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Biomedical subjects

J George

Publications and source records attributed to J George.

At least 343 records · Page 19Linked to original sources
PubMed1976

Neuropeptide MSH/ACTH 4-10 enhances attention in the mentally retarded.

Twenty adult mentally retarded men were randomly assigned to receive MSH/ACTH 4-10 or a vehicle control solution in a double blind procedure. After an intravenous injection the subjects were presented with an orienting sequence and a series of behavioral tests. Treatment with the peptide resulted in a significant decelerative heart rate response during the test stimulus of the orienting sequence. Improved performance of the intradimensional and extradimensional shift of a visual discrimination procedure was significant for subjects receiving MSH/ACTH 4-10. The pattern of response on the subproblem analysis of the extradimensional shift reflected greater dimensional attention in the subjects treated with the peptide. Attentive subjects given MSH/ACTH 4-10 evidenced significant improvement on a rhythm matching test, a test of spatial localization and a visual retention test. The data were interpreted as indicating that the peptide resulted in improved attention of stimulus processing. It was speculated that MSH/ACTH 4-10 may be unquely coded for perceptor/attentional functioning and may be useful as a treatment for disorders of attention.

Adrenocorticotropic Hormone↗
PubMed1976

Postural hypoxemia in quadriplegic patients.

Quadriplegic patients frequently undergo unusual positional changes, including head-down tilt. To determine if hypoxemia develops in this position and whether it is related to the duration of quadriplegia, five patients were studied within 1 year of injury (group A) and five after 1 year from injury (group B). Arterial blood gases were obtained in the seated and 45-degree head-down position. Group A patients had a decrease in arterial partial pressure of oxygen in the head-down position (p less than 0.025), while group B patients did not (p greater than 0.4). This study demonstrated that quadriplegic patients have positional hypoxemia early in their course. This probably results from relative hypoventilation of the upper lung fields caused by flaccid paralysis of the intercostal muscles. The positional hypoxemia disappears with time, presumably because of the change from flaccid to spastic paralysis of the intercostal muscles.

Humans↗
PubMed1975

Prophage induction and cell division in E. coli. III. Mutations sfiA and sfiB restore division in tif and lon strains and permit the expression of mutator properties of tif.

In E. coli K12, cell filamentation promoted by tif is enhanced by the lon mutation; in contrast, prophage induction and repair of UV-irradiated phage lambda, also promoted by tif, are not affected by lon. From a tif lon double mutant, "revertants" having recovered the ability to divide at 41 degrees were isolated, among which most (95%) had also lost their Lon filamentous phenotype after ultraviolet (UV) irradiation. From these 95% of revertants: (1) 94% are suppressed for the whole Tif phenotype, by additional mutations that render them deficient in DNA repair, as judged from their high UV sensitivity; some have been characterized as recA mutants. (2) 1% have recovered a control on cell division at 41 degrees or after UV irradiation by means of secondary mutations altering neither the other phenotypic properties of tif and lon, nor the repair and recombination ability of the cells: in particular, this class of "revertants" remains thermoinducible upon lysogenisation; the mutations which specifically suppress filamentation have been mapped at two loci, sfiA and sfiB, cotransducible respectively with pyrD and leu. In the remaining 5% of revertants that still exhibit an UV-induced filamentous growth, 3% can be tentatively classified as true tif+ revertants; 2% behave as tif thermodependent revertants, showing suppression of the Tif (and Lon) phenotype only at 41 degrees: 2recAts have been identified in this class. Non-lysogenic tif lon sfi and tif sfi strains remain viable during prolonged growth at 41 degrees. Under these conditions, tif expresses mutator properties, which can be conveniently analyzed in this sfi background. The action of lif, lon and sfi mutations is tentatively interpreted on the basis of a negative control of cell division specifically associated with DNA repair.

Cell Division↗
PubMed1975

Recovery of phage lambda from ultraviolet damage.

Recovery of phage lambda from ultraviolet damage can occur, in the dark, through three types of repair processes as defined by microbiological tests: (1) host-cell reactivation, (2) prophage reactivation, and (3) UV reactivation. This paper reviews the properties of the three repair processes, analyzes their dependence on the functioning of bacterial and phase genes, and discusses their relationship. Progress in the understanding of the molecular mechanisms underlying the three repair processes has been relatively slow, particularly for UV reactivation. It has been shown that host-cell reactivation is due to pyrimidine dimer excision and that prophage reactivation is due to genetic recombination (prereplicative). We provide evidence showing that neither of these mechanisms accounts for UV reactivation of phage lambda. Furthermore, UV reactivation differs from the other repair processes in that it is inducible and error-prone. Whether UV-damaged bacterial DNA is subject to a similar repair process is still an open question.

Cell Survival↗
PubMed1974

Indirect ultraviolet-reactivation of phage lambda.

When an F(-) recipient Escherichia coli K12 bacterium receives Hfr or F-lac(+) DNA from an ultraviolet-irradiated donor, its capacity to promote DNA repair and mutagenesis of ultraviolet-damaged phage lambda is substantially increased. We call this phenomenon indirect ultraviolet-reactivation, since its features are essentially the same as those of ultraviolet-reactivation; this repair process occurs in pyrimidine dimer excision-deficient strains and produces clear plaque mutations of the restored phage. Moreover, this process is similar to indirect ultraviolet-induction of prophage lambda, since it is promoted by conjugation. However, contrarily to indirect induction, it is produced by Hfr donors and occurs in recipients restricting the incoming ultraviolet-damaged donor DNA. The occurrence of indirect ultraviolet-reactivation provides evidence for the existence in E. coli of an inducible error-prone mechanism for the repair of DNA.

Coliphages↗