Objective To observe the effects of electrical acupuncture for the treatment of neurogenic detrusor overactivity (DO) caused by spinal cord injury (SCI).Methods Twenty SCI patients with DO were included in this study. There were 18 males and 2 females;age ranged from 17 to 58 years. Patients were given electro-acupuncture treatment at the bilateral S3 foramen at the lateral position during the vidio-urodynamic investigation when the detrusor of the patients began to contract.The different intensities of electrical stimulation were used when the DO appeared during cystometry and the most effective intensity to inhibit DO was determined. Then, the bladder was emptied and the stimulation with selected intensity was used at the beginning of cystometry. The changes of parameters in the urodynamics, the urinary incontinence times per day and the pad used per day were recorded. The acute effects were observed. Ten days were set as one course and after 3 courses and 9 courses the patients underwent urodynamic test again. The long-term effects were observed.Results After treatment, the urinary incontinence times per day and the pad used per day decreased obviously (P<0. 05). The bladder capacity increased significantly and the maximum intravesical pressure decreased significantly. There were 3 patients having the long terms treatment. Conclusions The Chinese electro-acupuncture at S3 foramen in the SCI patients with DO is demonstrated effective. After the treatment bladder capacity could increase and the times of the urinary incontinence per week decrease.

ObjectiveTo explore the effects of myoblast formation around the urethra of stress urinary incontinence (SUI) rats after treated with bone marrow mesenchymal stem cells(BMSCs) or musclelike cells/calcium alginate composite gel injection therapy.MethodsIsolation,cultivation and identification of Sprague-Dawley rat bone marrow mesenchymal stem cell were performed.5-azacytidine was introduced to induce muscle-like cells.Calcium alginate gel was initially prepared by 2％ sodium alginate and 1％ calcium chloride solution at a volume ratio of 5∶1.Compounds of stem cells or muscle-like cells were mixed with gel,respectively,and were prepared for microinjection.SUI was produced in 72 6-week-old female Sprague-Dawley rats.The rats were then divided into 4 groups:Gel group,stem cell-gel group,muscle-like cell-gel group and mock control group.Each group was further divided into 3 groups.Submucosal injection of gel was performed at urethra and bladder neck.After preparation of cross sections of rat urinary tract at 4 weeks and 8 weeks after injection,HE staining,fluorescent tracing,staining of Desmin and α-skeletal muscle actin (α-SMA) were performed.OD values of positive rates were compared.ResultsAt 4 weeks and 8 weeks after injection in stem cell-gel group and muscle-like cell-gel group,growth of blood vessels gradually increased at gel edge,BMSCs and muscle-like cells gathered around the new blood vessels observed by fl(u)orescence tracer,muscle-like cells grew into elongated spindle-like cells.Desmin and α-SMA staining were positive in these groups,and the OD values in the stem cell-gel group and muscle-like cell-gel group was significantly higher than that from the gel only group and control group,but no difference was found between stem cell-gel group and muscle-like cell-gel group.ConclusionsCompound of BMSCs,muscle-like cells and calcium alginate composite gel has the potential to differentiate into muscle cells in the microenvironment of SUI rat model.In short term,the myoblast formation potential is the same whether the BMSCs was introduced into the micro-environment in vivo directly,or the BMSCs was implanted into microenvironment after the formation of the muscles cells induced by 5-azacytidine in vitro.

Objective:To investigate the effects of intervention mapping on cardiopulmonary function for patients with acute heart failure in compensatory period, so as to provide references for their early rehabilitation activities.Methods:A total of 90 patients with acute heart failure admitted to Fuwai Central China Cardiovascular Hospital from October 2018 to October 2019 were enrolled in the present study. They were divided into experimental group and control group according to draw-lots-method, with 45 cases in each group. The control group received the routine care and activity plan, while the experimental group implemented intervention mapping-based stage early rehabilitation program. The indicators included 6MWT, forced expiratory volume in one second (FEV 1), brain natriuretic peptide (BNP) as well as Minnesota Living with Heart Failure Questionnaire (MLHFQ), and the intervention effects were compared between the two groups. Results:There were no significant differences in FEV 1, 6MWT, BNP and MLHFQ scores between the two groups at admission ( P>0.05). On discharge, FEV 1, 6MWT were (2.17±0.44) L, (273.09±55.80) m in the experimental group, significantly higher than (1.94 ± 0.39) L and (236.44 ± 50.99) m in the control group; the plasma BNP were (676.79 ± 78.75) ng/L in the experimental group, significantly lower than (736.05 ± 78.77) ng/L in the control group; in addition, the physical demention, emotional dimenson, other demension scores and total scores of MLHFQ in the experimental group were (65.39 ± 5.02), (67.56 ± 4.99), (66.05 ± 4.16) and (66.33 ± 2.63) points, significantly higher than (59.79 ± 5.94), (64.33 ± 5.93), (62.76 ± 4.47), (62.36 ± 2.98) points in the control group, the differences were statistically significant ( t values were 2.56-6.51, all P<0.05). Conclusions:Designing and implementing stage early rehabilitation program using intervention mapping can promote cardiopulmonary function and quality of life of patients with acute heart failure in compensatory period.

Objective To investigate the molecular mechanism of lectin-like oxidized low-density lipoprotein receptor 1(LOX-1)in the regulation of high glucose induced phagocytosis dysfunction of mouse microglia(BV2 microglia).Methods BV2 cells were cultured in vitro,lentivirus LOX-1RNAi vector(LV-LOX-1)and lentivirusempty vector(LV-Con)were constructed and divided into normal control(NC)group,HG group,LV-LOX-1 group and LV-Con group.After infecting BV2 cells with LV-LOX-1 and LV-Con,the cells were cultured with 25 mmol/L glucose for 24 h,and then divided into HG+LV-LOX-1 group and HG+LV-Con group.After treatment of HG+LV-LOX-1 and HG+LV-Con infected BV2 microglia with 15 μmol/L FH535(β-catenin inhibitor)and AEBSF(ATF6α inhibitor)for 24 h,respectively,they were denoted as HG+LV-LOX-1+FH535 group,HG+LV-Con+FH535 group,HG+LV-LOX-1+AEBSF group,and HG+LV-Con+AEBSF group.Transfection efficiency was determined by fluorescence microscopy,RT-PCR and Western blot.Cell viability was detected b CCK-8.RT-PCR and Western blot were used to detect the mRNA and protein expression of LOX-1,β-catenin,ATF6α and milk fat globular-surface growth factor Ⅷ(MFG-E8)in each group.Results After 72 h of LV-LOX-1 infection,the cells in LV-LOX-1 and LV-Con groups showed a lot of green fluorescence,but not in NC group.Compared with NC group,the mRNA and protein expression of LOX-1 and ATF6α were increased(P<0.05),while the mRNA and protein expression of MFG-E8 and β-catenin decreased in HG group(P<0.05).Compared with HG+LV-Con group,the mRNA and protein expression of LOX-1 and ATF6α were decreased(P<0.05),while the mRNA and protein expression of MFG-E8 and β-catenin increasedin HG+LV-LOX-1 group(P<0.05).Compared with HG+LV-LOX-1 group,the mRNA and protein expressions of MFG-E8 and β-catenin were decreased(P<0.05),and the mRNA and protein expressions of ATF6α and p-β-catenin and p-ATF6α were increased in HG+LV-LOX-1+FH535 group(P<0.05).Compared with HG+LV-LOX-1 group,the mRNA and protein expression were increased(P<0.05),ATF6α mRNA and protein expression and p-ATF6α protein expression were decreased MFG-E8 in HG+LV-LOX-1+AEBSF group(P<0.05).Conclusions LOX-1,MFG-E8,β-catenin and ATF6α are involved in the regulation of phagocytosis of BV2 cells.LOX-1 promotes the phagocytosis dysfunction of BV2 microglia induced by high glucose through β-catenin/ATF6α signaling pathway.

Plaque pH detection technology can detect the risk of caries and assist in the prevention of caries, with a mature theory and a relatively simple operation. With the increasing demand for clinical caries risk detection technology and the rapid development of microelectrode techniques, there is an increasing variety of types of microelectrodes that can detect the pH of dental plaque, including glass microelectrodes, metal oxide microelectrodes and ion-sensitive field effect transistors. The glass microelectrode was the first microelectrode to be applied in this field, but its structure is weak. Among the various options, the iridium oxide microelectrode has become the most promising caries risk detection electrode in recent years because of its high strength and excellent response. Metal oxide microelectrodes can also effectively compensate for the insufficient strength of glass microelectrodes. With advances in electrode technology, miniaturized, sensitive ion-sensitive field effect transistors have attracted the attention of researchers. Scientists have also recently developed a way to detect the pH of dental plaque with an optical no-contact technique. Optical contactless detection technology will not damage the dental plaque structure, so it has great research and clinical prospects. Future research will further improve the strength and performance of these electrodes on the premise of ensuring miniaturization and achieving noncontact detection.

Objective To investigate the mechanism by which lectin-like oxidized low density lipoprotein receptor-1(LOX-1)regulates hyperglycemic-induced myocardial fibroblast(CFs)fibrosis through the glycogen synthase kinase-3β(GSK-3β)/signal transducer and activator of transcription 3(STAT3)pathway.Methods CFs were isolated,cultured and identified.LOX-1 RNAi lentiviral vector was constructed and infected CFs.The experimental groups were as follows:Normal control(NC)group,High glucose(HG)group,LV-LOX-1,LV-Con group,Hypertonic(HPG)group.After LV-LOX-1 and LV-Con were infected with CFs,adding 25 mmol/L glucose to culture CFs for 24 h,they were denoted as HG+LV-LOX-1 group and HG+LV-Con group.Cells in HG+LV-LOX-1 group and HG+LV-Con group were treated with 10 μ mol/L SB216763 and 10 μ mol/L STATTIC for 24 h,respectively,and then they were recorded as HG+LV-LOX-1+SB216763 group,HG+LV-Con+SB216763 group,HG+LV-LOX-1+STATTIC group and HG+LV-Con+STATTIC group.CCK-8 was used to detect the activity of CFs,and the expression levels of mRAN and protein of LOX-1,collagen type I(COL-I),thioredoxin 5(TXNDC5),GSK-3β,STAT3,p-GSK-3β and p-STAT3 were detected by qRT-PCR and Western blot.Results CFs infected with LOX-1 RNAi lentiviral vector were obtained,which showed green under fluorescence microscopy.Compared with HG and HG+LV-Con groups,the mRNA expressions of LOX-1,COL-I and TXNDC5 were decreased in HG+LV-LOX-1 group(P<0.05).Compared with HG+LV-LOX-1 group,mRNA expressions of COL-I and TXNDC5 were decreased in HG+LV-LOX-1+SB216763 and HG+LV-LOX-1+STATTIC groups(P<0.05).Compared with HG and HG+LV-Con groups,p-GSK-3β protein expression was increased in HG+LV-LOX-1 group(P<0.05),while LOX-1,p-STAT3,COL-I,TXNDC5 protein expression was decreased in HG+LV-LOX-1 group(P<0.05).Compared with HG+LV-LOX-1 group,p-GSK-3β protein expression was increased in HG+LV-LOX-1+SB216763 group(P<0.05),while the protein expressions of p-STAT3,COL-I and TXNDC5 were decreased in HG+LV-LOX-1+SB216763 and HG+LV-LOX-1+STATTIC groups(P<0.05).Conclusion LOX-1,GSK-3β,STAT3,TXNDC5,and COL-I are involved in high glucose induced CFs fibrosis.LOX-1 promotes the expression of TXNDC5 and COL-I through GSK-3β/STAT3 pathway,and inhibition of LOX-1 can inhibit high glucose induced CFs fibrosis.

Acute kidney injury (AKI) is an important factor for the occurrence and development of CKD. The protective effect of dihydroartemisinin on AKI and and reported mechanism have not been reported. In this study, we used two animal models including ischemia-reperfusion and UUO, as well as a high-glucose-stimulated HK-2 cell model, to evaluate the protective effect of dihydroartemisinin on premature senescence of renal tubular epithelial cells in vitro and in vivo. We demonstrated that dihydroartemisinin improved renal aging and renal injury by activating autophagy. In addition, we found that co-treatment with chloroquine, an autophagy inhibitor, abolished the anti-renal aging effect of dihydroartemisinin in vitro. These findings suggested that activation of autophagy/elimination of senescent cell might be a useful strategy to prevent AKI/UUO induced renal tubular senescence and fibrosis.
Animals ; Kidney ; Acute Kidney Injury/chemically induced* ; Ischemia ; Reperfusion Injury/drug therapy* ; Autophagy ; Reperfusion