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C Nordström

Publications and source records attributed to C Nordström.

14 recordsLinked to original sources

Aspects on the cerebral perfusion pressure during therapy of a traumatic head injury.

An actively raised cerebral perfusion pressure by vasopressors is nowadays often advocated during therapy of a post traumatic brain oedema to improve oxygenation of the brain. In this paper we argue that the arterial pressure not uncritically can be raised as the subsequent increase in hydrostatic capillary pressure may favour transcapillary filtration if the blood-brain barrier is opened for solutes. Further, the use of vasoconstrictor drugs to increase the perfusion pressure may in fact impair oxygenation to the penumbra zones around brain contusions but also to other tissues of the body, like the intestinal mucosa and the kidney. An alternative therapeutical concept which both ensures an adequate oxygenation of the brain and controls the intracranial pressure (ICP) is given. In short, it implies active antistress and sedative treatment, adequate fluid therapy with blood and colloids to normal haemoglobine and albumin values, artificial ventilation to normal PaCO2 and PaO2, and this in combination with antihypertensive and catecholamine reducing treatment with alpha 2-agonist and beta 1-antagonist.

Adrenergic alpha-Agonists↗

The estrogen receptor cooperates with the TGF alpha receptor (c-erbB) in regulation of chicken erythroid progenitor self-renewal.

A unique combination of growth promoting factors is described that allows growth of large amounts (10(10)-10(11)) of normal erythroid progenitors from chick bone marrow. These erythroid progenitors express the estrogen receptor (ER) as well as the receptor tyrosine kinase TGF alpha R/c-erbB. They require both TGF alpha and estradiol for sustained self-renewal in vitro, but terminally differentiate upon withdrawal of TGF alpha and inactivation of the ER by an antagonist (ICI 164.384). Overexpression of the human ER in erythroblasts devoid of endogenous ER revealed that the hormone-activated ER alone arrested erythroid differentiation and repressed a large group of erythrocyte genes. When similarly overexpressed, TGF alpha R/c-erbB inhibited the expression of a distinct, but overlapping, set of genes. The endogenous ER and TGF alpha R/c-erbB affect erythrocyte gene expression in a similar, but less pronounced fashion. Surprisingly, suppression of ER function by antagonist efficiently inhibited erythroblast transformation by tyrosine kinase oncogenes, suggesting a role of the endogenous ER in leukemogenesis. We speculate that the oncogenes v-erbB and v-erbA cooperate in erythroleukemia induction by a mechanism that is employed by TGF alpha R/c-erbB and ER to regulate normal progenitor self-renewal in response to external signals.

Animals↗