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Biomedical subjects

M Baron

Publications and source records attributed to M Baron.

At least 163 records · Page 9Linked to original sources
PubMed1987

Phleomycin resistance encoded by the ble gene from transposon Tn 5 as a dominant selectable marker in Saccharomyces cerevisiae.

Phleomycin, a water-soluble antibiotic of the bleomycin family is as effective against Saccharomyces cerevisiae cells as against Escherichia coli cells. The ble gene of transposon Tn5, which confers resistance to phleomycin, was inserted in place of the iso-1-cytochrome C (CYC1) gene on an autonomously replicative multicopy E. coli-yeast shuttle plasmid. Higher resistance levels are obtained in S. cerevisiae when the region immediately upstream from the initiation codon conforms to the nucleotide sequence stringencies observed in almost every yeast gene. The expected regulation pattern of the whole CYC1 promoter confers different phleomycin resistance levels to the cell under varying physiological conditions. Partial deletions in the CYC1 promoter lead to changes in the resistance level of cells which are mostly accounted for by the removal of known positive and negative regulatory elements. Some of the vector constructions allow direct selection of phleomycin-resistant transformants on rich media.

Bleomycin↗
PubMed1987

The spectrum concept of schizophrenia: evidence for a genetic-environmental continuum.

Family data from 84 chronic schizophrenic, 11 schizotypal and 90 normal control probands were analyzed by multivariate-multifactorial genetic models using morbid risk statistics. The results were consistent with multifactorial inheritance whereby chronic schizophrenia and schizotypal personality disorder represent different phenotypic manifestations of the same underlying process; that is, the two disorders were found to have different thresholds on a single continuum of genetic-environmental liability. When subclassified according to Taylor and Abrams' criteria, chronic schizophrenic subjects who met these criteria (narrow schizophrenia) had a higher threshold of liability than those who did not (broad schizophrenia). The hypothesis of separate liabilities for the different disease states was rejected. Overall, the results suggest a gradation in multifactorial liability from schizotypal personality disorder (mild) to broad schizophrenia (moderate) to narrow schizophrenia (severe).

Adult↗
PubMed1987

Platelet 3H-imipramine binding and familial transmission of affective disorders.

We studied platelet 3H-imipramine binding and family history of affective illness in 26 patients with bipolar affective disorder and 24 patients with unipolar affective disorder. The density of platelet 3H-imipramine binding sites (Bmax) was significantly lower in bipolar patients with family history of affective illness than in healthy controls; however, there was a considerable overlap in Bmax values between the familial cases and the normal controls. A similar trend was observed in familial cases of unipolar disorder but the differences fell short of statistical significance. The nonfamilial cases of affective disorder did not differ from the healthy controls. The possible role of reduced platelet 3H-imipramine binding as a genetic vulnerability 'marker' in affective disorder was discussed.

Adult↗
PubMed1987

Hand function in the elderly: relation to osteoarthritis.

Hand function and osteoarthritis (OA) were assessed in 32 subjects, over 60-years-old. The Smith Hand Function Test bore a relation to age, coordination and hand strength but not to the degree of OA. Hand strength also was not related to OA. Subjective hand disability, measured with the Stanford Health Assessment Questionnaire, correlated with radiographic OA and joint tenderness as well as with sex and hand strength. OA does not contribute significantly to the objective decline in hand function in the elderly but may contribute to a subjective sense of functional limitation.

Aged↗
PubMed1986

Genetics of schizophrenia: II. Vulnerability traits and gene markers.

The author reviews research strategies for identifying biological vulnerability traits and gene markers. The application of these methods to schizophrenia are discussed. He concludes that, based on the available evidence, none of the proposed biological traits qualifies as a major factor in the genetic susceptibility to schizophrenia. Some of these traits (such as attentional, neurophysiological, and brain morphology measures) appear promising, but the data are inadequate to arrive at a firm conclusion. Studies with gene markers have not produced consistent results. The author presents the methodological issues that concern this area of research and offers recommendations for future studies.

Genetic Markers↗
PubMed1986

Modification of ligand binding to membranes by a soluble acceptor. Alpha-1-acid glycoprotein attenuates 3H-imipramine binding to cerebral membranes.

The effect of individual plasma proteins on the binding of 3H-imipramine (3H-IMI) was investigated, using rat cerebral membranes as the binding site source. Addition of alpha-1-acid glycoprotein (aAGLP) to an incubation medium containing 4 nm 3H-IMI resulted in a concentration-dependent inhibition of 3H-IMI binding, with an IC50 value of 0.53 microM. Albumin (0.7 mM) and gamma globulin (3 microM) had no apparent effect. Scatchard analyses of 3H-IMI binding in the presence and absence of 0.5 microM aAGLP revealed that the inhibition of 3H-IMI binding was associated with an increased Kd, with no appreciable change in Bmax. The inhibitory action of platelet-free plasma (PFP) on 3H-IMI binding to cerebral membranes was eliminated after treatment of PFP with specific antibodies to aAGLP. It is suggested that the inhibition of 3H-IMI binding to cerebral membranes by PFP is due, at least partially, to the presence of aAGLP in the plasma. The observed inhibitory effect is consistent with a competition for the ligand between the membrane binding site and the soluble protein acceptor. These findings may explain the serum effect confounding radioreceptor assays of various drugs.

Animals↗
PubMed1986

Genetics of schizophrenia: I. Familial patterns and mode of inheritance.

The purpose of this article is to review and condense the available literature on genetic modeling in schizophrenia research. The principles underlying genetic models and the various applications of these models to family data are reviewed. It is concluded that despite the advances in statistical genetics, the mode of inheritance of schizophrenia remains elusive. The conflicting results are attributed to variation in methods for data collection and analysis and to the heterogeneous nature of the disorder. The possibility is also raised that most previous genetic analyses of schizophrenia may have been compromised by methodological drawbacks. Although the use of advanced genetic models in conjunction with adequate data may shed more light on the genetic contribution to schizophrenia, the limitations of this approach in genetically heterogeneous disorders must be recognized. Alternative methods, such as studies with biological susceptibility traits and genetic markers, may be more useful in unraveling the specific genetic components that underlie the transmission of schizophrenia.

Genetic Counseling↗
PubMed1986

The horizontal cells in the retina of the owl, Tyto alba, and owlet, Carinae noctua.

One type of short-axon horizontal cell (HC) and one type of axonless HC are described in the retina of Carinae noctua, a crepuscular bird and Tyto alba, a pure nocturnal bird. The axonless HCs in both birds are similar to type II axonless HC found in diurnal birds. The short-axon HC of Carinae noctua is similar to the same cell type found in diurnal birds; the only difference being the axon length. The short-axon HC of the Tyto alba retina is morphologically different from the same cell type found in the retina of diurnal birds and Carinae noctua and very similar to the short-axon HC described in the mammalian retina and the primate retina in particular. The striking similarity between the short-axon HCs found in the retina of owl and primates may be related to the same rod-cone ratio found in these retinas.

Animals↗
PubMed1986

Assessing the role of X-linked inheritance in bipolar-related major affective disorder.

Data from a family study of bipolar affective illness in New York (1968-1972) are reexamined from the vantage point of X-linked dominant inheritance and genetic heterogeneity. For comparison, published data from a similar study in Bethesda (1974-1979) and from a literature summary are also re-analyzed. The New York data support the presence of a change in rates of affective illness over time (secular trend), with a substantial increase in risk at early ages for individuals born after 1920. Hence, risk ratios by sex of proband (male vs female) are calculated for each type of relative, thereby controlling simultaneously for generation and sex of relative. The risk ratios for all three studies are in the direction predicted by X-linkage. In addition, logistic regression is performed, incorporating the effects of generation, sex of relative, sex of proband, and X-linkage. In all three samples, the largest effect is due to X-linkage, which reaches statistical significance in the New York and literature summary samples. The results also suggest genetic heterogeneity, in that only a subgroup of bipolars carry the X-linked gene. Crude estimates predict that perhaps one-third of bipolars carry the X-linked gene. Analysis of the New York material also indicates that an X-linked subgroup may be associated with early onset (before 30 years old). These results are consistent with those from linkage analysis with markers on the long arm of the X chromosome.

Adult↗
PubMed1986

Inhibition of 3H-imipramine binding by plasma from depressed and normal subjects.

The inhibition by human plasma of 3H-imipramine (3H-IMI) specific binding to rat cerebral membranes was investigated using platelet-free plasma (PFP) from normal and depressed subjects. The specific binding of 3H-IMI at a ligand concentration of 4 nM decreased with increasing PFP volumes, reaching 50% inhibition following the addition of 10-13 microliters PFP to a final incubation volume of 250 microliters. The extent of this inhibition was the same using PFP from controls or depressed patients. The inhibitory activity was associated with plasma proteins. Scatchard analysis of 3H-IMI binding in the presence and absence of PFP indicated that the inhibitory effect was associated with an increased Kd without an appreciable change in Bmax. It is suggested that an endogenous acceptor in the PFP, such as alpha 1-acid-glycoprotein may be responsible for the observed inhibition of 3H-IMI binding to the cerebral membranes.

Adolescent↗
PubMed1986

Platelet [3H]imipramine binding in affective disorders: trait versus state characteristics.

Platelet [3H]imipramine binding (Bmax) was determined in 67 patients with major affective illness (33 euthymic bipolar, 34 depressed unipolar) and 58 normal control subjects. Bipolar patients had significantly lower Bmax values than did control subjects. The mean Bmax in the unipolar patients was lower than in the control subjects, but the difference was not statistically significant. Dissociation constant (Kd) values did not distinguish patients in either category from control subjects. The significantly lower Bmax in euthymic bipolar patients and the apparent state independence of Bmax in some but not all unipolar patients suggest that platelet imipramine binding may be a trait marker in a subset of affective disorders.

Adult↗
PubMed1985

Effect of membrane protein concentration on binding of 3H-imipramine in human platelets.

Binding of 3H-imipramine to platelet membranes has been implicated as a marker for depression. Comparing 3H-IMI binding between depressed patients and normal subjects we observed an increase in the dissociation constant Kd with increasing membrane protein. This phenomenon was studied more rigorously in five normal subjects. Platelet membranes were prepared and adjusted to four concentrations of protein ranging from 100 to 800 micrograms/ml. The 3H-IMI binding parameters of maximum binding sites number (Bmax) and Kd were obtained by Scatchard analysis at each membrane concentration. A positive linear relationship was found between Kd values and the concentration of membrane protein in the assay, but no change was observed in Bmax. The variability in Kd values reported in the literature may be accounted for in part by the different concentrations of membrane protein used in various studies.

Adult↗
PubMed1985

Platelet monoamine oxidase activity in patients with panic disorder.

Preliminary reports have indicated that platelet monoamine oxidase (MAO) activity is elevated in patients with anxiety disorder. We compared MAO activity in 20 drug-free patients with panic disorder with 20 age- and sex-matched normal controls. MAO activity in patients was significantly higher than in normals. MAO activity was not correlated with age or plasma catecholamine levels. The authors speculate about the possible significance of elevated MAO activity in patients with panic disorder.

Adult↗