CLDN1 regulates trophoblast apoptosis and proliferation in preeclampsia.

Preeclampsia is a gestational hypertensive disease; however, preeclampsia remains poorly understood. Bioinformatics analysis was applied to find novel genes involved in the pathogenesis of preeclampsia and identified CLDN1 as one of the most differentially expressed genes when comparing patients with preeclampsia and healthy controls. The results of the qRT-PCR, Western blotting and immunohistochemistry experiments demonstrated that CLDN1 was significantly downregulated in the chorionic villi in samples from patients with preeclampsia.

PDIA3 regulates trophoblast apoptosis and proliferation in preeclampsia via the MDM2/p53 pathway.

Protein disulfide isomerase 3 (PDIA3) is a chaperone protein that modulates the folding of newly synthesized glycoproteins, has isomerase and redox activity, and has been implicated in the pathogenesis of many diseases. However, the role of PDIA3 in pregnancy-associated diseases remains largely unknown. Our present study reveals a key role for PDIA3 in the biology of placental trophoblasts from women with preeclampsia (PE).

Investigations of the local distortions and EPR parameters for Cu in xNa O-(30-x)K O-70B O (5 ≤ x ≤ 25 mol%) glasses.

The local distortions and electron paramagnetic resonance parameters for Cu in the mixed alkali borate glasses xNa O-(30-x)K O-70B O (5 ≤ x ≤ 25 mol%) are theoretically studied with distinct modifier Na O compositions x. Owing to the Jahn-Teller effect, the octahedral [CuO ] clusters show significant tetragonal elongation ratios p ~19% along the C axis. With the increase of composition x, the cubic field parameter Dq and the orbital reduction factor k exhibit linearly and quasi-linearly decreasing tendencies, respectively, whereas the relative tetragonal elongation ratio p has quasi-linearly increasing rule with some fluctuations, leading to the minima of g factors at x = 10 mol%.

Epidermal growth factor receptor signalling mediates growth hormone-induced growth of chondrocytes from sex hormone-inhibited adolescent rats.

1. Growth hormone (GH) has been demonstrated to overcome the inappropriate deceleration of growth rate in children with central precocious puberty treated with gonadotropin-releasing hormone analogue (GnRHa). However, the underlying mechanisms remain largely unclear.

[Effects of AMPK on the transcriptional activity of FOXO1 and ubiquitin ligase MuRF1 expression in rat cardiomyocytes].

Objective: To investigate the effects of AICAR on the activity of transcription factor FOXO1 and expression of ubiquitin ligase MuRF1 in rat cardiomyocytes, and explore the possible role of AMP-activated protein kinase (AMPK) in proteolysis pathways.

Methods: In vitro cultured neonatal rat cardiac myocytes were treated with AICAR, and Western blotting was used to detect the phosphorylation of FOXO1 and expression of MuRF1 in the cells.

Results: AICAR activated AMPK in rat cardiac myocytes.

Metformin attenuates ventricular hypertrophy by activating the AMP-activated protein kinase-endothelial nitric oxide synthase pathway in rats.

1. Metformin is an activator of AMP-activated protein kinase (AMPK). Recent studies suggest that pharmacological activation of AMPK inhibits cardiac hypertrophy.

[Association between hemoglobin scavenger receptor CD163 expression and coronary atherosclerotic severity in patients with coronary heart disease].

Objective: To investigate the association between hemoglobin scavenger receptor (CD163) expression levels on monocytic surfaces and coronary atherosclerotic severity in patients with coronary heart disease (CHD) as well as the roles of CD163 in inflammation and lipidperoxidation.

Methods: Eighty-four patients were diagnosed as CHD according to the results of coronary angiography and ACC/AHA diagnostic criteria. The patients were divided into 3 groups: acute myocardial infarction (AMI) group (n = 30), unstable angina (UA) group (n = 30), stable angina (SA) group (n = 24).