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Biomedical subjects

K Sarkar

Publications and source records attributed to K Sarkar.

At least 73 records · Page 4Linked to original sources
PubMed1980

Ultrastructure of the common extensor tendon in tennis elbow.

In patients with tennis elbow, the common extensor tendon showed a pronounced reactive change consisting of mesenchymal cell proliferation along with aggregates of newly formed vascular channels. When studied ultrastructurally, many of the mesenchymal cells adjacent to the vascular channels were surrounded by a basal lamina, which is not normally seen around tenocytes. The cytoplasm of these cells showed features of both endothelial cells and tenocytes. It thus appeared, that the endothelial cells of the newly formed vascular channels were the source of proliferating mesenchymal cells differentiating toward tenocytes, and together they represented an intrinsic healing mechanism in the tendon.

Adult↗
PubMed1979

Renal oncocytoma. Study of eight cases.

Eight renal oncocytomas are described. Clinical manifestations were present in 3 cases, with hematuria occurring in 2 and flank pain in 2. Tumors were between 2.5 and 10.0 cm. in diameter and showed considerable variation in histologic pattern. The tan coloration of some tumors may permit a naked-eye distinction from renal cell carcinoma. All tumors appeared to be benign.

Adenoma↗
PubMed1979

Ultrastructural changes in the renal papillary cells of rats during maintenance and repair of profound potassium depletion.

In rats with long-term diet-induced potassium depletion, the cytoplasm of markedly enlarged papillary cells was mainly occupied by membrane-bound droplets, many of which acquired massive proportions. Both free and attached ribosomes were decreased, the Golgi apparatus was inconspicuous and there was a paucity of mitochondria. Despite the overwhelming accumulation of droplets with concomitant loss of normal metabolic organelles, cell death did not occur. With potassium repletion, the organelles readily proliferated regardless of the progression of droplet dissolution. The shrinkage of the droplets was accompanied either by disintegration of the limiting membrane or by disappearance of the constituents within an intact membrane. Microtubules were conspicuous in many of the cells undergoing gradual reduction in size. These cytoplasmic changes in renal medullary cells of rats during long-term potassium depletion and immediate post-repletion periods essentially represented the consequences of maintenance and repair of a storage process.

Animals↗
PubMed1978

Ultrastructural localization of calcium in calcifying tendinitis.

To determine the site of mineralization in calcifying tendinitis, we studied the ultrastructure of tendon fragments that were obtained during surgical interventions on ten patients with that condition. We found that calcification was occurring extracellularly and essentially in areas where the tendon had undergone cartilaginous transformation. Calcific crystals were present in matrix-vesicle-like structures that were seen either singly among collagen fibers or in aggregates. When they were in aggregates, the calcifying vesicles tended to fuse with each other. Thus, the process of mineralization in calcifying tendinitis resembled those calcifying conditions that have already been described in man and animals, both normal and pathological, in which the apatite crystals are initially localized in matrix vesicles.

Calcinosis↗
PubMed1978

Minimal medullary droplets in DOCA-induced potassium depletion of rats.

When potassium depletion is induced in rats administering desoxycorticosterone acetate instead of restricting potassium in the diet, the droplet accumulation in medullary cells is reduced, despite the similar degree and duration of potassium depletion. This finding indicates that the accumulation of droplets is more dependent on the inducing agent than on the severity or duration of potassium depletion.

Animals↗
PubMed1976

Effects on tissue and electrolytes of a mineralocorticoid blocker during DOCA-induced potassium depletion.

Chronic experiments were carried out on three groups of rats to evaluate tissue and electrolyte effects of a mineralocorticoid blocker canrenoate potassium (SC-14266) during DOCA-induced hypokalemic metabolic alkalosis. Group I animals received DOCA alone, group II received DOCA plus canrenoate, while group III received canrenoate alone. The daily dose ratio (per kilogram of body weight) was 180 mg canrenoate-0.45 mg DOCA. All animals ate a synthetic diet and drank 0.15 N NaHCO3. Group II animals demonstrated a lesser degree of metabolic alkalosis and a higher muscle potassium content when compared with group I rats. The most conspicuous histological abnormality was myocardial necrosis, the degree and extent of which was impressively reduced by the blocking agent.

Animals↗
PubMed1976

Persistence of a basal lamina-like structure following DOCA-induced myofibrillar degeneration in rats.

It is known that the myocardial necrosis of potassium depletion heals by reconstitution and not by scarring, when animals are replenished with potassium. In the course of studies on DOCA-induced myofibrillar degeneration, we found that a membrane-like structure persisted in the area where the disintegrating myofiber was being removed by macrophages. This structure resembled the basal lamina, and enclosed a space in which macrophages with phagosomes containing disintegrating myofibral constituents were seen in association with undifferentiated cells. We postulate that this basal lamina-like structure along with the undifferentiated cells, play a role in the reconstitution of the myocardium during the stage of potassium repletion, and that the scaffolding by basal lamina may be effective in myocardial reconstitution.

Animals↗
PubMed1975

A correlated study of kidney function and ultrastructure in potassium-depleted rats.

In order to provide an ultrastructural description of kaliopenic nephropathy in rats, potassium deficiency uncomplicated by chloride depletion or extracellular fluid volume expansion was induced by dietary means alone. After 12 days, serum and muscle analyses demonstrated severe potassium depletion, while urine concentrating ability was markedly impaired. Although micropuncture techniques demonstrated that net fluid transport in proximal tubules was normal, the epithelial cells showed the following morphological alterations: electron-lucent vacuoles and lysosome-like dense bodies were numerous, focal cytoplasmic degradation was present, and intercellular spaces were dilated in many proximal tubules. Medullary cell droplets were characterized by fusion, massive enlargement with sequestration of cytoplasmic components such as ribosomes, and occasional extrusion through ruptured plasma membranes--features not previously reported.

Animals↗