1.Characteristics of Polysomngraphy on Children with Obstructive Sleep Apnea Hypopnea Syndrome and Primary Snoring
pei-ru, XU ; xiao-ying, ZHANG ; li-kun, DUO
Journal of Applied Clinical Pediatrics 2003;0(10):-
Objective To explore the polysomnography(PSG) characteristice of obstructive sleep apnea hypopnea syndrome(OS-AHS) and primary snoring(PS) in children and clinical value of PSG in children with sleep disorders. Methods We analyzed 74 children with OSAHS and 62 with PS, every patient being monitored with PSG for 7 hours at night for 16 parameters, including apnea hypopnea index(AHI), periodic leg movement index(PLMI),and the lowest oxygen saturation(LSaQ2) etc. The parameters of the 2 groups were comparaed. Results Comparaed with PS group, there was statistically significant difference in parameters such as PLMI, AHI,LSaQ2,the moderate oxygen saturation(MSaO2).AHI in non- rapid eye movement (NREM)(P
2.Insulin protects isolated hearts from ischemia/reperfusion injury: cross-talk between PI3-K/Akt and JNKs.
Hai-Tao LIU ; Hai-Feng ZHANG ; Rui SI ; Quan-Jiang ZHANG ; Kun-Ru ZHANG ; Wen-Yi GUO ; Hai-Chang WANG ; Feng GAO
Acta Physiologica Sinica 2007;59(5):651-659
Our previous results have demonstrated that insulin reduces myocardial ischemia/reperfusion (MI/R) injury and increases the postischemic myocardial functions via activating the cellular survival signaling, i.e., phosphatidylinositol 3-kinase (PI3-K)-Akt-endothelial nitric oxide synthase (eNOS)-nitric oxide (NO) cascade. However, it remains largely controversial whether c-Jun NH2-terminal kinase (JNK) is involved in the effects of insulin on MI/R injury. Therefore, the aims of the present study were to investigate the role of JNK, especially the cross-talk between JNK and previously expatiated Akt signaling, in the protective effect of insulin on I/R myocardium. Isolated hearts from adult Sprague-Dawley rats were subjected to 30 min of regional ischemia and followed by 2 or 4 h of reperfusion (n=6). The hearts were pretreated with PI3-K inhibitor LY294002, or phosphorylated-JNK inhibitor SP600125, respectively, then perfused retrogradely with insulin, and the mechanical functions of hearts, including the heart rate (HR), left ventricular developed pressure (LVDP) and instantaneous first derivation of left ventricular pressure (+/-LVdp/dt(max)) were measured. At the end of reperfusion, the infarct size (IS) and apoptotic index (AI) were examined. MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with the control group, insulin treatment in MI/R rats exerted protective effects as evidenced by reduced myocardial IS [(28.9 +/- 2.0)% vs (45.0 +/- 4.0) %, n=6, P<0.01], inhibited cardiomyocyte apoptosis [decreased AI: (16.0 +/- 0.7) % vs (27.6 +/- 1.3) %, n=6, P<0.01] and improved recovery of cardiac systolic/diastolic function (including LVDP and +/-LVdp/dt(max)) at the end of reperfusion. Moreover, insulin resulted in 1.7-fold and 1.5-fold increases in Akt and JNK phosphorylation in I/R myocardium, respectively (n=6, P<0.05). Inhibition of Akt activation with LY294002 abolished, and inhibition of JNK activation with SP600125 enhanced the cardioprotection by insulin, respectively. And the abolishment by LY294002 could be partly converted by SP600125 pretreatment. In addition, SP600125 also decreased the Akt phosphorylation (n=6, P<0.05). These results demonstrate that insulin simultaneously activates both Akt and JNK, and the latter further increases the phosphorylation of Akt which attenuates MI/R injury and improves heart function; this cross-talk between Akt and JNK in the insulin signaling is involved in insulin-induced cardioprotective effect.
Animals
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Apoptosis
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Heart
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Insulin
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metabolism
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JNK Mitogen-Activated Protein Kinases
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MAP Kinase Signaling System
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Myocardial Infarction
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Myocardial Ischemia
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Myocardial Reperfusion Injury
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Myocardium
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Myocytes, Cardiac
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Nitric Oxide Synthase Type III
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Phosphatidylinositol 3-Kinase
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metabolism
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Phosphatidylinositol 3-Kinases
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metabolism
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Phosphorylation
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Proto-Oncogene Proteins c-akt
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Rats
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Rats, Sprague-Dawley
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Reperfusion Injury
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Signal Transduction
3.Protection of azithromycin against pulmonary II epithelial cell injuries induced by cigarette smoke extract and relevant mechanisms.
Xiao-Rong ZHANG ; Li-Kun DUO ; Pei-Ru XU ; Xiao-Mei LU ; Ya-Lou ZHANG ; Hui LIU
Chinese Journal of Contemporary Pediatrics 2007;9(1):63-66
OBJECTIVECigarette smoke extract (CSE) can induce injuries of pulmonary II epithelial cells, activate nuclear factor-kappaB and increase tumor necrosis factor-alpha(TNF-alpha) secretion. This study aimed to investigate whether azithromycin can protect pulmonary II epithelial cells from injuries induced by CSE and relevant mechanisms.
METHODSPulmonary II epithelial cells (A549 cells) were cultured in vitro. After 48 hrs of culture the cells were randomly treated with serum-free DMEM only (blank control group), azithromycin + serum-free DMEM, CSE+ serum-free DMEM or CSE+azithromycin. Eight hours later the morphology of A549 cells, the activity of NF-kappaB and the levels of TNF-alpha were measured by inverted microscope, immunohistochemistry and ELISA.
RESULTSThe morphology and structure of A549 cells were changed, NF-kappaB activity increased (dark brown staining ) and TNF-alpha levels (0.307 +/- 0.036 pg/mL vs 0.234 +/- 0.028 pg/mL)increased in the CSE+ serum-free DMEM group compared with the blank control group (P < 0.01). CSE together with azithromycin treatment recovered partly the morphological injuries of A549 cells. It also attenuated NF-kappaB staining and decreased TNF-alpha levels from 0.307 +/- 0.036 pg/mL (CSE+serum-free DMEM group) to 0.269 +/- 0.009 pg/mL (P < 0.05).
CONCLUSIONSAzithromycin may inhibit NF-kappaB activity, decrease TNF-alpha secretion and thus lessen cytotoxicity of CSE to A549 cells.
Anti-Bacterial Agents ; pharmacology ; Azithromycin ; pharmacology ; Cells, Cultured ; Epithelial Cells ; drug effects ; Humans ; Immunohistochemistry ; Lung ; drug effects ; metabolism ; pathology ; NF-kappa B ; analysis ; Smoke ; adverse effects ; Tobacco ; adverse effects ; Tumor Necrosis Factor-alpha ; analysis
4.Therapeutic effect of autologous platelet rich plasma combined with bone marrow mesenchymal stem cell transplantation on long shaft fracture bone nonunion
Song ZHANG ; Tao ZHANG ; Gui-Hong FU ; Shun-Hua LI ; Xue-Ru ZHOU ; Long-Kun CHEN
Chinese Journal of Tissue Engineering Research 2017;21(29):4716-4721
BACKGROUND:Autologous platelet rich plasma and bone marrow mesenchymal stem cells have certain effects on bone repair,but there are rare reports on the clinical treatment of long shaft fracture bone nonunion using autologous platelet rich plasma combined with bone marrow mesenchymal stem cell transplantation.OBJECTIVE:To investigate the therapeutic effect of autologous platelet rich plasma combined with bone marrow mesenchymal stem cell transplantation on long shaft fracture bone nonunion.METHODS:Forty-seven patients with long shaft fracture bone nonunion were randomly divided into two groups:monotherapy group (n=22) and combination group (n=25).In the monotherapy group,autologous bone marrow mesenchymal stem cell transplantation was performed in the bone nonunion site.In the combination group,autologous platelet rich plasma combined with bone marrow mesenchymal stem cell transplantation was implemented in the bone nonunion site.Callus score,clinical healing time,local complications and limb function grade were recorded and compared between the two groups.RESULTS AND CONCLUSION:The healing properties and limb function in the combination group were significantly superior to those in the monotherapy group [healing time:(4.2±1.5) vs.(5.6±1.1) months,P < 0.05;healing rate:92% vs.86%,P < 0.05;callus score:2.74±0.36 vs.2.32±0.53,P < 0.05;limb function recovery rate:77% vs.84%,P < 0.05].Complications like local skin redness or infection were not found in the two groups.In conclusion,both of the two methods can promote bone healing,but autologous platelet rich plasma combined with bone marrow mesenchymal stem cell transplantation has a better clinical effect on bone healing.
5.The effect of HSPB8 gene mutation on cell viability in Charcot-Marie-Tooth disease type 2L.
Shu-jian LI ; Bei-sha TANG ; Guo-hua ZHAO ; Ru-xu ZHANG ; Kun XIA ; Qian PAN
Chinese Journal of Medical Genetics 2011;28(5):528-531
OBJECTIVETo study the effect of Charcot-Marie-Tooth 2L disease causing gene K141N mutation in heat shock protein B8 gene (HSPB8) on cell viability.
METHODSBy using liposome transfection technique, (wt)HSPB8, (K141N)HSPB8 eukaryotic expression vector and green fluorescent protein (GFP) vector were transfected into SHSY-5Y cell, respectively. Twenty-four hours later, the cells were treated with 44 degree centigrade lethal heat shock for 40 minutes. The relative viability of SHSY-5Y cells in each group was tested by using tetrazole blue colorimetric method (methyl thiazolyl tetrazolium, MTT).
RESULTSThere were significant differences among the light absorption value of GFP, pEGFP-(wt)HSPB8 and pEGFP-(K141N)HSPB8 transfected groups after heat shock (P<0.05), indicating that the relative viability of cells overexpressed with (wt)HSPB8 and (K141N)HSPB8 was different from that of control cells. The viability of cells overexpressing (wt)HSPB8 was highest, followed by cells overexpressed with (K141N)HSPB8. The viability of cells tranfected with GFP only was the lowest.
CONCLUSIONHSPB8 may play an important role in the protection of cells under lethal heat shock treatment, and the K141N mutation can impair the protective effect.
Cell Line, Tumor ; Cell Survival ; genetics ; Charcot-Marie-Tooth Disease ; genetics ; metabolism ; Gene Expression Regulation ; Genetic Vectors ; genetics ; Heat-Shock Proteins ; genetics ; metabolism ; Humans ; Mutation ; genetics ; Protein-Serine-Threonine Kinases ; genetics ; metabolism
6.Identication of pearl powder and conch powder from different origins by differential scanning calorimetry.
Jia CHEN ; Ming-hua LI ; Kun-zi YU ; Ya-juan DONG ; Nan-ping ZHANG ; Xiao-ru HU ; Feng WEI ; Shuang-cheng MA
China Journal of Chinese Materia Medica 2015;40(8):1459-1462
The paper is aimed to establish a methods for identication of pearl powder and conch powder from different origins. Hermetic aluminum pan was used to encapsulate samples. The optimal testing conditions were: heating rate 10 degrees C x min(-1), sample weight 3 mg and nitrogen gas flow rate 40 mL x min(-1). The enthalpy values of pearl powder and conch powder was obvious different. Identication of pearl powder and conch powder by DSC is a practical method for its accuracy, convenience and practificality.
Animal Shells
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chemistry
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Animals
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Calorimetry, Differential Scanning
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methods
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China
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Discriminant Analysis
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Pinctada
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chemistry
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classification
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Powders
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chemistry
7.A study involving antioxidizability and cytotoxicity of two kinds of phenol from Ajania Salicifolia and their mechanisms of apoptosis.
Wei ZHANG ; Hong-ru WU ; Qiang-kun LIANG ; Yun-xia LI ; Yan-yu LU ; Yao LONG ; Yao ZHU ; Hong-fang LI
Chinese Journal of Applied Physiology 2015;31(5):422-426
OBJECTIVETo extract two kinds of phenols 4-hydroxy-3, 5-dimethoxy-4-(2-oxopropyl) cyclohexa-2, 5-dien-l-one and 6-methoxy-5,7-dihydroxy coumarin (named as I and H compounds respectively) from Ajania salicifolia and to investigate their antioxidation and cytotoxicity to tumors and explore their pro-apoptosis mechanism.
METHODSThe antioxidant activities of two compounds were assessed by ABTS and DPPH radical-scavenging assays. Two compounds were evaluated for their cytotoxicity against human chronic myelogenous leukemia (K562) cells using the MIT assay. The expression of NF-kappaB P65 mRNA in K562 apoptotic cells was measured by reverse transcription-polymerase chain reaction (RT-PCR), real-time quantitative PCR. In addition, protein expression levels of the NF-ICB P65, p-Akt, Fas, P-catenina and E-cadherin were also measured by Western blot.
RESULTS(1) We found that compound I displayed significant inoxidizability, while compound II had no obvious antioxidizability. (2) In cytotoxicity experiments, compound I didn't display cytotoxicity while compound H displayed obvious cytotoxicity. (3) Compared with the blank group, the expression of NF-kappaB P65 mRNA in K562 cell after treatment with compound II was obviously up-regulated. (4) Compared with the blank group, the expression levels of NF-kappaB P65, Fas, beta-catenina and E-cadherin were significantly increased in compound II treated groups and it appeared obvious dose-effect relationship between the expression of protein and drug concentration.
CONCLUSIONTwo phenols have obvious antioxidizability and cytotoxicity respectively. On the one hand, the tumor-suppressing mechanism of compound II maybe act by up-regulation the expression of NF-kappaB P65 and Fas protein; thereby, affecting the classical Fas apoptosis signaling pathways. On the other hand, it can also up-regulate the expression of protein beta-catenin and E-cadherin, which participate in the adhesion between cells, and accordingly, playing an important role in preventing the proliferation and metastasis of cancer cells.
Apoptosis ; Asteraceae ; chemistry ; Cadherins ; metabolism ; Humans ; K562 Cells ; Oncogene Protein v-akt ; metabolism ; Phenols ; chemistry ; Signal Transduction ; Transcription Factor RelA ; metabolism ; Up-Regulation ; beta Catenin ; metabolism ; fas Receptor ; metabolism
8.Expression and role of mitogen activated protein kinases signaling pathway in lung injury induced by phosgene.
Yi-ru SHAO ; Jie SHEN ; Zhen YUAN ; Dai-kun HE ; Lin ZHANG
Chinese Journal of Industrial Hygiene and Occupational Diseases 2012;30(4):278-283
OBJECTIVEThis study aimed to investigate the expression and role of the mitogen activated protein kinases (ERK1/2, P38, JNK) in phosgene induced lung injury in rats in vivo.
METHOD30 male wistar rats were randomized into the group as follows, Gas inhalation control group, Phosgene inhalation group, and the following groups of the inhibitors of MAPK, involving SP600125, PD98059 and SB203580, 6 animals in each group, we copy the model of phosgene-induced lung injury, used the directional flow-inhalation device, the air control group inhaled the air, and the intervention groups were given PD98059 (intraperitoneal injection), SB203580 (hypodermic injection), SP600125 (intravenous) respectively before the inhalation of phosgene. The locations and quantities of three subfamilies of MAPKs (ERK1/2, P38, JNK) and p-MAPKs (p-ERK1/2, p-P38, p-JNK) were analyzed by immunohistochemistry and Western Blot analysis respectively; The histopathological changes of lung tissues, the number of neutrophil cells and the W/D were examined.
RESULTThere were rare p-ERK1/2, p-P38 and p-JNK positive expression in alveolar and airway epithelial cells in control group. while the positive cells increased strikingly in phosgene inhalation groups, these cells involved in this process mainly included alveolar epithelial cells, air way epithelial cells, pleural mesothelial cells, infiltrative inflammatory cells, interstitium fibrocytes. After the intervention of the specific inhibitor, the positive cells decreased. As Western Blot analysis show, Protein quantities of p-P38 and p-JNK were higher in phosgene inhalation groups than those in control group, and the differences were significant (P < 0.05). Protein quantities of p-ERK1/2, p-P38 and p-JNK were lower in intervention groups than phosgene inhalation group, and the differences were significant (P < 0.05, P < 0.01). The lung injury in phosgene inhalation groups was more severer compared with the control group, the typical pathological characters of acute lung injury were discovered, the increase of the number of neutrophil cells and W/D. After the intervention of the specific inhibitor SP600125 and SB203580, the number of neutrophil cells and W/D reduced, and the differences were significant (P < 0.05, P < 0.01).
CONCLUSIONPhosgene inhalation may activate the MAPK signaling pathway, and the expression of the phosphorylation of MAPKs increased, especially the P38 ang JNK. The results may contribute to the lung injury induced by phosgene.
Animals ; Inhalation Exposure ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Lung ; metabolism ; pathology ; Lung Injury ; etiology ; metabolism ; MAP Kinase Signaling System ; Male ; Mitogen-Activated Protein Kinase 3 ; metabolism ; Mitogen-Activated Protein Kinases ; metabolism ; Phosgene ; adverse effects ; Rats ; Rats, Wistar ; p38 Mitogen-Activated Protein Kinases ; metabolism
9.Thoraco-abdominal aorta revascularization through a retroperitoneal approach.
Zheng YUE-HONG ; Yu KUN ; Zhang JIE-FENG ; Choi NIM ; Deng HONG-RU ; Rui FURTADO
Chinese Medical Sciences Journal 2010;25(4):233-236
OBJECTIVETo investigate the application of the retroperitoneal approach in aortic surgery.
METHODSWe collected and analyzed data of 7 patients in Macau who presented with aortic diseases from 2007 to 2008 and were treated with aorta repair through retroperitoneal approach. Demographic features as well as intraoperative and postoperative data were analyzed. One case of thoracoabdominal aneurysm and 4 cases of abdominal aneurysm received artificial graft, among which hybrid iliac artery reconstruction with Zenith stent covering the ostium of the left subclavian artery was performed in 2 cases of infrarenal abdominal aneurysm. Aortic-iliac artery bypass was performed in 2 cases of aortoiliac occlusion.
RESULTSNo operative or early postoperative death was observed. No perioperative intestinal adhesion or ureteral obstruction was found. One case reported delayed paraplegia and graft infection as postoperative complications. The complications were partially removed 3 months later after rehabilitation.
CONCLUSIONRetroperitoneal approach is a safe and feasible technique, which associated with a low incidence of postoperative pulmonary complications.
Aged ; Aorta ; surgery ; Humans ; Myocardial Revascularization ; methods ; Peritoneal Cavity ; Treatment Outcome ; Vascular Surgical Procedures ; methods
10.Optimal conditions for transfecting Wharton's Jelly-derived mesenchymal stem cells with electroporation method
Ze WANG ; Chun-Hua LI ; Ning-Kun ZHANG ; Lian-Ru GAO ; Yu CHEN
Chinese Journal of Tissue Engineering Research 2018;22(17):2717-2721
BACKGROUND: Wharton's Jelly-derived mesenchymal stem cells are relatively primitive stem cells that are ideal vectors for gene therapy. However, there is a lack of studies on the conditions for the electrotransfection of Wharton's Jelly-derived mesenchymal stem cells. Therefore, exploring the optimal conditions for the electrotransfection of Wharton's Jelly-derived mesenchymal stem cells occupies an important position. OBJECTIVE: To investigate the effects of different electroporation conditions on the transfection efficiency of Wharton's Jelly-derived mesenchymal stem cells, and to explore the optimal conditions for cell electroporation. METHODS: By controlling the transfection conditions such as voltage, pulse duration and cell status, EEV-EGFP plasmids were transfected into Wharton's Jelly-derived mesenchymal stem cells by electroporation under different conditions. Transfection efficiency was detected by flow cytometry. RESULTS AND CONCLUSION: (1) The transfection efficiency was intended to increase when the voltage ranged from 125 V to 150 V, and the maximum transfection efficiency was obtained when the voltage was 150 V. However, when the voltage was further increased to 170 V, the transfection efficiency began to decrease considerably. (2) The maximum transfection efficiency was obtained when the pulse duration was 5.0 ms, while it was certainly decreased when the pulse duration was 2.5 and 7.5 ms. (3) The transfection efficiency of the cells cultured under normoxia was higher than that under hypoxic culture. These findings reveal that normally cultured Wharton's Jelly-derived mesenchymal stem cells can achieve higher electroporation efficiency via two pulse sessions at a voltage of 150 V, pulse duration of 5.0 ms, and pulse interval time of 50 ms.