Biomedical subjects
Publications and source records attributed to J S Wilson.
Pancreatic lipid composition was found to be altered in rats fed a protein-deficient diet for 4 wk. Increases in triglycerides and cholesteryl ester content were found in association with a decrease in phospholipids. Alterations in these lipids may adversely affect membrane function and predispose to pancreatic injury.
The role of mitochondria in the initiation or promotion of pancreatic pathologic conditions has not been clearly delineated. In this context, it has recently been suggested that abnormal mitochondrial function may account for the fat accumulation observed in pancreatic acinar cells in alcoholism. To study these issues, we developed a method for the isolation of functional mitochondria from the rat pancreas. The resultant mitochondrial pellet possessed oligomycin-insensitive Mg2+-adenosine triphosphatase (ATPase) activity, and coupled respiration could be demonstrated in the presence of EDTA only after Mg2+ had been excluded from the incubation medium. Albumin was also a requirement for the demonstration of coupled respiration in vitro. When this new technique was applied to a rat model of alcohol-induced pancreatic steatosis, no mitochondrial dysfunction was demonstrated, suggesting that some other mechanism is responsible for fat accumulation in pancreatic acinar cells after long-term ethanol consumption. In contrast, DL-ethionine administration to rats produced partial or total uncoupling of mitochondrial respiration in the absence of morphologic evidence of mitochondrial injury.
The effects of baclofen, a gamma-aminobutyric acid (GABA) analogue, were studied on the intracellular responses of caudate neurons to cortical and thalamic stimulation. Systemic or intracaudate injections of baclofen did not reduce the initial excitatory postsynaptic potential (EPSP) to these stimuli; however, it did completely block evoked hyperpolarizations. These results suggest that the GABA-b receptor (one possible site of baclofen action) is not found on the corticostriate synaptic terminals. Furthermore, our results clearly indicate that evoked hyperpolarizations recorded in caudate neurons are not the result of cortical disfacilitation.
Rats fed pelleted nonpurified diets had significantly higher hepatic gamma-glutamyltranspeptidase (GGTP) activities than those fed liquid diets, with no difference in serum GGTP activities. However, levels of both hepatic and serum GGTP activity were higher in rats fed ethanol than in those fed liquid diets without ethanol. In addition, hepatic GGTP levels varied inversely with dietary carbohydrate content. These findings suggest that factors other than a mere increase of liver GGTP may be responsible for the elevated serum levels of this enzyme seen after chronic ethanol consumption and that dietary carbohydrate levels influence hepatic GGTP levels.
To determine whether increased intakes of fat and protein or particular drinking habits are associated with the development of alcoholic pancreatitis, a dietary study has been conducted. Patients with clinically evident alcoholic pancreatitis were compared with individuals with clinically evident alcoholic cirrhosis with respect to dietary and drinking habits before the onset of clinical illness. There was no significant difference between the two groups regarding intake of nutrients, drinking habits or type of alcoholic beverage consumed.
A technique for the isolation of functional rat pancreatic mitochondria is described. The resultant mitochondrial preparations contained oligomycin-insensitive Mg2+-ATPase activity and coupled respiration could only be demonstrated in the absence of Mg2+ and in the presence of EDTA.
To investigate the role of heredity in alcoholic pancreatitis, an HLA typing study has been performed. Patients with alcoholic pancreatitis exhibited an increased frequency of HLA Bw 39 when compared with the general population [13.6% vs 3.3%, P (corrected) less than 0.02; relative risk 4.7]. Alcoholics without pancreatitis did not differ from the general population with respect to HLA status, indicating that the increased incidence of HLA Bw 39 was related to alcoholic pancreatitis rather than to alcoholism itself. Thus, this study has provided evidence for a genetic predisposition to alcoholic pancreatitis.
Our results of 112 pectoralis major flaps used alone or in combination have been reviewed. Also, other anatomic studies have been described which led to the development of a true island flap with a more mobile, less bulky pedicle. The use of the flap in full-thickness reconstruction by modification of the flap or bilateral flaps has been discussed. The place of the flap when used in combination with the deltopectoral and forehead flaps in the repair of major postexcisional defects has been illustrated.
In a previous study, a rat model of ethanol-induced pancreatic steatosis was developed in which chronic ethanol feeding resulted in a twofold increase in pancreatic cholesteryl ester content. The studies reported here were performed in order to elucidate the mechanism of this cholesteryl ester accumulation. Rats were pair fed ethanol or control diets for 3 weeks. Ethanol feeding resulted in an increased accumulation of serum cholesterol in the pancreas. Ethanol feeding also resulted in increased in vitro incorporation of labeled acetate and mevalonate into the sterol moiety of pancreatic cholesteryl ester and increased incorporation of labeled acetate into its fatty acid component. These results suggest that chronic ethanol feeding causes pancreatic cholesteryl ester accumulation by affecting exchange of cholesterol between serum and pancreatic tissue.
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Stimulation of the exocrine pancreas is associated with marked changes in pancreatic phospholipid metabolism. It has been previously established that de novo synthesis of phospholipids constitutes part of this "phospholipid effect". This study has demonstrated that in vitro stimulation of the rat pancreas utilising bethanecol and pancreozymin results in increased incorporation of labelled glucose into phosphatidyl inositol and, to a lesser extent, other phospholipids, suggesting increased de novo synthesis of these compounds. However, secretin which is believed to act via a different intracellular pathway, did not exert such an effect. The relevance of this animal model is indicated by the demonstration of increased incorporation of labelled glucose into phospholipids of human pancreas stimulated in vitro by bethanecol or sincalide (the active carboxy terminal octapeptide of pancreozymin).
Quantitative analyses of the intracellular responses to peripheral stimuli were made in a 172 neurons recorded in the head of the caudate nucleus (Cd) of cat. Responsiveness of Cd neurons was tested using auditory and somatosensory stimuli which were presented unilaterally. We found that most cells (99%) responded to both auditory and somatosensory stimuli. Excitation followed by inhibition (i.e. E-I response) was the primary pattern of intracellular response occurring approximately 75% of the time. Qualitative and quantitative analyses revealed marked similarities in the amplitudes and time courses of the intracellular responses following supramaximal stimulation of the peripheral stimuli studied. Similarly, analyses of 40 pairs of simultaneously recorded neurons revealed a marked homogeneity in the intracellular responses to the same stimulus even though the recordings were made several mm apart. The most striking feature of the simultaneous recordings was that the peaks of the initial E-I response and the afterpotentials often occurred in register after a peripheral stimulus. Furthermore, changes in the responses of pairs of simultaneously recorded neurons co-varied. Because the striatum typically demonstrates spontaneous rhythmic activity, these data suggest that a peripheral stimulus has the potential of briefly synchronizing Cd's neuronal activity.
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The pathogenesis of alcoholic pancreatitis continues to be a puzzle. Of the many theories as to how alcohol might cause pancreatic damage, none satisfactorily explains why only a minority of alcoholics develop clinical pancreatitis. Hypertriglyceridemia and inherited factors could be important antecedents in some individuals, and high fat and protein diets may favour the development of the disease. Disturbances of the sphincter of Oddi have been postulated, but there are experimental and theoretical objections to the view that alcoholic pancreatitis generally results from sphincter dysfunction (obstruction-hypersecretion, biliary-pancreatic reflux and duodeno-pancreatic reflux). Biochemical studies of the effect of alcohol on pancreatic tissue have so far been relatively unrewarding. The most widely held view is that alcohol causes the deposition of protein in peripheral ducts leading to obstruction, inflammation and degeneration. However, it remains to be shown that these deposits are the cause rather than a result of pancreatic inflammation. Research might be facilitated by the development of a suitable animal model of the disease.
A better understanding of the detailed blood supply of skin and its underlying soft tissue has provided the reconstructive surgeon with a wider choice of reliable skin and muscle flaps for the reconstruction of head and neck defects after ablative surgery. The forehead, cervical and delto-pectoral flaps have been the standard flaps used for head and neck reconstruction. More recently, myocutaneous flaps like the pectoralis major myocutaneous flap and the latissimus dorsi myocutaneous flap have been used for head and neck reconstruction. The skin of these flaps provides the lining tissue and the muscle provides support as well as bulk and therefore greatly increases the scope of functional as well as cosmetic reconstruction. Finally, fat sculpturing techniques done as a secondary procedure on these myocutaneous flaps enables defects in the contour of the reconstructed face to be symmetrical with the normal side. This paper summarises the various flaps used in reconstruction of the head and neck region and discusses in detail the most promising myocutaneous flap for head and neck reconstruction in use today - the pectoralis major myocutaneous flap.
The effects of hyperbaric compression on heart rate, rectal temperature, respiratory rate, bubble formation, and survival were studied in three groups of anesthetized golden hamsters (Mesocricetus auratus). Group I (15 animals) breathed air while exposed to 7 ATA of pressure for 1 h in a hyperbaric chamber; Group II (13 animals), at the same pressure level (7 ATA) and for the same time period (1 h), breathed an oxygenated fluorocarbon liquid (temperature 27 degrees C) that was open to the chamber atmosphere; Group III (10 animals), at the same pressure and time period as the other groups, were sealed in a flexible plastic bag filled with oxygenated fluorocarbon as a breathing mixture. A fourth, Group IV (12 animals), breathed oxygenated fluorocarbon for 1 h at 1 ATA. Survival after rapid decompression in each group varied, 9 animals died in Group I, 12 animals in Group II, whereas none of the animals died in either Groups III or IV. Thirty minutes after decompression postmortem examinations of all the animals demonstrated the presence of large amounts of gas bubbles in the right ventricle and some gas bubbles in the left ventricle of all the hamsters in Groups I and II. No gas bubbles were found in the hearts of the Group III animals. Group III animals, breathing a liquid unsaturated by an inert gas, survived rapid explosive decompression without the signs and symptoms of decompression sickness. Immersion in the liquid fluorocarbon produced a profound decrease in heart rate, rectal temperature, and respiration in Groups II, III, and IV.
The phagocytosis of uniform fluorescent latex particles by pulmonary macrophages in the rat was analyzed by flow cytometric methods. The percentage of phagocytic macrophages and the number of particles per cell were determined from cell-size and fluorescence histograms. A comparison of in vivo and in vitro phagocytosis data showed that the percentage of phagocytic lavaged macrophages reflected the availability of instilled particles. With sodium azide used to model phagocytosis inhibition, it was shown that the percentage of phagocytic cells and the number of particles per cell can be determined simultaneously.