TLR9 mediates the activation of NLRP3 inflammasome and oxidative stress in murine allergic airway inflammation.

Toll-like receptor 9 (TLR9) has been reported to mediate airway inflammation, however, the underlying mechanism is poorly understood. In the present study, our objective was to reveal whether TLR9 regulates NLRP3 inflammasome and oxidative stress in murine allergic airway inflammation and Raw264.7 cells.

Histone deacetylase-2 expression and activity in children with nephrotic syndrome with different glucocorticoid response.

Background: Glucocorticosteroid (GC) is one of the most effective drugs available for the treatment of primary nephrotic syndrome (PNS) in children. However, some patients show little or no response to GC. The purpose of our research was to observe and describe the different levels of histone deacetylase-2 (HDAC2) expression in peripheral blood lymphocytes in children with PNS compared with various responses to the GC treatment, with the primary aim to assess the correlation between HDAC2 and GC resistance in PNS children.

Sequential invasive-noninvasive mechanical ventilation weaning strategy for patients after tracheostomy.

Background: Because the continuity and integrity of the trachea are likely damaged to some extent after tracheostomy, the implementation of sequential ventilation has certain difficulties, and sequential invasive-noninvasive ventilation on patients after tracheostomy is less common in practice. The present study aimed to investigate the feasibility of invasive-noninvasive sequential weaning strategy in patients after tracheostomy.

Methods: Fifty patients including 24 patients with withdrawal of mechanical ventilation (conventional group) and 26 patients with sequential invasive-noninvasive weaning by directly plugging of tracheostomy (sequential group) were analyzed retrospectively after appearance of pulmonary infection control (PIC) window.

Reversed expression of GRIM-1 and GRP78 in human non-small cell lung cancer.

Gene associated with retinoid and interferon-induced mortality 1 (GRIM-1) acts as a tumor growth suppressor via apoptosis induction. However, GRIM-1 expression in human non-small cell lung cancer (NSCLC) and its potential interaction with another apoptosis-associated protein-glucose-regulated protein 78 (GRP78)-are as yet unknown. Using 40 surgical specimens, we showed significantly lower expression of GRIM-1 in NSCLC at both protein and messenger RNA (mRNA) levels compared with that in normal tissues (P < .

The combination of angiotensin II and 5-azacytidine promotes cardiomyocyte differentiation of rat bone marrow mesenchymal stem cells.

Bone marrow mesenchymal stem cells (BMMSCs) are ideal seed cells for tissue engineering and regenerative medicine. Many studies have shown that 5-azacytidine (5-aza) can induce BMMSCs to differentiate into cardiomyogenic cells, but some issues still remain to be resolved. In this study, we investigated the effects of angiotensin II (Ang II) on the proliferation and differentiation of BMMSCs induced by 5-aza in vitro.

Gene associated with retinoid-interferon-induced mortality-19 suppresses growth of lung adenocarcinoma tumor in vitro and in vivo.

Lung cancer is currently the leading cause of cancer-related death in the world. Signal transducers and activators of transcription 3 (STAT3) is a major oncogenic transcription factor involved in the development and progression of a number of human tumors including lung denocarcinoma. Gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) is known to functionally interact with STAT3 and inhibit its transcriptional activity.

Chronic all-trans retinoic acid administration induced hyperactivity of HPA axis and behavioral changes in young rats.

Although clinical reports suggest a possible relationship between excess retinoids and the development of depression, the effect of retinoids on mood-related behavior remains controversial. Hyperactivity of the hypothalamus-pituitary-adrenal (HPA) axis plays a key role in the development of affective disorders. The present study aimed to elucidate the effect of retinoid on the activity of HPA axis in rat and whether this goes together with behavioral changes.

Increased expression level of corticotropin-releasing hormone in the amygdala and in the hypothalamus in rats exposed to chronic unpredictable mild stress.

Objective: Corticotropin-releasing hormone (CRH) plays an important role in neuroendocrine, autonomic and behavioral responses to stressors. In the present study, the effect of chronic unpredictable mild stress (CUMS) on CRH neurons was investigated in rat brain.

Methods: The rats were exposed to one of the stressors each day for 21 d.

Several interleukin-4 and interleukin-13 gene single nucleotide polymorphisms among Chinese asthmatic patients.

Asthma is a common respiratory disease associated with airway hyperactivity and high total serum immunoglobulin E (IgE) levels. The asthmatic phenotypes are widely considered to be caused by environmental effects on genetically predisposed individuals. Interleukin (IL)-4 and IL-13 act on B cells and regulate the IgE production, and the single nucleotide polymorphisms (SNPs) in the IL-4 and IL-13 genes are implicated in the pathogenesis of asthma.

Lithium regulates hippocampal neurogenesis by ERK pathway and facilitates recovery of spatial learning and memory in rats after transient global cerebral ischemia.

Recent studies have demonstrated that lithium has a neuroprotective effect against brain ischemia. Whether this effect is mediated by hippocampal neurogenesis remains unknown. The ERK (extracellular signal-regulated kinase) pathway plays an essential role in regulating neurogenesis.

Mifepristone repairs region-dependent alteration of synapsin I in hippocampus in rat model of depression.

Clinical investigations present much evidence that the glucocorticoid receptor (GR) antagonist mifepristone leads to a rapid amelioration of depression. The molecular mechanisms of mifepristone involved in the treatment of depression are not fully understood. Depression is associated with hippocampal plasticity, for which increased excitatory amino acid (EAA) release in CA3 induced by chronic stress is responsible, and glucocorticoids have a permissive role and act synergistically with EAAs in producing neuronal damage.

Lithium improves the behavioral disorder in rats subjected to transient global cerebral ischemia.

Previous study has indicated that chronic treatment with lithium protects brain against ischemic injury by reducing apoptotic death. To investigate whether lithium improves the behavioral disorder induced by transient global cerebral ischemia, we examined the effects of lithium treatment on the performance of rats in a set of behavioral tests, i.e.

Alterations of hHrd1 expression are related to hyperphosphorylated tau in the hippocampus in Alzheimer's disease.

The degradation of aberrantly phosphorylated tau in neurons plays an important role in the pathogenesis of Alzheimer's disease (AD). hHrd1 is a newly identified ubiquitin ligase involved in the endoplasmic reticulum (ER)-associated protein degradation. The expression and function of hHrd1 in AD brain remains elusive.

Brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase by Ca(2+)/calmodulin-dependent protein kinase II in rat hippocampus.

Aim: To investigate whether brain ischemia induces serine phosphorylation of neuronal nitric oxide synthase (nNOS) by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and the interaction between CaMKII? and nNOS in rat hippocampus.

Methods: Brain ischemia was induced by bilateral carotid artery occlusion procedure. Phosphorylation and the interaction of proteins were studied by immunoprecipitation and immunoblotting.

PSD-95 promotes CaMKII-catalyzed serine phosphorylation of the synaptic RAS-GTPase activating protein SynGAP after transient brain ischemia in rat hippocampus.

Recent studies have indicated that cerebral ischemia induces rapid serine phosphorylation of synaptic RAS-GTPase activating protein (SynGAP) by calcium/Camodulin-dependent protein kinase II (CaMKII) in rat hippocampus. To further illustrate the mechanisms underlying these processes, we examined the effects of transient (15 min) brain ischemia followed by reperfusion (0, 30 min, 6 h, 1, 3 days) on serine phosphorylation of SynGAP and interactions involving SynGAP, postsynaptic density protein 95 (PSD95) and CaMKII in rat hippocampus. Transient brain ischemia was induced by the method of four-vessel occlusion in Sprague-Dawley rats.

Competitive binding of postsynaptic density 95 and Ca2+-calmodulin dependent protein kinase II to N-methyl-D-aspartate receptor subunit 2B in rat brain.

Aim: To investigate the interactions among postsynaptic density 95 (PSD-95), Ca2+-calmodulin dependent protein kinase IIalpha (CaMKIIalpha), and N-methyl-D-aspartate receptor subunit 2B (NR2B) during ischemia and reperfusion in hippocampus of rats.

Methods: Brain ischemia was induced by four-vessel occlusion procedure in rats. Immunoprecipitation and immunoblotting were performed to study the interactions and phosphorylation of proteins.

Postsynaptic density protein 95 mediates Ca2+/calmodulin-dependent protein kinase II-activated serine phosphorylation of neuronal nitric oxide synthase during brain ischemia in rat hippocampus.

Recent study has indicated that postsynaptic density protein 95 (PSD95) promotes Ca2+/calmodulin-dependent protein kinase II (CaMKII)-mediated serine phosphorylation of neuronal nitric oxide synthase (nNOS). To investigate whether PSD95 is involved in the brain ischemia-induced enhancement of serine phosphorylation of nNOS by CaMKII in rat hippocampus, we examined the interactions among CaMKIIalpha, PSD95 and nNOS, and the effects of suppression of PSD95 expression on both the increased serine phosphorylation of nNOS and the interactions mentioned above by immunoprecipitation and immunoblotting. The following results were observed: (1) brain ischemia increased markedly the interactions of CaMKIIalpha and nNOS with PSD95.