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Biomedical subjects

P Bischof

Publications and source records attributed to P Bischof.

At least 145 records · Page 8Linked to original sources
PubMed1979

Measurement of pregnancy associated plasma protein A (PAPP-A).

A method is described for measuring pregnancy associated plasma protein A (PAPP-A) in the maternal circulation during the 3rd trimester of pregnancy. The method used is a modification of Laurell's electroimmunodiffusion technique.

Antibody Specificity↗
PubMed1979

Purification and characterization of pregnancy associated plasma protein A (PAPP-A).

Pregnancy Associated Plasma Protein A (PAPP-A) has been isolated from late pregnancy plasma using ammonium sulphate precipitation, ion exchange chromatography, affinity chromatography on Concanavalin-A, gel filtration and negative affinity chromatography. It was found that PAPP-A is an alpha 2-glycoprotein of 750-820 000 MW, probably a dimer with each monomer being composed of 2 polypeptide chains of 218 000 MW. The amino acid composition as well as other physicochemical characteristics are similar to human alpha 2-macroglobulin. PAPP-A exhibits in vitro an inhibition of the activity of the complement system, of the caseinolytic activity of plasmin and possibly of the urokinase activation of plasminogen. The hypothesis that PAPP-A plays a role in the regulation of fibrinolysis during pregnancy is put forward.

Amino Acid Sequence↗
PubMed1979

Studies on pregnancy-associated plasma protein A in the third trimester of pregnancy.

The plasma concentration of pregnancy-associated plasma protein A (PAPP-A) was measured in 34 women during the last 10 weeks of pregnancy. From 30 to 36 weeks the concentration of this protein increased steadily. Thereafter the concentration of PAPP-A rose more steeply, the highest amounts being found in early labour. The concentration of PAPP-A in peripheral venous blood and in the uterine vein was much the same. It was less in the retroplacental blood and a great deal less in the peritoneal fluid. The day-to-day variation was small; the coefficient of variation at 38 weeks was only 7.3 per cent. After delivery, the concentration of PAPP-A fell more slowly than other placental proteins and steroids, the average half-life being 51 hours. Although there is no doubt that PAPP-A is a product of the syncytiotrophoblast, our findings suggest that it is not simply secreted by the chorionic villi directly into the intervillous space but makes its way into the maternal circulation by a more circuitous route.

Ascitic Fluid↗
PubMed1976

[Problems of rheumatic therapy in pregnancy (author's transl)].

Almost every drug that is given to a pregnant woman can pass into the developing fetus and possibly cause harm. A well-founded corticoid therapy is not contra-indicated. The administration of pyrazole derivatives in considered largely unobjectionable. Damage has been observed very recently with salicylates. Also indometacin is not absolutely free from teratogenic effects. Harmful effects have not yet been seen with the rest of the preparations for symptomatic treatment. During treatment with the basic drugs: gold, D-penicillamine and chloroquine, pregnancy should be avoided. The administration of cytostatics during pregnancy and the lactation period is contraindicated. Departures from this rule are only permissible in severe systemic lupus erythematodes.

Adrenal Cortex Hormones↗
PubMed1976

[Lactic acidosis after administration of buformine (author's transl)].

An 85-year-old female diabetic was admitted in coma, having been on antidiabetic treatment with the biguanide derivative "Silubin retard", 600 mg/d, for one-and-a-half months. The anion deficiency was 57 mmol/l, pH 6.9, suggesting the diagnosis of lactic acidosis in the absence of other causes of metabolic acidosis. Blood lactic acid levels of more than 16.65 mmol/l (150 mg/100 ml) confirmed the diagnosis. Administration of 875 mmol sodium bicarbonate over 12 hours corrected the deficiency. On admission to hospital there had been slight pre-renal failure. Myocardial infarction developed as a result of tissue hypoxia but did not prove clinically important. On the second day there were signs of a compensated disseminated intravascular coagulopathy with upper gastro intestinal haemorrhage. The woman died suddenly 18 days later of pulmonary embolism.

Acidosis↗
PubMedDate not supplied

Pregnancy-associated plasma protein-A: an inhibitor of the complement system.

Pregnancy-associated plasma protein-A (PAPP-A) was purified to homogenicity from third-trimester pregnancy plasma using ion exchange chromatography and affinity chromatography on con A-Sepharose and anti-human serum-Sepharose. The elution of PAPP-A, alpha 2-macroglobulin, Cl-inhibitor and alpha 1-antitrypsin was followed by immuno-diffusion. the eluates were tested for stimulation or inhibition of complement-induced haemolysis. PAPP-A markedly inhibits the haemolytic activity of complement.

Chromatography, Affinity↗
PubMedDate not supplied

Immunohistochemical localization of pregnancy-associated plasma protein A in decidua and trophoblast: comparison with human chorionic gonadotrophin and fibrin.

In an immunoperoxidase study, pregnancy-associated placental protein A (PAPP-A) was localized to the cytoplasm of decidual stromal cells, the villous syncytiotrophoblast and on the surface of placental trophoblast. A decidual and a trophoblastic origin is suggested for PAPP-A, and its presence on the surface of the syncytiotrophoblast is interpreted as a possible immunoprotective layer.

Chorionic Gonadotropin↗
PubMedDate not supplied

Pregnancy-associated plasma protein A (PAPP-A) specifically inhibits the third component of human complement (C3).

Pregnancy-associated plasma protein A (PAPP-A), a macromolecular glycoprotein associated with pregnancy, was shown to inhibit complement-induced haemolysis and to bind heparin reversibly. Because of the inhibitory effects of heparin on the complement cascade it was not clear if the inhibition of complement activity observed with PAPP-A (isolated from heparin plasma) was attributable to the heparin moiety bound to PAPP-A. This work demonstrates that heparin exerts an inhibitory effect on complement activity but that heparin-free PAPP-A is also inhibitory. PAPP-A specifically inhibits C3 by binding to this complement subcomponent and not by inhibiting C3 convertase as demonstrated for C3 inactivator.

Complement C3↗
PubMedDate not supplied

Paracrine and autocrine regulators of trophoblast invasion--a review.

Cytotrophoblastic cells (CTBs) from first trimester placenta follow one of two existing differentiation pathways: villous CTBs (vCTBs) form a monolayer of polarized epithelial stem cells which proliferate and eventually differentiate by fusion to form a syncytiotrophoblast (STB) covering the entire surface of the villus, or they can break through the STB at selected sites (in anchoring villi) to form multilayered columns of non-polarized but invasive CTBs. In vitro, CTBs invade a reconstituted basement membrane, they thus behave like metastatic cells. This invasive behaviour is due to the ability of CTBs to secrete matrix metalloproteinases (MMPs) since tissue inhibitor of MMP (TIMP) inhibits their invasiveness. MMPs are a family of at least 17 human zinc-dependent endopeptidases collectively capable of degrading essentially all components of the extracellular matrix (ECM). Although CTBs behave like metastatic cells, in vivo they are only transiently invasive (first trimester) and their invasion is normally limited only to the endometrium and to the proximal third of the myometrium. This temporal and spatial regulation of trophoblast invasion is believed to be mediated in an autocrine way by trophoblastic factors and in a paracrine way by uterine factors. Several types of regulators have been investigated: hormones, cytokines, growth factors and ECM glycoproteins. This review is not intended to be an exhaustive catalogue of all the potential regulators but is aimed at emphasizing those factors relevant in trophoblast-endometrial interactions.

Carrier Proteins↗
PubMedDate not supplied

Regulation of trophoblastic gelatinases by proto-oncogenes.

During the first trimester of pregnancy, certain cytotrophoblastic cells (CTB) of anchoring villi invade the underlying decidua. Regulation of this invasive behaviour depends on cytokines and growth factors secreted by decidua and trophoblast, which modulate metalloproteinase (MMP) secretion of CTB. Since MMP-9 expression by CTB is a prerequisite for matrigel invasion and since the promoter region of the MMP-9 gene contains two AP-1 binding sites, we hypothesized, that transient activation of c-jun and c-fos oncogenes (which bind to form AP-1) by tumour necrosis factor (TNFalpha), or the phorbol ester TPA will promote the invasive phenotype of CTB and induce the production of MMP-9.TNFalpha or TPA when added to primary cultures of CTB increase MMP-9 activity and MMP-9 mRNA. This effect is inhibited by cycloheximide indicating the necessity of protein synthesis. TPA or TNFalpha induces also the binding of nuclear proteins (extracted from treated CTB) to a radiolabelled oligonucleotide corresponding to the consensus sequence of the TPA responsive element. Antibodies to Jun and Fos can displace this binding. Transient transfection of antisense mRNA to jun or fos into CTB inhibits the immunoreactivity and gelatinolytic activity of MMP-9. We conclude that AP-1 is necessary but may not be sufficient for transactivation of the MMP-9 gene in human CTB.

Adult↗