Disease relevance of CSH1

• Analysis of insect mRNA revealed that intron D-retaining PL-A2 cDNA was expressed without splicing in the baculovirus expression system [1].
• Hybrid hGH-N, hGH-V and hCS-A genes containing 5'-flanking sequences, including the endogenous promoter, are preferentially expressed in rat pituitary tumor (GC) cells, after gene transfer [2].
• Induction of CSH1 (chorionic somatomammotropin hormone 1) by NECC1 expression suggested differentiation of choriocarcinoma cells to syncytiotrophoblasts [3].
• Mutations in the CSA or CSB complementation genes cause the Cockayne syndrome, a severe genetic disorder that results in patients' death in early adulthood [4].
• Finally, CSB(-/-) but not CSA(-/-) mice fed with food containing di(2-ethylhexyl)phthalate (causing elevated levels of oxidative DNA damage in the liver) show weight reduction [5].

Psychiatry related information on CSH1

• Risk factors for CSA were male gender (odds ratio [OR] 3.50; 95% confidence interval [CI], 1.39 to 8.84), atrial fibrillation (OR 4.13; 95% CI 1.53 to 11. 14), age > 60 yr (OR 2.37; 95% CI 1.35 to 4.15), and hypocapnia (PCO(2 )< 38 mm Hg during wakefulness) (OR 4.33; 95% CI 2.50 to 7. 52) [6].
• METHODS: Polysomnograms with digitized video surveillance of 20 consecutive patients with heart failure and CSA-CSR were analyzed for total apnea-hypopnea index, mean event duration, and mean oxygen desaturation according to sleep stage and position [7].
• Pharyngeal compliance, defined as the slope of the regression CSA versus PPH, was significantly increased during NREM sleep compared with wakefulness and REM sleep, with the compliance during both tonic and phasic REM sleep being similar to that observed in wakefulness [8].
• DISCUSSION: The validation of the CSA and MM monitors against AEE and their calibration for sedentary, light, moderate, and vigorous thresholds certify these monitors as valid, useful devices for the assessment of physical activity in children [9].
• CONCLUSIONS: The results suggest that adolescence is a crucial time for the influence of CSA experiences on substance abuse [10].

High impact information on CSH1

• Finally, there are indications that the genes CSA and CSB, which are implicated in the human hereditary disease Cockayne syndrome, may have a role in transcription [11].
• It therefore appears that PL affects fetal growth both by exerting effects on the fetus and the mother [12].
• Subsequently, during the latter half of pregnancy, the metabolic actions of PL in the mother and fetus may predominate, ensuring the optimal supply of nutrients to the fetus and utilization of the nutrients by fetal tissues [12].
• Infusion of cyclosporine (CSA) hemodynamically parallels ET action, and knowing that CSA effects EC, we hypothesize that the vasoconstrictive effects of CSA are a result of ET synthesis by EC [13].
• These findings may help in the understanding of CSA-induced hypertension and vasculopathy [13].

Chemical compound and disease context of CSH1

• Sequentially measured coronary flow average peak velocity ([APV, cm/s] 0.018 in Doppler guide wire) and epicardial luminal cross-sectional area ([CSA, mm2] 4.3F 30-MHz ultrasound catheter) data were obtained at baseline and during peak hyperemia after administration of 12 to 18 micrograms IC adenosine and 150 to 200 micrograms IC nitroglycerin [14].
• We report reversal of severe neutropenia associated with T-LGL leukemia in five patients treated with cyclosporine (CSA) [15].
• CONCLUSION: CSA is effective in reversing CBDCA resistance in A2780 ovarian cancer cells [16].
• A partial correlation analysis controlling for the effects of serum cholesterol uncovered a significant relationship between average CSA level and proteinuria change (r = -0.76, P < 0.05) [17].
• Nine of the CSA patients were changed to azathioprine and prednisone because of suspected CSA toxicity, and eight of these kidneys began functioning within days, even though they had been oliguric for 21 to 83 days [18].

Biological context of CSH1

• The CSH1 gene is member of the growth hormone (GH) gene cluster on 17q, which consists of two growth hormone genes and three CSH genes [19].
• We also studied the regions of the hCS-L and hCS-A genes which are highly similar to the hCS-B enhancer [20].
• When the hGH-N or hCS-A gene, together with all previously identified cis-acting regulatory sequences, was integrated into the mouse genome, it was expressed only sporadically and at low levels in the transgenic target organs [21].
• Starting from approximately equal levels at 8 weeks of gestation, hCS-A is expressed 5-fold more abundantly than hCS-B by term [22].
• A small percentage of hCS transcripts stably retain intron 4 through gestation, the majority derived from the hCS-A gene. hCS-L transcripts undergo two distinct, developmentally stable, splicing pathways between exons 2 and 3 [22].

Anatomical context of CSH1

• By the use of confocal microscopy recombinant hPL-A2 was localized in the cell membrane [1].
• In addition, two longer alternatively spliced, (intron D retaining) mRNAs isoforms, termed PL-A2 and GH-V2, have been described in placenta and testis [1].
• Similarly, quadriceps muscle strength (MVC) of the GHD patients was 63.2 +/- 12.4% that of controls (P < 0.01), while no significant differences in the force per unit area (F/CSA) and per body mass (F/BM) were found [23].
• Thigh muscle + bone cross-sectional area (CSAM+B) and lower limb muscle plus bone volume (LLVM+B) of the GHD patients were 66.1 +/- 13.7% and 47.6 +/- 6.8% of those recorded in the controls (P < 0.01), whereas no difference in CSA/height2 was found between the two groups [23].
• Here we demonstrate by microinjection of antibodies against CSB and CSA gene products into living primary fibroblasts, that both proteins are required for TCR and for recovery of RNA synthesis after UV damage in vivo but not for basal transcription itself [24].

Associations of CSH1 with chemical compounds

• The translocation of CSA was also induced by treatment of the cells with cisplatin or hydrogen peroxide, both of which produce damage that is subjected to TCR but not induced by treatment with dimethyl sulfate, which produces damage that is not subjected to TCR [25].
• Coincubation of either cremophor alone or cycloheximide with CSA resulted in minimal ET present in the EC supernatants (P less than 0.01 each) [13].
• All patients also received GVHD prophylaxis with the combination of cyclosporine (CSA), methotrexate (MTX), and prednisone (PSE) [26].
• Eleven of 50 children treated with cyclosporin (CSA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF) developed MDS/AML; 8 of these were within 36 months of the diagnosis of AA, much earlier than previous reports [27].
• GVHD prophylaxis consisted of cyclosporine (CSA) and steroids, tacrolimus (FK506) and steroids, or FK506 and methotrexate [28].

Other interactions of CSH1

• There is a developmentally regulated switch in the relative expression of the two chorionic somatomammotropin genes, hCS-A and hCS-B [22].
• In accordance to previously reported data, the hGH-V, the hCS-A and the hCS-B genes which are expressed in placental tissue give rise to the 22-K mRNA but not to 20-K mRNA [29].
• These data indicate that rat Pit 1 binds to the placental hGH-V and hCS-A genes and correlates with their promoter activity in GC cells after gene transfer.(ABSTRACT TRUNCATED AT 250 WORDS)[2]
• DKFZp451B033 (AL831971.1) was the representative cDNA derived from human FCHO2 gene, while FLJ32208 (AK056770.1) was a chimeric cDNA generated by the recombination between FCHO2 and CSH1 genes [30].
• In the corresponding region of the hCS-A enhancer, which is known to be inactive, this element is inactivated by a naturally occurring single base mutation that disrupts hTEF-5 binding [31].

Analytical, diagnostic and therapeutic context of CSH1

• Gel filtration of repair- and transcription-competent whole cell extracts provided evidence that CSB and CSA are part of large complexes of different sizes [24].
• We predict that future patients with COFS syndrome will be found to have mutations in the CSA or XPB genes, and we document successful use of DNA repair for prenatal diagnosis in triplet and singleton pregnancies at risk for COFS syndrome [32].
• The presence of characteristic labeled bands, visualized by autoradiography, determined that hPL-4 and hPL-3, but not hPL-1, contribute to the production of mature hPL [33].
• Since Myo CSA is a function of wall thickness and wall circumference, overestimation of SWT by echocardiography would be expected to produce an overestimation of ES Myo CSA relative to ED Myo CSA [34].
• There was no development of MDS/AML among 41 children treated with either CSA or rhG-CSF or among 48 children who underwent bone marrow transplantation [27].

References