Biomedical subjects
P Garg
Publications and source records attributed to P Garg.
Stomach jolt--a possible mechanism for gastrosplenic injury in blunt abdominal trauma.
We report a 30-year-old man was involved in a road accident and had a gastric lesser curve tear and multiple splenic tears near the short gastric vessels. We believe that these resulted from sudden deceleration of a full stomach with sudden rise in intragastric pressure.
Perforation in acute acalculus Salmonella cholecystitis.
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Herniation of ureter in inguinal hernia.
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HIV-1 gp160 protein-macrophage interactions modulate mesangial cell proliferation and matrix synthesis.
Patients with HIV infection often develop glomerular lesions (focal segmental glomerular sclerosis). Because mesangial expansion (enhanced mesangial cell (MC) growth and matrix accumulation) has been demonstrated to precede the development of focal segmental glomerulosclerosis, we studied the effect of the interaction between HIV-1 proteins such as gp160 envelope protein and macrophages on mesangial cell proliferation and matrix synthesis. We determined the effect of control media, serum-free macrophage supernatant (MSP), and serum-free HIV-1 gp 160 protein-treated MSP (gp 160-MSP) on the proliferation of MC and synthesis of collagen type IV (a component of mesangial matrix). MSP (20%) enhanced (P < 0.01) MC proliferation (control, 7.58 +/- 0.29 versus MSP, 9.06 +/- 0.25 x 10(4) cells/ml), whereas gp 160-MSP (20%) inhibited (P < 0.001) MC proliferation (gp160-MSP, 5.58 +/- 0.14 x 10(4) cells/ml). gp160-MSP modulated MC proliferation in a dose-dependent manner; it enhanced cell proliferation at a lower concentration but inhibited cell proliferation at a higher concentration. Anti-TGF-beta antibody attenuated the effect of gp160-MSP on MC proliferation at lower as well as higher concentrations. Bromodeoxyuridine incorporation studies also showed the modulation of MC proliferation by gp160-MSP. Interaction of other HIV proteins such as HIV-1 Gag4 and HIV-1 Tat with macrophages did not affect MC proliferation when compared with MSP alone. gp160-MSP also enhanced (P < 0.001) synthesis of type IV collagen by MC (control, 467.8 +/- 9.0; MSP, 501.0 +/- 25.0; gp160-MSP, 775.5 +/- 39.0 ng/mg protein). The effect of gp160-MSP on collagen synthesis by MC was dose-dependent. Anti-TGF-beta antibody attenuated the gp160-MSP-induced mesangial cell collagen synthesis. The present study provides a basis for speculation that macrophage-gp160 interaction products have the potential to cause expansion of the mesangium.
Vasoactive agents modulate matrix metalloproteinase-2 activity by mesangial cells.
Vasoactive agents alter proteinuria by modulating glomerular hemodynamics. The authors hypothesized that vasoactive agents may be altering degradation of the collagen component of glomerular basement membrane, which also may be contributing to proteinuria. Mesangial cells treated with 10(-6) M angiotensin II had higher (P < 0.01) metalloproteinase activity (MA) when compared with control cells. This effect of angiotensin II was dose dependent. Amlodipine (10(-6) M), a calcium channel blocker, inhibited MA (control, 5.86 +/- 0.08 microgram versus 4.13 +/- 0.06 microgram gelatin degraded/mg protein, P < 0.001). The decrease in mesangial MA caused by amlodipine also occurred in a dose dependent manner. Amlodipine attenuated (P < 0.05) angiotensin II-stimulated MA (control, 6.69 +/- 0.30 micrograms, angiotensin II, 10.68 +/- 0.49 micrograms, angiotensin II+amlodipine 8.29 +/- 0.30 micrograms gelatin degraded/mg protein). Prostaglandin E2 increased (P < 0.001) MA (control, 10.22 +/- 0.9 micrograms versus prostaglandin E2, 17.9 +/- 0.9 micrograms gelatin degraded/mg protein), whereas indomethacin, a prostaglandin inhibitor, attenuated the metalloproteinase activity (control, 9.67 +/- 0.32 micrograms vs. 10(-6) M indomethacin, 4.22 +/- 0.31 micrograms gelatin degraded/mg protein, P < 0.001). Indomethacin also inhibited angiotensin II-stimulated MA (angiotensin II, 18.66 +/- 0.46 vs. angiotensin II+indomethacin, 11.86 +/- 0.56 micrograms degraded/mg protein, P < 0.001). Similarly, meclofenamate, another prostaglandin inhibitor, attenuated (P < 0.001) angiotensin II-induced MA. Because angiotensin II increases prostaglandin E2 synthesis by mesangial cells, it appears that increased MA, induced by angiotensin II, may be mediated partly through the generation of prostaglandin E2.
Human immunodeficiency virus-1 gp120 and gp160 envelope proteins modulate mesangial cell gelatinolytic activity.
Patients with human immunodeficiency virus (HIV) infection often develop glomerular lesions (mesangial expansion and sclerosis). Modulation of matrix degradation may be important in the expansion of the mesangium. We studied the effect of HIV sera and HIV-1 envelope glycoproteins on gelatinolytic activity of human mesangial cells. HIV serum-treated cells showed lower (P < 0.01) gelatinolytic activity when compared with cells treated with control serum (control serum, 4.3 +/- 0.1 versus HIV serum, 3.3 +/- 0.1 micrograms gelatin degraded/mg protein). Mesangial cells incubated with HIV-1 gp120 protein also showed decreased (P < 0.01) gelatinolytic activity (control, 4.6 +/- 0.2 versus HIV-1 gp120 protein, 1.7 +/- 0.2 micrograms gelatin degraded/mg protein). HIV-1 gp160 protein also inhibited (P < 0.05) mesangial cell gelatinolytic activity as judged by a biotin-avidin assay as well as by a 3H gelatin degradation assay. In contrast, gp alpha-1 acid, a nonviral glycoprotein, did not modulate mesangial cell gelatinolytic activity. These results suggest that the serum contents of HIV patients decrease gelatinolytic activity of mesangial cells. This effect of HIV sera seems to be mediated through HIV-1 gp proteins.
Malignant fibrous histiocytoma of renal capsule.
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The helix-loop-helix protein Id-2 enhances cell proliferation and binds to the retinoblastoma protein.
Cell growth and differentiation are usually antagonistic. Proteins of the basic helix-loop-helix (bHLH) family bind DNA and play important roles in the differentiation of specific cell types. Id proteins heterodimerize with bHLH transcription factors, blocking their activation of lineage-specific gene expression and thereby inhibiting cellular differentiation. To examine the effect of Id-2 on cell proliferation, we overexpressed Id-2 in the human osteosarcoma cell line U2OS. Id-2 expression in U2OS reduced the serum requirement for growth and stimulated cellular proliferation by shortening the doubling time and increasing the percentage of cells in S phase. We demonstrated that Id-2 expression was able to reverse the inhibition of cellular proliferation and the block in cell cycle progression mediated by the product of the retinoblastoma tumor suppressor gene pRB. This effect was not associated with changes in the state of pRb phosphorylation in transfected cells. In vitro, unphosphorylated pRb from cell lysates specifically bound Id-2 but was not able to bind a mutated form of Id-2 lacking the HLH domain that also did not antagonize the growth arrest by pRb. In vitro-synthesized pRb containing mutations within the E1A/large T-binding pocket did not bind Id-2. However, wild-type pRb was able to bind to a region of Id-2 corresponding to only the HLH domain. In vivo, a physical association between Id-2 and pRb was seen in cross-linked extracts from SAOS-2 cells transfected with Id-2 and pRb. Our data identify a role for Id-2 in the regulation of cellular proliferation and suggest that the interaction between Id-2 and pRB is a molecular pathway over which synchronous changes in growth and differentiation are mediated in vivo.
Comparative evaluation of commonly used catheters through histopathological changes induced in bladder urothelium.
There is growing concern about the toxic potential of chemicals coating various catheter materials, especially due to lack of international standards for toxicity testing. The present study evaluates the toxicity potential in terms of pathological changes induced by the catheters commonly used in practice, i.e. latex-, silicone- and Teflon-coated catheters. Teflon-coated catheters appear to be superior to others in the present study.
An improved method for rapid fixation and embedding of pteridophyte plant materials.
A rapid method for fixation and embedding of plant materials, especially pteridophytes, is suggested. Addition of tannic acid following osmication improved the visualization of membranes. Staining en bloc with uranyl acetate between osmication and tannic acid is suggested for tissues infected with fungi and bacteria.
Long-term effects of thrombolytic therapy on clinical course and left ventricular function after acute myocardial infarction.
Sixty five cases of Acute Myocardial Infarction, of which 40 cases received thrombolytic therapy, were followed up for a period of one year for clinical course and left ventricular function. Reperfusion was achieved in 65% cases who received thrombolytic therapy. At discharge and at one year treated group fared well on Killip Scale, and ejection fraction (EF), and the overally mortality was lower. This difference was more significant in the group who achieved reperfusion. Male sex, Anterior wall infarctions, deep Q wave infarctions as also low EF at the time of discharge and late cardiac events had adverse effect on the course of infarction during follow up.
Alkaptonuria: early detection.
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Mesenteric fibromatosis presenting as ovarian tumour.
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Retroperitoneal sponge causing painless haematuria.
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Assessment of intravenous streptokinase therapy in acute myocardial infarction.
Ten patients presenting within 6 hours of myocardial infarction, without contraindication for thrombolytic therapy, were given intravenous (IV) streptokinase (STK) 750,000 units in 15-30 min by infusion followed by anticoagulant therapy. Treatment was started within 241-360 min after the onset of symptoms. Fifteen other patients were given standard treatment without STK. Reperfusion was observed after a mean duration of 46 min in 7 patients in the STK group and none in the non-STK group. The results of IV STK thrombolytic therapy are comparable with those of previous studies using IV STK.
Bone mineral content in normal and malnourished children.
Bone mineral content (BMC) was determined at the distal radius in 70 children aged 2-14 years; Group I comprising 34 normal healthy children and Group II 36 malnourished children by the method of single photon absorptiometry. The mean value of BMC in Group I was 0.3 +/- 0.04 g/cm in 2-5 year, 0.52 +/- 0.08 g/cm in 6-10 year and 0.77 +/- 0.88 g/cm in 11-14 year age groups. No significant difference in the BMC was seen between boys and girls. An increase of BMC corresponded to growth spurts in 2-5 year and 11-14 year age groups. There was a significant reduction of BMC in Group II and in grade III malnutrition in 2-5 year and 11-14 year age groups as compared to Group I children. The study provides normal BMC data for Indian children and suggests that this can help to detect undemineralization of bones in malnourished children during the growth periods.