117 results match your criteria: "First Hospital Affiliated to the Chinese PLA General Hospital[Affiliation]"

HSF-1 is involved in attenuating the release of inflammatory cytokines induced by LPS through regulating autophagy.

Shock

May 2014

*Department of Pathophysiology, Xiangya School of Medicine, Central South University, Hunan; and †Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, China.

Autophagy plays a protective role in endotoxemic mice. Heat shock factor 1 (HSF-1) also plays a crucial protective role in endotoxemic mice by decreasing inflammatory cytokines. The purpose of this study was to determine whether HSF-1 is involved in attenuating the release of inflammatory cytokines in lipopolysaccharide (LPS)-stimulated mice and peritoneal macrophages (PMs) through regulating autophagy activity.

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Advances in sepsis-associated liver dysfunction.

Burns Trauma

September 2016

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, No.51 Fucheng Road, Haidian District, Beijing, 100048 China.

Recent studies have revealed liver dysfunction as an early event in sepsis. Sepsis-associated liver dysfunction is mainly resulted from systemic or microcirculatory disturbances, spillovers of bacteria and endotoxin (lipopolysaccharide, LPS), and subsequent activation of inflammatory cytokines as well as mediators. Three main cell types of the liver which contribute to the hepatic response in sepsis are Kupffer cells (KCs), hepatocytes and liver sinusoidal endothelial cells (LSECs).

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Increasing evidence shows that dysregulation of microRNAs is correlated with tumor development. This study was performed to determine the expression of miR-141 and investigate its clinical significance in pancreatic ductal adenocarcinoma (PDAC). Taqman quantitative RT-PCR was used to detect miR-141 expressions in 94 PDAC tissues and 16 nontumorous pancreatic tissues.

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Background: Our aim was to analyze clinicopathologic and prognostic values of microRNA (miR)-218 in pancreatic ductal adenocarcinima (PDAC).

Methods: TaqMan quantitative RT-PCR was used to determine the expression of miR-218 in human PDAC cells and tissue samples. The association of miR-218 expression with clinicopathologic variables was analyzed.

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The tumor necrosis factor-alpha-induced protein 8 family in immune homeostasis and inflammatory cancer diseases.

J Biol Regul Homeost Agents

November 2013

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, People's Republic of China.

Within the immune system homeostasis is maintained by a myriad of mechanisms that include the regulation of immune cell activation and programmed cell death. The breakdown of immune homeostasis may lead to fatal inflammatory diseases. We set out to identify genes of tumor necrosis factor-alpha-induced protein 8 (TNFAIP8) family that has a functional role in the process of immune homeostasis.

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Objectives: We aimed to investigate subjective sleep quality and polysomnographic sleep structure features in patients with vascular cognitive impairment-no dementia (VCIND).

Methods: Fifty-six patients with VCIND, 48 patients with simple stroke (without cognitive impairment), and 48 control subjects were included. The Pittsburgh Sleep Quality Index (PSQI) and polysomnography (PSG) were used to analyze their sleep characteristics.

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The significance and regulatory mechanisms of innate immune cells in the development of sepsis.

J Interferon Cytokine Res

January 2014

1 Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, People's Republic of China .

Sepsis with subsequent multiple organ dysfunction is a pronounced systemic inflammatory response to concealed or known infection and is a leading cause of death in intensive care units. The survival rate of severe sepsis and septic shock has not markedly improved in recent decades despite a great number of receptors and molecules involved in its pathogenesis have been found and taken as therapeutic targets. It is essential to thoroughly understand the host cell-mediated immunity involved in the development of sepsis and sepsis-related organ injury.

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High mobility group box-1 protein (HMGB1), which is a nuclear protein, participates in chromatin architecture and transcriptional regulation. When released from cells, HMGB1 also plays a well-established role as a pro-inflammatory mediator during innate immune responses to injury. In the initial stage of injury, there is a release of large quantities of early pro-inflammatory mediators to initiate or perpetuate immune responses against pathogens, but this pro-inflammatory period is transient, and it is followed by a prolonged period of immune suppression.

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Objective: To investigate the effects of PNU282987, a α7 nicotinic acetylcholine receptor agonist (α7nAChR), on organ function and survival rate in dogs with lethal burn shock.

Methods: Twelve adult male Beagle dogs were subjected to 50% total body surface area (TBSA) full-thickness flame injury, and then they were randomly divided into a burn group and a PNU282987 group (PNU group), each n=6. The dogs in PNU group received PNU282987 (0.

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Gelsolin is an actin filament-severing and capping protein, affecting cellular motility, adhesiveness and apoptosis. Whether it is expressed in the brain of burned mice has not yet been characterized. Mice were subjected to a 15% total body surface area scald injury.

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The role of regulatory T cells in the pathogenesis of sepsis and its clinical implication.

J Interferon Cytokine Res

August 2012

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, People's Republic of China.

Sepsis is denoted as a complex syndrome that results from a serious infection followed by amplified and dysregulated inflammatory response. The complex immune response associated with sepsis results in a high rate of morbidity and mortality, despite substantial basic science and clinical advances. Recently, accumulating evidence have demonstrated that regulatory T cells (Tregs) play important roles in suppression of immune response, as demonstrated by the number increase and functional enhancement following the onset of severe sepsis or septic shock.

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This study examined the effect of intensive insulin therapy on immune function and inflammatory factors at the early phase after severe trauma. At day 1, 3, 5, 7 after admission, subsets of CD4(+) helper T lymphocytes (Th1/Th2) and human leukocyte antigen (HLA)-DR expression on CD14(+) monocytes were flow cytometrically measured. Levels of cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-10 (IL-10) and other immunity markers, such as IgA, IgG, IgM, C3, C4 and C reaction protein (CRP) were examined in two groups.

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Update on the immunological pathway of negative regulation in acute insults and sepsis.

J Interferon Cytokine Res

July 2012

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing, People's Republic of China.

Sepsis with subsequent multiple organ dysfunction is a distinctly systemic inflammatory response to concealed or known infection and is a leading cause of death in intensive care units. In the initial stage of sepsis, a phase of immune activation can be evident, but a marked apoptosis-induced depletion of lymphocytes and a nonspecific anergy of immune function after severe trauma and burns might be responsible for the increased susceptibility of the host to subsequent septic complications. Recent studies indicated that negative regulation of immune function plays a pivotal role in the maintenance of peripheral homeostasis and regulation of immune responses; therefore, an understanding of the basic pathways might give rise to novel insights into the mechanisms of sepsis and immune homeostasis.

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High mobility group box-1 protein (HMGB1) had been proved to induce maturation and activation of dendritic cell (DC), however, the endogenous changes and mechanisms underlying are unknown. Since endoplasmic reticulum stress (ERS) activates an adaptive unfolded protein response (UPR) that facilitates cellular survival and repair, we hypothesized that HMGB1 may regulate the function of DC by modulating ERS. In our study, HMGB1 stimulation induced significant ERS responses in DCs in a time- and dose-dependent manner, demonstrated by the up-regulation of a number of ERS markers.

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Background: Depletion of the circulating actin-binding protein, plasma gelsolin (pGSN) has been described in critically ill surgical patients. We hypothesized that the extent of pGSN reduction might correlate with different outcome of burn patients. The study was performed to evaluate the prognostic implications of pGSN levels on the development of multiple organ dysfunction syndrome (MODS) and fatal outcome in a group of severely burn patients.

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Tumor necrosis factor-α induced protein 8 like-2 (TNFAIP8L2, TIPE2), a lately discovered negative regulator of innate immunity and cellular immunity, shares considerable sequence homology with members of the tumor necrosis factor-α induced protein 8 (TNFAIP8) family. It is preferentially expressed in lymphoid-derived and marrow-derived cells. However, it is unclear whether TIPE2 is expressed in the regulatory T cells (Tregs) to contribute to its negative regulatory property in immune response.

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Background: Burn survivors develop long-term cognitive impairment with increased inflammation and apoptosis in the brain. Gelsolin, an actin-binding protein with capping and severing activities, plays a crucial role in the septic response. We investigated if gelsolin infusion could attenuate neural damage in burned mice.

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Since 1991, the first laparoscopic liver resection (LLR) was reported by Reich, LLR had been applied and improved by different scholars like Wayand (1993), Ferzli (1995), Cherqui (2002), Descottes (2003). Zhou Weiping reported the first LLR in China in 1994. In 2004, after ten years development, LLR became more and more mature and international exchange happens.

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Background: Astragalus polysaccharides (APS) isolated from one of the Chinese herbs, Astragalus mongholicus, are known to have a variety of immunomodulatory activities. However, it is not yet clear whether APS can exert an effect on the immune functions of regulatory T cells (Tregs). This study was carried out to investigate the effect of APS on the immune function of peripheral blood Tregs in postburn sepsis.

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Introduction: High mobility group box-1 protein (HMGB1), a recently recognized mediator of immune response might contribute to immune suppression when released extracellularly. The present study was performed to clarify effects of HMGB1 on regulatory T cells (Tregs) and the involvement of toll-like receptor (TLR) 4 signaling.

Methods: CD4(+)CD25(+)Tregs, isolated from spleens of normal mice and treated with HMGB1 in vitro, and those isolated from HMGB1-treated C3H/HeN (wild type) or C3H/HeJ (TLR4 mutant type) mice, were analyzed for expressions of cytotoxic T lymphocyte-associated antigen (CTLA)4, forkhead/winged helix transcription factor p3 (Foxp3) and interleukin (IL)-10 secretion.

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[The central mechanism for estrogen receptor to mediate nutrients and energy metabolism].

Sheng Li Ke Xue Jin Zhan

October 2010

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Beijing 100048, China.

Estrogen is demonstrated to be involved in the development and progress of diabetes mellitus. Recently studies have indicated that estrogen receptor (ER) play a crucial role in the modulation of nutrients and energy metabolism. Estrogen could regulate the expressions of anorexia and hyperphagic neuropeptide in the hypothalamus by genomic actions via nuclear ER, or via membrane ER linking to the phosphatidylinositol 3-kinase (PI3-K)/Akt and ERK1/2 mitogen-activated protein kinase (MAPK) pathways.

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Objective: To study the effect of intensive insulin therapy on serum high mobility group box 1 (HMGB1) levels and its relationship with the prognosis in early phase of severe trauma.

Methods: Eighty severe trauma patients [injury severity score (ISS)≥ 16] were divided into groups according to injury to matched anatomical regions. Forty patients of intensive therapy group were given early intensive insulin therapy, while another 40 patients of the conventional treatment group received routine treatment based on clinical experience with insulin treatment.

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Aim: High mobility group box 1 protein (HMGB1) has been identified as a late proinflammatory cytokine and plays a key role in immune regulation. However, it is not yet clear whether HMGB1 can induce the activation and differentiation of dendritic cell (DC) subsets and subsequently modulate immune function of T cells. This study was performed to investigate the effect of HMGB1 on the differentiation of splenic DCs and its influence on T cell-mediated immunity in terms of DC subsets CD11c(low)CD45RB(high) DCs and CD11c(high)CD45RB(low) DCs in male BALB/c mice spleens in vitro.

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Association of high mobility group box-1 protein levels with sepsis and outcome of severely burned patients.

Cytokine

January 2011

Department of Microbiology and Immunology, Burns Institute, First Hospital Affiliated to the Chinese PLA General Hospital, Fucheng Road 51, Haidian District, Beijing 100048, People's Republic of China.

Background: The study was performed to observe the systemic release and kinetics of high mobility group box-1 protein (HMGB1) in burned patients.

Methods: 106 patients were included, and they were divided into three groups with different burn sizes: group I, group II and group III. Healthy volunteers served as normal controls (n=25).

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