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Biomedical subjects

J Kim

Publications and source records attributed to J Kim.

At least 1,189 records · Page 66Linked to original sources

Renal concentration defect following nonoliguric acute renal failure in the rat.

The mechanism of impaired renal concentrating ability following nonoliguric ischemic acute renal failure was studied in the rat. Fifty min of complete occlusion of the renal artery and vein with contralateral nephrectomy resulted in reversible, nonoliguric acute renal failure. Eight days following induction of acute renal failure, a defect in 30 hr dehydration urine osmolality was present when experimental animals were compared with uninephrectomized controls (1,425 +/- 166 versus 2,267 +/- 127 mOsm/kg water respectively, P less than 0.001). Comparable postdehydration plasma vasopressin levels in experimental and control animals and an impaired hydro-osmotic response to exogenous vasopressin in experimental animals documented a nephrogenic origin of the defect in urine concentration. Lower urinary excretion of prostaglandin E2 in experimental animals and a failure of cyclo-oxygenase inhibition with 10 mg/kg of indomethacin to improve dehydration urine osmolality suggested that prostaglandin E2 antagonism of vasopressin action did not contribute to the concentration defect. Postdehydration inner medullary (papillary) interstitial tonicity was significantly reduced in experimental animals versus controls (870 +/- 85 versus 1,499 +/- 87 mOsm/kg water respectively, P less than 0.001). To determine if this decreased interstitial tonicity was due to vascular mechanisms, papillary plasma flow was measured and found to be equivalent in experimental and control animals. To examine a role for biochemical factors in the renal concentration defect, cyclic nucleotide levels were measured in cytosol and membrane fragments. A decrease in vasopressin and sodium fluoride-stimulated adenylate cyclase was found in outer medullary tissue of experimental animals. In contrast, vasopressin-stimulated adenylate cyclase activity was comparable in the inner medullary tissue of control and experimental animals. Our study suggests a defect in generation of renal inner medullary interstitial solute as a mechanism of the impaired urinary concentration observed in this model of acute renal failure.

Acute Kidney Injury↗

Effect of fatty acid modification of cultured hepatoma cells on susceptibility to natural killer cells.

Rat hepatoma (Morris 7777) cells modified with either oleic or linoleic acid exhibited greater susceptibility to normal spleen cell-mediated lysis in a 16-hr 51Cr release assay. At effector:target cell ratios of 300:1, the specific lysis of fatty acid-enriched target cells (cultured for 2 days in fatty acid-supplemented medium) by the normal rat spleen cells was 60% higher than the untreated target cells (P less than 0.01). Prolonging the culture in fatty acid-supplemented medium up to 6 days produced similar effects. Analysis of the fatty acid composition of cellular lipids revealed that an elevation of oleic or linoleic acid was the only significant alteration in the hepatoma cells grown in the oleic or linoleic acid-supplemented medium, respectively. The percentage of the acids was increased in the total cellular phospholipids, the choline, ethanolamine, serine, and inositol phosphoglyceride fractions, and the neutral lipids. In conclusion, we suggest that the elevation of oleic acid and linoleic acid contents in the membranes of the fatty acid-modified hepatoma cells may contribute to the increased susceptibility of these cells to natural killer cell-mediated cytotoxicity.

Animals↗

Periodic transfusions for sickle cell anemia and CNS infarction.

Recurrences of CNS infarction often lead to progressive neurologic disability in sickle cell anemia. To prevent such reccurrence, a periodic blood transfusion program was begun in 1969. Currently, 27 patients are on this regimen. Before inclusion in the program, 12 patients had had one to nine CNS recurrences each. Since the program was started, two patients have had transient CNS ischemia. There were no other recurrences and none of the patients have shown progression of neurologic abnormalities. In addition, there was a striking decrease in bacterial infection and pain. We conclude that periodic transfusions are effective in preventing recurrent CNS infarction in sickle cell anemia. The benefits must be weighed against the potentially serious problem of iron overload, as evidenced by moderately elevated serum ferritin values.

Adolescent↗

Opticociliary veins in a primary optic nerve sheath meningioma.

A 59-year-old man developed painless visual loss in his left eye over a one-year period, with rapid progression to blindness over three months. Ocular examination of the left eye revealed proptosis, marked optic disk pallor, dilated retinal veins, and congeries of vessels at the disk margin (opticociliary veins). His right eye was unremarkable. Fluorescein angiography and histopathologic examination confirmed the presence of opticociliary veins communicating between branches of the central retinal vein and the adjacent choroidal vasculature. Primary orbital optic nerve meningioma associated with opticociliary veins was diagnosed.

Cranial Nerve Neoplasms↗

Reconstitution of lipid vesicles associated with HVJ (Sendai virus) sikes. Purification and some properties of vesicles containing nontoxic fragment A of diphtheria toxin.

A mixture of HVJ (Sendai virus) spike proteins, the nontoxic fragment A of diphtheria toxin, lecithin, and cholesterol was solubilized in sucrose solution containing a nonionic neutral detergent. The liposomal vesicles which formed on removal of the detergent by dialysis were purified by gel filtration and centrifugation on a sucrose gradient. The resulting purified vesicles had hemagglutinating activity, hemolytic activity and, after solubilization, the enzymic activity of fragment A. The vesicles had no cell fusion activity. Electron microscopy showed that both the outside and inside of membranes of the vesicles were associated with the spikes. When the vesicles were freeze-fractured, no large aggregates of particles were seen on either face. Such fragment A-containing lipid vesicles (liposomes) with HVJ spikes bound to mamalian cell membrane and released their fragment A into the cytoplasm causing cell death. Neither fragment A-containing liposomes without spikes nor empty liposomes with spikes were toxic.

Cell Fusion↗

Repair of major cranio-orbital defects with an elastomer-coated mesh and autogenous bone paste.

We present a method for repairing defects in the craniofacial region in which an elastomer-coated mesh is used as a template with bone paste. The method was developed by animal experimentation first, and then successfully used in the maxillofacial and mandibular regions. We have used this method to repair 16 craniofacial defects with satisfactory results, and complications have been kept to a minimum.

Adolescent↗

Serial propagation of Creutzfeldt-Jakob disease in guinea pigs.

The transmission and serial propagation of Creutzfeldt-Jakob disease from man to guinea pigs are reported. The latency, symptomatology, and morphology of the infection during the first four passages are presented. The incubation period between the first and subsequent passages was halved. One hundred percent take, morbidity, and mortality were achieved in all inoculated animals. All guinea pigs developed a subacute spongiform virus encephalopathy with marked neuronal destruction in the cerebral cortex and subcortical grey structures. The neuronal loss resulted in cerebral atrophy and hydrocephalus ex vacuo.

Animals↗

Phosphodiesterase inhibitors and cerebral vasospasm.

Experimental cerebral vasospasm was studied in cat and monkey models. In the cat, the basilar artery was exposed by a transclival approach and spasm induced by the application of blood to the vessel. In the monkey, spasm was produced by injecting blood into the subarachnoid space. Vessel size was determined in the cat by direct observation and, in the monkey, by cerebral angiography. Several agents known to alter the synthsis and degradation of cyclic adenosine monophosphate (AMP) were used to modity the vasospasm produced. Isoproterenol (Norisodrine) and aminophyline were effective in reversing cerebral vasospasm when applied topically and when administered parenterally. It is suggested that manipulation of the cyclic AMP pathways may be an effective method of controlling cerebral vasospasm.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗