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Biomedical subjects

Y Sagawa

Publications and source records attributed to Y Sagawa.

At least 37 records · Page 2Linked to original sources
PubMed1989

Breathing during sleep with mild hypoxia.

To investigate ventilatory response to mild hypoxia during non-rapid-eye-movement sleep, we administered approximately 16% O2 (which corresponds to concentrations found in commercial high altitude air craft) to 12 normal subjects by using a Venturi mask, which did not alter the breathing pattern during this study. Under mild hypoxia, inspiratory minute ventilation during sleep showed an initial rapid increase (P less than 0.001) but then declined significantly (P less than 0.001) and stabilized. Stable levels differed among individuals and, compared with those measured before hypoxia, were significantly lower in some subjects, higher in one, and essentially unchanged in the others. The initial rapid increase in minute ventilation after mild hypoxia during sleep correlated with the respective values of hypoxic ventilatory response during the awake state (P less than 0.01), but the final lowered levels did not. We conclude that the ventilatory response after mild hypoxia during sleep is biphasic and hypoxic depression exerts considerable influence on ventilation under mild hypoxia during sleep. So we should take hypoxic depression into consideration to evaluate the response to hypoxia during sleep.

Adult↗
PubMed1988

Angular homeostasis II: Pursuit of a moving target in a plane and some implications for cardiac teratology.

A model of cardiac ontogenesis is analyzed. It is cast in terms of the geometry of the pursuit of a linearly moving target by the growth of a chain of cells in the same plane, the pursuer, which at each step adjusts its direction of growth towards the current position of the target. The endpoint is the fusion between them, which can occur in 2 modes: either by the leading cell of the pursuer catching up with the target (pursuer-mediated fusion, or PMF) or by the target running into the preformed side of the pursuer (target-mediated fusion, or TMF). The causal specifications are the step size, the speed of the pursuer, the speed of the target, the restoration constant, and the initial direction of the pursuer; the outcome variables are the number of steps to fusion and the mode of fusion. The pattern of behavior is complicated, being more-or-less regular over large tracts of values, interspersed with abrupt, threshold-like changes that may generate a dichotomous pattern of inheritance despite a continuous gradation of genetic or other causes. The temporary abolition of the correction process (a change introduced to simulate the pattern of the effect of a teratogen) may delay fusion and suggest how a septum may fail to fuse, the ductus arteriosus to close, or an endocardial cushion to form. But the model also predicts that under certain plausible conditions, the "teratogen" would speed up fusion and hence perhaps offset a genetic predisposition to a congenital defect.

Heart Defects, Congenital↗
PubMed1988

Angular homeostasis. V: Some issues in genetics, ontogeny, and evolution.

We discuss a provisional model that deals with aspects of normal control of the direction in which cells grow; hence, the organization of structure. The interacting issues of genetics, ontogeny, and phylogeny in relationship to normal development and its defects are addressed. Our main goal is to define a model with a small and sufficient set of conditions that would make it possible to undertake statistically efficient genetic studies of certain congenital defects. But to do so in plausible and heuristic terms, one must address two classical questions: 1) How is the genome translated (or sometimes mistranslated) into a phenotype that is clinically conspicuous and that can be the object of genetic selection, and hence of evolution? 2) Granted that evolution of species occurs in small, rare steps, what is the path that calls for the smallest number of mutations through which ontogenesis could have developed, the intermediate stages being conserved because of actual phenotypic advantage?

Cell Division↗
PubMed1985

Report of a case with fulminant hepatitis A associated with acute renal failure.

A 34-year-old male presented with fulminant hepatitis A associated with acute renal failure. The patient was admitted four days after flu-like symptoms developed. Physical examination was unremarkable except for icteric sclerae. Laboratory studies showed SGOT 10719 U/l, SGPT 5780 U/l, prothrombin time 22%, BUN 25.5 mg/dl, and creatinine 2 mg/dl. Serum complements were within normal ranges, and circulating immune complexes were not detected. Anti-HAV IgM was positive. He developed hepatic coma on the fourth hospital day, and his renal function deteriorated progressively. He was treated with hemodialysis, but there was no improvement in consciousness. Although acute liver failure improved, he died on the 74th hospital day of subendocardial infarction. Autopsy examination showed acute renal tubular necrosis. The liver was enlarged and was in the residual stage of acute hepatitis without submassive necrosis. The development of fulminant hepatitis in hepatitis A has been rare, but in recent years acute renal failure in hepatitis A has been reported. Although the mechanisms responsible for renal failure in liver diseases are uncertain but could be multifactorial, immune complex-mediated nephritis and/or endotoxemia have been considered.

Acute Kidney Injury↗
PubMed1978

Doxapram hydrochloride in the treatment of acute exacerbation of chronic respiratory failure. A patient with four episodes treated without use of a respirator.

A 51-year-old woman with chronic respiratory failure (status after tuberculosis) was given an infusion of doxapram hydrochloride (1 to 2 mg/kg of body weight per hour) for four episodes of acute exacerbation of her condition. Treatment with the drug prevented worsening of hypercapnia in the four episodes, when administration of 24 percent oxygen had occasioned rises in the arterial carbon dioxide tension of 23, 10, 9, and 7 mm Hg.

Carbon Dioxide↗