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A Cohen

Publications and source records attributed to A Cohen.

At least 721 records · Page 40Linked to original sources
PubMed1985

The myosin alkali light chains of mouse ventricular and slow skeletal muscle are indistinguishable and are encoded by the same gene.

We have isolated a cDNA recombinant plasmid (pA29) identified as encoding part of the ventricular muscle myosin light chain MLC1v. This cDNA contains a 300-base pair fragment which under conditions of moderate stringency shows specific hybridization to MLC1v mRNA with no detectable cross-hybridization with the mRNAs encoding the fast skeletal muscle isoforms MLC1F and MLC3F, or the atrial muscle isoform MLC1A. Under these conditions hybridization is seen with an abundant mRNA present in slow skeletal muscle (soleus) which is indistinguishable from ventricular MLC1V mRNA on the basis of size and of thermal stability of hybrids formed with plasmid pA29. The mouse MLC1V and MLC1S proteins are found to co-migrate on two-dimensional gels. We therefore conclude that these isoforms are the same and are encoded by the same mRNA. Analysis of mouse DNA has identified a single region of the genome which hybridizes to this same fragment of pA29. This region has been isolated in a recombinant phage and has been shown to contain a single gene showing homology with MLC1V mRNA by R-loop analysis. We therefore conclude that MLC1V and MLC1S are encoded by a single gene. The pattern of segregation of a restriction fragment length polymorphism identified for this gene between Mus musculus and Mus spretus has been followed in an F1 backcross between these two mouse species. The results show the MLC1V/MLC1S gene to be closely linked to a marker at the distal end of mouse chromosome 9.

Animals↗
PubMed1985

Evidence for distinct catabolic pathways for deoxy-GTP and GTP in purine-nucleoside phosphorylase-deficient mouse T lymphoblasts.

The catabolism of deoxy-GTP and GTP was compared in purine-nucleoside phosphorylase-deficient mouse T lymphoblasts. It was found that guanine ribonucleotides and deoxyribonucleotides are degraded by distinct pathways in cells cultured under both physiological and induced catabolic conditions. In T lymphoblasts, cultured under physiological conditions, 50% of the GMP formed during GTP catabolism was dephosphorylated and 50% was deaminated, whereas in the presence of the catabolic inducer deoxyglucose 90% of the GMP formed was dephosphorylated and only 10% was deaminated. These results indicate that GTP catabolism in lymphoblasts proceeds by alternative pathways, either via GMP dephosphorylation or via GMP reductive deamination, and physiological conditions determine with pathway will be used. In contrast, deoxy-GTP catabolism proceeds exclusively via deoxy-GMP dephosphorylation under both physiological and induced catabolic conditions. The lack of deoxy-GMP deamination may contribute to the accumulation of cytotoxic levels of deoxyguanosine found in purine-nucleoside phosphorylase-deficient patients.

Animals↗
PubMed1985

The graded and quantal nature of opioid analgesia in the rat tailflick assay.

Opioid agonists routinely increase the latency to respond in the rodent tailflick assay. The nature of this effect was investigated in 5 experiments using several parametric variations and routes of administration. Morphine and methadone were found to produce both quantal and graded effects in all experiments. In cases where quantal effects were observed, the majority of animals also responded in a graded manner during subsequent testing. The increase in latency to respond in the tailflick assay produced by opioid agonists is not accurately characterized as predominantly quantal.

Animals↗
PubMed1985

Anticonvulsant properties of 3-hydroxy-2-quinoxalinecarboxylic acid, a newly found antagonist of excitatory amino acids.

Various aromatic acids have been investigated as putative ligands of excitatory amino acid receptors. 3-Hydroxy-2-quinoxalinecarboxylic acid (HQC), at 1 mM, was found to antagonize the 22Na+ efflux produced in 22Na+-preloaded brain slices by N-methyl-D-aspartate and kainate. The response to glutamate was also affected but not that to quisqualate. The apparent KI value of HQC for suppression of the N-methyl-D-aspartate response was 0.27 mM. The anticonvulsant action of HQC was investigated in mice and rats. HQC administered intracerebroventricularly caused a dose dependent delay in the occurrence of picrotoxin induced convulsions and afforded protection against picrotoxin induced death. These results confirm the proposition that antagonists of excitatory amino acids possess anticonvulsant properties.

Animals↗
PubMed1985

Co-mitogenic tumor promoters suppress the phosphatidylinositol response in lymphocytes during early mitogenesis.

The tumor-promoting agents 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and phorbol-12,13-dibenzoate inhibited the increased accumulation of [32P]phosphatidylinositol (PI) induced in mouse spleen lymphocytes by mitogenic lectins in the presence of [32P]orthophosphate. Similar inhibition of [32P]PI levels by TPA was seen in human tonsil T-lymphocytes stimulated with phytohemagglutinin. Only co-mitogenic phorbol esters prevented the [32P]PI accumulation during early mitogenesis. No increased 32P-labelling due to mitogen or decreases due to TPA was observed when cells were equilibrated with [32P]orthophosphate for 24 h prior to stimulation with mitogen, from which it is concluded that the total concentrations of phosphatidylcholine (PC) and PI are unaffected by mitogen or co-mitogen. The [32P]PI elevation but not the [32P]PC elevation was proportional to T-cell mitogenic potency for the lectins concanavalin A, divalent succinyl concanavalin A and phytohemagglutinin, and was prevented in each case by 5 X 10(-8) M TPA. Escherichia coli lipopolysaccharide did not give increased 32P incorporation into PI or PC, and TPA had no effect on 32P labelled phospholipid levels in the presence of this B-cell mitogen. The results indicate that the phosphatidylinositol response is not an invariable correlate of T-cell mitogenesis by polyclonal mitogens.

Animals↗
PubMed1985

Attentional deficit disorder and short-term visual memory.

Twenty-four children with Attentional Deficit Disorder (ADD) were compared to a control group of 17 children with emotional problems. All the subjects were tested on the Wechsler Intelligence Scale for Children-Revised (WISC-R), along with an adaptation of the Coding subtest to measure short-term visual memory. The results showed superiority of the control group on the short-term visual memory task. The correlations of short-term visual memory with each of the subtests of the WISC-R were different for each group. For the emotional group short-term visual memory correlated significantly with the WISC-R verbal scores, while in the ADD group visual memory more often significantly correlated with performance subtests. In the discussion an attempt was made to explore the reasons for these differences and their implications for academic tasks.

Adolescent↗
PubMed1985

Purine nucleotide metabolism in resident and activated rat macrophages in vitro.

The overall purine metabolism was studied in detail in resident peritoneal macrophages (M phi) and in thioglycolate elicited peritoneal M phi in vitro. The salvage of purine bases (adenine, hypoxanthine and guanine) was active in both M phi populations, whereas purine biosynthesis de novo was low. Purine nucleosides (inosine, guanosine and adenosine) were efficiently degraded to uric acid and only adenosine was directly salvaged into nucleotides. Purine salvage was markedly increased in elicited M phi as compared to resident M phi whereas purine degradation pathways were enhanced only slightly. These results clearly indicate that salvage of purine bases is the main source for purine nucleotide biosynthesis in M phi, but nucleotide catabolism is the predominant pathway.

Adenine↗
PubMed1985

Characterization of mouse lymphoma cells with altered nucleoside transport.

A mutant clone (NT-1) of a T-cell lymphoma was selected for its ability to grow in HAT medium (hypoxanthine, aminopterin and thymidine) in the presence of the nucleoside transport inhibitor P-nitrobenzyl-6-mercaptoinosine (NBMI). NT-1 cells contain half the number of NBMI binding sites present on the parental S49 cells and are partially able to transport nucleosides in the presence of the transport inhibitor (NBMI). These observations suggest that the mutant cells are heterozygous for nucleoside transport proteins and contain two types of transport proteins: the first protein can both bind and is inhibited by NBMI similar to the wild type phenotype, and the second is an altered protein. The altered transport protein apparently lost its NBMI binding sites without a parallel loss of nucleoside transport ability suggesting that the nucleoside transported sites are separate from the binding sites of the transport inhibitor.

Adenosine↗
PubMed1985

Analysis of the drug synergism between thymidine and arabinosyl cytosine using mouse S49 T lymphoma mutants.

The synergism between arabinosyl cytosine (araC) and thymidine is characterized using two mutant S49 T lymphoma cell populations with altered deoxyribonucleotide metabolism. AraC-1-6 cells are deficient in dCMP deaminase activity resulting in a secondary elevation of intracellular dCTP pools, whereas dGuo-200-1 cells have a mutation in the Ml subunit of ribonucleotide diphosphate reductase, which also results in elevation of dCTP levels. These two mutant cell populations are partially resistant to araC cytotoxicity as compared to the wild type cells. The resistance to araC is contributed to the elevation of dCTP levels in these mutants which prevent araC incorporation into the DNA due to feedback inhibition of deoxycytidine kinase. Addition of extracellular thymidine to dCMP deaminase deficient cells causes a decrease in dCTP levels and in parallel increase their sensitivity to araC. In contrast, extracellular thymidine does not reduce dCTP levels in the mutant cells with altered ribonucleotide reductase and no synergism between araC and thymidine is observed in these cells. The expansion of dTTP pools in the presence of thymidine is similar in the two mutants. These results suggest that the depletion of dCTP pools by thymidine is responsible for the synergistic action of thymidine on araC cytotoxicity and that dTTP does not directly enhance the incorporation of araC into the DNA of T lymphoma cells.

Animals↗
PubMed1985

Rubella virus RNA: effect of high multiplicity passage.

Evidence for the amplification of defective interfering particles of rubella virus after passage at high multiplicity has been obtained. The process is associated with the production of subgenomic rubella RNA species.

Animals↗