Comparison of acid volatile sulphide, metal speciation, and diffusive gradients in thin-film measurement for metal toxicity assessment of sediments in Lake Chaohu, China.

The toxicity of heavy metals in sediments is inseparable from their forms in the environment. Traditional sediment toxicity assessment systems, such as total metals, dissolved metals in pore water, metals extracted by the Community Bureau of Reference procedure, and acid volatile sulphide (AVS)-simultaneously extracted metal (SEM), have their own limitations. This study revealed the horizontal and vertical distribution characteristics of AVS and SEM in Lake Chaohu and three typical groups of two-dimensional profiles of diffusive gradients in thin-film (DGT)-labile S(-II) were obtained at representative sampling sites.

Involvement of kisspeptin in androgen-induced hypothalamic endoplasmic reticulum stress and its rescuing effect in PCOS rats.

Endoplasmic reticulum (ER) stress, with adaptive unfolded protein response (UPR), is a key link between obesity, insulin resistance and type 2 diabetes, all of which are often present in the most common endocrine-metabolic disorder in women of reproductive age, polycystic ovary syndrome (PCOS), which is characterized with hyperandrogenism. However, the link between excess androgen and endoplasmic reticulum (ER) stress/insulin resistance in patients with polycystic ovary syndrome (PCOS) is unknown. An unexpected role of kisspeptin was reported in the regulation of UPR pathways and its involvement in the androgen-induced ER stress in hypothalamic neuronal cells.

Abnormal CFTR Affects Glucagon Production by Islet α Cells in Cystic Fibrosis and Polycystic Ovarian Syndrome.

Glucagon, produced by islet α cells, functions to increase blood glucose. Abnormal glucose levels are often seen in cystic fibrosis (CF), a systematic disease caused by mutations of the CF transmembrane conductance regulator (CFTR), and in polycystic ovarian syndrome (PCOS), an endocrine disorder featured with hyperandrogenism affecting 5-10% women of reproductive age. Here, we explored the role of CFTR in glucagon production in α cells and its possible contribution to glucagon disturbance in CF and PCOS.

Bronchial hyperresponsiveness and obesity in middle age: insights from an Australian cohort.

The association between obesity and bronchial hyperresponsiveness (BHR) is incompletely characterised. Using the 2006 follow-up of the Tasmanian Longitudinal Health Study, we measured the association between obesity and BHR and whether it was mediated by small airway closure or modified by asthma and sex of the patient.A methacholine challenge measured BHR.

Involvement of small G protein RhoB in the regulation of proliferation, adhesion and migration by dexamethasone in osteoblastic cells.

Long-term exposure to therapeutic doses of glucocorticoids (GCs) results in bone remodeling, which frequently causes osteoporosis and fracture healing retardation because of the abnormality of osteoblastic proliferation and differentiation. The mechanisms of GCs' effect on osteoblasts are largely unknown. In this present study, we found that dexamethasone (Dex) could induce the expression of the small G protein, RhoB, in mRNA and protein levels in the osteoblast-derived osteosarcoma cell lines MG-63.

Up-regulation of stomatin expression by hypoxia and glucocorticoid stabilizes membrane-associated actin in alveolar epithelial cells.

Stomatin is an important lipid raft-associated protein which interacts with membrane proteins and plays a role in the membrane organization. However, it is unknown whether it is involved in the response to hypoxia and glucocorticoid (GC) in alveolar epithelial cells (AEC). In this study we found that hypoxia and dexamethasone (dex), a synthetic GC not only up-regulated the expression of stomatin alone, but also imposed additive effect on the expression of stomatin in A549 cells, primary AEC and lung of rats.

Therapeutic effects of inhaling aerosolized surfactant alone or with dexamethasone generated by a novel noninvasive apparatus on acute lung injury in rats.

Background: Pulmonary surfactant (PS) administration has been attempted for the treatment of adults with acute lung injury (ALI)/adult respiratory distress syndrome. Aerosolized surfactants inhaled by spontaneous breathing may be an effective method of surfactant-based therapies. Using a noninvasive apparatus, we evaluated the therapeutic effects of aerosolized PS alone or together with dexamethasone (Dex) on a rat model of ALI.

RhoB is involved in lipopolysaccharide-induced inflammation in mouse in vivo and in vitro.

Small GTPase RhoB has been well documented in regulating cell adhesion, motility, proliferation, and survival, but to date, there is little information about the relationship between RhoB and inflammation. In this study, the mRNA and protein levels of RhoB were induced by lipopolysaccharide (LPS) in RAW264.7 cells determined by real-time PCR and Western blot.

Dexamethasone enhances cell resistance to chemotherapy by increasing adhesion to extracellular matrix in human ovarian cancer cells.

Glucocorticoids (GCs) are widely used as co-medication in the therapy of solid malignant tumors to relieve some of the side effects of chemotherapeutic drugs. However, recent studies have shown that GCs could render cancer cells more resistant to cytotoxic drug-induced apoptosis, but the mechanism is largely unknown. In the present study, we found that the treatment of human ovarian cancer cell lines HO-8910 and SKOV3 with synthetic GCs dexamethasone (Dex) significantly increased their adhesion to extracellular matrix (ECM) and their resistance to apoptosis induced by cytotoxic drugs cisplatin and paclitaxel.

Expression of Gli1 correlates with the transition of breast cancer cells to estrogen-independent growth.

The failure of breast cancer treatment is largely due to the development of estrogen independence. Current data illustrate that Hedgehog (Hh) signaling may play an important role in breast cancer development. Here, we show that the expression of the Hh effector protein, Gli1 was significantly higher in estrogen-independent breast cancer cells than in estrogen-dependent cells.

Signal regulatory protein alpha1 is involved in the inhibitory effect of glucocorticoid receptor on the proliferation of murine macrophage RAW264.7 cell and mouse peritoneal macrophage.

Glucocorticoid (GC) effectively suppresses immune and inflammatory responses and inhibits the growth of several types of cells, but the role of GC and its receptor on macrophage proliferation is unclear. In our previous work, we found RAW-GR(-) cells (murine macrophage RAW264.7 cells stably transfected with GR-siRNA expression vector by RNA interference) grew faster by about twofold.

Role of glucocorticoids and glucocorticoid receptor in priming of macrophages caused by glucocorticoid receptor blockade.

We previously reported that glucocorticoid receptor (GR) blockade (injected with GR antagonist RU486) primed the host responses to lipopolysaccharide. Since decrease of GR and elevated glucocorticoids (GCs) have been always reported as parallel responses, we hypothesize that both GCs and GR play important roles in GR blockade induced priming. We first confirm that the production of nitric oxide (NO), superoxide (O2-), and PKCalpha expression are all increased in peritoneal macrophages from GR blockade rats, indicating that macrophages are primed by GR blockade.

Lipopolysaccharide primes macrophages to increase nitric oxide production in response to Staphylococcus aureus.

Sepsis, the leading cause of death in intensive care units, is associated with overproduction of nitric oxide (NO). The mechanism concerning the NO production in the sepsis caused by both Gram-negative and Gram-positive bacteria is largely unknown. The present study examines the effect of lipopolysaccharide (LPS) on Staphylococcus aureus-induced NO production in macrophages.

Up-regulation of RhoB by glucocorticoids and its effects on the cell proliferation and NF-kappaB transcriptional activity.

Although there is ample evidence that glucocorticoids (GCs) have an antiproliferative effect on many cell types, the molecular mechanism remains elusive. We reported in our previous study that Dex treatment led to cell growth arrest in a human ovarian cancer cell HO-8910. RhoB, as a member of Rho GTPases, have been implicated to be a negative regulator of cell proliferation.

[Mechanism of inhibiting proliferation of human ovarian cancer cells of the line HO-8910 by dexamethasone: the role of RhoB signaling pathway].

Objective: To observe the effect of dexamethasone (Dex) on the proliferation of human ovarian cancer cells of the line HO-8910, and explore the role of RhoB signaling pathway in this process.

Methods: Human ovarian cancer cells of the line HO-8910he were cultured in culture fluids with or without different concentrations of Dex. The cell growth levels in anchor-dependent and anchor-independent manner were detected by MTT and soft agar assay.