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Biomedical subjects

A Cohen

Publications and source records attributed to A Cohen.

At least 577 records · Page 32Linked to original sources
PubMed1990

Lexical priming deficits as a function of age.

The effects of age on implicit memory were assessed in elderly young adults using 2 priming procedures. Subjects also completed the WAIS-R, 3 tests to assess frontal lobe function, and 2 recall and 2 recognition tests of explicit memory. In Experiment 1, subjects were exposed to the low-frequency member of a homophone pair in a test purported to assess general knowledge. Subsequently, subjects completed a spelling test that contained the previously presented homophones to assess priming. Young subjects demonstrated priming (p less than .01). Elderly subjects demonstrated a high baseline that may have obscured priming. In Experiment 2, subjects from each decade of life from the 20s through the 80s were given a word-stem completion test of priming. All age conditions demonstrated an effect of priming (p less than .01). However, subjects in their 70s and 80s demonstrated lower priming scores (p less than .05). Elderly subjects were also impaired on immediate-and delayed-recall tests. These results suggest an age-related decline in both implicit and explicit memory.

Adolescent↗
PubMed1990

Extensive nuclear lobulation in the cells of a patient with acute myelomonocytic leukemia. The role of electron microscopy for establishment of a correct diagnosis.

Extensive nuclear convolution and lobulation was found in the peripheral blood cells of a patient with acute leukemia. While the morphology of the cells, such as observed with the light microscope, was compatible with the diagnosis of acute myeloid leukemia, the finding of Sezary-like cells with the electron microscope helped to establish the diagnosis of acute myelomonocytic leukemia. This report emphasizes the importance of the electron microscope for the correct diagnosis of leukemias.

Aged↗
PubMed1990

Changes in amniotic fluid concentrations of prostaglandins E2 and F2 alpha in women with preterm labor.

There is a paucity of data regarding the concentration of prostaglandins (PGs) in the amniotic fluid of women with preterm labor. The purpose of this study was to determine if preterm labor is associated with changes in amniotic fluid concentration of prostaglandins E2 and F2 alpha. Amniotic fluid was retrieved by transabdominal amniocentesis from women with preterm labor and intact membranes. Patients were classified into three groups according to the response to tocolysis and the presence or absence of intra-amniotic infection. PGE2 and PGF2 alpha were measured using specific and sensitive RIA kits. Amniotic fluid concentrations of PGE2 and PGF2 alpha were significantly higher in women with preterm labor and intra-amniotic infection than in women without infection, regardless of the response to tocolysis. These data suggest that both PGs are involved in the mechanism of preterm labor and may have prognostic value.

Amniotic Fluid↗
PubMed1989

Depletion of CD8+ cells in human thymic medulla results in selective immune deficiency.

CD8 molecules expressed on the surface of a subset of T cells participate in the selection of class I MHC antigen-restricted T cells in the thymus, and in MHC-restricted immune responses of mature class I MHC antigen-restricted T cells. Here we describe an immune-deficient patient with lack of CD8+ peripheral blood cells. The patient presented with Pneumocystis carinii pneumonia and was unable to reject an allogeneic skin graft, but had normal primary and secondary antibody responses. Examination of the patient's thymus revealed that the loss of CD8+ cells occurred during intrathymic differentiation: the patient's immature cortical thymocytes included both CD4+ and CD8+ cells while the mature medullary cells expressed the CD4 but not the CD8 protein on their surface. Northern blot and polymerase chain reaction analyses revealed the presence of CD8 alpha and beta mRNA in the patient's thymus but not in the peripheral blood. Both class I MHC antigen expression and the expressed TCR V beta repertoire are normal in this patient. These data are consistent with an impaired selection of CD8+ cells in the patient's thymus and support the role of the CD8 surface protein in thymic selection previously characterized in genetically manipulated and inbred mice.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1989

Rearrangements in the p53 gene in Philadelphia chromosome positive chronic myelogenous leukemia.

Molecular structural analysis of the p53 gene in patients with Philadelphia chromosome-positive chronic myelogenous leukemia (CML) indicates a significant incidence of gene rearrangements in patients at either accelerated phase or blastic crisis. Southern blot analysis of genomic DNA hybridizing with either genomic or cDNA p53 specific probes indicated that 30% of the CML patients at blastic crisis phase exhibited rearrangements, mostly mapping downstream to the first non-coding exon. This is compatible with the observation that the progression of CML from the chronic to the acute phase involves frequent aberrations in chromosome 17, to which the p53 oncogene has been mapped. Therefore, we suggest that one of the pathways of development of CML to the acute phase is associated with aberrations in the p53 nuclear oncogene.

Blast Crisis↗
PubMed1989

Establishment and characterization of adenosine deaminase-deficient human T cell lines.

We have established long term cell lines from a patient with adenosine deaminase (ADA)-deficient severe combined immunodeficiency by stimulation of blood and bone marrow cells with PHA and IL-2 followed by transformation of the activated cells with the human retrovirus HTLV-I. Despite the absence of detectable T cells in the patients blood, cell lines grew that carried the phenotype of mature activated T cells. TJF-2, the line established from blood, was characterized in detail. The concentration of ADA in TJF-2 cells was less than 1% of normal (3.2 U vs 413.0 U). Studies with pharmacologic inhibitors of ADA suggest that the residual adenosine deaminating activity of TJF-2 is from an enzyme distinct from true ADA, a nonspecific aminohydrolyase. Growth of TJF-2 cells was hypersensitive to inhibition by 2'-deoxyadenosine compared to normal T cells (ID50, 55 microM vs greater than 1000 microM). Analysis of 2'-deoxyadenosine-challenged cells showed that TJF-2 cells accumulated significant levels of deoxyadenosine triphosphate, whereas normal T cells did not unless they were also incubated with the ADA inhibitor deoxycoformycin. Southern and Northern blot analysis of these cells revealed a grossly intact ADA gene that produced a normal size ADA mRNA. Yet, despite ADA deficiency, cells of the TJF-2 line were otherwise indistinguishable from HTLV-I-transformed T cells derived from normal donors with respect to dependence on exogenous IL-2 for growth, clonal rearrangement patterns of TCR beta-chain genes, response to PHA, and rapid restoration of cellular volume after hypotonic challenge. The TJF-2 line thus represents a unique HTLV-I-transformed human T cell line exhibiting ADA deficiency and its expected metabolic consequences.

Adenosine Deaminase↗
PubMed1989

Long-term effect of splenectomy on transfusion requirements in thalassemia major.

Splenectomy reduces transfusion requirements in the first year after surgery in patients with thalassemia major and hypersplenism. To determine whether this response is maintained, we have studied transfusion requirements in 16 patients with thalassemia major for 2-17 years after splenectomy. Transfusion requirements remained stable (mean yearly change -0.1%) after the predictable fall in the first year after surgery. The mean change between the first postoperative year and the most recent year was -7 ml/kg. Transfusion requirements and the magnitude of change from year to year were unrelated to the time since splenectomy. These studies indicate that the effect of splenectomy on transfusion requirements is long-lasting and that large variations in annual transfusion requirements after splenectomy should prompt a search for accessory spleens or other causes of red cell destruction.

Adolescent↗
PubMed1989

Absolute bioavailability and noncompartmental analysis of intravenous and intramuscular Cefotan (cefotetan) in normal volunteers.

Cefotetan (1 g) was administered to 12 normal volunteers as a 30 minute intravenous infusion and as an intramuscular injection. The pharmacokinetic parameters were estimated using noncompartmental analysis. The mean +/- SD maximum plasma concentration, terminal half-life, and systemic clearance after intravenous infusion were 158 +/- 21 micrograms/mL, 4.54 +/- 1.05 hours, and 29.1 +/- 3.8 mL/min/1.73 m2, respectively. Renal clearance and nonrenal clearance accounted for 63.1% and 36.9% of the systemic clearance, respectively. The mean +/- SD maximum plasma concentration, time to maximum concentration, terminal half-life, and absolute bioavailability after intramuscular injection were 75.5 +/- 8.7 micrograms/mL, 1.33 +/- 0.48 hours, 4.32 +/- 0.77 hours, and 0.931 +/- 0.193, respectively. Moment analysis gave average +/- SD mean residence times (MRT) of 4.98 +/- 0.75 and 5.86 +/- 0.77 hours after intravenous and intramuscular administration, respectively. The average +/- SD mean absorption time (MAT) after intramuscular injection was 1.11 +/- 0.57 hours. The mean +/- SD steady-state volume of distribution after intravenous infusion was 0.129 +/- 0.024 L/kg. The mean +/- SD cumulative percentage of the dose excreted in the urine in 24 hours were 61.1 +/- 11.4% and 50.4 +/- 13.5% after intravenous and intramuscular dosing, respectively. The maximum urinary cefotetan concentrations occurred during the first 2 hours after dosing by both routes of administration. Cefotetan tautomer was detected in the plasma and urine of all subjects after both routes of administration, but the mean concentrations were only minimal compared to those for cefotetan. In conclusion, intramuscular cefotetan (1 g) is rapidly and almost completely absorbed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Conditioned media of regenerating fish optic nerves modulate laminin levels in glial cells.

Adult injured optic nerves of mammals show an increased distribution of laminin in the extracellular matrix after application of soluble substances in the form of conditioned media originating from growing nerves (Zak, et al., 1987). This increase could result from direct or an indirect activation of glial cells or from activation of other cellular elements. In the present study, we show that the conditioned media derived from regenerating fish optic nerves contain factors that directly modulate the level of laminin in C-6 glioma cells. The identity of the laminin was confirmed by metabolic labeling of the treated cells with [35S]methionine and by subsequent immunoprecipitation and gel electrophoresis. The level of other extracellular matrix proteins, such as fibronectin, is also increased. The significance of the presence of glial-activating substances in the conditioned media of regenerating nerves for the process of regeneration is discussed.

Culture Media↗
PubMed1989

Comparison of correlated correlations.

We consider a problem where kappa highly correlated variables are available, each being a candidate for predicting a dependent variable. Only one of the kappa variables can be chosen as a predictor and the question is whether there are significant differences in the quality of the predictors. We review several tests derived previously and propose a method based on the bootstrap. The motivating medical problem was to predict 24 hour proteinuria by protein-creatinine ratio measured at either 08:00, 12:00 or 16:00. The tests which we discuss are illustrated by this example and compared using a small Monte Carlo study.

Humans↗
PubMed1989

Chromosomal assignment of two myosin alkali light-chain genes encoding the ventricular/slow skeletal muscle isoform and the atrial/fetal muscle isoform (MYL3, MYL4).

In all eukaryotes, myosin plays a major role in the maintenance of cell shape and in cellular movement; in association with actin and other contractile proteins it is also a major structural component of the muscle sarcomere. Several isoforms of myosin alkali light chain have been identified, associated with different muscle types. We have recently localized the gene encoding the fast skeletal muscle alkali light-chain isoforms MLC1F and MLC3F (HGM symbol, MYL1) to human chromosome 2q32.1-qter (Cohen-Haguenauer 1988). We present here the chromosomal assignment of two loci encoding the ventricular muscle isoform MLC1V (equivalent to the slow skeletal muscle isoform MLC1Sb) and the atrial muscle isoform MLC1A (equivalent to the fetal isoform MLC1emb) using a panel of 25 independent man-rodent somatic cell hybrids. The MLC1V gene (HGM symbol, MYL3) was mapped to human chromosome 3 using a human full-length cDNA probe that hybridizes to a single major human TaqI2.8-kb fragment. The MLC1A probe (HGM symbol, MYL4) was a 360-bp mouse cDNA fragment that gave a distinct signal with human DNA using low stringency conditions of hybridization and washings and after presaturation of the Southern blots with rodent DNA. A single PstI 7.8-kb fragment gives an intense signal, and its presence correlates with the presence of chromosome 17 among the hybrids. These data are in keeping with the localizations of the MLC1V gene to mouse chromosome 9, and of the MLC1A gene to mouse chromosome 11, which share some markers in common with human chromosomes 3 and 17 respectively.

Animals↗
PubMed1989

Inflammatory competence of fetal rat: acute-phase plasma protein response of the fetus treated by turpentine in utero.

Using crossed immunoelectrophoresis, immunoelectrodiffusion, autoradiography, and equilibrium binding techniques, we demonstrate that the rat fetus, directly challenged in utero at 18 days by a single subcutaneous turpentine injection, presents a complex acute-phase plasma inflammatory response. A number of fetal serum proteins, 48 h after the injection, increase in concentration by factors of about 2-5. These positive acute-phase reactants (APR) are alpha 1-acute-phase globulin (alpha 1-AP), alpha 2-macroglobulin (alpha 2-M), alpha 1-acid glycoprotein (alpha 1-AG), haptoglobin (Hp), and hemopexin (Hpx). A number of proteins decrease, behaving like negative APRs. These are albumin, alpha 1-fetoprotein (AFP), transferrin, GHR-P63, thyroxine-binding prealbumin (TBPA), and transcortin (CBG). The marked fall in concentration of two of the high-affinity hormone-binding proteins of the fetal rat, i.e., the estrophilic AFP and TBPA, induce significant decreases (by 25-40%) of the estrogen- and thyroxine-binding abilities of the fetal serum. While the plasma inflammatory response of the fetus is qualitatively similar to that of the adult, the fetal reactions are, as a rule, quantitatively weaker. The characteristics of the plasma inflammatory response of the fetus are discussed in relation to the highly dynamic state of its development.

Acute-Phase Proteins↗