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Publications and source records attributed to Y Page.

At least 55 records · Page 3Linked to original sources
PubMed1990

[Calibrated side-to-side portacaval anastomosis in the treatment of bleeding from ruptured esophageal varices. Results in 38 cirrhotic patients].

We report the clinical results of 38 calibrated side-to-side portocaval shunts performed in patients with hemorrhagic liver cirrhosis (alcoholic in 90 percent of cases). The operative mortality (at 2 months) was 10.5 percent. The rate of recurrent bleeding was 2.6 percent; hepatic encephalopathy was encountered in 16 percent (acute encephalopathy: 6.5 percent; chronic encephalopathy: 9.6 percent; this rate decreased to 3.2 percent after anastomotic narrowing). Hepatopedal portal blood flow was maintained in 74.3 percent of cases in the early postoperative period (83.3 percent since the portacaval pressure gradient was maintained at 2/3 of the initial gradient) and disappeared with time in 75 percent of cases. The survival rates at 1 and 4 years were 79.4 percent and 60 percent, respectively, for all patients (94.4 and 83.3 percent for Child A patients) with a normal social activity in 90 percent of cases. Twelve patients developed hepatocellular carcinoma. These clinical results are similar to those observed after selective shunts and suggest that the side-to-side calibrated portacaval shunt is an excellent procedure for the treatment of bleeding esophageal varices in case of failure or contraindication to endoscopic sclerotherapy or in patients with chronic ascites and good liver function.

Adult↗
PubMed1986

Influence of SLO4 on the leucocyte migration inhibiting factor and on the DTH response.

This phase I study demonstrates the immunostimulating properties of SLO4 administered by the oral route in the healthy volunteer. Responses to the test of DTH (delayed type hypersensitivity) were enhanced by SLO4 and the production of MIF (migration inhibiting factor) involved in this response was stimulated. These properties could be correlated with the previously demonstrated induction of interferon by SLO4.

Adjuvants, Immunologic↗
PubMed1985

SLO4, a new interferon inducer isolated from Klebsiella pneumoniae and Escherichia coli.

A product isolated from Klebsiella pneumoniae and Escherichia coli, coded SLO4, has been shown to be effective in endogenous interferon induction in vivo in mouse when administered IP or IV, and in vitro with human leukocyte cultures. In these two systems induced interferon was defined. The inducer has not yet been characterized but seems not to belong to any components known to be interferon inducers such as viral particles, nucleic acids or endotoxins. An analytical study will be carried out to specify the constitution of this interferon inducer.

Animals↗
PubMed1983

[Acute ajmaline poisoning. Study of 7 cases].

Seven cases of acute ajmaline overdose admitted over a 3 year period to a polyvalent intensive care unit are reported. The severity of this condition is related to the membrane stabilising and depolarising effects of ajmaline on the myocardium. The dose ingested varied from 10 to 40 mg/kg. The delay between ingestion and hospital admission ranged from 3 to 6 1/2 hours. The first cardiac disturbances can appear one hour after ingestion. Three cardiac arrests and one hypovolemic shock occurred. Three atrioventricular blocks, six intraventricular blocks, three ventricular tachycardias, and six prolongations of the QT interval were observed. Serum ajmaline levels varied from 0,8 to 6 mg/l. Symptomatic therapy was mainly based on sodium, temporary cardiac pacing, external DC shock, sympathomimetics and external cardiac massage with assisted ventilation. Cardiac bypass should be a part of the therapeutic arsenal. Elimination of the drug is assisted by a complete digestive evacuation. Renal or extrarenal dialysis is not indicated. One of the seven patients died. Prophylaxis is based on the non-prescription of ajmaline for benign cardiac disturbances.

Adolescent↗
PubMed1981

[Glucose intolerance in injured patients (author's transl)].

Glucose intolerance occurring in injured patients is known to be a part of the general response to injury described by Cuthbbertson: early "ebb phase" with a decrease of energy production, then "flow phase" with hypermetabolism. Several processes can be responsible for the abnormalities observed: 1) Alterations in peripheral glucose uptake. 2) Absolute or relative insulin lack in connection with increased catecholamine release which is know to inhibit insulin secretion. 3) Decreased sensitivity and responsiveness to insulin in connection with increased levels of counter regulatory hormones (catecholamines, glucagon, growth hormone). 4) Non-suppressibility of hepatic gluconeogenesis by glucose. Glucose intolerance decreases glucose utilisation and leads to increased proteolysis always unfavorable for patients.

Glucose↗