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Results for “PLACENTAL EXTRACTS”

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At least 937 records · Page 52Linked to original sources
PubMed1982

Dose-dependent induction of embryonic abnormalities in vitro by tissue homogenates of placenta and decidua.

Homogenate preparations from normal rat placental and decidual tissue induced abnormalities when included in the culture medium of rat embryos between Day 9.5 and Day 11.5. Abnormal embryos were produced between doses of 2.5 and 4 mg/ml for the placental homogenate and between doses of 1.2 and 4 mg/ml for the decidual homogenate, but were not produced by a solution of bovine serum albumin or by a protein preparation of rat lung tissue at the same concentration. The degree to which the embryos were malformed depended on the dose and which of the two homogenates was used. The decidual homogenate preparation was more pathogenic than the placental homogenate, but both were able to produce neural-tube defects and a severe reduction in embryonic size. The possible association between these findings and some known proteins within such homogenates is discussed.

Abnormalities, Drug-Induced↗
PubMed1993

Chromatographic, immunochemical and electrophoretic studies of human uterotrophic placental factor (hUTPF).

The human uterotrophic placental factor (hUTPF) is a protein obtained from human term placentae and acts on uterine growth, mammary gland, and blastocyst development and implantation. In the present work, we further define some molecular characteristics of hUTPF using chromatographic, electrophoretic and immunochemical methods. It is concluded that in human term placenta a high molecular weight hUTPF is present, bound to albumin and immunoglobulins, which could represent a storage or transport form of this factor. hUTPF presents several molecular forms, one of them of 270 kDa and others of approximately 90 kDa and 27 kDa.

Animals↗
PubMed1994

[Intravenous placental immunoglobulin for treatment of chronic graft versus host disease].

Intravenous placental immunoglobulin (IV Pt IG) was used for the treatment of chronic graft versus host disease (CGVHD) in 30 patients who are refractory to steroid and cyclosporinic A. 15 (50%) patients showed excellent response and 11 (36.66%) good response. The total response rate is 86.66%. The dosage of IV Pt IG was 4 gm/day in adults by intravenous infusion. Effectiveness of IV PtIG was discerned within 2 weeks. The plasma levels of IgG, IgA and IgM were tested before and after IV PtIG treatment. There was no significant statistical difference between the plasma IgG, IgA, IgM levels in pre- and post-treatment period. The efficacy of IV PtIG against CGVHD is therefore ascribed to its pharmacological effect.

Adolescent↗
PubMed1994

Subtle differences in human pregnancy-specific glycoprotein gene promoters allow for differential expression.

Eleven pregnancy-specific glycoprotein (PSG) genes reside on human chromosome 19. The sequence of these genes is extremely similar and that similarity extends to their putative control regions. However, the expression pattern of each PSG gene differs in the placenta, the primary site of PSG synthesis. To understand the molecular mechanisms underlying differential PSG expression, we characterized promoter elements of six PSG genes. We have shown previously that nucleotides -172 to -34 with respect to the translation start site constitute a minimal promoter in the PSG12 gene (class 1). We now show that PSG1-I and PSG3 are also members of class 1 genes. In contrast, only nucleotides -172 to -80 are necessary for promoter activity in PSG5, PSG6, and PSG11 genes (class 2). Class 2 genes contain a perfect Sp1 recognition sequence (CCCCGCCC) at nucleotides -148 to -141 which is necessary for promoter activity. Placental cell extracts formed three protein-DNA complexes with nucleotides -172 to -80 of all six PSG genes. One of the components of these complexes is an Sp1-like molecule. We have previously reported activator sequences within nucleotides -83 to -34 in PSG12. We now show that a 50-kDa protein binds to this region of PSG12, and the resultant complex can be supershifted by a monoclonal antibody to PEA3.

Base Sequence↗
PubMed1993

Hypothesis for endometrial carcinoma carcinogenesis. Preventive prospects.

Considering endometrial carcinoma as a natural experimental model for in vivo study of carcinogenesis, a hypothesis of endometrial type A carcinogenesis and some preventive prospects are advanced. Under the name of endometrial carcinoma two different types are considered: A) hormone dependent type, and B) autonomous type. Aging, obesity, hypertension and/or diabetes, persistent exposure to unopposed exogenous or endogenous estrogens are recognized epidemiological factors for endometrial carcinoma. Experimental and clinical studies have shown that in pregnancy associated with clinical conditions characterized by a compromised maternal circulation in the intervillous space, a state of true or relative hypoxia stimulates syncytial hyperplasia, as adaptive process, in order to increase the exchange area of the placenta. Vaginosonographic studies have shown in patients with endometrial thickness greater than or equal to 4 mm complex and atypical hyperplasia than endometrial carcinoma in a higher percentage than in patients with endometrial thickness less than 3 mm. It seems that hypoxia in endometrial thickness, greater than 3 mm promoted by estrogens, would be a supplementary proliferating factor. Immunological studies have shown, in patients with complex or atypical hyperplasia of the endometrium and/or endometrial carcinoma, a host immunological reaction (DTHS-reactivity test) to a pharmaceutical placental suspension, when injected intradermally. An extract prepared from placental suspension is also recognized in vitro, by patients' serum (Ouchterlony's technique). To conclude, hypoxic insult, as common pathophysiological factor in most predisposing diseases for endometrial cancer, leads to a persistent multicellular hyperplasia of the endometrium. Sometimes populations with an altered growth pattern develop.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Management of vitiligo.

Vitiligo is a disease of unknown origin that causes destruction of melanocytes in the skin, mucous membranes, the eyes, and occasionally in hairbulbs and in the ears. The loss of melanocytes alters both structure and function of these organs. The goals of therapy are multifold. The primary goal is to restore melanocytes to the skin so that the epidermis has a normal morphology. Such repigmented skin regains its normal immune/inflammatory functions.

Administration, Cutaneous↗