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Biomedical subjects

P Garg

Publications and source records attributed to P Garg.

At least 73 records · Page 4Linked to original sources
PubMed1998

"EXPATH" an expert system for pathology for the diagnosis of jaundice.

Computers are increasingly playing an important role in the field of medicine. A computer aided expert system has been developed for the differential diagnosis of jaundice. In this article the major features and application of this modular software are discussed.

Diagnosis, Computer-Assisted↗
PubMed1997

Dorsal penile frenulum.

A dorsal frenulum with a normal penis lacks description in the available English literature. We report 1 such case and its genesis is also postulated.

Adult↗
PubMed1997

Daughter diverticula from Meckel's diverticulum.

Daughter diverticula arising from the body of Meckel's diverticulum are rare. We detected such an occurrence in a 35-year-old man at appendectomy. These are probably primary and not pulsion or traction diverticula, as they do not have a muscle wall.

Adult↗
PubMed1997

Comparative evaluation of conservative management versus early surgical intervention in appendicular mass--a clinical study.

The management of appendicular mass seems to be taking turn with the availability of better antibiotics, care and anaesthesia. Quite a few workers turned to the other extreme of traditional conservative approach and reported acceptable results with immediate intervention during phlegmonous stage. But practically, surgeons still continue to adopt the same old regime. To alleviate this fear and circumvent the disadvantages of immediate intervention a midpath regime called early appendicectomy has been clinically evaluated. With this new approach in the present study preventing misdiagnosis (15%), no chance of recurrence as also of missing in the follow-up and shorter overall hospital stay with economy are some strong reasons to adopt this regime.

Acute Disease↗
PubMed1997

Ophthalmic antiviral chemotherapy: an overview.

Antiviral drug development has been slow due to many factors. One such factor is the difficulty to block the viral replication in the cell without adversely affecting the host cell metabolic activity. Most of the antiviral compounds are analogs of purines and pyramidines. Currently available antiviral drugs mainly inhibit viral nucleic acid synthesis, hence act only on actively replicating viruses. This article presents an overview of some of the commonly used antiviral agents in clinical ophthalmology.

Antiviral Agents↗
PubMed1997

Ultrasonically guided percutaneous drainage of breast abscess.

Percutaneous drainage of abscess under ultrasound guidance is a well established modality. Its use in breast abscess has still not found wide application. The present study on 25 consecutive cases of breast abscess with success rate of 84% is an attempt to recommend routine use of this modality wherever the facilities exist.

Abscess↗
PubMed1996

Nitric oxide stimulates the activity of a 72-kDa neutral matrix metalloproteinase in cultured rat mesangial cells.

We recently demonstrated that stimulation of inducible nitric oxide synthase (iNOS) activity reduced the accumulation of collagen and fibronectin in cultured rat mesangial cells. Therefore, we examined whether nitric oxide (NO) influenced the activity of a 72 kDa neutral matrix metalloproteinase by these cells in vitro. Enzyme activity was assessed in a biotin-avidin ELISA and by zymography. Exposure of mesangial cells to the cytokines, interferon (IFN)-gamma and lipopolysaccharide (LPS), increased gelatinolytic activity by 325 +/- 60% (P < 0.025). Co-incubation with 20 mM L-arginine caused a further increase in matrix metalloproteinase levels. Addition of L-NAME, an inhibitor of iNOS, reversed the IFN-gamma/LPS-induced rise in gelatinolytic activity. Incubation with the exogenous NO donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP), resulted in a dose dependent increase in metalloproteinase activity (P < 0.01). The NO-induced changes in metalloproteinase activity were also demonstrable by zymography. These data indicate that NO modulates the activity of a 72 kDa neutral matrix metalloproteinase and suggest that altered NO production may contribute to the development of glomerulosclerosis and tubulointerstitial fibrosis in chronic renal disease states.

Animals↗
PubMed1996

Morphine-induced macrophage activity modulates mesangial cell proliferation and matrix synthesis.

Glomerular mesangial injury is the predominant renal lesion in patients with heroin addition. We studied the effect of morphine (an active metabolite of heroin)activated macrophages on mesangial cell (MC) proliferation and matrix synthesis. We prepared conditioned media containing either vehicle along (CSP), macrophage secretory products (MSP) and secretory products of morphine treated macrophages (M-MSP), M-MSP increased (P < 0.01) the proliferation of MC when compared with MSP alone. M-MSP increased synthesis of laminin by MC at concentrations of 10 to 50% when compared with cells treated with MSP alone (at 50% concentration, MSP, 126 +/- 19 vs. M-MSP, 312 +/- 14 ng/mg protein, P < 0.001). M-MSP also increased the synthesis of collagen type IV by MC. This effect of M-MSP was attenuated (P < 0.05) by anti-TGF-beta antibodies. Since M-MSP also increased mRNA expression for TGF-beta by MC, it appears that the effected of M-MSP on MC may be mediated through the generation of TGF-beta.

Animals↗
PubMed1996

Morphine modulates migration of monocytes.

Macrophages seem to play an important role in the development of glomerulosclerosis. In the present study we evaluated the effect of morphine, an active metabolite of heroin, on the migration of monocytes across a filter in a modified Boyden chamber. Morphine-mesangial cell interaction enhanced (p < 0.004) the migration of monocytes across the filter (control 14.2 +/- 0.6 vs. morphine 22.1 +/- 1.7 monocytes/HPF). Dimethylthiourea (DMTU), a free radical scavenger, attenuated this effect of morphine. Morphine-monocyte secretory products (MMSP) did not modulate the migration of monocytes. However, the products of interaction between mesangial cells and MMSP enhanced (p < 0.001) the passage of monocytes across the filter. Mesangial cells treated with MMSP showed mRNA expression for monocyte chemoat-tractant peptide-1 (MCP-1). Superoxide also induced mRNA expression for MCP-1 on MC. DMTU attenuated this effect of superoxide. Since morphine activates MC to produce superoxide and DMTU attenuated the effect of superoxide on MC, the effect of morphine on the migration of macrophages may be mediated through superoxide-induced generation of MCP-1. We conclude that morphine enhances the migration of monocytes. This effect of morphine may be contributing to the development of glomerulosclerosis in patients with heroin addiction.

Animals↗
PubMed1996

Simulated glomerular pressure modulates mesangial cell 72 kDa metalloproteinase activity.

Glomerular hypertension has been considered to play an important role in the development of glomerulosclerosis. Mesangial expansion, a precursor of glomerulosclerosis, may be dependent not only on synthesis of matrix but also on degradation of the deposited matrix. In the present study we investigated the effect of simulated glomerular pressure on 72 kDa metalloproteinase activity (measured as degradation of gelatin) of mesangial cells. To simulate glomerular pressure conditions we have used an in vitro mechanical stretch/relaxation system as well as an alternative system which allowed direct application of pressure on mesangial cells. Mesangial cells were grown either under control (no added pressure), stretch/relaxation, or direct mean pressure of 45-50 mm Hg (physiologic glomerular pressure) conditions. Mesangial cells grown under stretch/relaxation showed a higher (P < 0.02) level of 72 kDa metalloproteinase activity when compared with control cells (control, 6.9 +/- 0.8 vs. stretch, 9.9 +/- 0.5 ng gelatin degraded/micrograms protein). Similarly, direct stimulated glomerular pressure increased (P < 0.01) mesangial cell 72 kDa metalloproteinase activity when compared with control cells. The effect of mechanical strain on mesangial cell 72 kDa metalloproteinase activity peaked at the end of the third day (control, 4.5 +/- 1.1 vs. stretch 15.3 +/- 1.1 ng gelatin degraded/micrograms protein, P < 0.001). Both mechanical strain and direct pressure to mesangial cells modulated 72 kDa metalloproteinase activity in a dose dependent manner. Mechanical stretch equivalent to normal simulated glomerular pressure increased mesangial 72 kDa metalloproteinase activity by 88%; whereas mesangial cell 72 kDa metalloproteinase activity declined to basal levels at higher simulated glomerular pressure (equivalent to 100 mm Hg). Likewise, direct higher pressure (100 mm Hg) also lowered 72 kDa metalloproteinase activity to basal levels. These results indicate that higher glomerular pressure inhibits degradation of type IV collagen. This may cause an accumulation of extracellular matrix and may thus be contributing to the expansion of the mesangium.

Animals↗