[Prolonged hospitalization of children].
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Biomedical subjects
Publications and source records attributed to G Mitchell.
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Stimulation of the intracerebral noadrenergic pathway (INP) increases hypothalamic blood flow as measured in conscious rabbits using a 133xenon washout technique. This increase is abolished by the intra-hypothalamic injection of 0.65 micrograms of the muscarinic antagonist atropine and by 5 micrograms of the nicotinic antagonist mecamylamine. Further, 1 micrograms of the cholinomimetic methacholine produces a similar vasodilation. While methacholine enhances the vasodilatation on stimulation of the INP, destruction of the pathway abolishes the entire vasodilator response to methacloline. Removal of the superior cervical sympathetic ganglia does not abolish vasodilatation. A role for endogenous acetylcholine in the INP-induced vasodilatation is thus proposed. This vasodilatation appears to act via an increase in neuronal activity with a resultant lowering of local pH, as 60 micrograms barbiturate and intra-hypothalamic bicarbonate abolish the dilatation completely. The cholinergic vasodilatation reported here is probably an excitatory effect on the INP and is not likely to be due to an inhibition of sympathetic vasoconstrictor tone.
Serum creatine phosphokinase (CPK) activity was measured in 10 German Landrace pigs from 11 to 28 weeks of age. A pronounced age dependence of serum enzyme activity was observed, peak activity occurring at 19 weeks of age. At the end of the growth period, when the pigs were challenged with halothane to detect the malignant hyperthermia syndrome, 3 pigs were found to be susceptible. Singificant increases in the serum enzyme levels in the susceptible pigs were observed only at 11 and 28 weeks of age. Serum enzyme levels measured during the rapid phase of growth could not be used to predict the malignant hyperthermia syndrome. Elevated serum CPK levels were also observed in two litters of Large White and Landrace x Large White pigs, breeds known to be stress-resistant. No pigs in these litters were susceptible to halothane, even though CPK levels were similar to those of the German Landrace pigs. The results indicate that serum CPK levels can be used as evidence of predisposition to the malignant hyperthermia syndrome but cannot be relied on as a single ultimate test.
Elizabeth Murray describes a new flexible learning programme currently being piloted in Nottingham. Its open and distance learning approach makes it accessible to a variety of those involved in caring for elderly people.
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Both clinical trials and everyday experience indicate that most hypertensive patients will need two or more drugs to reach target blood pressures. The current framework for the selection of drugs for combination therapy is based mainly on their interaction with the renin-angiotensin system. However, this approach would not fully exploit the range of drugs now available. This study, based on current primary care practice, confirms that the centrally acting drug moxonidine has efficacy as an add-on agent comparable to that of other drugs such as beta-blockers and ACE inhibitors and that it can effectively be combined with these agents. It also shows that moxonidine is as well tolerated as the other drugs and much better than older centrally acting agents such as clonidine and methyldopa. The study reinforces the view that moxonidine can be considered as an effective and well-tolerated drug for use in combination with any other class of antihypertensives.
Carnitine Palmitoyl Transferase (CPT) deficiencies are found in 2 different clinical forms: muscular and hepatic. The study of fibroblasts of 2 patients corresponding to each of these situations showed that these phenotypes are associated with different abnormalities of CPT, CPT I in the hepatic type and CPT II in the muscular type. The functional consequences of both abnormalities are different. In the hepatic type, CPT I deficiency induces a lack of long chain fatty acid (LCFA) oxidation in fibroblasts as well as, probably, in the patient's liver. In the muscular type, CPT II deficiency has no functional consequences in the fibroblast, contrary to what is observed in the patient's muscle. It is postulated that control of the mitochondrial LCFA oxidation in the liver and in the fibroblasts depends on CPT I, while it depends on CPT II in the muscle.
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