Myocardial glutamate dehydrogenase activity.
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Biomedical subjects
Publications and source records attributed to R L Jenkins.
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Forty-one patients, all in end stage hepatic failure, underwent 46 liver transplantations with a long-term survival rate of 63%. Six patients died of uncontrollable bleeding due to primary graft malfunction at or immediately after operation. Nine died early or late with overwhelming infection. In addition to clinical assessment, needle liver biopsy, central plasma clearance rate of amino acids (CPCR-AA), and routine "liver function tests" were employed to aid in selection of patients for transplantation and for guidance in postoperative management. Although liver biopsies usually afforded an exact diagnosis, neither they nor the routine liver function tests quantitated the extent to which hepatocyte function was impaired. CPCR-AA, which measures the rate of amino acid uptake by the liver and other central tissues for oxidation, gluconeogenesis, and protein synthesis was 91 +/- 9 ml/M2/min in the preoperative transplant group. This compares with a value of 97 +/- 16 in a previously studied series of cirrhotics who died following other forms of surgery and a CPCR-AA of 220 +/- 26 ml/m2/min in those who survived. In addition, the preoperative CPCR-AA was found to correlate with the in vitro hepatic protein synthetic rate of slices from the resected recipient liver (r = 0.72, p less than 0.02). After operation, serial hepatic needle biopsies were classified by histology into four grades of injury, ranging from normal liver transplant (Grade I) to mild hypoxic or rejection injury (Grade II), viral hepatitis (Grade III), and severe hypoxic or rejection injury (Grade IV). Significant relationships of the histological grades to ultimate mortality, CPCR-AA, and prothrombin times were found. CPCR-AA and prothrombin time correlate inversely (r = 0.57, p less than 0.001), further demonstrating the relationship of CPCR-AA to protein synthesis of clotting factors. These patterns of posttransplant response were delineated by serial CPCR-AA values. "Early" responders had values over 290 ml/M2/min and all survived. Twelve patients with delayed response were characterized by values of 150 +/- 12, rising to over 200 ml/M2/min after 2 weeks. Two who failed to increase CPCR-AA died. In six "poor" responders, CPCR-AA with Grade IV injury remained below 110 ml/M2/min. All died except for one whose CPCR-AA subsequently rose following retransplantation. It is concluded that percutaneous hepatic needle biopsies and CPCR-AA measurements in combination are of proven value, not only in understanding the nature of injury and functional impairment of the liver, but are also important as guides to selection of patients and for their posttransplant management.
Pulmonary complications following orthotopic liver transplantation (OLT) were prospectively evaluated in 18 individuals transplanted at the New England Deaconess Hospital. Of sixteen patients who survived the immediate postoperative period, 12 (75%) sustained a pulmonary complication. Of these complications, 64% were noninfectious--whereas 22% were infectious, and 14% probably infectious. Six of eight documented infections were caused by viruses of the herpes group. In four cases of viral pneumonitis other pulmonary pathogens were isolated (fungi-3, protozoan-1, bacteria-1). Unlike noninfectious complications, pulmonary infections were associated with a fatal outcome in five of six patients who died after OLT. Pulmonary complications are frequent and serious occurrences after OLT, and contribute to both the morbidity and mortality of this procedure. Compared with pulmonary complications seen after transplantation of other organs, OLT was associated with a higher proportion of noninfectious complications but a similar spectrum of pulmonary infections.
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Phenylalanine hydroxylation, tyrosine oxidation, and plasma appearance of phenylalanine and tyrosine were evaluated in a 49-yr-old woman with fulminant non-A, non-B hepatitis and encephalopathy using a continuous intravenous infusion of L-[ring-D5]phenylalanine and L-[U-14C]tyrosine. Despite marked elevations in plasma phenylalanine and tyrosine appearance and normal apparent albumin synthetic rates, phenylalanine clearance and hydroxylation to tyrosine were only 12% and 60%, respectively, of values observed in individuals with normal liver function. Three days after orthotopic liver transplantation, plasma phenylalanine and tyrosine appearances were not markedly changed. Phenylalanine clearance and conversion to tyrosine, however, were restored to normal. In addition, tyrosine oxidation and apparent albumin synthesis were increased. This case report represents the first in vivo demonstration of a selective diminution of enzyme function in an individual with fulminant liver disease. Liver replacement restored aromatic amino acid degradative capacity and increased albumin synthesis.
Liver replacement has become a viable treatment option for select patients with severe acute or chronic hepatic failure. Evaluation of potential candidates is discussed along with current techniques for donor organ retrieval, recipient implantation, and postoperative immunosuppression.
The management of portal hypertension focuses on control of its complications, the most important of which is bleeding esophageal varices. Other complications, such as ascites, bleeding intestinal stomas, and hypersplenism, rarely require surgical intervention. Other than medical management, the three basic procedures now available for the treatment of bleeding esophageal varices include decompression of varices with a portosystemic shunt, nonshunting operations that attack directly the esophageal variceal-bearing area, and liver transplantation as the procedure of choice in selected patients. Patients who present with episodes of acute bleeding are usually treated initially with medical therapy including acute sclerotherapy or balloon tamponade techniques when necessary. If the patient fails to respond or if episodes of bleeding recur, further therapy is required. Although selection of therapy remains controversial, it is based on multiple factors. These include the basic pathogenic mechanism of portal hypertension in the individual patient, status of the patient as defined by Child's classification, elective or urgent nature of the operation, hemodynamic stability of the patient at the time of the procedure, site of the block in the portal system, and caliber and anatomic relationship of the vessels available for anastomosis in the portal system. Additional factors include the presence and severity of ascites or encephalopathy, age of the patient, site of bleeding (esophageal or gastric), severity of associated hypersplenism, and techniques and expertise available at a given institution. Shunting procedures achieve the best long-term control of bleeding, but they can precipitate the development of encephalopathy. Nonshunting procedures do not induce encephalopathy, but they are usually associated with a high rate of rebleeding. Also, with the possible exception of sclerotherapy, they are still associated with a high operative mortality rate in alcoholic patients classified as Child's C. Although sclerotherapy controls acute variceal bleeding more successfully than conventional methods, it is not readily applicable in patients with bleeding gastric varices. Also, it has not yet clearly been proved to be an effective method of permanent control of gastroesophageal bleeding and has not been demonstrated to increase survival. The new methods of extensive esophagogastric devascularization (for example, porta-azygos disconnection using the Sugiura procedure) are attractive because of the low late recurrence rate for bleeding without the induction of encephalopathy.(ABSTRACT TRUNCATED AT 400 WORDS)
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The problem we studied relates to the inheritance of Gilles de la Tourette's syndrome. The method was the investigation, including blood studies, of a pair of twins who both were affected with the syndrome. It was concluded that the twins were identical and this added to the evidence of the heritability of the disorder. The twins were affected with other but related problems of behavior; considerable similarities were found in their behavior and behavioral problems. No family history of this or tic-like disorders could be obtained. Reduction of tics occurred when haloperidol treatment began.
Giant neural cell systems (dendrites, cell bodies, and axons) are present among more usual structures in the retina and optic nerve of the small whale (dolphin) Tursiops truncatus retina. Giant cell body dimensions range up to 75 microns in diameter. Nuclei of the cells are frequently larger (greater than 20 microns) than nearby ganglion, bipolar, and receptor cell bodies. The presence of the giant cell system and giant elements in the nerve fiber layer agree with the unusually broad fiber spectrum of the dolphin optic nerve where more than 6% of the axons are greater than 15 microns in diameter. Smaller axons in the size distribution are typical of dimensions found in terrestrial mammals. The axon estimate totaled 157,000 per optic nerve. The giant cell-axon systems of the whale retina may be a unique expression of the large ganglion cell-axon (transient or "Y" functional unit) systems recently identified in terrestrial mammals.
Administered the Memory-for-Designs Test and a verbal and visuospatial paired associate learning test to separate groups of alcoholics (N = 32) 3 and 11 weeks abstinent from alcohol and to a matched control group (N = 16). Alcoholics were not impaired in verbal learning. Alcoholics 3 weeks abstinent performed significantly less well than controls on all nonverbal tasks and less well than 11-weeks alcoholics on one nonverbal measure. No significant differences were found between 11-week alcoholics and controls. The results suggest that some recovery of function may occur in alcoholics after 10 weeks of abstinence. The data also support the hypothesis of impaired right hemisphere in alcoholics.
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To examine the hypothesis that the functioning of the right hemisphere is disrupted as a result of prolonged alcohol abuse, male middle-aged alcoholic patients and nonalcoholic controls were tested on the standard Tactual Performance Test (TPT) from the Halstead-Reitan Neuropsychological Test Battery or on a modified form of the TPT employing stimuli of low verbal codability. On the standard TPT, alcoholic patients were impaired relative to controls on timed performance and memory for TPT figures but not for location. Analysis of the pattern of timed performance indicated the presence of an alcohol-related deficit for the left hand; however, right-hand scores were not impaired in alcoholic patients. For the modified TPT, alcoholic patients were impaired relative to controls for level but not pattern of timed performance; memory for TPT figures was impaired in alcoholic patients although location scores were not. The standard and modified TPT were found to discriminate alcoholic and control subjects with equal accuracy. The results support the hypothesis that chronic alcoholism leads to a disruption in the normal function of the right cerebral hemisphere.
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We examined the subsequent criminal activities of delinquent boys classified as having either socialized conduct disorder, undersocialized conduct disorder, aggressive type, or undersocialized conduct disorder, unaggressive type. A follow-up study of more than ten years revealed profound differences in the likelihood of criminal convictions or incarcerations between socialized and undersocialized delinquents. The socialized delinquents have less chance of being either convicted of a crime or being imprisoned. This difference supports the previous studies that demonstrated that these classifications could be distinguished on the basis of differences in behavior, personality, psychological test results, and characteristic family backgrounds, and reinforces this method of classifying conduct disorders. Differences between the undersocialized aggressive and unaggressive groups appear qualitative and indicate that subjects in the former group are involved in more crimes of violence subjects in the latter.
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Two-hundred broiler-type chickens were reared under either normal lighting or darkness for 16 weeks. Each week, birds were subjected to applanation tonometry for measurement of intraocular pressures (IOP). The birds were then weighed, eye enucleated, and dimensions measured. All eyes were prepared for histological examination. Chickens reared in darkness for 4 to 6 weeks displayed an abnormal eye enlargement, accompanied by an increase in IOP in comparison to chickens reared under conventional management. From the 6th to the 16th week, the eyes of dark-reared chickens continued to enlarge while IOP decreased. The sclera, choroid, retina, and retinal layers of dark-reared chicks were not as thick as controls throughout the 16 weeks. Two principle retinal pathologies were induced by darkness. One appeared as darkened areas of the peripheral retina. In histological sections the darkened retinal areas had a thin choroid and thin retinal layers. The second retinal abnormality was one or more white, nonpigmented bands directed perpendicular to the pectin. Histologically, the depigmented bands were areas in which the vessels of the choroid, the pigmented epithelium, and the outer retinal layers were absent. The corneas of dark-reared chicks exhibited a reduction in their curvature and thickness compared to control corneas.