Guorong Lv

Cerebral vascular resistance and left ventricular myocardial performance in fetuses with Ebstein's anomaly.

We sought to determine whether cerebral vascular resistance and left ventricular myocardial performance (LVTei) are abnormal in fetuses with Ebsteins anomaly. The pulsatility index of the middle cerebral artery (MCAPI) and umbilical artery (UAPI), LVTei, left ventricular ejection fraction (LVEF), and fetal cardiovascular profile score in 11 fetuses with Ebsteins anomaly were evaluated by fetal echocardiography. MCAPI/UAPI values were calculated for the Ebsteins anomaly group. The control group included 44 healthy fetuses of uncomplicated pregnancies matched for gestational age (according to 1:4). MCAPI and MCAPI/UAPI were significantly lower in fetuses with Ebsteins anomaly than in controls (all P < 0.001). UAPI and LVTei were higher in fetuses with Ebsteins anomaly than in control fetuses ( P < 0.001, P < 0.05, respectively). No significant between group difference was observed for LVEF ( P > 0.05). The median cardiovascular profile score (CVPS) for the fetuses with Ebsteins anomaly (median, 7.0; interquartile range [IQR], 5.0 to 8.0) was a full point lower than for controls (median, 10.0; IQR 10.0 to 10.0). This difference was statistically significant ( P < 0.001). MCAPI and LVTei were both correlated with fetal CVPS in fetuses with Ebsteins anomaly (correlation coefficient (1) = 0.477, P < 0.05; correlation coefficient (2) = -0.602, P < 0.05). In fetuses with Ebsteins anomaly in utero, cerebral vascular resistance is decreased; global LV performance, as assessed by the Tei index, is abnormal.

Triptolide triggers the apoptosis of pancreatic cancer cells via the downregulation of Decoy receptor 3 expression

PurposeTriptolide (TPL) is a diterpenoid triepoxide that effectively induces apoptosis in a wide variety of cancer cells. However, the detailed mechanism by which TPL activates caspase cascade remains elusive. This study aimed to examine the antitumor effects of TPL against pancreatic cancer and investigate the underlying mechanism.MethodsCell proliferation was evaluated by sulforhodamine B assay. The apoptosis was evaluated by caspase activity assay, Western blot and flow cytometry. DcR3 level was measured by ELISA. AsPC-1 xenografts were established to compare the in vivo antitumor effects of TPL and Gemcitabine.ResultsTPL inhibited the proliferation and induced the apoptosis of pancreatic cancer cells in a dose- and time-dependent manner. TPL also inhibited DcR3 expression in a dose- and time-dependent manner. siRNA-mediated DcR3 knockdown sensitized pancreatic cancer cells to TPL-induced apoptosis. In vivo, DcR3 siRNA significantly enhanced TPL-induced apoptosis and tumor growth inhibition. Moreover, TPL showed less toxicity compared to Gemcitabine in mice model.ConclusionsTPL induces the apoptosis of pancreatic cancer cells via the downregulation of DcR3 expression and has the potential as an effective agent against pancreatic cancer.

Maternal Hypoxia Increases the Susceptibility of Adult Rat Male Offspring to High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease

Exposure to an adverse intrauterine environment increases the risk for adult metabolic syndrome. However, the influence of prenatal hypoxia on the risk of fatty liver disease in offspring is unclear. The purpose of the present study was to evaluate the role of reduced fetal oxygen on the development and severity of high-fat (HF) diet-induced nonalcoholic fatty liver disease (NAFLD). Based on design implicating 2 factors, ie, maternal hypoxia (MH) and postnatal HF diet, blood lipid and insulin levels, hepatic histology, and potential molecular targets were evaluated in male Sprague Dawley rat offspring. MH associated with postnatal HF diet caused a significant increase in plasma concentration of triglycerides, free fatty acids, low-density lipoprotein cholesterol, and insulin. Histologically, a more severe form of NAFLD with hepatic inflammation, hepatic resident macrophage infiltration, and progression toward nonalcoholic steatohepatitis was observed. The lipid homeostasis changes and insulin resistance caused by MH plus HF were accompanied by a significant down-regulation of insulin receptor substrate 2 (IRS-2), phosphoinositide-3 kinase p110 catalytic subunit, and protein kinase B. In MH rats, insulin-stimulated IRS-2 and protein kinase B (AKT) phosphorylation were significantly blunted as well as insulin suppression of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase. Meanwhile, a significant up-regulation of lipogenic pathways was noticed, including sterol-regulatory element-binding protein-1 and fatty acid synthase in liver. Our results indicate that maternal hypoxia enhances dysmetabolic liver injury in response to an HF diet. Therefore, the offspring born in the context of maternal hypoxia may require special attention and follow-up to prevent the early development of NAFLD.

Effect of Triptolide on Malignant Peripheral Nerve Sheath Tumours In Vitro and In Vivo

Objective: Malignant peripheral nerve sheath tumours (MPNSTs) are invasive, hard-to-treat, soft tissue sarcomas. In this study, in vitro and in vivo effects of triptolide were investigated using human MPNST cell lines. Methods: Cultured STS-26T and ST88-14 cells were treated with 0 - 100 ng/ml triptolide (for determination of cell proliferation by sulphorhodamine B assay), with 12.5 ng/ml or 25 ng/ml triptolide (for analysis of caspase activity, effects on apoptotic pathway intermediates [by Western blots and flow cytometry], and for measurement of vascular endothelial growth factor [VEGF] and epidermal0 growth factor receptor [EGFR] levels by enzyme-linked immunosorbent assay). A xenograft model was established by injection of STS-26T cells into nude mice, and the effects of 250 μg/kg triptolide on tumour growth and apoptosis were compared with controls. Results: Triptolide significantly inhibited cell proliferation and induced apoptosis in vitro, through activation of caspases, in a dose- and time-dependent manner; VEGF and EGFR levels were suppressed. In vivo, triptolide inhibited the growth of STS-26T xenografts and reduced apoptosis. Conclusion: Triptolide may have a therapeutic benefit in MPNST treatment.

Hypoxia during pregnancy in rats leads to the changes of the cerebral white matter in adult offspring.

The aim of the present study is to evaluate the effect of reduced fetal oxygen supply on cerebral white matter in the adult offspring and further assess its susceptibility to postnatal hypoxia and high-fat diet. Based on a 3 x 2 full factorial design consisting of three factors of maternal hypoxia, postnatal high-fat diet, and postnatal hypoxia, the ultrastructure of myelin, axon and capillaries were observed, and the expression of myelin basic protein (MBP), neurofilament-H+L(NF-H+L), and glial fibrillary acidic protein (GFAP) was analyzed in periventricular white matter of 16-month-old offspring. Demyelination, injured axon and damaged microvasculars were observed in maternal hypoxia offspring. The main effect of maternal hypoxia lead to decreased expression of MBP or NF-H+L, and increased expression of GFAP (all P<0.05). Moreover, there was positive three-way interaction among maternal hypoxia, high-fat diet and postnatal hypoxia on MBP, NF-H+L or GFAP expression (all P<0.05). In summary, our results indicated that maternal hypoxia during pregnancy in rats lead to changes of periventricular white matter in adult offspring, including demyelination, damaged axon and proliferated astroglia. This effect was amplified by high-fat diet and postnatal hypoxia.

Reference ranges of fetal spleen biometric parameters and volume assessed by three‐dimensional ultrasound and their applicability in spleen malformations

The aims of this article are to establish three‐dimensional ultrasonographic nomograms of normal fetal spleen size and to evaluate the clinical application value.

Evaluation of Gastric Emptying in Diabetic Gastropathy by an Ultrasonic Whole Stomach Cylinder Method

In order to explore the accuracy of ultrasonic whole stomach cylinder measurement (UWSCM) in the evaluation of gastric emptying, we measured the gastric emptying times (ET) at 25% (T1), 50% (T2) and 75% (T3) of healthy subjects and patients with diabetic gastropathy by UWSCM and scintigraphy. The ET of patients were compared with their clinical symptom scores. We found that the ET measured by UWSCM showed no significant difference with scintigraphy (p > 0.05). The correlation between them was good, and the correlation coefficient of T3 reached 0.744 (p < 0.05). All emptying times in the diabetic patients were longer than those in the healthy subjects (p < 0.05). The T3 in the diabetic group measured by UWSCM had the best correlation with the symptom index (r = 0.469, p < 0.05). We conclude that ET measured by UWSCM is accurate and T3 combining the symptoms index provides an accurate clinical basis for gastropathy.

Intermittent maternal hypoxia has an influence on regional expression of endothelial nitric oxide synthase in fetal arteries of rabbits

Background:Maternal hypoxia induces sustained fetal adaptations associated with changes in gene expression. We hypothesized that intermittent maternal hypoxia has an influence on regional expression of endothelial nitric oxide synthase (eNOS) in fetal arteries of New Zealand White rabbits.Methods:Timed-pregnant New Zealand White rabbits (term = 30 ± 1 d) were randomly assigned to a normoxic control group (n = 5) or a hypoxia group (12% O2, n = 5) during days 10–29 of pregnancy. At the end of pregnancy (29 d gestation), blood samples were collected from mothers and fetuses. Carotid and femoral arteries of fetuses were extracted for eNOS mRNA and protein concentration and analysis of total NOS activities.Results:Our data demonstrate that chronic intermittent maternal hypoxia significantly increased eNOS mRNA and protein concentrations and total NOS activities in carotid artery segments but decreased eNOS mRNA and protein concentrations and total NOS activities in femoral artery segments in the same fetuses. Vascular endothelial cells, but not smooth muscle cells, of fetal rabbits exhibited positive immunostaining for the eNOS protein.Conclusion:These observations suggest that chronic hypoxia can regulate regional expression of eNOS as an adaptive response to hypoxic stress in fetal arteries.

The effect of fetal congenital heart disease on in utero urine production rate

To evaluate the influence of congenital heart disease (CHD) or congestive heart failure (CHF) on fetal urine production rate (UPR) and to establish normal reference intervals.

Ultrasound probe pressure but not maternal Valsalva maneuver alters Doppler parameters during fetal middle cerebral artery Doppler ultrasonography.

To determine the effects of increased ultrasound probe pressure and maternal Valsalva maneuver (VM) on the middle cerebral artery (MCA) Doppler ultrasonography in fetuses.