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Biomedical subjects

S Sollid

Publications and source records attributed to S Sollid.

4 recordsLinked to original sources
PubMed1999

[Decompression craniectomy--life-saving treatment in acute cerebral infarction].

Massive cerebral infarction is often accompanied by early death secondary to transtentorial herniation. Decompressive hemicraniectomy has been suggested as a lifesaving procedure. We report the case of a 61 year old man who had an acute infarction in the distribution area of the right middle cerebral artery. Initially, he was awake and suffered from total left-sided hemiparalysis. Over the next two days, his level of consciousness deteriorated to a Glasgow Coma Scale score of 5. Intracranial pressure (ICP) monitoring was then established. Three days later, the ICP increased from 20 to 40 mm Hg. We performed a right-sided decompressive hemicraniectomy, and the ICP was normalized immediately. Ten months after surgery the patient was at home and functioning with minimal assistance. He had moderate paresis of the left leg and was able to walk, but his left arm was paralytic. The presented case confirms that decompressive hemicraniectomy may prevent death and allow survival without severe disability in patients with massive cerebral infarction.

Acute Disease↗
PubMed1996

Arginine 210 is not a critical residue for the allosteric interactions mediated by binding of cyclic AMP to site A of regulatory (RIalpha) subunit of cyclic AMP-dependent protein kinase.

The guanidinium groups of conserved arginines in the two intrachain cAMP-binding sites of regulatory (R) subunit of cAMP-dependent protein kinase have been implicated in the allosteric interactions by which cAMP binding leads to kinase activation. We have investigated the functional role of Arg-210, the conserved arginine in site A of murine type Ialpha R subunit, by analyzing the effects of nine different substitutions at this residue on cAMP binding and allosteric properties of bacterially expressed RIalpha subunits. All substitutions reduced the cAMP binding affinity of site A, but the magnitude of reduction varied from several hundredfold to 10(6)-fold. The differential effects of the different substitutions could not easily be rationalized by interactions with cAMP and might, in part, reflect interactions with other residues in the unoccupied cAMP-binding pocket. None of the Arg-210 substitutions appeared to disrupt the allosteric interaction by which occupation of site A slows dissociation of cAMP from site B, although the effect was difficult to elicit in full with mutations that had strong effects on cAMP binding. The two weakest substitutions, Arg-210 --> Ile and Arg-210 --> Thr, could be shown to have essentially no effect on the allosteric interaction by which occupation of site A reduces the affinity of R subunit for the catalytic subunit. The weaker mutations had a smaller effect on kinase activation by the suboptimal activator Rp-adenosine cyclic 3',5'-phosphorothioate than by cAMP, suggesting that the analog largely bypasses interactions with the guanidinium group of Arg-210.

Allosteric Regulation↗