Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In 1970, Field and Caspary reported that lymphocytes from patients with malignant disease can be stimulated by a basic protein from human brain (human encephalitogenic protein--HEP). The stimulated lymphocytes are capable of releasing the macrophage-slowing factor, which reduces the electrophoretic mobility of guinea-pig macrophages. In general, this effect was not found with lymphocytes from patients without malignant disease. This paper deals with the application of the MEM test using HEP and HCG as antigen in the diagnosis of trophoblastic disease. We have found cellular sensitization against HCG in all patients with gestational trophoblastic tumours and against HEP in patients with hydatidiform moles of the group II or III as well as choriocarcinoma. Patients with malignant tumours of different localization showed a cellular sensitization against HEP, but only some against HCG. In pregnant women no cellular sensitization against HEP as well as HCG was detected. The results of the MEM test using HEP as antigen in patients with gestational trophoblastic tumours are compared with the clinical findings and the histological diagnosis. By means of this combination a more exact evaluation of the biological activity of the trophoblastic disease was obtained.
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PMID:The macrophage electrophoretic mobility (MEM) test for the diagnosis of hydatidiform mole and choriocarcinoma. Preliminary report. 7 73

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

We have developed a simplified quick semiquantitative determination for urinary estrogen in non-pregnant female by utilizing Amberlite XAD-2 and E3 LAIR-KIT. The whole procedure required only 20 minutes. Interassay variance of this method was 10% and intraassay variance was 7%. The recovery was 85%. There was a highly significant correlation between the data obtained by this method and those by RIA (r = 0.944). We applied this method to the monitoring of follicular maturation in the HMG-HCG therapy. Urinary estrogens obtained from 28 anovulatory women (60 cycles) were determined by this method in order to decide the appropriate timing for the HCG injection following the HMG. Our data indicate that it is possible to induce ovulation without the risk of ovarian hyperstimulation syndrome if the HCG was injected on the day when the urinary estrogen level rose to between 70 and 100 ng/ml for 2 consecutive days. This method could well be applied to prospective monitoring in ovulation induction with HMG-HCG therapy.
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PMID:[A simplified quick semi-quantitative determination of urinary estrogen in non-pregnant female: the application for monitoring of follicular maturation at HMG-HCG therapy]. 308 68

On the basis of results of our research and review of literature, the complex of immuno logical influences, operating during the development of the human fetus, were evaluated. It is obvious that during the early stages of pregnancy the conceptus is protected by non-specific mechanisms, i.e. hormonally (HCG, progesterone) and by certain properties of the trophoblast (barrier function, immunologically inert surface). Specific immunological tolerance is formed by gradual penetration of trophoblast particles and later by penetration of fetal blood cells into maternal circulation. Thus a specific suppression of maternal T lymphocytes against fetal antigens develops, other immunological functions being intact. - Following a strong antigenic stimulus (e.g. Rh-D), isoimmunization of the mother and serious risk for the fetus occur. Immunological causes of abortion could not be unequivocally proved in recurrent abortions. The explanation of the origin of EPH-gestosis on the basis of toxic action of immunocomplexes is highly probable, however the laboratory and experimental proof is still lacking.
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PMID:The development of immunological relationship between mother and fetus under physiological and pathological conditions. 314 89

Chromosome 17q is frequently rearranged in breast cancer. Allelotyping studies have proposed the existence of at least four regions of allelic imbalance (AI). Here we present a study combining allelotyping using 19 CA repeat markers mapping in the 17q21-25 region and molecular cytogenetics (CGH and FISH). Allelotyping was undertaken on 178 pairs of cognate tumor and normal DNA in order to determine the number of regions of AI and define the shortest overlaps. AI ranged from 34-54% of the informative cases according to the marker and, overall, 66% of the tumors presented AI at one of the markers tested. Analysis of the patterns of imbalances revealed at least five common regions of imbalance respectively defined by markers: D17S855, which is intragenic of BRCA1 (SRO 1), D17S1607 (SRO 2), D17S1855 (SRO 3), between D17S789 and D17S785 (SRO 4) and D17S784 (SRO 5). In order to characterize the nature of the genetic events revealed by allelotyping we performed CGH analysis on a subset of 43 tumors presenting variable patterns of imbalance. CGH showed that AI at 17q could represent four different types of genetic events: loss of chromosome 17, gain of 17q, gain of 17q22-q24, loss of 17q11-q21 and/or 17q25-qter. Some of these anomalies could occur concomitantly within the same tumor. Since 35% of the tumors analysed by CGH presented gains, these data indicated that AI at 17q were not solely indicative of losses of genetic material and could also represent DNA amplification. Gains were most commonly observed in the 17q23-q24 regions. This suggested that AI in SRO 2 and SRO 3 corresponded to DNA amplification. To assess this, we isolated BAC clones by PCR screening for markers D17S1607 and D17S1855 and used these in FISH experiments on six breast tumor cell lines and 14 breast cancer specimens. FISH results showed that both D17S1607 and D17S1855 were frequently involved in DNA amplification (8-30 copies). Altogether, our data show that allelotyping can be efficiently used in amplicon mapping. Clinico-pathological correlations indicated that imbalance at 17q preferentially occurred in high grade, PR- and ERBB2 amplified tumors.
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PMID:17q21-q25 aberrations in breast cancer: combined allelotyping and CGH analysis reveals 5 regions of allelic imbalance among which two correspond to DNA amplification. 1059 24

It is known that, following radiotherapy, secondary cancer may occur after a long latent period. Few cytogenetic studies have been reported on tumors of the central nervous system occurring after radiotherapy. We report the cytogenetic study of six cases of radiation-induced meningiomas. In all cases, we observed the same chromosome abnormality, der(1)(1qter-->1p11::22q12-->22pter). SKY and CGH techniques allowed us to identify the chromosomal abnormalities. We suggest that a gene localized on 1p13 is involved in radiation-induced meningiomas.
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PMID:Cytogenetic study of six cases of radiation-induced meningiomas. 1137 99

Soft tissue sarcomas constitute a heterogeneous group of malignant tumors of mesenchymal origin, the classification of which may present a diagnostic challenge. We present here the cytological, histopathological, immunohistochemical, and cytogenetic findings of an unusual case of a highly aggressive sarcoma. Based on the morphology and the immunohistochemical profile, this primitive tumor and its metastases could not be conclusively classified as any of the defined subtypes of sarcomas, although the findings were suggestive of a variant of rhabdomyosarcoma. Cytogenetic characterization using G-banding, SKY, FISH, and CGH revealed almost identical chromosomal compositions of the primary tumor and the metastasis. The hypertetraploid karyotype was characterized by numerical imbalances as well as by an unbalanced translocation t(1;19)(q12;q13.2), which has not been previously reported.
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PMID:A highly aggressive primitive mesenchymal tumor with a translocation (1;19)(q12;q13.2). 1142 51

We have applied the method of genomic microarray to investigate amplification of oncogenes throughout the genome of nasopharyngeal carcinoma (NPC). Array based comparative genomic hybridization (array CGH) allows simultaneous examination of 58 oncogenes commonly amplified in various human cancers. In the present study, we have examined 15 NPC samples including five cell lines, two xenografts and eight primary tumours with array CGH to reveal the particular oncogenes associated with this cancer. This is the first genome wide survey of multiple oncogene amplifications involved in the development of NPC. Non-random gene amplifications were identified for the first time in NPC on MYCL1 in 1p34.3 and on TERC and PIK3CA at 3q26.3. Other high level amplified oncogenes included NRAS, RAF1, MYB, EGFR, FGF4, EMS1, and D17S167. Highest frequencies of gain of novel oncogenes were detected on MYCL1 (66.7%), TERC (46.7%), ESR (46.7%), PIK3CA (40%), LAMC2 (33.3%), and CSE1L (33.3%).
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PMID:Genome wide detection of oncogene amplifications in nasopharyngeal carcinoma by array based comparative genomic hybridization. 1183 56

Ovarian hyperstimulation syndrome (OHSS) is an iatrogenic complication of treatment with fertility drugs. Using human lung microvascular endothelial cells (HUMEC-L) as an in-vitro model of OHSS, we have tested the hypothesis that the endothelium is a target of HCG in the pathogenesis of OHSS. Since OHSS is characterized by increased capillary permeability, we have investigated the production and action of vasoactive agents. When HUMEC-L were cultured with high doses of estradiol (E(2)), no significant changes were observed in the secretion of vascular endothelial growth factor (VEGF), interleukin (IL)-6 or IL-1 beta. However, the addition of HCG resulted in a significant increase in the secretion of VEGF and IL-6. Time-course experiments showed that VEGF was secreted within minutes of HCG addition, whereas IL-6 was significantly increased only after 48 h in culture. The secretion of IL-1 beta was unchanged by these hormonal conditions. The presence of HCG receptors was demonstrated in HUMEC-L in basal conditions as well as after the addition of E(2). The expression of VEGF receptors was also investigated. High doses of E(2) were unable to increase the expression of KDR, flt-1 and sfl-t, but the addition of HCG significantly upregulated the KDR concentration in endothelial cells, while no change was observed for flt. Permeability assays demonstrated that while E(2) alone did not change the arrangement of HUMEC-L in vitro, the presence of HCG caused changes in the actin fibres corresponding to increased capillary permeability. Anti-human VEGF antibodies were able to overcome these changes. In conclusion, these experiments show that the endothelium may be a primary target of HCG, causing an acute release of VEGF and a significant increase in IL-6 and resulting in an autocrine-paracrine action that may increase vascular permeability.
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PMID:The role of endothelial cells in the pathogenesis of ovarian hyperstimulation syndrome. 1199 37


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