Cardiopulmonary Resuscitation ; China ; Humans ; Time Factors

OBJECTIVETo explore the correlation of low-dose radiation with endoplasmic reticulum stress and the activation of the PERK-CHOP signaling pathway in mouse testicular cells.

METHODSHealthy Kunming mice were randomly assigned to time-effect (0, 3, 6, 12 and 24 h of irradiation at 75 mGy) and dose-effect (12 h of irradiation at 0, 50, 75, 100 and 200 mGy) groups. The contents of H202 and MDA were measured by colorimetry with the agent kits, the expressions of GRP78, PERK and CHOP mRNA detected by quantitative RT-PCR, and the levels of GRP7B, PERK, phosphorylated PERK (pho-PERK) and CHOP proteins determined by Western blotting and image analysis.

RESULTSAfter whole-body irradiation of the mice with 75 mGy, the content of H2 02 in the testis tissue was increased with time prolongation, while that of MDA decreased slightly at 3 and 6 h and then increased with the lengthening of time, both increased significantly at 12 and 24 h as compared with those at 0 h (P < 0. 05, P < 0. 01). Apart from reduced levels of GRP78 mRNA at 3 and 24 h and GRP78 protein at 6 h after irradiation, significant increases were found in the mRNA expressions of GRP78 at 12 h, PERK at 3,6, 12 and 24 hand CHOP at 12 and 24 h (P < 0.05, P < 0.01), as well as in the protein levels of GRP78 at 12 and 24 h, pho-PERK at 3, 12 and 24 h and CHOP at 3, 6, 12 and 24 h in comparison with those at 0 h (P < 0. 05, P < 0. 01). No obvious regularity was observed in the change of the PERK protein expression. After 12 h of whole-body irradiation, the content of H202 was increased at 50, 75 and 100 mGy, but decreased slightly at 200 mGy, while that of MDA was increased with dose increasing, with significant increases in the content of H2 02 at 75 and 100 mCy and in that of MDA at 75, 100 and 200 mGy as compared with the 0 mGy group. Apart from the reduced levels of GRP78 mRNA at 50 and 200 mCy, significant increases were found in the mRNA expressions of PERK at 75, 100 and 200 mGy and CHOP at 50, 75, 100 and 200 (P c 0. 05, P < 0.01) as well as in the protein levels of GRP78 at 100 and 200 mGy, pho-PERK at 50, 100 and 200 mGy and CHOP at 50, 75, 100 and 200 mCy as compared with those at 0 mGy (P < 0. 05, P < 0. 01). There were differences in the changes of different protein expressions, but no obvious regularity was seen in the change of the PERK protein expression.

CONCLUSIONLow-dose radiation can induce endoplasmic reticulum stress in mouse testicular cells, and activate the PERK-CHOP signaling pathway.

Animals ; Endoplasmic Reticulum Stress ; radiation effects ; Heat-Shock Proteins ; metabolism ; Male ; Mice ; Mice, Inbred Strains ; Radiation Dosage ; Radiation, Ionizing ; Signal Transduction ; radiation effects ; Testis ; cytology ; metabolism ; radiation effects ; Transcription Factor CHOP ; metabolism ; Whole-Body Irradiation ; eIF-2 Kinase ; metabolism

Objective To investigate whether the effect of puerarin on right ventricle hypertrophy of pulmonary hypertensive rats induced by chronic hypoxia-hypercapnia was related to new peptide Apelin or its receptor(APJ).Methods Thirty male Sprague-Dawley rats were randomly divided into three groups, they are control group,hypoxia-hypercapnia 4-week model group,and hypoxia-hypercapnia 4-week plus puerarin group.The concentrations of Apelin-36 protein in plasma and homogenate of right ventricular muscle were detected by radioimmunoassay.The mRNA expressions of Apelin and APJ in right ventricu- lar muscle were measured by semi-quantitive reverse transcription polymerase chain reaction(RT-PCR). Results The weight ratio of right ventricle to left ventricle plus septum[RV/(LV+S)] in model group was significantly higher than that in control group(P0.05).The plasma concen- tration of Apelin-36 protein in model group was significantly higher than that in control group(P

OBJECTIVETo investigate clinical efficacy and significance of gluteal muscle contracture release for the treatment of gluteal muscle contracture induced knee osteoarthritis.

METHODSFrom January 2008 to June 2010,52 patients with gluteal muscle contracture induced knee osteoarthritis were reviewed. Among the patients,15 patients were male and 37 patients were female, ranging in age from 15 to 45 years, with an average of 35 years. Eighteen patients had left knee osteoarthritis, 30 patients had right osteoarthritis, and 4 patients had double knee osteoarthritis. All the patients were treated with gluteal muscle contracture release. Lysholm knee score was used to evaluate therapeutic effects before and after operation.

RESULTSAll the patients were followed up,and the duration ranged from 12 to 37 years,with a mean of 15 months. The Lysholm knee score improved from preoperative (68.12 +/- 0.78) points to postoperative (91.23 +/- 0.47) points at the last follow-up, the difference had statistical difference (t=31.269, P<0.01).

CONCLUSIONGluteal muscle contracture release is effective to relieve symptoms of gluteal muscles contracture and knee osteoarthritis. The patients with gluteal muscle contracture should be treated early so as to prevent effects of gluteal muscle contracture on knee joint, slow down degeneration of knee joint at early stage, and prevent occurrence of knee osteoarthritis.

Adolescent ; Adult ; Buttocks ; Contracture ; complications ; diagnostic imaging ; therapy ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Osteoarthritis, Knee ; diagnostic imaging ; etiology ; therapy ; Tomography, X-Ray Computed ; Young Adult

Objective To evaluate the clinical diagnosis and treatment of acute renal infarction.Methods Two cases (3 sides) of acute renal infarction were reported.The patients were 1 male and 1 female,with the age of 62 and 54 years.Case 1 presented acute left flank pain,and enhanced CT showed a non-enhanced area in the upper and mid pole of the left kidney.The diagnosis of focal renal infarction was made and treated with low-molecular heparin (6000 U ).Case 2 presented acute both right abdominal and flank pain,and enhanced CT showed right renal artery embolism and right renal complete infarction.Digital subtraction angiography (DSA) and catheter thrombolytic therapy was applied.4 months later,the patient presented acute left flank pain,and enhanced CT showed a low density area in left kidney without enhanced by contrast,and DSA and catheter thrombolytic therapy was applied again.Results In case 1,contrastenhanced MRI showed a still low signal area like enhanced CT after 2 days of treatment.The renal function remained normal in the follow-up of 36 months.In case 2,the right kidney resorted to moderate blood flow but became atrophy later.In the follow-up of 4 months,a recurrent focal infarction was confirmed in left kidney by enhanced CT.The left kidney also resorted to moderate bloodflow after DSA and catheter thrombolytic therapy.The renal function became normal after follow-up of 10 months and no new infarction was observed.Conclusions The diagnosis of acute renal infraction could be made by enhanced CT or MRI.Early diagnosis and location of the infraction renal artery is critical for recovery of the impaired renal function.Acute renal infraction should be suspected in patients with unexplained persistent and steady flank or abdominal pain in emergence department.

OBJECTIVETo investigate the effect of glycine on CD14 and NF-kappa B in Kupffer cells from rat liver grafts after ischemia-reperfusion injury (IRI).

METHODSThe rats were randomly divided into an IRI group, saline solution preconditioning group, and glycine preconditioning group. Their survival rates, graft functions, and hepatic histopathologic examinations were observed after IRI. Kupffer cells (KCs) following IRI were isolated and cultured to detect CD14 mRNA, NF-kappa B binding activity, and the TNF alpha and IL-1 level in the supernatant of the media.

RESULTS(1) Glycine preconditioning greatly enhanced the one-week survival rate (chi2 = 6.67 and 8.57 respectively), improved graft function, and ameliorated the histopathologic signs of injury. (2) The CD14 mRNA expression level (F = 7.64), NF-kappa B binding activity (F = 11.47), TNF alpha and IL-1 production (F = 14.08 and 9.56 respectively) in the glycine group were significantly lower than those in the other two groups.

CONCLUSIONGlycine could efficiently protect rat liver grafts from ischemia-reperfusion injury by repressing the expression of CD14 and NF-kappa B binding activity in Kupffer cells and inhibiting the productions of TNF alpha and IL-1.

Animals ; Cells, Cultured ; Glycine ; pharmacology ; Kupffer Cells ; metabolism ; pathology ; Lipopolysaccharide Receptors ; biosynthesis ; genetics ; Liver ; blood supply ; metabolism ; Liver Transplantation ; adverse effects ; NF-kappa B ; metabolism ; RNA, Messenger ; biosynthesis ; Random Allocation ; Rats ; Rats, Wistar ; Reperfusion Injury ; metabolism ; pathology

OBJECTIVETo investigate the protective effect of limited fluid resuscitation against intestinal ischemia- reperfusion injury in postpartum rabbits with severe uncontrolled obstetrical hemorrhagic shock.

METHODSTwenty- four postpartum rabbits were randomly assigned into sham shock group (group P), shock group without interventions (group P0), conventional fluid resuscitation group (group PNL), and limited fluid resuscitation group (group PLH), and the model of severe uncontrolled hemorrhagic shock was established in the latter 3 groups. The rabbits were sacrificed 4 h later, and SOD activity and MDA content in the intestinal mucosa and the degree of injury to the intestinal mucosa were observed.

RESULTSIschemia-reperfusion injury of the intestine due to uncontrolled hemorrhagic shock resulted in decreased SOD activity and increased MDA content. The MDA content was significantly lower and SOD activity was significantly higher in group PLH than in group PNL (P<0.05), and the intestinal mucosal tissue morphology and intestinal mucosa barrier lesion increased in group PLH.

CONCLUSIONInitial limited fluid resuscitation can relieve intestinal ischemia-reperfusion injury in postpartum rabbits with severe uncontrolled obstetrical hemorrhagic shock.

Animals ; Disease Models, Animal ; Female ; Fluid Therapy ; methods ; Intestines ; blood supply ; Pregnancy ; Rabbits ; Reperfusion Injury ; etiology ; prevention & control ; Shock, Hemorrhagic ; complications

OBJECTIVESTo study the role of cyclooxygenase 2 (COX 2) and prostaglandin I2 (PGI2) in the development of portal hypertensive gastropathy (PHG).

METHODSForty Wistar rats were divided into surgery group (32) and control group (8). Partial portal vein ligation method was used to narrow the sectional area of portal vein to establish the experimental model of PHG in surgery group rats. Then they were divided into four groups (8 rats in each). The free pressure of portal vein was determined at the 1st, 2nd, 3rd, 4th weeks after the operation, and 8 rats were killed to observe the pathological change of gastric mucosa. The levels of 6-keto-PGF1 alpha, a stable metabolite of PGI2, were determined by radioimmunoassay in gastric mucosa homogenate and the blood of portal vein. The expression of COX 2 in gastric mucosa was determined by immunohistochemistry.

RESULTSThe free pressure of portal vein increased rapidly after partial portal vein ligation and maintained a high stable level after 1 week. They were (2.40+/-0.15) kPa, (2.38+/-0.17) kPa, (2.52+/-0.21) kPa, and (2.46+/-0.17) kPa at the 1st, 2nd, 3rd, and 4th weeks after partial portal vein ligation, while it was (0.90+/-0.16) kPa in control group (t>or=17.356, P<0.05). The gastric mucosa appeared pale, edema, hyperaemia, surface erosion, punctate hemorrhage and these lesions were more apparent with the time after the operation. The pathological examination showed that the gastric mucosa and submucosa thickened. The vessels of gastric mucosa and submucosa expanded and increased. There were lymphocytes and neutrophils infiltration around the vessels in the gastric mucosa and submucosa. The 6-keto-PGF1 alpha levels in gastric mucosa and the blood of portal vein increased rapidly and maintained a high level after partial portal vein ligation,which were higher than those in control group (104.52pg/ml+/-25.11pg/ml vs 73.62pg/ml+/- 20.33pg/ml, t=2.710, P<0.05; 180.21pg /ml+/-37.56pg /ml vs 142.11pg /ml+/-31.51pg /ml, t=2.198, P<0.05). The results of immunohistochemistry showed that the intensity and degree of the COX 2 staining in gastric tissue increased at the 1st, 2nd, 3rd, 4th weeks after partial portal vein ligation, while the COX 2 in control group rats was negative.

CONCLUSIONSThe expression of COX 2 and PGI2 in gastric tissue increased in portal hypertension. PGI2 as an inflammatory medium, damages the gastric mucosa by expanding vessels and other mechanisms in portal hypertension. It may be one of the important factors contributing to the development of PHG.

Animals ; Cyclooxygenase 2 ; Disease Models, Animal ; Epoprostenol ; physiology ; Hypertension, Portal ; complications ; pathology ; Isoenzymes ; physiology ; Male ; Prostaglandin-Endoperoxide Synthases ; physiology ; Rats ; Rats, Wistar ; Stomach Diseases ; etiology ; pathology

OBJECTIVETo explore the effects of HBsAg pulsed dendritic vaccination on anti-HBs production in immunosuppressed rats after liver transplantation (LT).

METHODSBrown-Norway liver allografts were transplanted into Lewis recipients. The transplanted Lewis rats were injected with EK506 (2 mg/kg) and randomly divided into two groups: rats in HBsAg-DCs group (n = 15) were intraperitoneally injected with HBsAg pulsed DCs at 14 d and 28 d after LT, and rats in the HBsAg group (n = 15) were injected with HBsAg (200 mul) once a week for 12 weeks. Rats without any immunosuppressive treatment after LT served as controls (n = 5). IL-2 and IFN-gamma mRNA expression in spleen were analyzed by RT-PCR, serum IL-2, IFN-gamma and anti-HBs were detected by ELISA.

RESULTSHigh dose of FK506 resulted in the immunosuppressed in LT rats, as evident by low production of IL-2 and IFN-gamma, and without liver rejection compared to rats in the control group. HBsAg-DCs induced high titer of anti-HBs antibody, however, titer of anti-HBs were seldom detectable in the HBsAg group at 1, 2 and 3 mouth after vaccination.

CONCLUSIONThe capacity of HBsAg-DCs to induce anti-HBs in immunosuppressed rats suggested that DC vaccine may prevent HBV recurrence in liver transplanted patients.

Adjuvants, Immunologic ; pharmacology ; Animals ; Cytokines ; blood ; genetics ; metabolism ; Dendritic Cells ; immunology ; Disease Models, Animal ; Hepatitis B ; immunology ; prevention & control ; Hepatitis B Antibodies ; blood ; immunology ; Hepatitis B Surface Antigens ; immunology ; Hepatitis B Vaccines ; Immunosuppression ; Immunosuppressive Agents ; administration & dosage ; Liver Transplantation ; immunology ; Male ; RNA, Messenger ; genetics ; metabolism ; Random Allocation ; Rats ; Rats, Inbred BN ; Rats, Inbred Lew ; Secondary Prevention ; Spleen ; immunology ; metabolism

OBJECTIVETo investigate the role of autophagy inhibitor chloroquine (CQ) in the proliferation of pulmonary arterial smooth muscle cells (PASMCs) in hypoxia conditions.

METHODSThe following groups in this study were set up: control group, hypoxia group, 50 micromol/L CQ + hypoxia group, 50 micromol/L CQ group. The viability of PASMCs in every group was detected by MTT assay. Autophagic vacuoles in the cells were observed by MDC staining. Protein expression of microtubule associated protein light chain 3 (LC3) was measured by Western blot. Migration of PASMCs was detected by wound healing assay.

RESULTSCompared with control group, no effect on the viability of PASMCs was observed treated by CQ alone. In 1% hypoxia group, cell viability increased significantly compared with that in control group. The number of autophagic vacuoles and the rate of cell migration and also protein expression of LC3-II were also markedly increased. Compared with hypoxia group, addition of CQ increased the number of autophagic vacuoles and the levels of LC3-II protein, but decreased the proliferation and migration of PASMCs.

CONCLUSIONHypoxia could activates autophagy and contributes to proliferation and migration of PASMCs, and autophagy inhibitor CQ could decrease the effect of hypoxia on PASMCs through inhibiting autophagy process.

Autophagy ; drug effects ; Cell Hypoxia ; Cell Movement ; Cell Survival ; Cells, Cultured ; Chloroquine ; pharmacology ; Humans ; Microtubule-Associated Proteins ; metabolism ; Myocytes, Smooth Muscle ; drug effects ; Pulmonary Artery ; cytology