Meishan, China

Anhui Medical University

www.ahmu.edu.cn
Meishan, China

Anhui Medical University is a key provincial university in Hefei, Anhui province, China. Wikipedia.


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The anti-malaria drug chloroquine is well known as autophagy inhibitor. Chloroquine has also been used as anti-inflammatory drugs to treat inflammatory diseases. We hypothesized that chloroquine could have a dual effect in liver ischemia/reperfusion (I/R) injury: chloroquine on the one hand could protect the liver against I/R injury via inhibition of inflammatory response, but on the other hand could aggravate liver I/R injury through inhibition of autophagy. Rats (n=6 per group) were pre-treated with chloroquine (60 mg/kg, i.p.) 1 h before warm ischemia, and they were continuously subjected to a daily chloroquine injection for up to 2 days. Rats were killed 0.5, 6, 24 and 48 h after reperfusion. At the early phase (i.e., 0-6 h after reperfusion), chloroquine treatment ameliorated liver I/R injury, as indicated by lower serum aminotransferase levels, lower hepatic inflammatory cytokines and fewer histopathologic changes. In contrast, chloroquine worsened liver injury at the late phase of reperfusion (i.e., 24-48 h after reperfusion). The mechanism of protective action of chloroquine appeared to involve its ability to modulate mitogen-activated protein kinase activation, reduce high-mobility group box 1 release and inflammatory cytokines production, whereas chloroquine worsened liver injury via inhibition of autophagy and induction of hepatic apoptosis at the late phase. In conclusion, chloroquine prevents ischemic liver damage at the early phase, but aggravates liver damage at the late phase in liver I/R injury. This dual role of chloroquine should be considered when using chloroquine as an inhibitor of inflammation or autophagy in I/R injury.


The human major histocompatibility complex (MHC) region has been shown to be associated with numerous diseases. However, it remains a challenge to pinpoint the causal variants for these associations because of the extreme complexity of the region. We thus sequenced the entire 5-Mb MHC region in 20,635 individuals of Han Chinese ancestry (10,689 controls and 9,946 patients with psoriasis) and constructed a Han-MHC database that includes both variants and HLA gene typing results of high accuracy. We further identified multiple independent new susceptibility loci in HLA-C, HLA-B, HLA-DPB1 and BTNL2 and an intergenic variant, rs118179173, associated with psoriasis and confirmed the well-established risk allele HLA-C*06:02. We anticipate that our Han-MHC reference panel built by deep sequencing of a large number of samples will serve as a useful tool for investigating the role of the MHC region in a variety of diseases and thus advance understanding of the pathogenesis of these disorders. © 2016 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.


Rong C.,Anhui Medical University
Molecular and cellular biochemistry | Year: 2012

Cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases, including rheumatoid arthritis (RA). Increasing evidence has revealed the importance of IL-23, which closely resembles IL-12 structurally and immunologically, in linking innate and adaptive immunity. IL-23, a newly identified heterodimeric pro-inflammatory cytokine, is composed of a p40 subunit in common with IL-12 and a unique p19 subunit. Recent evidence suggests that IL-23, rather than IL-12, is the crucial factor in the pathogenesis of various immune-mediated disorders. In addition, recent studies have explored the role of IL-23 in patients with RA. An elevated expression of IL-23 has been demonstrated in the synovial fibroblasts and plasma of patients with RA. Moreover, an association between IL-23 and IL-23R polymorphisms with susceptibility to RA has been reported. Therefore, the targeting of IL-23 or the IL-23 receptor has been proposed as a potential therapeutic approach for RA. In this review we will discuss the biological features of IL-23, and summarize recent advances in our understanding of the role of IL-23 in the pathogenesis and treatment of RA.


Zhang X.,Anhui Medical University
Journal of Dermatological Science | Year: 2012

Complex diseases are caused by both genetic and environmental factors. Over decades, scientists endeavored to uncover the genetic myth of complex diseases by linkage and association studies. Since 2005, the genome-wide association study (GWAS) has been proved to be the most powerful and efficient study design thus far in identifying genetic variants that are associated with complex diseases. More than 230 complex diseases and traits have been investigated by this approach. In dermatology, 10 skin complex diseases have been investigated, a wealth of common susceptibility variants conferring risk for skin complex diseases have been discovered. These findings point to genes and/or loci involved in biological systems worth further investigating by using other methodologies. Certainly, as our understanding of the genetic etiology of skin complex diseases continues to mature, important opportunities will emerge for developing more effective diagnostic and clinical management tools for these diseases. © 2012 Japanese Society for Investigative Dermatology.


Hao J.-Q.,Anhui Medical University
Inflammation | Year: 2014

Interleukin-22 (IL-22) is an IL-10 family cytokine that was recently discovered to be released by T helper 17 (Th17) cells, Th22 cells, etc. Recently, there is emerging evidence that IL-22 is involved in the development and pathogenesis of psoriasis. For instance, IL-22 can inhibit keratinocyte terminal differentiation and can induce psoriasis-like epidermis alterations; serum IL-22 levels were correlated with the disease severity of psoriasis patients, and IL-22 mRNA was positively expressed in the psoriatic skin lesions, but negatively expressed in the normal controls. All these findings suggest that IL-22 may be implicated in psoriasis; therapeutics targeting IL-22 may have promise as a potential therapeutic target for treating psoriasis. In the present review, we summarize recent advances on the role of IL-22 in the pathogenesis and treatment of psoriasis. © 2013 Springer Science+Business Media.


Xu W.D.,Anhui Medical University
Expert reviews in molecular medicine | Year: 2013

Systemic lupus erythematosus (SLE) is a severe multi-system autoimmune disease, whereas interferon regulatory factor (IRF) 5 belongs to the family of transcription factors that modulate immune system activities. Recently, many lines of investigations suggested that IRF5 gene polymorphisms are closely associated with the disease onset of SLE. Indeed, expressed in B cells, dendritic cells (DCs), monocytes and macrophages, IRF5 could significantly affect these immune cells participating in the pathogenesis of SLE, and numerous studies implied that this transcription factor is mechanistically linked to the disease progression. Here, we comprehensively review the updated evidence indicating the roles of IRF5 in autoimmune lupus. Hopefully, the information obtained will lead to a better understanding of the pathogenesis and development of novel therapeutic strategies for the systemic autoimmune disease.


Fei G.H.,Anhui Medical University
Respiratory research | Year: 2013

Cognitive impairment has been found in chronic obstructive pulmonary disease (COPD) patients. However, the structural alteration of the brain and underlying mechanisms are poorly understood. Thirty-seven mild-to-moderate COPD patients, forty-eight severe COPD patients, and thirty-one control subjects were recruited for cognitive test and neuroimaging studies. Serum levels of S100B,pulmonary function and arterial blood gas levels were also evaluated in each subject. The hippocampal volume was significantly smaller in COPD patients compared to the control group. It is positively correlated with a mini mental state examination (MMSE) score, SaO2 in mild-to-moderate COPD patients, the levels of PaO2 in both mild-to-moderate and severe COPD patients. Higher S100B concentrations were observed in mild-to-moderate COPD patients, while the highest S100B level was found in severe COPD patients when compared to the control subjects. S100B levels are negatively associated with MMSE in both mild-to-moderate and severe COPD patients and also negatively associated with the hippocampal volume in the total COPD patients. Hippocampal atrophy based on quantitative assessment by magnetic resonance imaging does occur in COPD patients, which may be associated with cognitive dysfunction and the most prevalent mechanism accountable for hippocampal atrophy is chronic hypoxemia in COPD. Higher serum S100B levels may be peripheral biochemical marker for cognitive impairment in COPD.


Yan L.,Anhui Medical University
European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery | Year: 2013

To evaluate the efficacy and safety of the right vertical infra-axillary mini-incision (RVAI) used for the repair of simple congenital heart defects. We performed a retrospective 1:1 matched-pair analysis on the patients with simple congenital heart defects who were operated on from February 2003 to October 2010. All the recruited patients were treated through either RVAI (RVAI group) or median sternotomy incision (MSI group). In order to balance the major prognostic factors between the two groups, the MSI group was selected by a pair-matched case-control methodology and matched for heart defects, the year of surgery, body weight and patching. A total of 104 patients were included. The demographics and preoperative clinical characteristics of the patients in the RVAI group (n = 52) and in the MSI one (n = 52) were similar. There were no operative or late mortalities and no special care in the intensive care unit (ICU) or rehospitalization. The mean duration time of surgical operation (skin-to-skin) was 147 ± 21 min (range from 100 to 190 min) in the RVAI group and 174 ± 35 min (range from 120 to 270 min) in the MSI one (P < 0.001), respectively. No significant difference was found between the two groups in the consuming time for cardiopulmonary bypass, aortic cross-clamp, postoperative ventilation, ICU stay, postoperative hospital stay and drainage. No significant residual defects were found in patients of both groups. No asymmetrical development of the breast, thoracic deformity or scoliosis has been found during the follow-up. All the patients or the parents of young children (100%) in the RVAI group and 34 patients or the parents of young children (65.4%) in the MSI one were satisfied with the cosmetic results (P < 0.001). The RVAI surgical approach to simple congenital heart defects was a safe procedure and could be performed with excellent cosmetic and clinical outcomes. It provided a good alternative to the standard MSI for simple congenital heart defects.


The present invention provides are a gold nanoflower structure and a preparation method therefor. The gold nanoflower structure is a gold nanoflower particle, with round-head columns being uniformly distributed at the periphery thereof, obtained by using gold octahedrons, gold balls or gold tetrahedrons as seed crystals and reducing chloroauric acid by using weak reductant in an environment of high-concentration polyvinylpyrrolidone. In addition, also provided in the present invention are a gold nanoflower/quantum dot composite probe for living cell immunofluorescent labeling and photothermal therapy, a preparation method therefor and a use thereof. In comparison with traditional probes, the probe, incorporates the features of photothermal therapy and fluorescent labeling, and is capable of killing cancer cells in an effective and directional way. Two light sources are adopted to bring a tremendous photothermal conversion efficiency and a greater enhancement on fluorescence intensity of quantum dots respectively, thus mutual interference of two effects are avoided tactfully. The coating of silicon dioxide averts the biotoxicity of the gold nanoflower and the quantum dot effectually, enabling the surface of the composite probe to be easily functionalized and also imparting an extraordinarily excellent biocompatibility to the composite probe.


Toxoplasma gondii infection in pregnant women may result in abortion or in fetal teratogenesis; however, the underlying mechanisms are still unclear. In this paper, based on a murine model, we showed that maternal infection with RH strain T. gondii tachyzoites induced elevated production of reactive oxygen species (ROS), local oxidative stress, and subsequent apoptosis of placental trophoblasts. PCR array analysis of 84 oxidative stress-related genes demonstrated that 27 genes were upregulated at least 2-fold and that 9 genes were downregulated at least 2-fold in the T. gondii infection group compared with levels in the control group. The expression of NADPH oxidase 1 (Nox1) and glutathione peroxidase 6 (Gpx6) increased significantly, about 25-fold. The levels of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) increased significantly with T. gondii infection, and levels of glutathione (GSH) decreased rapidly. T. gondii infection increased the early expression of endoplasmic reticulum stress (ERS) markers, followed by cleavage of caspase-12, activation of ASK1/JNK, and increased apoptosis of trophoblasts, both in vivo and in vitro. The apoptosis of trophoblasts, the activation of caspase-12 and the ASK1/JNK pathway, and the production of peroxides were dramatically inhibited by pretreatment with N-acetylcysteine (NAC). The upregulation of Nox1 was contact dependent and preceded the increase in levels of ERS markers and the activation of the proapoptosis cascade. Thus, we concluded that apoptosis in placental trophoblasts was initiated predominantly by ROS-mediated ERS via activation of caspase-12, CHOP, and the JNK pathway in acute T. gondii infection. Elevated ROS production is the central event in T. gondii-induced apoptosis of placental trophoblasts.

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