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Biomedical subjects

K Kitazawa

Publications and source records attributed to K Kitazawa.

At least 73 records · Page 4Linked to original sources
PubMed1990

[A case of cerebral gigantism with cerebellar atrophy].

A 37-year-old housewife, who had physical characteristics of cerebral gigantism, such as the tall stature, acromegaly, macrocephalia, high arched palate and antimongoloid slant, developed cerebellar ataxia and dysarthria. Her mother, uncle and grandmother were also reported to have slowly progressive gait disturbance. Her mother was also tall. Endocrinological studies failed to show any definite abnormality. CT and MRI revealed remarkable cerebellar atrophy. Though cerebral gigantism is often associated with clumsiness and incoordination, the etiology of the ataxia is poorly understood. This case indicates that the ataxia in cerebral gigantism may be, at least partly, caused by cerebellar atrophy.

Adult↗
PubMed1988

Studies on cell proliferation and tracer localization in the kidneys of guinea pigs with experimental autoimmune anti-tubular basement membrane nephritis.

The mitotic activity in kidneys of guinea pigs with experimental autoimmune anti-tubular basement membrane (TBM) nephritis was investigated using autoradiographic techniques to determine the uptake of [3H]thymidine by actively dividing cells. It was observed in these animals that cells of proximal tubules, distal tubules, cortical and medullary interstitium, medullary collecting ducts, and loops of Henle took up significantly greater amounts of [3H]thymidine when compared with normal animals. In addition, the behaviour of horseradish peroxidase (HRP) and goat anti-HRP IgG in extraglomerular sites in the kidneys of these animals was studied. Contrary to what was expected, these tracers appeared to be less concentrated in the tubules and interstitium of animals with anti-TBM disease, with tracer movement restricted in areas of disrupted TBM. The significance of these observations is discussed.

Animals↗
PubMed1988

Effects of methylprednisolone on acute lung paraquat toxicity in sheep.

Infused into sheep, paraquat causes increased flow of protein-rich lung lymph, increased prostanoid production, and neutrophil accumulation in the lung. The effects of high-dose methylprednisolone on the response to paraquat infusion were studied in awake sheep with chronic lung lymph fistulas. Seven sheep were infused with paraquat (30 mg/kg) alone. Six sheep received methylprednisolone (1.0 g plus 0.5 g/h intravenously), beginning 30 min before paraquat (pretreatment), and 5 received methylprednisolone, beginning 4 h after paraquat (post-treatment). Neutrophil accumulation in the lung was measured in biopsy tissue taken at baseline and at postmortem. Methylprednisolone pretreatment significantly prevented the increase in lung lymph flow (paraquat, from 4.4 +/- 0.3 to 11.1 +/- 0.8 ml/h, p less than 0.05; pretreatment, from 4.8 +/- 0.9 to 3.7 +/- 0.3, NS), and the increase in lymph-to-plasma protein concentration ratio (paraquat, from 0.69 +/- 0.02 to 0.80 +/- 0.02, p less than 0.05; pretreatment, from 0.66 +/- 0.06 to 0.60 +/- 0.02, NS) during 8 h after paraquat infusion. Treatment with methylprednisolone after paraquat also reduced the changes in lung lymph flow and protein clearance. Methylprednisolone prior to paraquat significantly inhibited accumulation of 6-keto-PGF1 alpha in lymph and plasma, but did not significantly inhibit accumulation of TxB2 in lymph or plasma. The number of neutrophils in the paraquat lungs was 3 to 4 times that in the control lungs, with or without methylprednisolone. Methylprednisolone pretreatment prolonged the survival time, but did not prevent death within 48 h after paraquat infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1988

[Tissue distribution of beta-lactam antibiotics, cefotiam and cefmenoxime in the lungs of sheep].

The present study was performed to investigate the distribution of beta-lactam antibiotics, cefotiam (CTM) and cefmenoxime (CMX) in pulmonary tissue of sheep. The animals were prepared to form chronic lung-lymph fistula for the collection of lung lymph. CTM and CMX were administered bolus-intravenously at doses of 20 mg/kg and 40 mg/kg, respectively, and serum and lymph levels of each drug were measured by bioassay method. Antibiotic levels of serum or lymph increased to a peak within 15 minutes after injection and then decreased rapidly. Measurable concentrations persisted for 240 minutes after the injection. Ratios of lung lymph to serum concentrations of CTM and CMX within 1 hour after the injection ranged 0.7 to 1.3, and 0.9 to 1.3, respectively. In addition, CMX levels in serum, lung lymph and tissues of both right and left lung were compared in anesthetized sheep to which CMX 50 mg/kg was given. Ratios of lung lymph and tissue concentrations of CMX in right and left lung to serum concentration were 0.76, 0.14 and 0.13, respectively. These results indicate that CTM and CMX were well distributed in interstitial fluid (lung lymph), and the levels of CMX in tissues of both right and left lung were markedly lower than those of lung lymph.

Animals↗
PubMed1986

Reabsorption of horseradish peroxidase by proximal tubules in rats with Heymann nephritis.

The distribution of the histochemical protein tracer, horseradish peroxidase, was studied in proximal tubules of rats with Heymann nephritis. Peroxidase reabsorption was substantially reduced in stage 2 of Heymann nephritis, a period during which the brush border of proximal tubules is severely damaged by specific antibodies. Impairment of the reabsorption function could not be attributed either to proteinuria or disturbances of proximal tubule metabolism and appeared to result from loss of microvilli. Recovery of brush border membrane morphology in stage 4 of Heymann nephritis was not accompanied by recovery of the normal capacity to reabsorb peroxidase. Functional deficits resulting from immunologic injury to proximal tubules in Heymann nephritis may persist despite waning of the anti-brush border antibody response and regeneration of the brush border of proximal tubule cells.

Animals↗
PubMed1984

Studies on the metabolic fate of sucrose esters in rats.

The metabolism in rats of sucrose esters of stearic acid and palmitic acid was studied in vivo and in vitro using esters labelled with 14C at the sucrose of fatty-acid moiety. In excretion studies, the ratio of expired radioactivity to absorbed radioactivity after oral administration of the sucrose esters labelled at the sucrose moiety was similar to that after the administration of [14C]sucrose. A similar correlation between the ester labelled at the fatty-acid moiety and the free [14C]fatty acid was also observed. No intact sucrose ester was detected in the urine. Studies in vitro using everted intestinal sacs showed that there was virtually no transport of 14C-labelled sucrose esters from the mucosal to the serosal solution through the intestinal tissues, and that the enzymes in the intestinal mucosa played a more important role in the hydrolysis of sucrose esters than did those in the digestive fluid. In studies of intestinal absorption through the mesenteric lymphatic system, during the 24 hr after ingestion 1.8% of the administered radioactivity was recovered in the lymph after dosing with [U-14C]sucrose monostearate whereas 20% was recovered in the lymph after dosing with sucrose [1-14C]monostearate. This difference in levels of recovery of administered radioactivity indicated that sucrose monostearate was absorbed only after hydrolysis. No intact ester was detected in the lymph or in the portal or femoral blood. The results of all of these experiments show that the sucrose esters are hydrolysed to sucrose and fatty acids prior to intestinal absorption.

Absorption↗