Dehydrooligopeptides. V. Synthesis of N-carboxy alpha-dehydroamino acid anhydrides and their transformation to alpha-dehydroamino acid and dehydrooligopeptide derivatives.
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Amino Acids↗
Biomedical subjects
C Shin
Publications and source records attributed to C Shin.
Evidence implicating substantia nigra in regulation of kindled seizure threshold.
We studied the effects of microinjected drugs and brainstem lesions on motor and limbic seizures in the kindling model of epilepsy. The duration of motor seizures was determined by timing the colonic and tonic movements of the extremities. The duration of limbic seizures was determined by measuring afterdischarge recorded on the electroencephalogram. Bilateral microinjection of a gamma-aminobutyric acid (GABA) agonist, muscimol, into the area of the substantia nigra (SN) markedly suppressed both motor and limbic seizures induced by stimulation of amygdala, olfactory structures, or lateral entorhinal cortex. Microinjection of saline did not suppress seizures. The suppressive effect of muscimol: (i) dissipated after several hours and was dependent on dose; (ii) was due to an elevation of the seizure threshold, since typical seizures could be elicited with electrical current far exceeding the threshold; and (iii) exhibited spatial specificity since muscimol injections 1 to 2 mm dorsal to the SN or into neocortex did not suppress the seizures. The actions of muscimol were probably mediated by its GABA agonist properties, since microinjection of an irreversible inhibitor of GABA transaminase (gamma-vinyl GABA) into the area of the SN also suppressed kindled seizures. Destruction of brainstem structures was produced by microinjection of the neurotoxin, N-methyl-D,L-aspartate. Seizures were markedly suppressed in animals with bilateral destruction of the SN but not in animals in which the SN was spared bilaterally. We interpret the data to indicate that the SN is the site at which the GABA agonists and lesions act to raise the threshold for kindled seizures. The suppression of limbic seizures indicates that this brainstem nucleus can regulate the intrinsic neuronal excitability of hemispheric sites.
Aminocaproates↗
Conversion of ischemic to hemorrhagic infarction by anticoagulant administration. Report of two cases with evidence from serial computed tomographic brain scans.
Anticoagulant therapy is appropriate for embolic cerebral infarction due to valvular heart disease or cardiac dysrhythmia, as well as for stroke-in-evolution. Various incidences of hemorrhagic complications have been cited in patients given anticoagulants after stroke or transient cerebral ischemia. Conversion of ischemic to hemorrhagic infarction has been shown to occur experimentally. We describe two patients in whom this conversion occurred in the absence of hypertension or excessive anticoagulation and was substantiated by serial computed tomographic brain scans. This finding suggests that conversion of ischemic to hemorrhagic infarction may occur even with appropriate and carefully administered anticoagulation therapy.
Adult↗
Interference with virus infection induced by RNA in chick embryo cells.
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Alkalies↗
Studies on the blood of an MiV/Mk proposita and her family.
An individual (J-1) was shown to be heterozygous for the MiV and Mk genes. Her red cells typed as M+(weak), N-, S-, s+(strong), U+, Hil+, Wr(a-b-), En(a+weak). Polyacrylamide gel electrophoresis analysis of her red cell membranes revealed absence of PAS-staining bands corresponding to normal MN and Ss sialoglycoprotein (SGP), and presence of a hybrid MNSs SGP [(alpha-delta)MiV] similar but not identical to that reported for an MiV homozygote. However, J-1 cannot be homozygous for MiV since the red cells of two of her children are Hil- and s-, carry only a single dose of M antigen, and have a sialic acid content that is consistent with the presumption that they are Mk heterozygotes. J-1's hybrid MNSs SGP is considered to be gene-fusion product resulting from unequal crossover between a normal alpha M and delta gene, and her red cells lack that portion of the Ena antigen that is resistant to ficin. Her hybrid MNSs SGP differs, therefore, from that reported for the MiV homozygote, which probably arose from unequal crossover between alpha N and delta genes. Further, the red cells of the MiV homozygote carry the ficin-resistant Ena determinant.
Aged↗