Objective:To investigate the effects of pulsed electromagnetic field(PEMF)on sevoflurane-induced cognitive dysfunction in elderly rats and also explore its related mechanism.Methods:Thirty elderly male rats were randomly divided into the control group,sevoflurane treatment group(SEV),and sevoflurane+PEMF treatment group(SEV+PEMF).Rats in the sevoflurane group and sevoflurane+PEMF group passively inhaled 2.5％sevoflurane for 4 h,while rats in the SEV+PEMF group were stimulated with 2 mT,15 Hz PEMF for 14 d(2 h/day).The cognitive function of rats was evaluated via the Morris water maze testing.The serum concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1β),IL-6,neuron specific enolase(NSE),and β amyloid protein(Aβ),as well as the levels of nerve growth factor(NGF)and brain-derived neurotrophic factor(BDNF)in hippocampal tissue,were de-termined via ELISA.Western blot was used to detect the expression of autophagy-related biomarkers in rat hippocampal tissue.Secondly,30 elderly male rats were randomly divided into three groups:SEV group,SEV+PEMF group,and SEV+3-MA(the autophagy inhibitor)+PEMF group.The Morris water maze experiment was used to evaluate the change of PEMF-induced improvement of cognitive function sevoflurane-inhaled elderly rats following the autophagy inhi-bition.Results:PEMF inhibited sevoflurane-induced increase in escape latency and overall swimming distance,as well as the decrease in the number of crossing target quadrant(P＜0.05);PEMF decreased the levels of serum Aβ and NSE in elderly rats inhaled with sevoflurane(P＜0.05),decreased the levels of TNF-α,IL-1β,and IL-6(P＜0.05),increased the levels of NGF and BDNF in hippocampal tissue(P＜0.05),inhibited neuronal apoptosis in hip-pocampal tissue and increased its autophagy level(P＜0.05).Following inhibition of autophagy with 3-MA,the im-provement of PEMF on the decreased learning and memory ability induced by sevoflurane in elderly rats was significantly inhibited(P＜0.05).Conclusion:PEMF can effectively inhibit sevoflurane-induced cognitive dysfunction in elderly rats by regulating the autophagy of hippocampal neuronal cells.

Objective:To investigate the effects of pulsed electromagnetic field(PEMF)on sevoflurane-induced cognitive dysfunction in elderly rats and also explore its related mechanism.Methods:Thirty elderly male rats were randomly divided into the control group,sevoflurane treatment group(SEV),and sevoflurane+PEMF treatment group(SEV+PEMF).Rats in the sevoflurane group and sevoflurane+PEMF group passively inhaled 2.5％sevoflurane for 4 h,while rats in the SEV+PEMF group were stimulated with 2 mT,15 Hz PEMF for 14 d(2 h/day).The cognitive function of rats was evaluated via the Morris water maze testing.The serum concentrations of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1β),IL-6,neuron specific enolase(NSE),and β amyloid protein(Aβ),as well as the levels of nerve growth factor(NGF)and brain-derived neurotrophic factor(BDNF)in hippocampal tissue,were de-termined via ELISA.Western blot was used to detect the expression of autophagy-related biomarkers in rat hippocampal tissue.Secondly,30 elderly male rats were randomly divided into three groups:SEV group,SEV+PEMF group,and SEV+3-MA(the autophagy inhibitor)+PEMF group.The Morris water maze experiment was used to evaluate the change of PEMF-induced improvement of cognitive function sevoflurane-inhaled elderly rats following the autophagy inhi-bition.Results:PEMF inhibited sevoflurane-induced increase in escape latency and overall swimming distance,as well as the decrease in the number of crossing target quadrant(P＜0.05);PEMF decreased the levels of serum Aβ and NSE in elderly rats inhaled with sevoflurane(P＜0.05),decreased the levels of TNF-α,IL-1β,and IL-6(P＜0.05),increased the levels of NGF and BDNF in hippocampal tissue(P＜0.05),inhibited neuronal apoptosis in hip-pocampal tissue and increased its autophagy level(P＜0.05).Following inhibition of autophagy with 3-MA,the im-provement of PEMF on the decreased learning and memory ability induced by sevoflurane in elderly rats was significantly inhibited(P＜0.05).Conclusion:PEMF can effectively inhibit sevoflurane-induced cognitive dysfunction in elderly rats by regulating the autophagy of hippocampal neuronal cells.

Obesity is an important manifestation of the imbalance of energy regulation, and its complications can cause irreparable damage to the body. Finding the pathogenesis of obesity at the molecular level can help fundamentally avoid these irreversible complications. Extended synaptotagmins (E-Syts) are proteins related to the formation of endoplasmic reticulum (ER) and plasma membrane (PM). Because of the short discovery time, there is huge room for exploration. In terms of the role of the established structure of E- Syts at the molecular level, it has a non-negligible link with the pathogenesis of obesity. Starting with the structure of hypothalamus, this paper reviews the literature evidence of this connection, hoping to find a new research angle for reducing the incidence of obesity.

Objective To investigate the effect of dexmedetomidine(Dex)on bone loss in tail-suspended rats and primarily explore its regulatory mechanism on bone metabolism.Methods A total of 30 male rats were randomly divided into a control group,a model group,and a Dex group,with 10 animals in each group.Rat model of osteoporosis was established by hind limb suspension for 4 weeks.Dex at a dose of 10 μg/kg was given intraperitoneally,once every other day from the day of tail suspension.And equal amount of normal saline was given to the control and model group.Bone histological staining was used to observe the trabecular bone area fraction.Biomechanical three-point bending test was employed to measure the maximum load,stiffness,and fracture energy.Dual calcein/alizarin red fluorescence labeling and tartrate resistant acid phosphatase(TRAP)staining were applied respectively to detect the mineral apposition rate and bone formation rate as well as the number of osteoclasts on bone surfaces.Secondly,after primary osteoblasts were isolated from the tibiae of tail-suspended rats and then treated with 1 nmol/L Dex,the proportion of alkaline phosphatase(ALP)-positive osteoblasts and the activity of the enzyme were detected by ALP staining and activity test.qRT-PCR was applied to measure the expression of osteogenic activity-related factors,including osteocalcin(Ocn),Runt related transcription factor 2(Runx2),Osterix protein(Osx),and type 1 collagen(Col1).Results The animal experiments revealed that Dex treatment significantly increased the tibial trabecular bone area fraction,inhibited the decrease in bone mechanical strength,and enhanced the mineralization deposition rate and new bone formation rate of trabecular bone in the tail-suspended rats(all P＜0.001).The in vitro experiments showed that Dex treatment obviously improved ALP activity and the number of ALP-positive osteoblasts in primary osteoblasts isolated from tail-suspended rats(P＜0.01),and up-regulated the expression levels of osteogenic differentiation-related genes,such as Ocn,Runx2,Osx and Col1(P＜0.01).Conclusion Dex exerts anti-bone loss effect in tail-suspended rats,which may be associated with its stimulation on osteoblast-mediated bone formation.

Objective To investigate the ameliorative effect and the related mechanism of rotating magnetic fields(RMF)on sevoflurane(SEV,a commonly used inhalational anesthetics in clinics)-induced cognitive impairments in elderly rats.Methods The cognitive functions of 24 elderly male SD rats which were allocated into 3 experimental groups(Control group,SEV group,and SEV+RMF group;n=8 per group)were assessedviawater maze testing,and the damage and repair of hippocampal neurons were detected using ELISA and Western blotting assays.Water maze testing was also conducted on additional 24 elderly male SD rats which were randomized into 3 groups(SEV group,SEV+RMF group,and SEV+autophagy inhibitor+RMF group;n=8 per group)for assessing their cognitive functions.Results Compared with SEV group,RMF intervention significantly reduced the escape latency and swimming distance in water maze test(P<0.01),while increasing the number of platform crossovers(P<0.001).RMF downregulated the serum levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in SEV-treated rats(P<0.001),and led to remarkable reductions in both serum neuron-specific enolase and β-amyloid protein levels(P<0.001).Moreover,RMF upregulated the expressions of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons(P<0.001),suppressed the expression of apoptotic protein caspase-3 and autophagy related protein p62 in the hippocampus,and upregulate the expression of autophagy related protein Beclin-1(P<0.001).However,the administration of autophagy inhibitor 3-MA abolished the ameliorative effects of RMF on SEV-induced cognitive impairments in elderly rats(P<0.001).Conclusion RMF can effectively improves SEV-induced cognitive dysfunction in elderly rats,and this neuroprotective effect is mediated by the autophagy activation in hippocampal neurons.

Objective To investigate the ameliorative effect and the related mechanism of rotating magnetic fields(RMF)on sevoflurane(SEV,a commonly used inhalational anesthetics in clinics)-induced cognitive impairments in elderly rats.Methods The cognitive functions of 24 elderly male SD rats which were allocated into 3 experimental groups(Control group,SEV group,and SEV+RMF group;n=8 per group)were assessedviawater maze testing,and the damage and repair of hippocampal neurons were detected using ELISA and Western blotting assays.Water maze testing was also conducted on additional 24 elderly male SD rats which were randomized into 3 groups(SEV group,SEV+RMF group,and SEV+autophagy inhibitor+RMF group;n=8 per group)for assessing their cognitive functions.Results Compared with SEV group,RMF intervention significantly reduced the escape latency and swimming distance in water maze test(P<0.01),while increasing the number of platform crossovers(P<0.001).RMF downregulated the serum levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 in SEV-treated rats(P<0.001),and led to remarkable reductions in both serum neuron-specific enolase and β-amyloid protein levels(P<0.001).Moreover,RMF upregulated the expressions of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons(P<0.001),suppressed the expression of apoptotic protein caspase-3 and autophagy related protein p62 in the hippocampus,and upregulate the expression of autophagy related protein Beclin-1(P<0.001).However,the administration of autophagy inhibitor 3-MA abolished the ameliorative effects of RMF on SEV-induced cognitive impairments in elderly rats(P<0.001).Conclusion RMF can effectively improves SEV-induced cognitive dysfunction in elderly rats,and this neuroprotective effect is mediated by the autophagy activation in hippocampal neurons.

Objective:To investigate the effectiveness and safety of domestic upper gastrointestinal endoscopic ultrasound (EUS).Methods:A total of 160 patients undergoing EUS at Shengjing Hospital of China Medical University (Center1) and Shenzhen People's Hospital (Center 2) from March to July 2021 were randomly selected by stratified blocked randomization, and were treated with SonoScape EG-UG5T (the test group) or Fujifilm EG-580UT (the control group). The primary outcome was the ultrasound image quality excellence rate, and the comparison was verified by non-inferiority. The secondary outcomes were the endoscopic image quality excellence rate, the operational performance excellence rate, and the system stability evaluation. The safety evaluation was based on the occurrence of intraoperative and postoperative adverse events in the subjects.Results:In the intention-to-treat analysis set (ITT), the excellence rate of ultrasound image quality in the test group and the control group was 100.0% (78/78) and 100.0% (77/77), respectively. The rate difference between the two groups was 0.0% (95% CI: -4.7%-4.8%). In the per protocol analysis set (PPS), the excellence rate of ultrasound image quality in the test group and the control group was 100.0% (78/78) and 100.0% (75/75), respectively. The rate difference between the two groups was 0.0% (95% CI: -4.7%-4.9%). The lower limit of the confidence interval of ultrasound image quality excellence rate of both data sets was greater than the non-inferiority threshold value of -8%, which inferred that the non-inferiority hypothesis of the test machine non-inferior to the control machine was valid. The endoscopic image quality excellence rate and the operational performance excellence rate of the test group and the control group was 100.0% in both the ITT and PPS analyses, and there was no statistically significant difference between the two groups ( P=1.000). The system instability event rate was 0.0% (0/78) in the test group and 3.9% (3/77) in the control group ( P=0.120). No adverse event occurred in either group. Conclusion:The domestic upper gastrointestinal endoscopic ultrasound is standard-compliant for clinical application under normal conditions in terms of effectiveness, safety, and stability.

Aim To investigate the neuroprotective effect of picroside Ⅱ(PIC)on cyto C/caspase-9/caspase-3 signal pathway following ischemia/reperfusion(I/R)injury in rats.Methods Atractyloside(Atr)was selected as negative control,cyclosporin A(CsA)was selected as positive control,and PIC was selected as the treatment medicine.The I/R model was made by inserting a monofilament suture into internal carotid artery for 2 h,and then reperfused for 24 h.The cerebral infarction volume was detected by TTC staining,and the expression of cyto C,caspase-9 and caspase-3 were determined by immunohistochemical assay and Western blot.Results In model group,the cerebral infarct volume was obviously large;the expression of cyto C,caspase-9 and caspase-3 was increased significantly more than that in sham group(P<0.05).In PIC group,the cerebral infarct volume was significantly improved;the expression of cyto C,caspase-9 and caspase-3 was significantly decreased than that in model group(P<0.05).In Atr+PIC group,the rat infarction volume was reduced,and the expression of cyto C,caspase-9 and caspase-3 was significantly decreased than that in Atr group(P<0.05).Conclusion The mechanism of PIC inhibiting neuron apoptosis in focal cerebral I/R rats might be through down-regulating the expression of cyto C,caspase-9 and caspase-3.

Objective To study the association between CYP2C9 gene polymorphism and warfarin maintenance dosage in anticoagulation therapy.Methods 200 Han patients admitted to our hospital for heart valve replacement were included in this study.CYP2C9 * 2,CYP2C9 * 3,CYP2C9 *c65 in CYP2C9 gene were sequenced using the CAPS technique and conventional DNA sequencing method.Dosages of warfarin used in patients carrying different genes were analyzed.Results No mutation of CYP2C9 * 2 but only one kind of allele C was detected in 200 patients.The genotype of CYP2C9 * 2 was C/C wild type.Allelic gene was detected at CYP2C9 * 3 A and C,with A/A wild type detected in 171 patients,A/C heterozygote mutation type detected in 18 patients,and C/C heterozygote mutation type detected in 11 patients respectively.The frequency of allelic genes A and B was 94.3 ％ and 5.7 ％ respectively.A significant difference was found between CYP2C9 * 3 mutation and warfarin dosage (P＜0.05).The dosage of warfarin reduced 18.46％ and 76.0％ respectively in patients carrying A/C heterozygote mutation type and in those carrying C/C heterozygote mutation type.Two kinds of allelic gene were detected at CYP2C9 * c65 G and C,with G/G wild type detected in 182 patients and G/C heterozygote mutation type detected in 18 patients respectively.No significant association was found in warfarin maintenance dosage for patients carrying G/G wild type and G/C heterozygote mutation type.Conclusion CYP2C9 gene polymorphism is associated with warfarin maintenance dosage in anticoagulation therapy.

Objective To investigate the effect ofpicroside Ⅱ on mitochondria cytochrome C (CytC) expression and its significance in rats after ischemia/reperfusion.Methods Ninety-six Wistar rats were randomly divided into sham-operated group,model group,picroside Ⅱ group,Cyclosporin A (CsA,specific antgonist of CytC) group,CsA+picroside Ⅱ group,atractyloside (Atr,selective agonist of CytC) group,Atr+picroside Ⅱ group and DMSO group (n=12);the middle cerebral artery occlusion/reperfusion models referring to Longa's method with medications were adopted,which were established by inserting a monofilament suture into the internal carotid artery for 2 h and then reperfusion for 24 h.After 24 h of ischemia/reperfusion,modified neurological severity scale (mNSS) scores were observed,contents of reactive oxygen species (ROS) in brain tissues were measured by enzyme-linked immunosorbent assay (ELISA),morphology of brain tissues was observed by hematoxylin-eosin staining,ultrastructures ofmitochondria were observed by transmission electron microscopy,apoptotic cells were counted by terminal deoxynucleotidyl transferase dUTP nick end labeling assay (TUNEL),and CytC expression was determined by immunohistochemical assay and Western blotting.Results As compared with the sham-operated group,the model group had significantly increased mNSS scores,ROS contents,number ofapoptotic cells and CytC expression (P＜0.05),and the mitochondria structure was seriously destroyed.The picroside Ⅱ group had obviously decreased mNSS scores,ROS contents,number of apoptotic cells and CytC expression,and the morphology of brain tissue was improved and the mitochondria damage was reduced as compared with the model group,with significant differences (P＜0.05).The Atr+picroside Ⅱ group had significantly decreased mNSS scores,ROS contents,number of apoptotic cells and CytC expression (P＜0.05),and the mitochondria damage in the Atr+picroside Ⅱ group was reduced as compared with that in the Atr group with significant difference (P＜0.05).Conclusion The mechanism of picroside Ⅱ protecting against focal cerebral ischemia reperfusion might attribute to decrease of ROS contents,protection of mitochondria structure and down-regulation of CytC expression in middle cerebral artery occlusion/reperfusion rats.