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Biomedical subjects

S S Shapiro

Publications and source records attributed to S S Shapiro.

At least 19 recordsLinked to original sources
PubMed1992

Tumor necrosis factor-alpha modulation of glycoprotein Ib alpha expression in human endothelial and erythroleukemia cells.

Glycoprotein Ib alpha (GpIb alpha) is a platelet membrane Gp that binds von Willebrand factor and mediates platelet adhesion to subendothelium. We have found both GpIb alpha mRNA and protein in human umbilical vein endothelial cells (HUVEC). In previously published work we reported that combined treatment with interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) markedly increased the GpIb alpha mRNA level in HUVEC. We have now documented that TNF-alpha alone induces GpIb alpha mRNA and protein expression, studied the kinetics of this response, and investigated potential mechanisms of the TNF-alpha effect. GpIb alpha mRNA induction by TNF-alpha is detectable as early as 2 hours after exposure to this cytokine, and reaches a maximal level after 20 to 24 hours. Using a nuclear run-on assay we found that GpIb alpha gene transcription is increased approximately 10-fold after 2 hours of TNF-alpha treatment. Furthermore, using two monoclonal antibodies that recognize different epitopes of GpIb alpha, we found that the protein expression in endothelial cells is markedly increased by TNF-alpha. Interleukin-1 (IL-1) and the phorbol ester phorbol myristate acetate, which mimic many effects of TNF-alpha on endothelial cells, have no effect on endothelial or human erytholeukemia (HEL)-cell GpIb alpha mRNA. TNF-alpha treatment for 24 hours increases the HEL cell GpIb alpha mRNA level approximately fourfold, showing a time- and dose-dependent effect similar to that seen in HUVEC. TNF-alpha-induced GpIb alpha mRNA and protein synthesis may play a role in mediating platelet or other cell interaction with activated endothelium. Unlike other endothelial pro-thrombotic and pro-adhesive proteins induced by TNF-alpha, GpIb alpha is not induced by IL-1 treatment, which suggests a novel pathway for induction of this protein.

Blotting, Western↗
PubMed1992

Longitudinal study of semen quality in Wisconsin men over one decade.

To determine whether there has been a time-related change in semen quality, we examined a Wisconsin population of men over a 10-year period. The semen quality of potential sperm donors was assessed between the years 1978 and 1987. The semen analyses included sperm concentration, motility, and morphology. No significant changes over time were observed for sperm concentration or motility. The percentage of morphologically abnormal sperm rose sharply between 1982 and 1983. This, however, coincided with a change in criteria used to identify abnormal sperm, and was, therefore, due to a procedural artifact. In summary, we found no evidence of a decline in semen quality in our Wisconsin population over a 10-year period.

Humans↗
PubMed1979

The value of hysterosalpingography prior to donor artificial insemination.

The value of hysterosalpingography as a tool in the pretreatment evaluation of candidates for donor artificial insemination has been retrospectively evaluated. In 89 consecutive artificial inseminations by donor candidates, hysterosalpingograms were evaluated for genital tract abnormalities. In only four of these studies was there a failure of dye to spill into the peritoneal cavity. The low incidence of significantly abnormal hysterosalpingographic studies, and the failure of these studies to correlate with pregnancy outcome, strongly argues against the use of hysterosalpingography in the preliminary evaluation of the patient considered for donor artificial insemination.

Adult↗
PubMed1979

Genetic causes and workup of male and female infertility. 1. Prenatal reproductive loss.

Studies show that the greatest check on human reproduction occurs prenatally in apparently fertile couples. Most chromosomally abnormal embryos are aborted spontaneously. This paper, to be published in three parts, reviews the major known anatomic, functional, genetic, and environmental causes of infertility and reproductive wastage. The second and third parts, to appear in succeeding issues, are concerned with chromosome abnormalities and congenital malformations in the period from birth to adult life and with the diagnostic workup of infertile men and women.

Abortion, Habitual↗
PubMed1979

Genetic causes and workup of male and female infertility. 2. Abnormalities presenting between birth and adult life.

At birth some 6/1,000 persons have chromosome abnormalities; in about 60% of cases these abnormalities cause death or infertility, and in one third fertility is reduced. Some 1.7% of persons (3.4% of couples) with recurrent spontaneous abortion, infertility, or both have a chromosome abnormality. Chromosome abnormalities are far more common in men than in women with infertility; 15% to 20% of men with azoospermia have the Klinefelter syndrome. Meiotic defects explain 20% of male infertility in patients with apparently normal somatic chromosomes. Congenital malformations of the genitalia are more common in males than in females; about 0.82% of liveborn males have hypospadias. Almost one sixth of women with primary amenorrhea have some form of müllerian atresia, usually with associated renal anomalies.

Chromosome Aberrations↗
PubMed1979

Genetic causes and workup of male and female infertility. 3. Details of the clinical evaluation.

In the evaluation of male and female infertility the history, family history, physical examination, and endocrine and gonadal functional evaluations are the most informative measures. The cause of the infertility is never found in some 17.5% of couples and in almost one fourth of males. In over one third of cases male infertility is attributed to varicocele. In 40% of women infertility can be attributed to ovulatory or cervical factors, uterotubal disease, endometriosis and other pelvic disease, or a combination of these factors. For couples with primary infertility the fertility rate after seven years is only 36%; in such cases the neonatal death rate, frequency of low birth weight, and incidence of major malformations are several time greater than in the normal population.

Adult↗
PubMed1978

Synthetic progestins: in vitro potency on human endometrium and specific binding to cytosol receptor.

The relative potency of six commonly used synthetic progestins has been evaluated in an organ culture system for human endometrium. The affinities of these progestins for endometrial progesterone receptor were also evaluated after removing the CBG-like protein by spheroidal hydroxylapatite chromatography. All six progestins induced an increase in tissue glycogen during culture at lower concentrations than did progesterone; only one (medroxyprogesterone acetate) had a relative affinity greater than progesterone. The relative potencies and affinities of the synthetic progestins were found to have the same relative order but to differ in relative magnitude.

Chromatography↗
PubMed1978

Alterations in human endometrial protein synthesis during the menstrual cycle and in progestone-stimulated organ culture.

The cytoplasmic protein content of endometrium from women at various times in the menstrual cycle has been examined by means of polyacrylamide gel electrophoresis using a double-label isotope technique. Analysis of the gels for altered label ratios suggests an increase in the concentration of a single protein band during the immediate postovulatory period that can be duplicated by the addition of progesterone to organ cultures of preovulatory endometrium. An alteration in the protein content is also observed in the same section of these gels when they are stained and scanned. The protein band of interest migrates on sodium dodecyl sulfate gels at a rate that establishes its approximate molecular weight as 51,500.

Electrophoresis, Polyacrylamide Gel↗
PubMed1978

Effect of retinyl acetate on sulfated glycosaminoglycan biosynthesis in dermal and epidermal cells in vitro.

The effects of retinyl acetate on the biosynthesis of sulfated glycosaminoglycans in dermal and epidermal cells isolated from newborn mice was investigated. Three compartments were analysed for [35S]-glycosaminoglycans; the culture medium, the cellular matrix, and the cells. The individual levels of chondroitin 4-sulfate, dermatan sulfate and heparin and/or heparan sulfate in these compartments as a function of retinyl acetate was also analysed. The addition of retinyl acetate resulted in a dose dependent increase 35SO4 incorporation in the cellular and matrix compartments of the dermis in vitro. At the optimum concentration of 1.8 X 10(-6) M, this increase was 50%. The levels of35SO4 incorporated into medium glycosaminoglycans were relatively constant. There were also changes in the levels of the individual sulfated glycosaminoglycans. The glycosaminoglycan profile was modified differently in each of the three compartments analysed. In the epidermal cells, retinyl acetate at an optimum concentration of 1.8 X 10(-6) M resulted in a dose dependent increase in 35SO4 incorporation in the cellular, matrix and medium compartments. There was no apparent change in the glycosaminoglycan profile, with heparin and/or heparan sulfate being the major sulfated glycosaminoglycan.

Cell Count↗
PubMed1978

Factor V antibody and disseminated intravascular coagulation.

A factor V inhibitor arose in a 79-year-old man within 1 month of an operation for a fractured leg. Absorption studies with solid-phase antibodies to human immunoglobulins showed the inhibitory activity to be primarily in the IgG class, but also in the IgA class, of immunoglobulins. This is the first report of an IgA immunoglobulin with factor V inhibitory activity. While the inhibitor was present, and at a time when no circulating Factor V activity was detectable, the patient developed septicemia and disseminated intravascular coagulation. The mechanism sustaining disseminated intravascular coagulation despite the absence of circulation factor V activity remains unexplained. The factor V inhibitor disappeared within 5 months of its initial detection. Possible origins of factor V inhibitors are discussed.

Aged↗