Who 'needs' community health? Planning for equity in the distribution of scarce resources.
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Biomedical subjects
Publications and source records attributed to S Duckett.
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Skeletal muscle ventricles (SMVs) were constructed from preconditioned latissimus dorsi muscles in eight dogs and then connected to each animal's systemic arterial circulation in short-term experiments. The lengths of time that SMVs could produce hemodynamic work as left ventricular assist devices were recorded. After 4 hr of continuous pumping at approximately 55 beats/min, six of eight SMVs were able to generate systolic pressures of 128 +/- 23 mm Hg and flows of 340 +/- 31 ml/min, representing 20 +/- 4% of the animals' cardiac output. After 8 hr of continuous pumping, five of the eight SMVs generated pressures of 110 +/- 15 mm Hg and flows of 308 +/- 88 ml/min, or 15 +/- 7% of the animals' cardiac output. The stroke work produced by the SMVs was intermediate between that of the animals' left and right ventricles. Although the SMVs were stimulated to contract at only about one-third the heart rate, the power output of the SMVs approximated that of the right ventricles because of the greater stroke work of the SMVs. Two SMVs functioned as LVADs for 14 hr. Deterioration in SMV function eventually occurred. In each case, however, complications such as anemia, hypoxia, and hypotension, which are inherent to prolonged short-term experiments of this type, contributed to the deterioration of SMV function. The results presented here suggest that skeletal muscle has the potential to directly support the circulation; however, the length of time such muscle pumps are capable of functioning has yet to be determined.
Three patients presented with encephalopathies: an undiagnosed degenerative disease of the brain, a degenerative cerebral disease in a patient with a myeloma but without a myelomatous deposit in the CNS and a malignant astrocytoma. Perivascular pallidal deposits (vascular siderosis) containing chromium, phosphorus and calcium plus sometimes traces of other elements were present in the three cases. Such deposits were present in the pallidal parenchyma and around vessels in the cerebellum in one case. Calcium and phosphorus are always present in any CNS calcification but the presence of chromium has not been reported. Chromium and its compounds (ingested, injected or inhaled) are toxic to humans and animals in trace doses. Approximately 900 cases of chromium intoxication have been reported and usually have had dermatological or pulmonary lesions (including cancer) but there is no report of involvement of the CNS. Sublethal doses of chromium nitrate injected intraperitoneally in rats and rabbits results in the presence of chromium in the brain. A thorough investigation was made to find the source of the chromium in these patients. Chromium was found to be present in trace amounts in the radiological contrast agents administered to these patients and in the KCl replacement solution and in mylanta, an antacid, given to one case. The evidence that chromium induced pathological changes in these three brains is circumstantial but shows that chromium can penetrate the human brain. This study indicates that vascular siderosis found in the brains of the majority of middle-aged and elderly humans is not simply an anecdotal pathological curiosity, but that it can serve as a route of entry for toxic products into the brain.
Placement of the intact omentum upon a recently traumatised spinal cord was found to be effective in lessening motor and neuroelectrical dysfunction in a group of cats. It was theorised that the beneficial effect of omental transposition was due to the establishment of a dynamic equilibrium between production of vasogenic oedema from the injured cord and its absorption through omental pathways. Removing vasogenic oedema at the omental/spinal cord interface is hypothesised to stabilise a rising tissue pressure within the cord during the acute phase of injury and at a later date to decrease scar formation at the injury site.
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A subtoxic quantity of radioactive 111indium and stable indium was injected once into young rats. Subsequently pairs of these rats were killed at intervals of 15 minutes to 3 days after the injection. Tissues from the central (CNS) and peripheral nervous system (PNS) and blood were removed from each rat and the amount of 111indium was measured in the tissues. Cryostat sections of the cerebrum, cerebellum, spinal cord, sciatic nerve, a blood smear and a kidney control from each rat were examined with an analytical ion microscope (secondary ion mass spectrometry analysis) and the presence of 113 and 115 indium was localized in the tissues. These observations show that indium penetrates all neural tissues and that the brain resists the entry of indium - a very toxic element - much more effectively than the sciatic nerve.
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An equal amount (per weight) of 127m tellurium (Te) was injected IP into weanling and adult rats, some intoxicated with a diet containing Te, others not. The young intoxicated rats presented a segmental demyelination of the sciatic nerve and paralysis of the hind limbs; the adult intoxicated rats did not. Quantitation of 127m Te in nervous and other tissues was done with a gamma counter. Correlative morphological examination of the nervous tissues was done with light and electron microscopy. This study shows that Te crosses the vascular wall without injuring endothelial cells and invades the surrounding sciatic nerve parenchyma following administration of 127m Te to a weanling or adult rat. However, Te damages the endothelium, crosses the vascular wall of endo and perineurial vessels in weanling rats, causes a perivascular oedema, cytoplasmic anomalies in the Schwann cells, destruction of myelin and apparently invades axones--according to autoradiographic studies--following the administration of 127m Te plus the Te-diet. It is concluded that Te penetrates more quickly and in larger amounts the walls of blood vessels in the sciatic nerve of weanling rats intoxicated with Te, than the same nerve in the other weanling and adults rats. Te in the amounts indicated here penetrates the parenchyma of the CNS but apparently does not cause injury.
This is a study of DNA synthesis of Schwann cells during the demyelination and the remyelination of peripheral nerves secondary to the intoxication of young rats with tellurium (Te). 3H-thymidine uptake of Schwann cells begins on day 4, reaches a zenith on day 7, and ends before day 20 on the Te diet despite continuation of the diet. The chronology of pathologic events is that myelin breakdown leading to segmental demyelination occurs first, followed within 24--48 h by the appearance of paralysis and by the beginning of DNA synthesis by the Schwann cells. A quantitative study on isolated nerve fiber preparations showed that more Schwann cells are produced than necessary to cope with the remyelination and that only one of four to six Schwann cells present in the demyelinated area at day 12 will participate in the remyelinating process.
Free-moving mice from the high-alcohol preference C57BL/6J strain and low-preference DBA/2J strain were slowly fed [2-14C]ethanol intragastrically until anesthesia was achieved. Behavior was monitored in a Plexiglas metabolic chamber while 14CO2 was simultaneously trapped to determine the rate of ethanol metabolism. Average time to the loss of the righting reflex in the DBA/2J was 21.9 min and 27.9 min for the C57BL/6J strain (p less than 0.005). Elimination of 14CO2 was slightly higher (n.s.) in the DBA/2J strain for the entire monitoring period. Infusion of ethanol via the tail vein yielded identical results indicating that the slower elimination rate in the C57BL/6J strain could not be the result of slower absorption across the gut wall. Infusion via the tail vein with radioactive sodium bicarbonate indicated that the DBA/2J strain has a higher rate of CO2 expiration (n.s.). Consequently, the higher rate of 14CO2 expiration from ethanol oxidation may not reflect a higher rate of metabolism. These results are discussed in terms of the apparent differences between these strains in neural sensitivity to ethanol.
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Adult white rats were injected daily for 1 month with aluminum chloride and killed. Aluminum was identified, quantitated, and localized in the brains of these rats. The only detectable anomalies were crystals of aluminum and phosphorus in lysosomes and lipofuscin granules in the cytoplasm of neurons.
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