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Li H.-D.,The 88th Hospital of the Chinese PLA | Zhang Q.-X.,The 148th Hospital of the Chinese PLA | Mao Z.,Chinese PLA General Hospital | Xu X.-J.,The Affiliated Hospital of Taishan Medical College | And 2 more authors.
Experimental Physiology | Year: 2015

New Findings: What is the central question of this study? It is not known whether treatment with interleukin-10 (IL-10) attenuates hyperoxia-induced acute lung injury in mice. What is the main finding and its importance? Our results showed that exogenous IL-10 treatment alleviated hyperoxia-induced acute lung injury in mice, possibly by regulating neutrophil recruitment and the subsequent generation of cytokines, nitric oxide and matrix metalloproteinases. Lung injury caused by breathing air enriched with oxygen continues to be a major problem in clinical medicine. Here, we investigated the therapeutic role of interleukin-10 (IL-10) in hyperoxia-induced acute lung injury in mice. In the first experiment, mice were exposed to room air or 95% O2 and treated with IL-10 simultaneously. In the second experiment, wild-type mice and IL-10-/- mice were exposed to room air or 95% O2. Exogenous IL-10 treatment attenuated hyperoxia-induced acute lung injury, evidenced by a reduced ratio of lung weight to body weight, ratio of lung wet weight to dry weight, cell numbers and protein content in bronchoalveolar lavage fluid and cell death. Interleukin-10 treatment markedly prolonged the survival of mice during oxygen exposure. Interleukin-10 treatment reduced the activity of myeloperoxidase and mRNA levels of interleukin-6, tumour necrosis factor-α and macrophage inflammatory protein 2, suppressed nuclear factor-κB activation and decreased inducible nitric oxide synthnase expression and nitric oxide formation in lungs of mice exposed to hyperoxia. Interleukin-10 treatment suppressed activities of matrix metalloproteinase 2 and matrix metalloproteinase 9 and reduced lung permeability in mice during oxygen exposure. Furthermore, absence of IL-10 aggravated hyperoxia-induced acute lung injury and reduced the duration of survival of mice during oxygen exposure, which was attenuated by treatment with IL-10. In conclusion, our results show that exogenous IL-10 treatment alleviates hyperoxia-induced acute lung injury in mice, possibly by regulating neutrophil recruitment and the subsequent generation of cytokines, nitric oxide and matrix metalloproteinases. This suggests that IL-10 treatment may be a promising therapeutic strategy to reduce lung injury in patients exposed to hyperoxia. © 2014 The Physiological Society.


PubMed | Peking Union Medical College, Qingdao University, Neonatal Screening Center and The Affiliated Hospital of Taishan Medical College
Type: | Journal: Oncotarget | Year: 2016

Mutations in the dual oxidase 2 gene (DUOX2) impair hydrogen peroxide (H2O2) production and cause dyshormonogenesis. In addition, these mutations have been implicated in autosomal recessive congenital hypothyroidism (CH) with goiter. In this study, we identified DUOX2 mutations that were causative for CH and explored the effects of these mutations on DUOX2 function. Blood samples were collected from 10 infants born with CH and goiter to unrelated parents. We extracted genomic DNA and sequenced all exons by polymerase chain reaction direct sequencing. The effects of DUOX2 mutations were characterized by H2O2 production assays and cycloheximide (CHX) chase experiments. Sequence analysis revealed one novel DUOX2 mutation and one known DUOX2 mutation in unrelated families: c.1060C>T (p.R354W) and c.3616 G>A (p.A1206T). Both mutations impaired H2O2 production. CHX chase experiments demonstrated the DUOX2 mutants had shorter half-lives and degraded more rapidly than wild-type DUOX2. Our study identified two novel DUOX2 mutations in Chinese patients with CH and goiter, which were responsible for the deficit in the organification process.


Bi Y.,Nanjing Medical University | Li X.,The Affiliated Hospital of Taishan Medical College | Yang D.,Sun Yat Sen University | Hao Y.,Sun Yat Sen University | And 3 more authors.
Journal of Diabetes Investigation | Year: 2012

Aims/Introduction: Although long-acting insulin analogs are recommended in type2 diabetics failing on oral agents, their efficacy is uncertain. Here we compared the efficacy and safety of regimens based on long-acting insulin analogs with other preparations in insulin-naïve type2 diabetics failing on oral agents. Materials and Methods: Data from 9548 participants in 22 English studies were included. Most of the studies were of short to medium duration and of low quality. Results: In terms of decreasing hemoglobin A1c, long-acting insulin analogs were not statistically significant to rapid-acting insulin analogs or intermediate neutral protamine Hagedorn (NPH) insulin or glucagon-like peptide-1 (GLP-1) analogs, and the differences between long-acting and biphasic insulin analogs were marginal. Compared with rapid-acting insulin analogs, long-acting insulin analogs were similar in the incidence of total hypoglycemia, and the superiority in less weight gain was inconsistent. Relative to biphasic insulin analogs, long-acting insulin analogs were associated with lower incidence of total hypoglycemia and less weight gain. Compared with NPH insulin, long-acting insulin analogs were associated with lower incidence of total and nocturnal hypoglycemia. Relative to GLP-1 analogs, long-acting insulin analogs were associated with lower incidence of treatment related adverse events but with greater weight gain. Conclusions: For type two diabetics failing on oral agents, initiating long-acting insulin analogues seems to provide glycemic control similar to rapid-acting insulin analogs or NPH insulin or glucagon-like peptide-1 analogs and slightly inferior to biphasic insulin analogs with fewer side-effects. © 2011 Asian Association for the Study of Diabetes and Blackwell Publishing Asia Pty Ltd.


Objective: Intracellular chloride concentration of a given cell within the central nervous system is determined by a delicate balance between the Cl- extrusion system and the Claccumulation system. In this study, we aim to investigate the expression profiles of cationchloride cotransporters (CCCs) mRNA in the mice model of lithium-pilocarpine induced status epilepticus (PISE) and the possible relationships between CCCs and epileptogenesis. Methods: Male adult Balb/c mice were randomly divided into two groups: the PISE group and the control. We used the mice of PISE group to establish the animal model of PISE and the PISE group could be subdivided into three time points: 1 d, 14 d and 45 d. Real-time fluorescence quantitative PCR (polymerase chain reaction) was used to explore the expression of CCCs family members mRNA in CA1 region. Results: These CCCs members all showed distinctive expression patterns. The expression levels of NKCC1 (sodium potassium cation-chloride cotransporter 1), KCC1 (potassium cation-chloride cotransporter 1), KCC3 (potassium cation-chloride cotransporter 3) and CIP1 (CCC-interacting protein type 1)mRNA were up-regulated while those of KCC2 (potassium cation-chloride cotransporter 2) and CCC9 (cation-chloride cotransporter) mRNA were downregulated after PISE. The expression of KCC4 (potassium cation-chloride cotransporter 4) remained unchanged. Conclusions: These data lead us to conclude that CCCs expression as a whole is under very strict transcriptional control in this model. Deregulation of their expression might break the balance of intracellular and extracellular chloride concentration which contributed to the mechanism of hyperexcitability that led to seizures. This may be due to some form of genetic program activated in response to epileptic seizure in the brain and may highlight which biological pathways are modulated.


PubMed | Nanjing Medical University, Sun Yat Sen University and The Affiliated Hospital of Taishan Medical College
Type: Journal Article | Journal: Journal of diabetes investigation | Year: 2014

Aims/Introduction: Although long-acting insulin analogs are recommended in type2 diabetics failing on oral agents, their efficacy is uncertain. Here we compared the efficacy and safety of regimens based on long-acting insulin analogs with other preparations in insulin-nave type2 diabetics failing on oral agents. Data from 9548 participants in 22 English studies were included. Most of the studies were of short to medium duration and of low quality. In terms of decreasing hemoglobin A1c, long-acting insulin analogs were not statistically significant to rapid-acting insulin analogs or intermediate neutral protamine Hagedorn (NPH) insulin or glucagon-like peptide-1 (GLP-1) analogs, and the differences between long-acting and biphasic insulin analogs were marginal. Compared with rapid-acting insulin analogs, long-acting insulin analogs were similar in the incidence of total hypoglycemia, and the superiority in less weight gain was inconsistent. Relative to biphasic insulin analogs, long-acting insulin analogs were associated with lower incidence of total hypoglycemia and less weight gain. Compared with NPH insulin, long-acting insulin analogs were associated with lower incidence of total and nocturnal hypoglycemia. Relative to GLP-1 analogs, long-acting insulin analogs were associated with lower incidence of treatment related adverse events but with greater weight gain. For type 2 diabetics failing on oral agents, initiating long-acting insulin analogues seems to provide glycemic control similar to rapid-acting insulin analogs or NPH insulin or glucagon-like peptide-1 analogs and slightly inferior to biphasic insulin analogs with fewer side-effects. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00187.x, 2011).


Hou X.,The Affiliated Hospital of Taishan Medical College | Hou X.,Shandong University | Zhang Y.,Shandong University | Wang X.,Shandong University | And 3 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Objective: This study is to investigate the effect of rosuvastatin on atrial nerve sprouting and electrical remodeling after myocardial infarction (MI). Methods: Rabbit MI model was established by anterior descending branch ligation. These models were divided into the sham (n = 9), MI model (n = 7), and rosuvastatin intervention (n = 8) groups. Immunohistochemistry was used to detect the autonomic atrial nerve distribution. Real-time PCR and Western blot analysis were performed to evaluate the mRNA and protein expression levels, respectively. Results: Our results from immunohistochemistry showed that, compared with the sham group, the densities of tyrosine hydroxylase (TH)- and choline acetyltransferase (CHAT)-positive nerve fibers were significantly elevated in the MI model group. However, TH- and CHAT-positive nerve fibers were significantly decreased by rosuvastatin treatment, suggesting that rosuvastatin could reduce autonomic nerve sprouting in acute MI. Moreover, rosuvastatin decreased the mRNA and protein expression levels of TH in atrial tissues following MI. Compared with the sham group, the mRNA expression level of KCND3 was significantly down-regulated in the MI model group. And, this down-regulation was restored by rosuvastatin treatment. These results suggested that rosuvastatin could inhibit the electrical remodeling in atrium after acute MI. Conclusion: Atrial nerve sprouting and electrical remodeling occur following MI, which could be suppressed by rosuvastatin treatment. Our findings provide insights into the understanding of the mechanism through which statins decrease the risk of atrium arrhythmia after MI. © 2015, E-Century Publishing Corporation. All rights reserved.


Li X.Q.,The Affiliated Hospital of Taishan Medical College
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban | Year: 2011

To observe the effects of rukangyin (RKY) on the lymphangiogenesis and lymph node metastasis of breast cancer transplantation tumor mice, thus exploring its anti-tumor metastasis mechanisms. Human breast cancer cell line MDA-MB-435S were in situ implanted into the mammary fat pad of 30 female nude mice to establish breast cancer transplantation tumor spontaneous metastasis model. They were randomly divided into six groups, i.e., the model control group, the 5-FU control group, the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, 5 in each. Normal saline was given to mice in the model control group at the daily dose of 0.4 mL/kg by gastrogavage. 5-FU was given to mice in the 5-FU control group at the daily dose of 30 mg/kg by peritoneal injection. RKY was given to mice in the small, medium, large dose RKY groups at the daily dose of 18, 45, and 90 g/kg by gastrogavage. 5-FU 30 mg/kg (by peritoneal injection) + RKY 45 g/( kg x d) (by gastrogavage) was given to mice in the medium dose RKY +5-FU group. All medication was carried out once daily for 6 successive weeks. The tumor volume, the tumor inhibition ratio, and the inhibition ratio of axillary lymph node metastasis were detected after medication. The lymphatic microvessel density (LMVD) and expressions of vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR-3) of the breast cancer tissues were detected using immunohistochemical assay. Compared with the model control group, the tumor volume was markedly reduced in the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, the expressions of VEGF-C and VEGFR-3 were significantly down-regulated and LMVD were obviously lowered, showing statistical difference (P < 0.05, P < 0.01). The inhibition rates of tumor and axillary lymph node metastasis were highest and the LMVD was the lowest in the medium dose RKY +5-FU group, showing statistical difference when compared with other medication groups (P < 0.05, P < 0.01). RKY might inhibit the lymph node metastasis of breast cancer possibly through intervening the expressions of VEGF-C and VEGFR-3, and suppressing lymphangiogenesis.


PubMed | The Affiliated Hospital of Taishan Medical College
Type: Journal Article | Journal: Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine | Year: 2012

To observe the effects of rukangyin (RKY) on the lymphangiogenesis and lymph node metastasis of breast cancer transplantation tumor mice, thus exploring its anti-tumor metastasis mechanisms.Human breast cancer cell line MDA-MB-435S were in situ implanted into the mammary fat pad of 30 female nude mice to establish breast cancer transplantation tumor spontaneous metastasis model. They were randomly divided into six groups, i.e., the model control group, the 5-FU control group, the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, 5 in each. Normal saline was given to mice in the model control group at the daily dose of 0.4 mL/kg by gastrogavage. 5-FU was given to mice in the 5-FU control group at the daily dose of 30 mg/kg by peritoneal injection. RKY was given to mice in the small, medium, large dose RKY groups at the daily dose of 18, 45, and 90 g/kg by gastrogavage. 5-FU 30 mg/kg (by peritoneal injection) + RKY 45 g/( kg x d) (by gastrogavage) was given to mice in the medium dose RKY +5-FU group. All medication was carried out once daily for 6 successive weeks. The tumor volume, the tumor inhibition ratio, and the inhibition ratio of axillary lymph node metastasis were detected after medication. The lymphatic microvessel density (LMVD) and expressions of vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR-3) of the breast cancer tissues were detected using immunohistochemical assay.Compared with the model control group, the tumor volume was markedly reduced in the small, medium, large dose RKY groups, and the medium dose RKY +5-FU group, the expressions of VEGF-C and VEGFR-3 were significantly down-regulated and LMVD were obviously lowered, showing statistical difference (P < 0.05, P < 0.01). The inhibition rates of tumor and axillary lymph node metastasis were highest and the LMVD was the lowest in the medium dose RKY +5-FU group, showing statistical difference when compared with other medication groups (P < 0.05, P < 0.01).RKY might inhibit the lymph node metastasis of breast cancer possibly through intervening the expressions of VEGF-C and VEGFR-3, and suppressing lymphangiogenesis.


PubMed | the Affiliated Hospital of Taishan Medical College
Type: Journal Article | Journal: PloS one | Year: 2014

Antibiotic abuse can lead to antibiotic resistance, which is a severe problem in China. The purpose of this study is to evaluate the short-term effects of antimicrobial stewardship strategies, including formulary restriction, preauthorization, perioperative quinolone restriction, and control of total antibiotic consumption in the ICU at a tertiary hospital in China. After implementation of antimicrobial stewardship, the total antibiotic consumption in the ICU significantly decreased. The defined daily doses (DDDs) per 100 patient-days decreased from 197.65 to 143.41; however, the consumption of cephalosporins increased from 53.65 to 63.17 DDDs. Significant improvements in resistance to amikacin, gentamicin, ciprofloxacin, ofloxacin, ceftriaxone, ceftazidime, and piperacillin in Enterobacteriaceae and resistance to ceftazidime, imipenem, and meropenem in non-fermenting Gram-negative rods were observed. In addition, the initial use of no antibiotics or of a single antibiotic significantly increased (P<0.001) and the use of two antibiotics in combination significantly decreased (P<0.001). Our results demonstrate that implementation of antimicrobial stewardship in a short period in the ICU dramatically reduced antibiotic consumption and significantly improved antibiotic resistance, which leads to more reasonable antibiotic selections by ICU physicians.


PubMed | the Affiliated Hospital of Taishan Medical College
Type: Journal Article | Journal: Neuro-Signals | Year: 2011

Protein kinase C (PKC) has been widely reported to participate in somatic pain; however, its role in visceral pain remains largely unclear. Using a colon inflammatory pain model by intracolonic injection of formalin in rats, the present study was to examine the role of PKC in visceral pain and determine which subtypes may be involved. The colon pain behavior induced by formalin injection could be enhanced by intrathecal pretreatment with a PKC activator (PMA), and alleviated by a PKC inhibitor (H-7). Wide dynamic range (WDR) neurons in the L6-S1 spinal dorsal horn that were responsive to colorectal distension were recorded extracellularly. It was found that neuronal activity was greatly increased following formalin injection. Microdialysis of PMA near the recorded neuron in the spinal dorsal horn facilitated the enhanced responsive activity induced by formalin injection, while H-7 inhibited significantly the enhanced response induced by formalin injection. Western blot analysis revealed that membrane translocation of PKC- and PKC-, but not other subtypes, in the spinal cord was obviously increased following formalin injection. Therefore, our findings suggest that PKC is actively involved in the colon pain induced by intracolonic injection of formalin. PKC- and PKC- subtypes seem to significantly contribute to this process.

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