Positive outcomes have been reported about the transcranial magnetic stimulation for aphasia. This paper reviewed the relat-ed literatures about repetitive transcranial magnetic stimulation used in clinical and research, and discussed the possible mechanisms in the recovery of aphasia, and the roles of hemispheres in brain.

Objective Resveratrol can improve nonalcoholic fatty liver disease , but its action mechanisms remain unclear . This study aimed to investigate the protective effect of resveratrol against the free fatty acid ( FFA)-induced apoptosis of human hepatic L02 cells and its possible mechanisms . Methods Human hepatic L02 cells were incubated with FFA and resveratrol for 24 hours.The prepared cells were divided into a blank control , an FFA ( 2 mmol/L) , and a resveratrol group ( 50 μmol/L resveratrol +2 mmol L/FFA).After treatment, we measured the triglyceride (TG), glutathi-one (GSH), and malonaldchyde (MDA) contents and caspase3 ac-tivity in the hepatocytes , determined the apoptosis of the cells by flow cytometry , and detected the protein expression of silent information regulator 1 (SIRT1) by Western blot as well as the mRNA expressions of catalase (CAT), Mn superoxide dismucase (MnSOD), Bcl-2, and Bax by qRT-PCR. Results The TG content and caspase 3 activity in the hepatocytes were significantly increased in the FFA ([3518.±64.2] μmol/L and [5.97 ±0.78] U/g) and the resveratrol group ([201.1 ±60.1] μmol/L and [3.60 ±0.73] U/g) as compared with those of the blank control ([40.2 ±7.4] μmol/L and [2.56 ±0.49] U/g) (both P<0.05), but the caspase3 ac-tivity was markedly decreased in the resveratrol group in comparison with that of the FFA group (P<0.05).Both early and late apop-tosis rates of the hepatocytes were remarkably higher in the FFA ([6.75 ±0.81]%and [8.52 ±0.54]%) and the resveratrol group ([4.94 ±0.44]%and [6.52 ±0.61]%) than those in the blank control ([3.38 ±0.33]% and [2.72 ±0.19]%) ( both P<0.05), with statistically significant differences between the former two groups (P<0.05).The resveratrol group showed significant differences in the GSH content ([100.2 ±8.8] nmol/g), the MDA level ([2.36 ±0.82] mg/g), and the relative expression of SIRT1 (0.84 ±0.04) from the FFA group ([73.8 ±13.1] nmol/g, [3.77 ±0.92] mg/g, and 0.61 ±0.07) and the control ([113.7 ±13.8] nmol/g, [1.85 ±0.41] mg/g, and 0.90 ±0.02) (all P<0.05).The resveratrol group also exhibited statistically significant differences in the relative expressions of the MnSOD , CAT, and Bax genes from the FFA and control groups (P<0.05). Conclusion Resveratrol attenuates FFA-induced apoptosis of human hepatic L 02 cells by activating SIRT1 and reducing the oxidative stress of hepatocytes .

AIM:To prepare the Lyophiled Royal Jelly Soft Capsule and study its stability and Influential factors.METHODS:The suspending agent and processing method were optimized using sedimentation volume rate as the index.Soft capsules were prepared and product stability under high temperature and high humidity environment was studied according to the determination of the content of 10-HAD by HPLC.RESULTS:The finished product yield in pilot test was more than 90%,the soft capsule products stored in cold were stable,while those stored under room temperature or high temperature and high humidity were unstable with a noticeable decrease in quality.Water content in capsule shell affects the 10-HDA content of the finished product.CONCLUSION:The preparative process is feasible and the products should be storaged in cold enviroment.

Objective To investigate the roles of TrkA and TrkB in radiation-induced hippocampal neurogenesis impairment.Methods Fifty-six rats were randomized into radiation group and sham control group.Radiation group received whole brain irradiation at a single dose of 10 Gy.The hippocampus were separated from rats in day 1,day 3,day 14 and 1 month after irradiation.Western blot and RT-PCR were applied to detect the protein levels and mRNA levels.Golgi staining was used to observe the dendritic spine of hippocampus.Immunofluorescence was performed to detect neural precursor's proliferation.Results Compared with control group,the numbers of dendritic spine significantly decreased after irradiation and its shape change obviously.Immunofluorescence showed a significant decrease in neural precursor's proliferation comparing with control group (t =6.49,P ＜ 0.05).Protein level of TrkA expression increased (t =2.64,3.06,4.80,2.64,P ＜ 0.05),while the levels of TrkB protein expression decreased significantly (t =4.59,3.06,2.81,2.57,P ＜ 0.05).The mRNA level of TrkA expressions increased (t =4.57,3.06,5.39,5.86,P ＜ 0.05),while the mRNA level of TrkB decreased (t =14.87,11.69,4.98,P ＜ 0.05).Conclusions As a signaling pathways downstream of NGF and BDNF,TrkA and TrkB may play an important role in radiation-induced neurogenesis impairment.

Objective To improve hand hygiene compliance among health care workers(HCWs)through continu-ous quality improvement,and effectively reduce the incidence of healthcare-associated infection(HAI).Methods Continuous quality improvement was performed by adopting plan-do-check-action(PDCA)cycle,all HCWs were trained,hand hygiene was stressed,periodical and random checking was conducted.Results After the implementa-tion of PDCA cycle,the acknowledge rate of hand hygiene enhanced from 48.00% to 63.99%;hand hygiene com-pliance rate enhanced from 65.11% to 82.40%,the difference were both significant(χ2=12.75,259.65,respective-ly,both P<0.05).The daily consumption of instant hand antiseptic per 1 000 bed day increased obviously,which was 2.95-fold of pre-implementation.Conclusion Continuous quality improvement through PDCA cycle can effec-tively improve hand hygiene compliance rate of HCWs.

Objective To evaluate the effects of dexmedetomidine on perioperative pulmonary compliance and the expression of Toll?like recep?tor(TLR)?2 and TLR?4 in the peripheral blood during perioperative period in patients undergoing open colorectal cancer radical surgery. Meth?ods Twenty patients with colorectal cancer underwent elective general anesthesia,with ASA gradeⅠ?Ⅱand body mass index(BMI)<30 kg/m2, aged 30 to 68 years old,were enrolled for the study. They were randomly divided into control group(group C,n=10)and dexmedetomidine group (group D,n=10). In group D,dexmedetomidine was infused at a rate of 0.4μg·kg-1·h-1 from the beginning of surgery till 30 min before the end of surgery. The patients in group C received same manipulation as in group D except dexmedetomidine was replaced by normal saline. The mean ar?terial pressure(MAP)and heart rate(HR)were recorded before anesthesia induction(T0),30 min(T2),60 min(T3),and 90 min(T4)after the beginning of surgery,extubation(T6),and 3 min after extubation(T7). Airway pressure and lung dynamic compliance were recorded at T1?T7 time points,respectively. Vein blood samples were drawn to analyze the TLR?2,TLR?4 and tumor necrosis factorα(TNF?α)concentration at T0,T4,T7 and the day after operation(T8),respectively. Results Compared with group C,MAP and HR increased in group D at T6(P<0.05);lung dynamic compliance increased in group D at T4(P<0.05);TLR?2 and TLR?4 concentration in serum decreased in group D at T4, T7 and T8(P<0.05);TNF?αconcentration in serum decreased in group D at T4,T7 and T8(P<0.05). Conclusion Continuous infusion of 0.4μg·kg-1·h-1 dexmedetomidine can help to stabilize hemodynamics,relieve inflammatory stress response,maintain the relative stability of intra?operative hemodynamic parameters,and also can improve the pulmonary dynamic compliance of patients.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

Purpose: Asthma is a serious inflammatory disease of the respiratory system in which airway smooth muscle cells (ASMCs) play a key role. This study aimed to investigate the expression of SLC26A2 in human ASMCs (HASMCs) and the regulatory mechanism of SLC26A2 in the proliferation and inflammatory factor production of HASMCs. Materials and Methods: We obtained the asthma-associated differential mRNA SLC26A2 by bioinformatics analysis in childhood acute asthma samples. To investigate its role in airway inflammation and airway remodeling, we treated HASMCs with plateletderived growth factor (PDGF) in an in vitro model and determined SLC26A2 expression in cells using western blotting. Cell proliferation was detected by MTT and EdU assays, and cell contractile phenotype marker proteins were measured. Cell migration and production of inflammatory factors were determined by Transwell and ELISA assays. Additionally, the upstream regulatory miRNA and LncRNA of SLC26A2 were identified by bioinformatics, luciferase reporter gene, and RIP analyses. Results: SLC26A2 was significantly upregulated in bioinformatics analysis of pediatric asthma-related sample. PDGF treatment up-regulated SLC26A2 expression in HASMCs, whereas the knockdown of SLC26A2 inhibited PDGF-stimulated proliferation, migration, and production of inflammatory factors, and enhanced the expression of cell contractile phenotype marker proteins in HASMCs. Luciferase reporter and RIP experiments validated that NEAT1 targeted miR-9-5p to regulate SLC26A2, thereby influencing the biological function of PDGF-induced HASMCs. Conclusion These findings indicate that NEAT1-mediated miR-9-5p targeting of SLC26A2 inhibits the PDGF-induced proliferation and production of inflammatory factors in HASMCs. These findings highlight potential therapeutic targets for asthma and airway inflammation.

The CRISPR-Cas (clustered regularly interspaced short palindromic repeats and CRISPR-associated) system is an "adaptive immune system" found in the genomes of bacteria and archaea which is mediated by RNA and resists foreign nucleic acid invasion.Take advantage of specific recognition of target nucleic acid, CRISPR-Cas system can efficiently edit their target site or accurately regulate gene expression, and now have been developed into a powerful tool for gene editing.According to the different compositions of the effector complex, the system has been divided into two categories: class 1 (type I, type IV, and type III) and class 2 (type II, type V, and type VI).Class 2 system, like the CRISPR-Cas9, is widely used in basic research due to the earliest discovery and best research.However, class 1 has not been maturely developed and utilized though it makes up 90% of the entire CRISPR-Cas system.In this essay, the classification of subtype, the assembly of Cascade complex, the cleavage and degradation mechanism of Cas3, and the application in gene editing of class 1 type I CRISPR-Cas system will be discussed and summarized to provide new ideas and methods for further mechanism studying and application of this category.