Inhibitory effect of receptor for advanced glycation end product‑specific small interfering RNAs on the development of hepatic fibrosis in primary rat hepatic stellate cells.

Specific small interfering RNAs (siRNAs) targeting receptor for advanced glycation end products (RAGE) inhibit the expression of RAGE, α-smooth muscle actin and type I collagen in the T6 hepatic stellate cells (HSCs), indicating that RAGE is important for the activation of HSCs and the expression of collagen. The present study aimed to investigate the effect of specific siRNAs targeting RAGE on the development of hepatic fibrosis (HF), using primary rat HSCs, which were isolated and cultured in vitro. The expression vectors for specific siRNAs targeting RAGE were constructed and transfected into primary rat HSCs.

Anti-fibrotic effects of specific-siRNA targeting of the receptor for advanced glycation end products in a rat model of experimental hepatic fibrosis.

Since the receptor for advanced glycation end products (RAGE)-ligand axis has been demonstrated to be important in fibrogenesis, rat models may be used to assess whether specific small interfering RNAs (siRNAs) that target RAGE are able to reduce the progression of hepatic fibrosis. However, the effect of RAGE-targeted siRNA on established hepatic fibrosis remains to be elucidated. In the present study, RAGE-specific siRNA expression vectors were constructed prior to the animal experiment.

In vivo and in vitro expression of the RASAL1 gene in human gastric adenocarcinoma and its clinicopathological significance.

Recent studies have suggested that the RAS protein activator like-1 (RASAL1) is a potential tumor suppressor, which is found to be reduced in certain human cancers. Its downregulation is involved in the progression of malignancies. However, whether or not RASAL1 plays a role in the development of gastric cancer remains to be determined.

Elevation of high-mobility group protein box-1 in serum correlates with severity of acute intracerebral hemorrhage.

High-mobility group protein box-1 (HMGB1) is a proinflammatory involved in many inflammatory diseases. However, its roles in intracerebral hemorrhage (ICH) remain unknown. The purpose of this study was to examine the correlation between changes in serum levels of HMGB1 following acute ICH and the severity of stroke as well as the underlying mechanism.

HMBG1 mediates ischemia-reperfusion injury by TRIF-adaptor independent Toll-like receptor 4 signaling.

High-mobility group protein box-1 (HMGB1) has recently been recognized as a novel candidate in a specific upstream pathway promoting inflammation after brain ischemia. However, its downstream pathway and underlying mechanism have yet to be elucidated. The HMGB1 level in the acute cerebral infarct (ACI) group was significantly increased compared with that of control group, and correlated with the severity of neurologic impairment of ACI patients.

Efficacy and safety of placing nasoenteral feeding tube with transnasal ultrathin endoscope in critically ill patients.

Background: The placement of an enteral feeding tube is the foundation for providing enteral nutrition. But due to the anatomic complexity of the stomach and the duodenum, to a certain degree, there are some technical difficulties in the placement of postpyloric feeding tube, especially in critically ill patients. This study aimed to evaluate the efficacy and safety of placing nasoenteral feeding tube with a transnasal ultrathin endoscope.

High-mobility group protein box-1 and its relevance to cerebral ischemia.

High-mobility group box-1 (HMGB1) was originally identified as a ubiquitously expressed, abundant, nonhistone DNA-binding protein. It has well-established functions in the maintenance of nuclear homeostasis. The HMGB1 can either be passively released into the extracellular milieu in response to necrotic signals or actively secreted in response to inflammatory signals.

Upregulated expression of toll-like receptor 4 in monocytes correlates with severity of acute cerebral infarction.

In the present study, we observed the expression of toll-like receptor 4 (TLR4) and its downstream signal pathway in peripheral blood monocytes (PBMs) from patients with acute cerebral infarct (ACI). The expression of TLR4 and MyD88 by PBMs was determined by flow cytometry and reverse transcriptase-polymerase chain reaction, and nuclear factor-kappaB (NF-kappaB) activity was detected by electrophoretic mobility shift assay. Ischemia/reperfusion injury-induced cerebral edema, infarction area, and neurologic impairment scores were determined in MyD88 gene knockout mice.

[Research progress in human artificial chromosomes(HACs) and the potentials in application].

Since the first report of the establishment of human artificial chromosome(HAC) was published in 1997, several types of HAC have been created by different strategies. Compared to other artificial chromosomes, such as yeast artificial chromosome (YAC) and bacterial artificial chromosome(BAC), HAC exists in a cell independently, in other words, HAC does not integrated into the cellular genome, and can undergo normal mitosis and meiosis from generation to generation in vitro and in vivo. Recent results proved that HAC, as a DNA carrier, is able to host a large fragment of DNA or mini-chromosome, thus it could be a very important tool in the study of human gene expression and regulation, human chromosome function and minimum functional elements and animal models for human diseases.

[Cloning and identification of NF-kappaB p50 Rel homology domain and detection of its autonomous reporter gene activity].

Aim: To clone NF-kappaB p50 Rel homology domain (RHD) gene and construct the "bait" vector in yeast two-hybrid system, and detect the yeast cell toxicity and autonomous reporter gene activity of target gene.

Methods: Total RNA was extracted from human peripheral blood mononuclear cells and NF-kappaB p50 RHD gene was amplified by RT-PCR, and cloned into pGBKT7. The recombinant plasmid was transformed into yeast AH109.

[Changes in human leukocyte antigen-DR expression on monocytes and its value of prediction on infection complication in trauma patients].

Objective: To observe the changes of human leukocyte antigen DR (HLA-DR) expression in monocytes of trauma patients and its value of prediction on infection complications.

Methods: Fifty-four trauma patients were divided into three groups according to severity of injury: severe trauma group injury severity score (ISS) >or=25, moderate trauma group (16or=16) were divided into three groups according to infection or not: no infection group, localized infection group and systemic infection group.

Effect of decoy-oligodeoxynucleotides on expression of inflammation mediators in pMPhi cells from rats.

Objective: To study the effect of decoy-oligodeoxynucleotides (decoy-ODNs) in dumbbell shape with the oligodeoxynucleotide sequence similar to nuclear factor kappa B (NF-kappaB) cis-elements on expression of inflammation mediators in pMPhi cells from rats.

Methods: With carriers of cationic liposomes, decoy-ODNs were transfected into pMPhi cells of rats. Then the inhibiting effects of the decoy-ODNs on tumor necrosis factor alpha (TNFalpha), interleukin-6 (IL-6) and IL-10 were analyzed.