ObjectiveTo compare the clinical effects of laparoscopically assisted vaginal hysterectomy (LAVH) and transabdominal hysterectomy (TAH).MethodsOne hundred and twenty-six cases operated with hysterectomy were classified into LAVH group and TAH group by random digits table with 63 cases each.The operation time,intraoperative bleeding amount,exhaust time,hospitalization time and postoperative complications were observed and compared.ResultsThe operation time,intraoperative bleeding amount,exhaust time and hospitalization time was ( 115.6 ± 13.8 ) min,(92.5 ± 11.3 ) ml,(21.8 ±4.8) d and (6.1 ± 1.7) d in LAVH group,( 82.5 ± 8.7) min,( 112.3 ± 17.8) ml,(28.9 ± 6.2) d and (9.6 ±2.2) d in TAH group,there were significant differences between two groups (P＜0.05).The incidence of incision pain,delayed wound healing,vaginal stump infection,thrombophlebitis,and gastrointestinal disorders was 9.5％(6/63),0,1.6％(1/63),0 and 7.9％(5/63) in LAVH group,which was significantly lower than that in TAH group [52.4％(33/63),7.9％(5/63),11.1％(7/63),7.9％(5/63) and 22.2％ ( 14/63 ) ] (P ＜ 0.05).ConclusionCompared with TAH,LAVH can shorten exhaust time,hospitalization time,reduce intraoperative bleeding amount,decrease complication rate,which can be further applied in clinic.

ObjectiveTo examine the expressions of amplified in breast cancer 1(AIB1) and epithelial cadherin (E-cadherin) in ovarian carcinoma (OC) tissues,and determine the correlation between the expression and clinical pathological features.MethodsThe expression of AIB 1,E-cadherin,estrogen receptor (ER),progesterone receptor (PR) and Ki-67 in tissues of 50OCs and 13 normal ovarians tissues were detected by immunohistochemistry(IHC) EnVision two step process analysis.ResultsPositive expression of AIB1 in OC tissues[68％(34/50) ] was obviously higher than that in normal ovarian tissues [8％ (1/13)] (P ＜0.01).Down-regulation of E-cadherin expression was 60％ (30/50).The positive expression of AIB1 was significantly higher in stage Ⅲ and Ⅳ than in stage Ⅰand Ⅱ according to International Federation of Gynecology and Obstetrics (FIGO) stage (P =0.036),in lymph node metastasis group than in none lymph node metastasis group ( P =0.027 ),in stage G3 than in stage G1 and G2 according to Silverberg stage (P =0.003),and in serous adenocarcinoma group than in non-serous adenocarcinoma group (P=0.049);positive rates of ER and Ki-67 were higher than negative rates of ER(P=0.000) and Ki-67 (P =0.009) respectively.Down-regulation of E-cadherin expression was higher in FIGO stage Ⅲ and Ⅳ than in stage Ⅰ and Ⅱ (P =0.044),in serous adenocarcinoma group than in non- serous adenocarcinoma group ( P =0.022) ; positive rates of ER and Ki-67 were higher than negative rates of ER ( P =0.02 1 ) and Ki-67 (P=0.035) respectively.The expression of AIB1 was negatively correlated with E-cadherin expressioh (P =0.026).ConclusionsThe expressions of AIB1 and E-cadherin in OC tissues is closely related to clinical stage.Therefore,AIB1 and E-cadherin may be important moleculars involved in the progression of OC.

ObjectiveTo study the pathogcncsis of gastrointestinal vascular malformation (GIVM) and the potential mechanism of thalidomide in the treatment of gastrointestinal bleeding due to GIVM.Methods We collected the surgical intestinal specimens from 10 patients who suffered from massive hemorrhage of gastrointestinal tract owning to GIVM and the normal intestinal mucosa around the lesions,as well as normal intestinal mucosa from healthy subjects.Immunohistochemical(IHC) staining was carried out to investigate the differences of angiopoietin 2 ( Ang2 ),Notch1 and delta like ligand 4 (Dll4) in the above three intestinal mucosa to find the relationship with the pathogenesis of GIVM. Human umbilical vein endothelial cells(HUVECs) were cultured with 0,25,50,100 and 200 mg/L thalidomide for 24 or 48 hours to observe their mRNA and protein expressions of Ang2,Notch1,Dll4 by real-time PCR and Western blot.ResultsBy IHC staining,more expressions of Ang2,Notch1 and Dll4 in the lesions were detected than those in the normal intestinal mucosa around the lesions and the normal intestinal mucosa in healthy people.The expressions of Ang2,Notch1 and Dll4 were significantly correlated (P =0.016,r =0.732),and the expressions of Notch1 and Dll4 were absolutely correlated ( P =0.000,r =1.000).Real-time PCR and Western blot showed that thalidomide could down-regulate the expressions of them,which were in a concentration-dependent manner.ConclusionAng2,Notch1 and Dll4 may correlate with the pathogenesis of GIVM,while thalidomide can concentration-dependently down-regulate the expression of Ang2,Notch1 and Dll4,which may be one of the mechanism that thalidomide play a therapeutic role in GIVM.

Objective To estimate prenatal diagnoses strategy with abnormal results of non-invasive prenatal testing (NIPT) based on a case of mosaic for trisomy 22.Methods The pregnanct woman was recruited from Department of Prenatal Diagnosis Center of Xinhua Hospital.Ultrasound scans suggested fetal nuchal translucency was 3.5 mm.Peripheral venous blood was drawn from the pregnant woman for NIPT at 12+2 weeks gestation.For further prenatal diagnosis, amniocentesis was conducted at 16+2 weeks gestation, and karyotype analysis combination with chromosome microarray analysis (CMA) was executed to analysis amniocytes.Results NIPT results suggested that chromosome 21, 18 and 13 were normal and supplementary reports suggested that chromosome 22 were slightly above the normal range.Karyotype analyzed 35 cultured cells.Each of them revealed a normal female karyotype.However, CMA results suggested that chromosome 22 gain mosaic and its copy number was 2.26.The fetus was diagnosed as high possibility of mosaic for trisomy 22.Conclusions Combined with the NIPT results, which was slightly gain mosaic of chromosome 22, a prenatal diagnosis strategy were proposed.When NIPT results suggest chromosomal abnormities, karyotype analysis combination with CMA to diagnose were recommended.

Objective:To explore the regulatory effect of glutathione S-transferase P1(GSTP1) on the radiosensitivity of mouse Lewis lung cancer (LLC) cells.Methods:GSTP1-shRNA lentivirus and negative control lentivirus were used to respectively infect the LLC cells, and stable transgenic strains were selected. Real-time PCR and Western blot were conducted to quantitatively measure the expression levels of GSTP1 mRNA and protein in the LLC cells to verify the knockdown effect. The cell counting kit-8(CCK-8) assay was used to detect cell viability after irradiation. The colony formation assay was utilized to assess the cell proliferation ability after irradiation. Flow cytometry was performed to assess the level of cell apoptosis after irradiation. The tumor-bearing mice were established and irradiated to detect the changes in the tumor volume after irradiation. TUNEL staining was employed to detect the level of tumor apoptosis after irradiation. Immunofluorescence was used to detect the number of CD 4+ CD 8+ T cells in the tumor after irradiation. Results:Real-time PCR and Western blot showed that after shRNA lentivirus interference, the expression levels of GSTP1 mRNA and protein were significantly down-regulated. Down-regulation of GSTP1 reduced cell viability and proliferation, and increased the rate of cell apoptosis after irradiation. The tumor volume of the tumor-bearing mice after irradiation in the GSTP1 knockdown group was significantly smaller than that in the NC group, whereas the tumor apoptosis rate was significantly higher and the number of infiltrating CD 4+ CD 8+ T cells in the tumor was remarkably higher compared with those in the control group. Conclusion:Knockdown of GSTP1 can significantly increase the radiosensitivity of LLC cells and enhance the infiltration of lymphocytes in tumor tissues.

Objective To evaluate the effects of body position and cuffed endotracheal tube (cETT) position on the intracuff pressure during tonsillectomy in the pediatric patients.Methods Sixty pediatric patients,aged 3-12 yr,scheduled for elective tonsillectomy under general anesthesia,were divided into group A and group B using a random number table,with 30 patients in each group.The cETTs were placed on one side of the blade of Davis retractor in group A.The cETTs were placed between the blade of Davis retractor and the body of tongue in group B.The intracuff pressure was recorded when the head was in the neutral position (T1),after changing to the head back position (T2) and when the retractor was placed for operation (T3).Results The intracuff pressure was significantly higher at T2 than at T1 in the two groups (P＜0.01).The intracuff pressure was significantly higher at T3 in group A and lower at T3 in group B than at T2 (P＜0.01).Compared with group A,the intracuff pressure was significantly decreased at T3 (P＜0.01),and no significant change was found in the intracuff pressure at T1,2 in group B (P＞0.05).Conclusion The intracuff pressure is affected by body position and cETT position during tonsillectomy in the pediatric patients,and routine monitoring of the intracuff pressure is recommended.

Cerebral organoids are three-dimensional nerve cultures induced by embryonic stem cells(ESCs)or induced pluripotent stem cells(iPSCs)that mimic the structure and function of human brain.With the continuous optimization of cerebral organoid culture technology and the combination with emerging technologies such as organ transplantation,gene editing and organoids-on-chip,complex brain tissue structures such as functional vascular structures and neural circuits have been produced,which provides new methods and ideas for studying human brain development and diseases.This article reviews the latest advances in brain organoid technology,describes its application in neurological diseases and advances in stroke modeling and transplantation treatment.

Post-stroke cognitive impairment(PSCI)is mainly manifested as learning and memory disorders.Highly enriched RNA m6A methylation modification in mammalian brain is involved in glial cell-mediated neuroinflammation.Given that neuroinflammation is the main mechanism for neural damage and spatial and memory impairment of PSCI,it is speculated that RNA m6A methylation modification can regulate the inflammatory response of glial cells after stroke to improve PSCI.This review summarizes and analyzes the role of RNA m6A methylation modification in the development of PSCI and analyzes its detailed mechanism of regulating glial cell-mediated inflammation,which will provide reference for researchers in this field.

BACKGROUND:Long non-coding RNAs(lncRNAs),as important regulators of the inflammatory response,are involved in the immune-inflammation-brain crosstalk mechanism after ischemic stroke and have the potential to become a therapeutic agent for neurological dysfunction after ischemic stroke. OBJECTIVE:To analyze and summarize the molecular mechanism of lncRNA acting on glial cells involved in the neuroimmuno-inflammatory cascade response after ischemic stroke and the associated signaling pathways,pointing out that lncRNAs have the potential to regulate inflammation after ischemic stroke. METHODS:PubMed was searched using the search terms of"ischemic stroke,long non-coding RNA,neuroinflammation,immune function,signal pathway,microglia,astrocytes,oligodendrocyte,mechanism,"and 63 relevant documents were finally included for review. RESULTS AND CONCLUSION:In the early stage of ischemic stroke,the death of nerve cells due to ischemia and hypoxia activates the innate immune response of the brain,promoting the secretion of inflammatory factors and inducing blood-brain barrier damage and a series of inflammatory cascades responses.As an important pathogenesis factor in ischemic stroke,the neuroimmuno-inflammatory cascade has been proved to seriously affect the prognosis of patients with ischemic stroke,and it needs to be suppressed promptly in the early stage.Neuroinflammation after ischemic stroke usually induces abnormal expression of a large number of lncRNAs that mediate a series of neuro-immune-inflammatory crosstalk mechanisms through regulating the polarization of microglia,astrocytes and oligodendrocytes to exert post-stroke neuroprotective effects.LncRNAs,as important regulatory factors of the inflammatory response,inhibit the neuroimmuno-inflammatory cascade response after ischemic stroke through regulating nuclear factor-κB,lncRNA-miRNA-mRNA axis,Rho-ROCK,MAPK,AKT,ERK and other signaling pathways to effectively improve neurological impairment after ischemic stroke.Most of experimental studies on the interaction between lncRNAs and ischemic stroke are based on a middle cerebral artery occlusion model or a cerebral ischemia-reperfusion injury model,but no clinical trials have been conducted.Therefore,it remains to be further explored about whether lncRNAs can be safely applied in clinical practice.At present,there are many therapeutic drugs for the treatment of ischemic stroke,but there are relatively few studies on the application of lncRNAs,exosomes and other transplantation technologies for the treatment of ischemic stroke using tissue engineering technology,which need to be further explored.lncRNA has become an important target for the treatment of ischemic stroke with its relative stability and high specificity.In future studies,more types of inflammatory lncRNAs that function under ischemic-hypoxia conditions should continue to be explored,in order to provide new research directions for the treatment of neuroinflammation after ischemic stroke.

Post-stroke cognitive impairment(PSCI)is a common complication after stroke,which significantly affects quality of life.However,the pathogenesis has not been fully explained.Increasing evidence has shown that the mechanism of programmed cell death(PCD)is related to PSCI,including apoptosis,necroptosis,pyroptosis,PANoptosis,parthanatos,and ferroptosis.Therefore,it is crucial to clearly understand the various mechanisms of PCD and their relationship with PSCI,and to elucidate the role of PCD in PSCI pathogenesis.The article reviews six PCD pathways related to PSCI,summarizes their mechanisms of action in PSCI,and elucidates the possible crosstalk among pathways to provide a basis for clinical targeting of regulatory factors in the PCD pathway for PSCI treatment.