Gene/Protein Disease Symptom Drug Enzyme Compound
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The rate of utero-placental blood flow depends on functional components (perfusion pressure and flow resistance within the area of the vascular bed of the placenta), as well as on morphological factors (regressive changes in the placenta). Different primary maternal conditions and diseases may lower the rate of placental flow, leading to placental insufficiency; the highest percentage, by far, of placental dysfunction is found in patients suffering from gestosis. Hypocirculation initially present in cases of EPH gestosis and caused by arteriolar spasms triggers off a vicious circle involving placental infarction and severe reduction in the utero-placental perfusion rate. This in turn leads to fetal hypotrophy, a high rate of premature births and perinatal mortality. Verification of HPL, HCG, alpha-Fetoprotein or E3 in maternal serum and amniotic fluid or urine greatly improved the recording of partial placental functions. Along with ultrasonic biometry, cardiotocography and amnioscopy, these hormonal parameters allow only indirect assessment of the placental function. On the other hand, measurements of the utero-placental flow offers a direct approach. In order to evaluate the placental flow measurements it is imperative to obtain a curve indicating the course over the last third of the pregnancy-in addition to establishing a general normal range. In case of placental insufficiency, it is necessary to determine whether this is due to functional disorders alone, or to more extenisve morphological changes. A placental perfusion test (PPT) was developed in order to make this distinction. Beta2-mimetic treatment is indicated if functional factors predominate, whereby it appears essential to obtain the requisite experimental data for precise quantification of beta-mimetic action.
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PMID:[New aspects in diagnosis and therapy of placental insufficiency. Placental perfusion measurements; placental perfusion test (PPT) and betamimetic long term treatment (clinical and experimental data (authors transl)]. 1 7

Serum, cord blood and amniotic fluid beta2-microglobulin contents were measured from normal pregnancies complicated by EPH gestosis, Rh immunisation and pathological serum levels of HPL and alpha1-fetoprotein. We found no changes in high risk pregnancies from normal serum levels. beta2-microglobulin seems to be no parameter in managing complicated pregnancies and fetal growth retardation.
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PMID:[Serum, cord blood and amniotic fluid concentrations of beta2-microglobulin in patients with normal and complicated pregnancies (author's transl)]. 7 88

The digital estimation of utero-placental circulation by means of nuclear-medical examinations with help of 113 m In-Cl and regarding to the "region of interest" gives no depositions in cases with an intrauterine retardation. This concerns the activity as well in the placenta as in the uterus too. Exceptions represents intrauterine retardations on the base of heaviness EPH-gestosis and placenta previa. Herewith the rise of activity corresponds with the thickness in the III. trimester of pregnancy. A treatment about several weeks with Hepain under bed conditions leads to no proofed influence of the uteroplacental circulation, on the contrary to a rise of estriol and HPL-values, meaning a improvement of placental performance. The estimation of the utero-placental circulation by means of nuclear-medical examinations is situated to the problem of fetal condition by EPH-gestosis, placenta previa and other.
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PMID:[Performance of uteroplacental perfusion in contrast to hormone-analytic investigations in intrauterine retardation and under the influence of intravenous long-term application of heparin (author's transl)]. 60 45

Following a description of the three different functions of the placenta (respiratory, nutritive, endocrine) and their failures the most common function tests are presented. Special emphasis is put on the evaluation of a recently described pregnancy-specific protein (SP1) in the maternal serum. The amount of the substance produced by the placenta correlates well with the fetal weight and well-being in cases of EPH-gestosis and idiopathic placental insufficiency; correlation was not as well in mild EPH-gestosis, diabetes and RH-incompatibility. The validity of measuring SP1-production seems to be similar to that of HPL. The method of quantitative determination is simple and possible even in a smaller hospital.
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PMID:[Diagnosis of the placental function with special reference to the pregnancy-specific protein SP-1]. 84 69

In the serum of 145 women between the 34th and 42nd weeks of pregnancy, 209 radioimmunological determinations of human placental lactogen were made, using the Pharmacia, Uppsala, Sweden, HCS Phadebas Test. Following the determination of normal HPL levels in late pregnancy, the HPL values of high-risk pregnancies were investigated in relation to normal values and compared with the clinical pattern. A satisfactory relation was found between low HPL levels and fetal growth retardation. To some extent the HPL data can also be used in monitoring severe EPH-gestosis and postmaturity. Light cases of gestosis and pregnancies involving Rh-incompatibility do not affect HPL production. The clinical findings regarding HPL levels should not be overestimated in attempting to diagnose placental insufficiency.
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PMID:[The determination of human placental lactogen (HPL) for hormonal supervision in late pregnancy]. 98 89

EPH gestosis and placental insufficiency sui generis are cause of fetal hazards. Clinical symptomatology and anamnesis indicate different tests to detect pathological conditions for the fetus. HPL, HCG, urinary estriol, measuring the placental flow-rate, ultrasonic diagnosis as all other usual examinations during pregnancy were carried out. In EPH gestosis a reduction of all placental functions was found like as for thrombocytes and fibrinogen. Placental insufficiency showed an even greater reduction of placental function, only thrombocytes and fibrinogen remained constant. Weight and length of the newborn were according the pathological placental function reduced. Morphology of the placenta could proof the results of the previous done tests.
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PMID:[Optimal monitoring in EPH gestosis and idiopathic placentar insufficiency (author's transl)]. 118 12

Sp1, the pregnancy-specific beta 1-glycoprotein, was studied in normal and pathologic pregnancies. We developed a highly specific and sensitive double-antibody-radioimmunoassay by radioiodination of purified placental SP1. This RIA allowed the estimation of SP1 concentrations as low as 2 ng/ml. In a collective of 227 women with normal pregnancies we established the normal distribution curve in maternal plasma from the fifth week of gestation to term. The median value rose steadily from 3 microgram/ml in the 8th week to 140 microgram/ml in the 36th week when a plateau was formed. In more than 400 patients with pregnancies complicated by a variety of pathologic disorders the SP1 levels were controlled by either single assays or serial estimations throughout pregnancy and were compared with the normal distribution range. SP1 was also determined in about 200 samples of amniotic fluid gained by amniocentesis and during parturition of normal pregnant women from the 13th gestational week until term. The normal range was established up to the 20th w.o.p. The concentrations rose from below 0.2 microgram/ml in early pregnancy to 3 microgram/ml and generally amounted to approximately 1% of the respective serum value. Pathologic cases with diverse chromosomal anomalies, Rh-incompatibility, anencephaly, hydramnios and other abnormal conditions were examined. From these only twin-pregnancies with slightly elevated levels and cases with fetal trisomies with reduced SP1 concentrations showed aberrations from the normal distribution. The estimation of serum concentrations in mothers with diabetes or Rh-incompatibility were not significantly different from the normal collective. In diabetes a characteristic course of the follow-up curves was observed. Abortion in early pregnancy was frequently but not always indicated by reduced SP1 values. Threatened abortion with subsequent continuation of pregnancy exhibited SP1 values scattered within the normal range. Since the radioimmunological determination of SP1 is possible in the early stage of gestation (from week 8) it may serve as a useful tool for prediction at times when the determination of placental lactogen is not yet possible. In pregnancies with "small-for-date babies" the correlation between SP1 in maternal plasma and fetal growth retardation was reflected in a pronounced tendency to low SP1 levels. Serial determinations of SP1 in the serum of women with EPH-gestosis were compared with the corresponding HPL determinations and showed the equality of SP1 concerning the assessment of the placental function.
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PMID:Radioimmunoassay of SP1 (pregnancy-specific beta1-glycoprotein) in maternal blood and in amniotic fluid normal and pathologic pregnancies. 678 88

The ratio between fetal and placental weight is often thought to be a measure of the reserve capacity of the placenta. The aim of our study was to investigate the relationship between 1) endocrinologic parameters during pregnancy (serum placental lactogen - HPL, urinary estriol - E3), 2) the occurrence of fetal distress during labor, and 3) the severity of EPH gestosis, and the fetal/placental weight ratio at various gestational ages. The data from a total of 4911 consecutive pregnancies and deliveries were evaluated. Up to 37 weeks the mean fetal/placental weight ratio was significantly lower in infants with fetal distress. Up to 32 weeks there was a positive correlation between the percentage of women with low HPL and E2 levels and the percentage of infants with fetal distress, and the gestosis index. In addition there was a significant increase in the mean fetal/placental weight ratio in the group with moderate and severe gestosis. With advancing gestational age fetal/placental weight ratios were independent of the severity of EPH gestosis. It is concluded that until 37 weeks fetal distress is associated with a significant lower fetal/placental weight ratio. The morphologic and functional changes in placentas of gestotic pregnancies do not manifest themselves in either an increase or a decrease of the mean fetal/placental weight ratio after 33 weeks.
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PMID:Placental function, fetal distress, and the fetal/placental weight ratio in normal and gestotic pregnancies. 720 Apr 64

In the present studies, we demonstrate that heregulin is a potent and rapid activator of the serine/threonine kinase called Akt in the MCF-7 breast cancer cell line but not in 3 other breast cancer cell lines (T47D, HBL-100, and MDA-231). The extent of activation of Akt in the 4 cell lines correlated with the ability of heregulin to activate phosphatidylinositol 3-kinase and inhibition of the kinase blocked Akt activation. A monoclonal antibody to HER2 inhibited the ability of heregulin to activate Akt in the MCF-7 cells. BT474, a breast cancer cell line which overexpresses HER2, had high basal Akt enzymatic activity. This high basal activity was lowered when cells were pre-incubated with an anti-HER2 monoclonal antibody which is used to treat breast cancer patients. Our results indicate that heregulin is a potent activator of Akt and that overexpression of HER2 in breast cancers could also lead to activation of Akt.
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PMID:Heregulin regulation of Akt/protein kinase B in breast cancer cells. 1044 22

Ras genes, frequently mutated in human tumors, promote malignant transformation. Ras transformation requires membrane anchorage, which is promoted by Ras farnesylcysteine carboxymethylester and by a second signal. Previously we showed that the farnesylcysteine mimetic, farnesylthiosalicylic acid (FTS) disrupts Ras membrane anchorage. To understand how this disruption contributes to inhibition of cell transformation we searched for new Ras-interacting proteins and identified galectin-1, a lectin implicated in human tumors, as a selective binding partner of oncogenic H-Ras(12V). The observed size of H-Ras(12V)-galectin-1 complex, which is equal to the sum of the molecular weights of Ras and galectin-1 indicates a direct binding interaction between the two proteins. FTS disrupted H-Ras(12V)-galectin-1 interactions. Overexpression of galectin-1 increased membrane-associated Ras, Ras-GTP, and active ERK resulting in cell transformation, which was blocked by dominant negative Ras. Galectin-1 antisense RNA inhibited transformation by H-Ras(12V) and abolished membrane anchorage of green fluorescent protein (GFP)-H-Ras(12V) but not of GFP-H-Ras wild-type (wt), GFP-K-Ras(12V), or GFP-N-Ras(13V). H-Ras(12V)-galectin-1 interactions establish an essential link between two proteins associated with cell transformation and human malignancies that can be exploited to selectively target oncogenic Ras proteins.
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PMID:Galectin-1 binds oncogenic H-Ras to mediate Ras membrane anchorage and cell transformation. 1170 20


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