[Henley-Soupault technic of gastric transit reconstruction in the treatment of postgastrectomy syndromes].
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Biomedical subjects
Publications and source records attributed to M Matsuda.
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Hyperfunctioning platelets in the thrombocytotic patients after major surgery were satisfactorily controlled by a small dose of aspirin ingestion. Since aspirin is well documented as a potent inhibitor of platelet aggregation, a small dose of prophylactic administration of aspirin appeared to be a legitimate approach to a possible life-threatening thrombo-embolic complication after surgery, particularly when the platelets are excessively produced and hyperfunctioning.
Carboxyl groups of native human fibrinogen were modified with glycine methyl ester and 1-ethyl-3(3-dimethylaminopropyl)carbodiimide. It seemed likely that the modification occurred stepwise. Approximately 26% of the carboxyl groups of fibrinogen was modified finally. The modified fibrinogen had no interaction with cationic detergent, and did not form any complex with the detergent. In dilute acid, fibrinogen was observed to show only a slight interaction with cationic detergent. It is probable that the exposed and ionized carboxyl groups are essential for the formation of a complex between fibrinogen and cationic detergent.
Tetanus neurotoxin (molecular weight approximately 160,000) was purified from bacterial extracts (intracellular toxin) and mildly trypsinized and from culture filtrates (extracellular toxin). Both purified preparations could be dissociated reversibly into two polypeptide chains, with molecular weights of 53,000 (fragment alpha) and 107,000 (fragment beta), by treatment with 100 mM dithiothreitol (DTT) and 4 M urea with concomitant loss of toxicity. Upon removal of DDT and urea from the dissociated toxin preparation by dialysis, these fragments reassociated, forming the whole toxin. The two fragments were isolated and purified from the dissociated toxin by gel filtration on an Ultrogel AcA 44 column equilibrated with buffer containing 2 M urea and 1 mM DTT. The preparation of fragment alpha was nontoxic whereas that of fragment beta was slightly toxic. Immunodiffusion analyses, using horse antitoxin, showed that the antigenicities of fragment alpha and fragment beta were distinct from each other but were partially identical with that of undissociated toxin. The abilities of these fragments to precipitate antitoxin were lost on heating at 60 C for 5 min. The molecular substructure of tetanus neurotoxin is discussed on the basis of these findings.
A case of systemic-pulmonary arteriovenous fistula is described. Chest trauma with multiple bone fractures 9 years prior to this admission was the suspected cause. Three years after the trauma, chest X-rays revealed abnormal vessels in the right lung. Eight years after the trauma, the patient developed congestive heart failure. This has been well controlled with digitalis and occasional diuretics.
Cerebral autoregulation and vastomotor responsiveness to carbon dioxide (CO2) were measured quantitatively by the use of the autoregulation index and chemical index, respectively, in normal baboons before and after intravertebral and intracarotid infusion of the anticholinesterase agent, neostigmine methylsufate (Prostigmin). Continuous measurements were made of cerebral blood flow (measured as bilateral internal jugular venous outflow), arterial and cerebral venous pO2 and pCO2, cerebral arteriovenous oxygen differences, and endotracheal CO2. The effect of intravertebral infusion of neostigmine (12.5 mug/kg body weight) was compared to intravertebral infusion of neostigmine (25 mug/kg body weight) for assessment of any specific action of the drug on a hypothetical cholinergic vasomotor center, presumed to be located in the territory of the vertebrobasilar supply. No significant or persistent changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) followed either intravertebral or intracarotid infusion of neostigmine. Cerebral vascular resistance (CVR) and cerebral perfusion pressure (CPP), however, decreased significantly after intravertebral infusion. Cerebral autoregulatory vasoconstriction during increases of CCP was significantly reduced following both intravertebral and intracarotid infusion. Cerebral autoregulatory vasodilatation was not altered as CPP was lowered. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced following intravertebral neostigime but not following intracarotid neostigmine. Cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. These results support the view that central cholinergic cerebrovascular influences exist, and are vasodilatory in nature.
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