LncRNA uc003fir promotes CCL5 expression and negatively affects proliferation and migration of trophoblast cells in preeclampsia.

Objective: To evaluate the role of lncRNA uc003fir in the progression and development of preeclampsia (PE).

Design: Paired test using placental tissue collected from PE women and normally pregnant women.

Setting: First Hospital of Soochow University, Suzhou, China.

Prenatal high-salt diet impaired vasodilatation with reprogrammed renin-angiotensin system in offspring rats.

Aims: High-salt diet is linked to hypertension, and prenatal high-salt diet increases the risk of cardiovascular diseases in the offspring. The present study investigated whether and how prenatal high-salt diet influenced nitric oxide-mediated vasodilatation in the offspring.

Methods And Results: Pregnant rats were fed either normal-salt (1% sodium chloride) or high-salt (8% sodium chloride) diet during gestation.

Emerging evidence supports grouping by location of early gastric carcinoma for appropriate clinical management in Chinese patients.

Gastric cancer is common in China. At present, early detection with prompt resection of early gastric carcinoma (EGC) is crucial for improving patient's survival. Because of high heterogeneity of EGC in Chinese patients we reviewed recent clinicopathological and molecular evidence and proposed a grouping EGC in three subgroups according to their location for appropriate management.

Prenatal caffeine damaged learning and memory in rat offspring mediated by ARs/PKA/CREB/BDNF pathway.

Prenatal exposure to caffeine can cause developmental problems. This study determined chronic influence of prenatal caffeine at relatively higher doses on cognitive functions in the rat offspring. Pregnant Sprague-Dawley rats (4-month-old) were exposed to caffeine (20 mg/kg, twice a day) for whole pregnancy from gestational day 4.

Micropapillary early gastric carcinoma with distinct clinicopathological features, high risk for lymph node metastasis, and dismal prognosis: a multicenter clinicopathological study of 29 cases identified in 1890 early gastric carcinoma radical gastrectomies.

Clinicopathology and risk factors of lymph node metastasis (LNM) in micropapillary early (pT1) gastric carcinoma (MEGC) remain elusive because of the extreme rarity. In this multicenter study, we investigated 1890 consecutive radical resections of early gastric carcinoma diagnosed with the World Health Organization criteria and identified 29 (1.5%) MEGC cases with a small (≥5%) micropapillary component.

Magnesium Sulfate-Mediated Vascular Relaxation and Calcium Channel Activity in Placental Vessels Different From Nonplacental Vessels.

Background: Magnesium sulfate (MgSO) has been used as a common therapy for preeclampsia and eclampsia for many years. MgSO decreases peripheral vascular resistance so as to reduce maternal blood pressure. Whether placental blood vessels react to MgSO in the same patterns as that in maternal vessels is largely unknown.

Methylation-reprogrammed Wnt/β-catenin signalling mediated prenatal hypoxia-induced brain injury in foetal and offspring rats.

Prenatal hypoxia (PH) is a common pregnancy complication, harmful to brain development. This study investigated whether and how PH affected Wnt pathway in the brain. Pregnant rats were exposed to hypoxia (10.

Neural stem cell therapies and hypoxic-ischemic brain injury.

Hypoxic-ischemic brain injury is a significant cause of morbidity and mortality in the adult as well as in the neonate. Extensive pre-clinical studies have shown promising therapeutic effects of neural stem cell-based treatments for hypoxic-ischemic brain injury. There are two major strategies of neural stem cell-based therapies: transplanting exogenous neural stem cells and boosting self-repair of endogenous neural stem cells.

Downregulation of L-Type Voltage-Gated Ca, Voltage-Gated K, and Large-Conductance Ca-Activated K Channels in Vascular Myocytes From Salt-Loading Offspring Rats Exposed to Prenatal Hypoxia.

Background: Prenatal hypoxia is suggested to be associated with increased risks of hypertension in offspring. This study tested whether prenatal hypoxia resulted in salt-sensitive offspring and its related mechanisms of vascular ion channel remodeling.

Methods And Results: Pregnant rats were housed in a normoxic (21% O) or hypoxic (10.

Impact of prenatal hypoxia on fetal bone growth and osteoporosis in ovariectomized offspring rats.

Prenatal hypoxia causes intrauterine growth retardation. It is unclear whether/how hypoxia affects the bone in fetal and offspring life. This study showed that prenatal hypoxia retarded fetal skeletal growth in rats, inhibited extracellular matrix (ECM) synthesis and down-regulated of insulin-like growth factor 1 (IGF1) signaling in fetal growth plate chondrocytes in vivo and in vitro.

Chronic Prenatal Hypoxia Down-Regulated BK Channel Β1 Subunits in Mesenteric Artery Smooth Muscle Cells of the Offspring.

Background/aims: Chronic hypoxia in utero could impair vascular functions in the offspring, underlying mechanisms are unclear. This study investigated functional alteration in large-conductance Ca2+-activated K+ (BK) channels in offspring mesenteric arteries following prenatal hypoxia.

Methods: Pregnant rats were exposed to normoxic control (21% O2, Con) or hypoxic (10.

Clinical practice guidelines for post-stroke depression in China.

Post-stroke depression (PSD) is a very common complication that leads to increased physical disability, poor functional outcome, and higher mortality. Therefore, early detection and treatment are very important. Since there are currently no specific guidelines for this disorder in China, the purpose of this study was to develop PSD guidelines and provide suggestions for clinicians and related workers.

Synergetic Effects of Prenatal and Postnatal High Sucrose Intake on Glucose Tolerance and Hepatic Insulin Resistance in Rat Offspring.

Scope: High sucrose intake during pregnancy is linked to type 2 diabetes mellitus and altered insulin resistance.

Methods And Results: This study attempts to ascertain whether prenatal high sucrose intake (20% sucrose) alleviates the detrimental effects of high postnatal sugar consumption in the offspring, and the molecular mechanisms are investigated using a rat model. High prenatal sucrose exposure increases the body weight of the offspring at 1-3 weeks of age.

What is precise pathophysiology in development of hypertension in pregnancy? Precision medicine requires precise physiology and pathophysiology.

It is widely accepted that placental ischemia is central in the evolution of hypertension in pregnancy. Many studies and reviews have targeted placental ischemia to explain mechanisms for initiating pregnancy hypertension. The placenta is rich in blood vessels, which are the basis for developing placental ischemia.

Lower maternal and fetal vitamin D status and higher placental and umbilical vitamin D receptor expression in preeclamptic pregnancies.

Objective: To explore associations between maternal and fetal vitamin D status in preeclamptic pregnancies.

Methods: A case-control experiment was carried out with proportion ratio of 1:1 (controls: n = 60 vs cases: n = 60). Blood collection of both maternal and cord were performed before and during delivery, respectively, and 25(OH)D measurement was conducted.

Prenatal Hypoxia Induced Dysfunction in Cerebral Arteries of Offspring Rats.

Background: Hypoxia during pregnancy could cause abnormal development and lead to increased risks of vascular diseases in adults. This study determined angiotensin II (AII)-mediated vascular dysfunction in offspring middle cerebral arteries (MCA).

Methods And Results: Pregnant rats were subjected to hypoxia.

miR-144 may regulate the proliferation, migration and invasion of trophoblastic cells through targeting PTEN in preeclampsia.

Previous studies indicated that microRNAs (miRNAs) were aberrantly expressed in the placentas of patients with Preeclampsia (PE); however, the underlying mechanism still requires further investigation. The aim of this study is to investigate the roles of miR-144 in preeclampsia and the related mechanism. The expression of miR-144 and PTEN in 30 placentas of patients with PE and 30 normal placentas was compared; next, HTR8/SVneo cells were transfected with miR-144 mimics and miR-144 inhibitors and cultured for 48h, and the proliferation and apoptosis, cell migration and invasion of the cells were examined; furthermore, the expression PTEN, Caspase-3 and Bcl-2 was examined; next, dual luciferase reporter assay has been performed to confirm that PTEN is a direct target of miR-144; finally, HTR-8/SVneo cells were transfected with either PTEN overexpression plasmid or PTEN RNAi to determine whether knockdown or overexpression of PTEN can mimic the effect of miR-144 We have observed that the expression of miR-144 was significantly decreased and the expression of PTEN was markedly increased in placentas of patients with PE compared with normal placentas; moreover, transfection of miR-144 mimics in trophoblastic cells induced significant increase in cell proliferation, migration, invasion, and decrease in cell apoptosis, and also affected the cell cycles; on the other hand, transfection of miR-144 inhibitors has shown the opposite effects; furthermore, transient overexpression of miR-144 induced marked decrease in the expression of PTEN, Caspase-3 and increase in expression of Bcl-2 (P<0.

[Elevation of red cell distribution width during hospitalization predicts mortality in patients with sepsis].

Objective: To investigate the association of red cell distribution width (RDW) with prognosis in patients with sepsis.

Methods: Patients with sepsis admitted to intensive care unit (ICU) of the First Hospital of Soochow University from January 2011 to December 2016 were enrolled. All clinical data were collected for participants, which mainly included basic data, main underlying disease, site of infection, acute physiology and chronic health evaluation II(APACHE II) score, blood routine test, biochemical test, blood gas analysis, coagulation index, procalcitonin (PCT), hospitalization days, and 28-day and 90-day mortality.

Prenatal high sucrose intake affected learning and memory of aged rat offspring with abnormal oxidative stress and NMDARs/Wnt signaling in the hippocampus.

Maternal over-nutrition may predispose offspring to obesity, type 2 diabetes and other adult diseases. The present study investigated long-term impact of prenatal high sucrose (HS) diets on cognitive capabilities in aged rat offspring. The fasting plasma glucose concentration did not differ between the control and HS groups.

"Three Hits" Hypothesis for Developmental Origins of Health and Diseases in View of Cardiovascular Abnormalities.

"Fetal Origins of Adult Diseases" (FOAD) or "Barker hypothesis," also known as the developmental origins of health and diseases (DoHaD), was initially proposed by David Barker in the 1980s. Progress in past 2 to 3 decades demonstrated that many adult disorders, including hypertension, diabetes, obesity, cancer, and others, could be linked to poor development resulting from in utero insults. Utero-environments play a critical role in fetal development.

Prenatal exposure to the Great Chinese Famine and mid-age hypertension.

Background: One of the most terrible famines last century was Great Chinese Famine (GCF) in 1959~1961 when millions of people died from starving. Under-nutrition during famine between the Western and Eastern (Dutch Hungry vs. GCF) was similar, while cardiovascular consequences might not be the same.

Maternal high-sucrose diets altered vascular large-conductance Ca2+-activated K+ channels via reactive oxygen species in offspring rats.

Overnutrition during pregnancy could increase risks of cardiovascular diseases in late life. This study investigated whether and how reactive oxygen species (ROS) may influence functions of large-conductance Ca2+-activated K+ channels (BKCa) in the offspring exposed to prenatal high sucrose (HS). We found that prenatal HS diets significantly increased phenylephrine (PE)-induced vessel contractions in mesenteric arteries of the adult offspring.

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia.

The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.

Pregnancy Reprograms Large-Conductance Ca-Activated K Channel in Uterine Arteries: Roles of Ten-Eleven Translocation Methylcytosine Dioxygenase 1-Mediated Active Demethylation.

The large-conductance Ca-activated K (BK) channel is of critical importance in pregnancy-mediated increase in uterine artery vasodilation and blood flow. The present study tested the hypothesis that active DNA demethylation plays a key role in pregnancy-induced reprogramming and upregulation of BK channel β1 subunit (BKβ1) in uterine arteries. Uterine arteries were isolated from nonpregnant and near-term pregnant sheep.

Maternal high salt diet altered Adenosine-mediated vasodilatation via PKA/BK channel pathway in offspring rats.

Scope: High salt (HS) diets are related to cardiovascular diseases, and prenatal HS was suggested to increase risks of coronary artery diseases in the offspring. This study tested the hypothesis that prenatal HS may influence Adenosine-induced vasodilatation via protein kinase A (PKA) pathway in coronary arteries.

Methods And Results: Sprague-Dawley rats were fed with 8% salt diet for gestation, the control was fed with 0.