Objective: To investigate the differences of biochemical markers between the patients with pulmonary hypertension related to left heart disease (PH-LHD) and LHD; to explore the sensitive bio markers which may predict PH in LHD patients. Methods: A total of 355 LHD patients admitted to our hospital from 2014-01 to 2015-05 were enrolled. According to 2009 ESC/ERS guidelines, PH was deifned by pulmonary artery systolic pressure (PASP)>50 mmHg and patients were divided into 2 groups: LHD group,n=224 and PH-LHD group,n=131. The basic information with blood levels of biomarkers was recorded and their accuracy for predicting PH was analyzed. Results: The pathogenesis of LHD included 184 (51.83%) patients of coronary heart disease, 90 (25.35%) of dilated cardiomyopathy and 81 (22.81%) of cardiac valve heart disease. Compared with LHD group, PH-LHD group had increased ratio of NYHA III and IV degree (89.31% vs 45.54%), decreased LVEF [42.0 (33.0, 59.0) % vs 60.0 (42.0, 65.0) %], all P<0.001; PH-LHD group presented elevated blood levels of BNP, bilirubin, red cell distribution width (RDW), uric acid and cystatin C, while reduced lipoprotein (HDL), allP<0.001. PASP was positively related to biomarkers as BNP, bilirubin, RDW, uric acid and cystatin C, while negatively related to HDL. With the combination of BNP, direct bilirubin and RDW, the predictive value for PH-LHD under ROC curve was 0.828 with the sensitivity at 0.813, speciifcity at 0.708. Conclusion: Blood levels of biochemical markers were statistically different between the patients of PH-LHD and LHD; the combination of BNP, direct bilirubin and RDW showed the higher accuracy for predicting PH occurrence in LHD patients.

ASICs are H+-gated novel cation ion channels, which belong to the epithelial sodium channels (NaC/DEG) superfamily. As recent studies focus, ASICs are expected to be pharmacological targets on protecting the neuron from ischemia and damage, improving the ability of memory and study, curing epilepsy and analgesia. It is not until the most recentness that the subunits of ASICs have been cloned. Now, researchers have paid more attention to the distribution, expression, function and modulation of ASICs in the organism.

Objective To investigate the sequence variations of mitochondrial D-loop region in chronic glomerular nephritis patients and family members and their possible associations with chronic glomerular nephritis.Methods 20 patients with chronic glomerular nephritis and 48 unaffected pedigree members,as well as 122 cases of normal control were recruited.mtDNA extracted from peripheral blood were examined by PCR-based assay for D-loop sequence variations,followed by sequencing analysis.Results Compared with the normal control and standard sequence,a total of 61 sequence variants were detected,among these,three high variations were found,and the base variation rate of patients with chronic glomerular nephritis(CGN)and unaffected pedigree members(UAPM)(0.88%,0.72%)significantly increased compared with the control group(0.61%).The distibutional difference of base variation rate in the experimental groups were significantly higher than those in the control group(x2=21.220,7.964,all P<0.05).Especially in microsatellite variation in D310 region,the mutation frequency and base variation rate in patients with CGN were 100.00% and 30.00%,respectively,which of UAPM were 81.30% and 17.95%,respectively,while those in the normal control group were 53.30% and 6.05%,respectively.Among them,the patients with CGN compared with the control group had statistically significant differences(x2=15.610,150.047,all P<0.05).Likewise,UAPM also had statistically significant difference compared with the control group(x2=11.347,66.188,all P<0.05).Conclusion D-Loop of mitochondrial genome mutations may be related to the development of chronic glomerular nephritis.

OBJECTIVETo study measurement methods of acromioclavicular and coracoclavicular ligament injuries,its therapeutic effects and complications during internal fixation operation for the treatment of fresh acromioclavicular joint dislocations of Tossy type III.

METHODSFrom July 2003 to May 2012,127 patients with acromioclavicular joint dislocations of Tossy type III were treated with wire fixation from coracoid process to clavicle or hook-plate fixation. The patients were divided into group A (63 cases) and group B (64 cases) according to whether acromioclavicular ligament and coracoclavicular ligament were repaired or not. In group A (ligaments repaired), there were 39 males and 24 females with an average age of (33.25 +/- 8.46) years old (ranged from 17 to 59 years). And in group B (no ligaments repaired), there were 41 males and 23 females with an average age of (34.10 +/- 7.19) years (ranged from 19 to 57 years). The operation times, intraoperative blood loss, postoperative infections, internal fixation failure, recurrence and other complications, together with therapeutic effects were compared between two groups.

RESULTSThe outcome was analyzed according to Karlsson standard. In group A, 54 patients got an excellent result and 9 good according to Karlsson standard;the average operative time was (55.90 +/- 26.56) min; the average intraoperative bleeding amount was (99.80 +/- 50.30) ml; 1 patient had wire broken without re-dislocation at 16 weeks after operation, 3 patients got wound fat liquefaction and recovered after treatment, 1 patient had pain after shoulder joint motion and pain disappeared after implants were taken out. In group B, 52 patients got an excellent result and 12 good according to Karlsson standard; the average operative time was (49.50 +/- 23.14) min; the average intraoperative bleeding amount was (87.30 +/- 46.41) ml; 2 patients got wound fat liquefaction, and 2 patients had pain after shoulder joint motion. All the patients were followed up, and the duration ranged from 9 to 16 months. All internal steel-wire or hook plate were taken out during 4 to 9 months without acromioclavicular joint re dislocation. There were no significant difference in the average operative time, the average intraoperative blood less, complication recurrence rates of fixation failure, wound fat liquefaction, postoperative infection, acromioclavicular joint re-dislocation, and therapeutic effects between two groups.

CONCLUSIONBoth wire and clavicular hook plate fixation, performed for fresh acromioclavicular joint dislocation with Tossy type III, are simple, effective, less invasive method with less blood loss. In addition, the treatment without ligaments repaired could not increase incidence of complications.

Acromioclavicular Joint ; diagnostic imaging ; injuries ; surgery ; Adolescent ; Adult ; Case-Control Studies ; Clavicle ; Female ; Humans ; Joint Dislocations ; diagnostic imaging ; surgery ; Ligaments ; diagnostic imaging ; injuries ; surgery ; Male ; Middle Aged ; Orthopedic Procedures ; methods ; Tomography, X-Ray Computed ; Treatment Outcome ; Young Adult

In the present study, packaging system composed of pAAV-CMV-GFP, pAAV-RC and pHelper were transfected into human embryonic kidney 293 cells (HEK293 cells) mediated by polyethyleneimine (PEI) to explore an optimal transfection condition. Different total plasmid DNA dosages (1, 2, 3, 4, 5, 6 μg) and different PEI/Plasmid ratios (1:1, 3:1, 5:1, 7:1) were tested with detection of green fluorescence protein (GFP) with ImagePro Plus6. 0 Software. Then transfection efficiency of the optimized transfection system was further observed for different time periods(12, 24, 36, 48, 60, 72 h). The results showed that total plasmid dosage of 4 μg/well with PEI/plasmid ratio of 3 : 1-5 : 1 was an efficient transfection condition. Transfection efficiency-time curve was an S-shaped curve. Transfection efficiency reached a plateau at 60 h after transfection. The optimized conditions for PEI-mediated transfection at the optimal time result in enhanced transfection efficiency of triple plasmid into HEK293 cells.
Green Fluorescent Proteins ; HEK293 Cells ; Humans ; Plasmids ; Polyethyleneimine ; Transfection ; methods

Compounds with serotonin reuptake inhibition/5-HT(1A) dual activity were used to build 3D pharmacophore model as a training molecules by Discover Studio. Based on the model, 8 novel aryl piperazine benzo[b][1,4] oxazine derivatives were designed and synthesized, and their structures were confirmed by 1H NMR and HR-MS. Biological evaluation illustrated that compounds VI(1) and VI(7) showed potent functional activities at both 5-HT transporter and 5-HT(1A) receptor, which can be used as lead compounds to guide future research of design and synthesis of potent novel compounds.

Objective To evaluate the role of Janus kinase 2-signal transducer and activator of transcription 3 (JAK2-STAT3) signaling pathway in sevoflurane postconditioning-induced inhibition of mitochondrial permeability transition pore (mPTP) opening during myocardial ischemia-reperfusion (I/R)in rats.Methods Sixty pathogen-free healthy male Sprague-Dawley rats,weighing 250-300 g,were divided into 4 groups (n=15 each) using a random number table:I/R group,sevoflurane postconditioning group (group SP),AG-490 group (group AG) and sevoflurane postconditioning plus AG-490 group (group SP+AG).Myocardial I/R was induced by 30 min ligation of the left anterior descending branch of coronary artery followed by 120 min reperfusion.In group SP,2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.JAK2 inhibitor AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion in group AG.In group SP+AG,AG-490 3 mg/kg was intravenously injected at 10 min before reperfusion,and 2.8％ sevoflurane was inhaled for 15 min starting from 2 min before reperfusion.At 15 min of reperfusion,5 rats were sacrificed and myocardial specimens were obtained for determination of the expression of JAK2,phosphorylated JAK2 (p-JAK2),STAT3 and phosphorylated STAT3 (p-STAT3)in myocardial tissues by Western blot.The ratios of p-JAK2 to JAK2 expression (p-JAK2/JAK2) and pSTAT3 to STAT3 expression (p-STAT3/STAT3) were calculated.Five rats were sacrificed at the end of reperfusion for measurement of myocardial infarct size.The left 5 rats were selected and sacrificed,myocardial specimens were obtained,and the opening of mPTP was detected by a calcein-cobalt quenching method.Results Compared with group I/R,the myocardial infarct size and mPTP opening were significantly decreased,and JAK2/p-JAK2 and STAT3/p-STAT3 were increased in group SP (P＜0.05),and no significant change was found in the parameters mentioned above in SP+AG and AG groups (P＞0.05).Compared with group SP,the myocardial infarct size was significantly enlarged,the extent of mnPTP opening was aggravated,and JAK2/p-JAK2 and STAT3/p-STAT3 were decreased in SP+AG and AG groups (P＜0.05).Conclusion The mechanism by which sevoflurane postconditioning inhibits the opening of mPTP during myocardial I/R is related to activation of JAK2-STAT3 signaling pathway in rats.

Objective To study changes in synaptic plasticity in the contralesional mirror area of the cortexes of rats with cerebral infarction treated by low-frequency electrical stimulation(LFES)and to explore the therapeutic mechanism of LFES on the molecular level.Methods Forty-eight Sprague-Dawley rats were randomly allocated into a LFES group,a placebo group and a sham-operation group.Following middle cerebral artery occlusion(MCAO),rats in the LFES group were treated with LFES for 7 d(20 min/d),while the ones in placebo group were connected with the same LFES device but without electricity.Rats in the sham-operation group were subjected to a MCAO operation without occlusion and then received no special treatment.Synaptic ultra-structures and the expression levels of glia fibrillary acidic protein(CFAP)and synaptophysin in the contralesional mirror area of the cortexes of the rats in each group were measured with electron-microscopy and Western blotting.Results Compared with the placebo group or the rats before treatment,rats treated with LFES exhibited ultra-structural changes in the form of larger curvature of synaptic interfaces and narrower synaptic clefts.GFAP expression levels did not fluctuate significantly,but the expression of synaptophysin was significantly up-regulated.Conclusion LFES treatment can induce active changes in synaptic plasticity in the contralesional mirror area of the cortex of rats after cerebral infarction.

Objective To study the effects of low-frequency electrical stimulation(LFES)on motor function and the expression of glia fibrillary acidic protein(GFAP)around cerebral infarction sites in rats.Methods Fifty-four male adult Sprague-Dawley rats were randomly divided into a LFES group,a placebo group and a sham operation group(18/group).All groups were randomly divided into 3 treatment groups.A rat model of middle cerebral artery occlusion(MCAO)was established using intraluminal filament occlusion.Treatment was carried out 3 d after the operation.Rats in the LFES treatment groups were stimulated with LFES for 3,7 or 14 days (10 min/d);the placebo groups were treated in the same way without electric stimulation;the sham operation subgroups didn't receive any therapy.Scores on a beam-walking test,a rotating pole test and a screen test were assessed at each time point mentioned above.Expression of GFAP was also assessed using immunohistochemcal techniques.Results The paralysed limbs recovered motor function better in the LFES groups than in the control groups.GFAP-positive cells were more numerous at the margins of the infarction area in the treated groups than in the control groups.Conclusions LFES might increase the expression of GFAP,which might be an important mechanism in improving brain plasticity after cerebral ischemia,aiding the recovery of the central nervous system and rebuilding its functioning.

Objective To observe the PML protein expression of hepatocellar carcinoma tissue and cells lines and As 2 O3 regulate its expression .Methods Immunohistochemistry was used to examine the PML protein expression of hepatocellar carcinoma tissue . Western blot analysis were used to observe PML protein expression of hepatocellar carcinoma tissue of 12 cases ,5 hepatocellar car-cinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 ,MHC97H .Western blot analysis was used to detected the PML pro-tein expression of these hepatocellar carcinoma cell lines after 72-96 h treated with 0 .25 μg/mL of As2 O3 .Results Immunohisch-enmical staining showed that the PML protein was expressed in both cytoplasm and nucleus ,did not well-distributed in hepatocellar carcinoma cells .There was no significant differences of PML protein expressed among differently differentiated stages of hepatocel-lar carcinoma cells .Western blot analysis found that hepatocellar carcinoma tissues of 12 cases with hepatocellar carcinoma ex-pressed PML protein ,and there was significant difference of PML protein expressed among 12 cases suffer with hepatocellar carci-noma .hepatocellar carcinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H all expressed PML protein ,and there was little difference of PML protein expressed among hepatocellar carcinoma cell lines .The PML protein expression of HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H cell after 72-96 h treated with 0 .25 μg/mL of As2O3 significant decreased . Conclusion Hepatocellar carcinoma tissue and cells may express PML protein ,and As2 O3 may regulate this protein expression as well .PML protein may be the target molecule of As2 O3 treating HCC .