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Biomedical subjects

S Haberman

Publications and source records attributed to S Haberman.

At least 37 records · Page 2Linked to original sources
PubMed1978

The changing mortality of cerebrovascular disease.

Cerebrovascular disease mortality trends in England and Wales are discussed, concentrating on data relating to years after 1968. Cerebrovascular disease deaths have been found to comprise a decreasing proportion of all deaths and of all cardiovascular disease deaths. For ages under 85 the mortality rates have generally fallen for cerebrovascular disease, with females experiencing the greater improvement. Concerning the main diagnostic categories, the rates for cerebral haemorrhage and thrombosis have fallen, and have risen for subarachnoid haemorrhage and the vague rubrics (436, 437). Possible explanations for these trends are proposed including relationships to other cardiovascular diseases. In particular, the downward trend in cerebral haemorrhage mortality rates is found to be positively correlated at a significant level with that due to hypertensive disease. However, the trends in cerebral thrombosis and ischaemic heart disease mortality rates are found to be in opposite directions--a phenomenon which contradicts the widely-held view that these diseases have a common aetiology.

Age Factors↗
PubMed1978

The definition and classification of stroke. A new approach.

Accuracy of diagnosis, both anatomical and pathological, and disability scoring would add to the quality of certification data, and would help in comparing reports on strokes as well as with data regarding referral history and therapeutic trials. Considerable information could be made available by the use of new types of certification. The problems of existing definition and classification are discussed and a new classification for stroke is described.

Brain↗
PubMed1977

New classification of stroke: preliminary communication.

We describe a new method of classifying stroke using a cumulative numbering system. The method is simple and more explicit than currently used classifications, and could be useful for different agencies looking after patients with stroke in hospital or at home.

Cerebrovascular Disorders↗
PubMed1977

The effect of cyclic GMP on phosphofructokinase from rat tissues.

In view of the recently proposed hypothesis of biologic regulation through opposing influences of cyclic AMP and cyclic GMP, and since cyclic AMP is a well-known allosteric activator of phosphofructokinase (ATP:D-fructose-6-phosphate 1-phosphotransferase, EC 2.7.1.11), the effect of cyclic GMP on the activity of this enzyme from several rat tissues was investigated. It was found that cyclic GMP exerted an inhibitory effect on the activity of rat heart and skeletal muscle phosphofructokinase. This effect was most pronounced under conditions in which the enzyme was partially inhibited by ATP or by citrate. Cyclic GMP also antagonized the deinhibitory action of cyclic AMP and other allosteric activators, such as glucose 1,6-bisphosphate or AMP, on the ATP or citrate-inhibited heart or muscle phosphofructokinase. In contrast to the heart and skeletal muscle phosphofructokinase, the adipose-tissue enzyme was not affected by cyclic GMP to any significant degree. The antagonistic action of cyclic GMP to the activation of heart-phosphofructokinase, may suggest a mechanism by which the activity of phosphofructokinase is synchronized with the activity of glycogen phosphorylase, as a result of acetylcholine action in heart, to achieve a decrease in total glycogenolysis and glycolysis.

Adenosine Monophosphate↗
PubMed1975

Complementarity in the regulation of phosphoglucomutase, phosphofructokinase and hexokinase; the role of glucose 1,6-bisphosphate.

ATP and citrate, the well known inhibitors of phosphofructokinase (ATP: D-fructose 6-phosphate 1-phosphotransferase, EC 2.7.1.11), were found to inhibit the activities of the multiple forms of phosphoglucomutase (alpha-D-glucose 1,6-bisphosphate: alpha-D-glucose 1-phosphate phosphotransferase, EC 2.7.5.1) from rat muscle and adipose tissue. This inhibition could be reversed by an increase in the glucose 1,6-bisphosphate (Glc-1,6-P2) concentration. Other known activators (deinhibitors) of phosphofructokinase, viz. cyclic AMP, AMP, ADP or Pi, had no direct deinhibitory action on the ATP or citrate inhibited multiple phosphoglucomutases. Cyclic AMP and AMP, could however lead indirectly to deinhibition of the phosphoglucomutases, by activating phosphofructokinase which catalyzes the ATP-dependent phosphorylation of glucose 1-phosphate to form Glc-1,6-P2, the la-ter then released the multiple phosphoglucomutases from ATP or citrate inhibition. The Glc-1,6-P2 was also found to exert a selective inhibitory effect on hexokinase (ATP: D-hexose 6-phosphotransferase, EC 2.7.1.1) type II, the predominant form in skeletal muscle. This selective inhibition by Glc-1,6-P2 was demonstrated on the multiple hexokinases which were resolved by cellogel electrophoresis or isolated by chromatography on DEAE-cellulose. Based on the in vitro studies it is suggested that during periods of highly active epinephrine-induced glycogenolysis in muscle, the Glc-1,6-P2, produced by the cyclic AMP-stimulated reaction of phosphofructokinase with glucose 1-phosphate, will release the phosphoglucomutases from ATP or citrate inhibition, and will depress the activity of muscle type II hexokinase.

Adenosine Triphosphate↗
PubMed1967

Local and regional applications of hydrogen peroxide in the control of clostridial myositis in rabbits.

The intra-arterial infusion of hydrogen peroxide has been used as a method for producing a hyperoxic environment in experimental animals for the treatment of experimentally induced clostridial myositis. Eighty-five rabbits were employed in this study; 43 were controls and 42 were experimental animals. In the experimental study, 21 animals were treated with hydrogen peroxide by each route of administration. In this group, 52.4% of the animals receiving the intra-arterial infusion and 66.6% receiving intramuscular clysis survived. There were no survivors past 72 hr in the control group.

Animals↗