine models are being extensively studied to help define the importance of VCAM-1 in inflammatory disorders. We have cloned and characterized the murine Vcam1 gene including 3 kb of 5'-flanking sequences and mapped the gene to chromosome 3 near Amy1. cDNA clones isolated from a stimulated hepatic library were found to encode a truncated form of VCAM-1 (T-VCAM-1) which contains Ig domains 1 through 3 and has a unique alternative carboxyl terminus. This form arises by alternative splicing. High level expression of T-VCAM-1 in transfected L cells was sufficient to support adhesion of lymphocytes, and this adhesion was blocked by Abs to VCAM-1. Treatment of transfected COS cells with phospholipase C led to reduced levels of T-VCAM-1 on the cell surface consistent with glycosylphosphatidylinositol linkage. Northern blot analysis showed that mRNA for T-VCAM-1 is inducible in multiple tissues after stimulation with endotoxin. Both forms of VCAM-1 were expressed in cultured endothelial, fibroblast, and aortic smooth muscle cells, whereas neither form was observed in monocyte- and lymphocyte-derived lines. Differential regulation of both forms of VCAM-1 was observed in the three different cell types that are present in the vessel wall. Thus, expression of VCAM-1 is restricted and controlled at the level of transcription and by alternative splicing.
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Ehlers-Danlos syndrome (EDS) type IV results in a high incidence of vascular lesions. The extreme fragility of arteries is associated with multiple aneurysm formation, spontaneous rupture, and dissection. Surgical management of patients with this disorder is hazardous and often unrewarding. In this report we describe the difficulties encountered in the management of three patients with EDS-related vascular lesions. Three patients presented with pain and exhibited characteristic features of EDS. Diagnostic modalities included computerized tomography, transesophageal echocardiography, and magnetic resonance. Aortography was performed only in specific situations. One patient with pericardial and mediastinal hemorrhage was stabilized and treated conservatively, with a good outcome. An adolescent with a ruptured aortic pseudoaneurysm died at surgery. The third patient underwent successful surgical correction of multiple aortic and renal aneurysms. In view of the increased risk of fatal vascular complications, surgeons should identify patients with EDS before performing invasive procedures. Arteriography should be used only when necessary. Although operative mortality remains at a high level due to the tendency of vessels to tear with even minimal manipulation, mortality from hemorrhage without surgical intervention is even greater. The key to favorable outcomes lies in identification of the syndrome preoperatively, surgical intervention only in life- or limb-threatening situations, and appropriate modification of surgical technique.
Serum samples were collected from 140 cancer cervix patients aged between 25-60 years and also from 20 age matched, married, healthy women to serve as controls. These sera were tested for HSV-2 antibodies by ELISA test and HBsAg by RPHA test. HSV-2 antibodies were detected in 92 (65-71%) and HBsAg in 25 (17.8%) cancer cervix patients. Sera from control group were negative for HSV-2 antibodies and HBsAg.
Twenty-five cases of human anthrax, occurring after contact with a Jercy cow infected with B. anthracis and consumption of its improperly cooked meat after death, were reported. Cutaneous anthrax was the predominant variety in 18 persons, 7 had intestinal anthrax, out of them 2 children died, 5 adults survived and one among them developed associated cutaneous anthrax also. All the persons with cutaneous anthrax recovered with treatment.
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One hundred clinically diagnosed cases of Tinea capitis were studied to know the clinical types and the causative agents. The incidence of grey patch, Kerion and black dot being 60%, 31% and 9% respectively. Tinea capitis was found to be more common in males (58%) than in females (42%) and it is more prevalent in children aged between 6-15 years. Trichophyton violaceum is the predominant (63.15%) fungal species isolated.
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540 strains of bacteria isolated from various clinical materials comprising 440 strains of Gram negative bacilli and 100 strains of Gram positive cocci were tested for their susceptibility in vitro to Kanamycin, Gentamicin and a new aminoglycoside antibiotic Sisomicin (Ensamycin). The sensitivity pattern revealed that 68.88% of the strains were sensitive to Kanamycin, 82.9% to Gentamicin and 89.0% to Sisomicin. The effectiveness of Sisomicin is comparatively greater (6.1%) than the other two aminoglycosides. In particular a considerable number of Gentamicin resistant Pseudomonas aeruginosa (12.3%) were found to be sensitive to Sisomicin which is a highly desirable property. Existence of about 11% Sisomium resistant strains even before the wide usage of this antibiotic is note worthy.
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Our studies in vitro demonstrate that neutrophil mediated injury of isolated cardiac myocytes requires the presence of ICAM-1 on the surface of the myocyte and CD11b/CD18 activation on the neutrophil. In post-ischemic cardiac lymph, there is rapid appearance of C5a activity during the first hours of reperfusion. Interleukin-6 activity is present throughout the first 72 h of reperfusion and is sufficient to induce ICAM-1 on the surface of the cardiac myocyte. In situ hybridization studies suggest that ICAM-1 mRNA is found in viable myocardial cells on the edge of the myocardial infarction within 1 h of reperfusion. ICAM-1 protein expression on cardiac myocytes is seen after 6 h of reperfusion, and increases thereafter. Non-ischemic tissue demonstrates no early induction of ICAM-1 mRNA or ICAM-1 protein on myocardial cells. In our most recent experiments, we have determined that reperfusion is an absolute requirement for the early induction of myocardial ICAM-1 mRNA in previously ischemic myocardial cells. To further assess this, we have cloned and sequenced a canine interleukin-6 (IL-6) cDNA. The data suggest that early induction of IL-6 mRNA is also reperfusion dependent as it could be demonstrated in the same ischemic and reperfused segments in which ICAM-1 mRNA was found. Peak expression of IL-6 mRNA occurred much earlier than that for ICAM-1 mRNA. Similar experiments were then performed with a molecular probe for interleukin-8 (IL-8). This chemokine is a potent neutrophil stimulant and has a higher degree of specificity for neutrophils than classic chemoattractants such as C5a.(ABSTRACT TRUNCATED AT 250 WORDS)