BACKGROUND:Studies have shown that tea polyphenols have anti-inflammatory effects on multiple organs,but there are few studies on the effects of tea polyphenols on central nervous system inflammation caused by exercise fatigue.OBJECTIVE:To explore the central anti-inflammatory effect and mechanism of tea polyphenols in exercise fatigue.METHODS:7-week-old male Kunming mice were divided into quiet control group,fatigue model group,and tea polyphenols group.In the fatigue model group,mice were given exhaustive swimming at one time.In the tea polyphenols group,tea polyphenols were injected into abdominal cavity half an hour before exhaustive swimming.The exhaustive swimming time in mice of fatigue model group and tea polyphenols group was recorded.Samples were taken from mice in each group after two hours of exhaustive swimming.The changes of brain tissue morphology and structure in each group were observed by hematoxylin-eosin staining.Western blot assay or real-time fluorescence quantitative polymerase chain reaction were used to detect the expression of inflammation-related factors,the activation of microglia,and the activation of STAT3/nuclear factor-κB p65 inflammatory pathway in the brain tissue of mice.Enzyme-linked immunosorbent assay was used to detect the levels of plasma inflammatory factors.RESULTS AND CONCLUSION:(1)Compared with the fatigue model group,the swimming exhaustion time of mice in the tea polyphenols group was significantly prolonged.(2)No abnormality was found in the hematoxylin-eosin staining results of brain tissues of mice in each group.(3)Compared with the quiet control group,the expression levels of inflammatory factors tumor necrosis factor α protein,interleukin-1β protein,M1 activated microglia marker-inducible nitric oxide synthase protein,nuclear factor-κB p65 protein and mRNA,and p-STAT3 protein and STAT3 mRNA in the fatigue model group were significantly increased,while the expression levels of anti-inflammatory factor interleukin-10 protein and M2 activated microglia marker-arginase 1 protein were significantly decreased.Compared with the fatigue model group,the inflammatory reaction,microglia types and signal molecules showed opposite obvious changes in the tea polyphenols group.(4)The expression levels of tumor necrosis factor α,interleukin 1β,interleukin-10 in peripheral plasma and brain tissue were consistent in mice of each group.(5)To sum up,exercise fatigue can trigger inflammatory reaction of nerve center,and tea polyphenols can alleviate this inflammatory reaction,and then enhance the fatigue resistance time of mice.The effects of exercise-induced fatigue and tea polyphenols on the inflammatory reaction in the brain may be completed through STAT3/nuclearfactor-κB p65 pathway.

BACKGROUND:Studies have shown that tea polyphenols have anti-inflammatory effects on multiple organs,but there are few studies on the effects of tea polyphenols on central nervous system inflammation caused by exercise fatigue.OBJECTIVE:To explore the central anti-inflammatory effect and mechanism of tea polyphenols in exercise fatigue.METHODS:7-week-old male Kunming mice were divided into quiet control group,fatigue model group,and tea polyphenols group.In the fatigue model group,mice were given exhaustive swimming at one time.In the tea polyphenols group,tea polyphenols were injected into abdominal cavity half an hour before exhaustive swimming.The exhaustive swimming time in mice of fatigue model group and tea polyphenols group was recorded.Samples were taken from mice in each group after two hours of exhaustive swimming.The changes of brain tissue morphology and structure in each group were observed by hematoxylin-eosin staining.Western blot assay or real-time fluorescence quantitative polymerase chain reaction were used to detect the expression of inflammation-related factors,the activation of microglia,and the activation of STAT3/nuclear factor-κB p65 inflammatory pathway in the brain tissue of mice.Enzyme-linked immunosorbent assay was used to detect the levels of plasma inflammatory factors.RESULTS AND CONCLUSION:(1)Compared with the fatigue model group,the swimming exhaustion time of mice in the tea polyphenols group was significantly prolonged.(2)No abnormality was found in the hematoxylin-eosin staining results of brain tissues of mice in each group.(3)Compared with the quiet control group,the expression levels of inflammatory factors tumor necrosis factor α protein,interleukin-1β protein,M1 activated microglia marker-inducible nitric oxide synthase protein,nuclear factor-κB p65 protein and mRNA,and p-STAT3 protein and STAT3 mRNA in the fatigue model group were significantly increased,while the expression levels of anti-inflammatory factor interleukin-10 protein and M2 activated microglia marker-arginase 1 protein were significantly decreased.Compared with the fatigue model group,the inflammatory reaction,microglia types and signal molecules showed opposite obvious changes in the tea polyphenols group.(4)The expression levels of tumor necrosis factor α,interleukin 1β,interleukin-10 in peripheral plasma and brain tissue were consistent in mice of each group.(5)To sum up,exercise fatigue can trigger inflammatory reaction of nerve center,and tea polyphenols can alleviate this inflammatory reaction,and then enhance the fatigue resistance time of mice.The effects of exercise-induced fatigue and tea polyphenols on the inflammatory reaction in the brain may be completed through STAT3/nuclearfactor-κB p65 pathway.

BACKGROUND:The α7 nicotinic acetylcholine receptor is highly expressed in the cerebral cortex and hippocampus,and has been shown to play an important regulatory role in the pathological development of Alzheimer's disease,making it a potential therapeutic target for Alzheimer's disease.OBJECTIVE:To summarize the close relationship and interaction mechanism between α7 nicotinic acetylcholine receptor and Alzheimer's disease.METHODS:Retrieve relevant literature was searched in CNKI and PubMed databases using the search terms of"alpha7 nicotinic acetylcholine receptor,Alzheimer's disease,beta amyloid protein,agonist,positive allosteric modulator,antagonist"in Chinese and English,respectively.The search time was from database inception to July 2024.According to the inclusion criteria,the search results were accepted or excluded,and ultimately 83 articles that met the criteria were included for review.RESULTS AND CONCLUSION:The α7 nicotinic acetylcholine receptor interacts with β-amyloid protein to reduce the neurotoxicity of β-amyloid protein,such as promoting synaptic plasticity and rapid transmission of cholinergic synapses in Alzheimer's disease,alleviating central nervous system inflammation induced by β-amyloid protein,resisting neuronal apoptosis,and thus having a protective effect on the brain of patients with Alzheimer's disease.The α7 nicotinic acetylcholine receptor has great potential as a therapeutic target for Alzheimer's disease,but there are still a series of issues that need to be addressed,such as desensitization of α7 nicotinic acetylcholine receptor,stability of moderate activity,and gene polymorphism.Screening for drugs with high specificity,safety and multi-target binding action centered on the α7 nicotinic acetylcholine receptor will be a future direction for the treatment of Alzheimer's disease.

BACKGROUND:The α7 nicotinic acetylcholine receptor is highly expressed in the cerebral cortex and hippocampus,and has been shown to play an important regulatory role in the pathological development of Alzheimer's disease,making it a potential therapeutic target for Alzheimer's disease.OBJECTIVE:To summarize the close relationship and interaction mechanism between α7 nicotinic acetylcholine receptor and Alzheimer's disease.METHODS:Retrieve relevant literature was searched in CNKI and PubMed databases using the search terms of"alpha7 nicotinic acetylcholine receptor,Alzheimer's disease,beta amyloid protein,agonist,positive allosteric modulator,antagonist"in Chinese and English,respectively.The search time was from database inception to July 2024.According to the inclusion criteria,the search results were accepted or excluded,and ultimately 83 articles that met the criteria were included for review.RESULTS AND CONCLUSION:The α7 nicotinic acetylcholine receptor interacts with β-amyloid protein to reduce the neurotoxicity of β-amyloid protein,such as promoting synaptic plasticity and rapid transmission of cholinergic synapses in Alzheimer's disease,alleviating central nervous system inflammation induced by β-amyloid protein,resisting neuronal apoptosis,and thus having a protective effect on the brain of patients with Alzheimer's disease.The α7 nicotinic acetylcholine receptor has great potential as a therapeutic target for Alzheimer's disease,but there are still a series of issues that need to be addressed,such as desensitization of α7 nicotinic acetylcholine receptor,stability of moderate activity,and gene polymorphism.Screening for drugs with high specificity,safety and multi-target binding action centered on the α7 nicotinic acetylcholine receptor will be a future direction for the treatment of Alzheimer's disease.

BACKGROUND:The effect of electroacupuncture on the proliferation and differentiation of hippocampal oligodendrocytes in model mice with Alzheimer's disease remains poorly understood while demyelinating reaction related to oligodendrocytes is a common pathological reaction of Alzheimer's disease. OBJECTIVE:To investigate the effects and mechanism of electroacupuncture stimulation of"Baihui"(GV 20),"Fengfu"(GV 16)and bilateral"Shenshu"(BL 23)in Alzheimer's disease model mice on the proliferation and differentiation of endogenous neural stem cells to neurons and oligodendrocytes. METHODS:Forty 6-week-old SPF APP/PS1 transgenic male Alzheimer's disease model mice were randomly divided into electroacupuncture group(n=20)and Alzheimer's disease model group(n=20).Healthy male C57BL/6J mice of the same age were used as normal controls(n=20).The mice in the electroacupuncture group received electroacupuncture at"Baihui"(GV 20),"Fengfu"(GV 16)and bilateral"Shenshu"(BL 23)for 16 weeks(20 minutes/day and one day off a week).After electroacupuncture,Morris water maze was used to detect the changes of learning and memory function.Immunohistochemistry was utilized to detect hippocampal dentate gyrus β-amyloid senile plaques.The expression of BrdU/NeuN and BrdU/GALC in the hippocampal dentate gyrus was detected by immunofluorescence double labeling.Western blot assay was used to detect the expression levels of neuron specific protein Nestin and oligodendrocyte specific protein GALC in the hippocampus.mRNA and protein levels of Notch1 and Hes1 in the hippocampus were detected by real-time fluorescence quantitative PCR and western blot assay. RESULTS AND CONCLUSION:(1)Compared with the normal control group,the ability of learning and memory in the Alzheimer's disease model group decreased significantly;hippocampal dentate gyrus β-amyloid senile plaques increased significantly(P<0.01);the expression of GALC and Nestin in the hippocampus decreased significantly(P<0.01,P<0.05).(2)Compared with the Alzheimer's disease model group,the learning and memory ability of the electroacupuncture group was significantly increased;β-amyloid senile plaque in the hippocampal dentate gyrus decreased significantly(P<0.01).BrdU/NeuN double labeled positive cells in the hippocampal dentate gyrus and Nestin protein expression in the hippocampus increased significantly(P<0.01,P<0.05);GALC expression in hippocampus increased significantly(P<0.01).The mRNA and protein levels of Notch1 in the hippocampus were significantly increased(P<0.05,P<0.01).The mRNA and protein levels of Hes1 in the hippocampus decreased significantly(P<0.05).(3)These findings indicate that electroacupuncture at"Baihui"(GV 20),"Fengfu"(GV 16)and bilateral"Shenshu"(BL 23)of the Alzheimer's disease model infant mice can promote the proliferation and differentiation of endogenous neural stem cells to neurons and oligodendrocytes,which may be regulated through the Notch1/Hes1 pathway.

Objective:To investigate the predictive value of serum D-dimer combined with myocardial injury markers on admission for early identification of high-risk patients with acute myocarditis.Methods:Patients hospitalized for acute myocarditis in China-Japan Friendship Hospital were retrospectively enrolled from 2010 to 2021. Patients were divided into the high D-dimer level group and low D-dimer level group according to the median value of D-dimer measured by immunoturbidimetry within 24 h of admission. In-hospital adverse events were defined as death, cardiogenic shock, malignant ventricular arrhythmia and new-onset heart failure. Multivariate logistic analysis was used to explore the independent predictors of in-hospital adverse events, and receiver operating characteristic curve was used to evaluate the predictive value.Results:A total of 106 patients were analyzed, including 52 high level D-dimer patients and 54 low level D-dimer patients, with an average age of (36±16) years, and 62.3% were male. Compared with the low D-dimer level group, patients in the high D-dimer level group had lower mean systolic blood pressure [(114±21) mmHg vs. (121±14) mmHg] and diastolic blood pressure [(71±13) mmHg vs. (76±10) mmHg], higher heart rate [(97±26) beats/min vs. (79±15) beats/min], higher C-reactive protein levels [6.82 (1.61, 20.05) mg/dL vs. 1.30 (0.13, 8.93) mg/dL] and creatinine levels [86.95 (67.63, 117.83) μmol/L vs. 68.80 (60.18, 81.93) μmol/L] on admission. The proportion of patients having QRS interval >120 ms on electrocardiogram was higher in high D-dimer level group (25.0% vs. 7.4%). There was no significant difference in patients with positive myocardial injury biomarkers between the two groups. The incidence of in-hospital adverse events was higher in the high D-dimer level group (67.3% vs. 22.2%, P<0.001). Multivariate logistic analysis showed that serum D-dimer levels and elevated myocardial injury markers on admission were independently associated with in-hospital adverse events. The area under the curve (AUC) of elevated serum D-dimer level on admission for predicting in-hospital adverse events was 0.781 (95% CI: 0.690-0.873), the sensitivity was 74.5%, and the specificity was 71.2%. When combined with positive cardiac biomarkers, the AUC was 0.831 (95% CI: 0.752-0.910) with a sensitivity of 80.9% and a specificity of 78.0%. Conclusions:Elevated D-dimer level on admission can predict the risk of in-hospital adverse events in patients with acute myocarditis. The combination of cardiac injury biomarkers can improve the predictive value.

As China has not yet established a sound regional trauma treatment system and standardized trauma centers at all levels, the trauma treatment capability in China is poorer than that in the developed countries. At present, Shaanxi Province has not established a regional trauma treatment system and standardized trauma centers at all levels. Based on the analysis of the characteristics of geography, population and social environment in Shaanxi Province, the authors explore the concept of the trauma treatment system and the construction of trauma centers at all levels in Shaanxi Province on the platform of the trauma center of Shaanxi People's Hospital ( Grade I trauma center) . The authors clarify the respective hardware facilities, team structure, treatment process and quality control goals, training and management system of professional trauma teams in trauma centers at all levels, so as to provide reference for improving the overall level of trauma treatment in Shaanxi Province.

To investigate the resistance mechanisms of tigecycline-non-susceptible Acinetobacter baumannii and for providing the evidence of the control of nosocomial infection and rational use of antibiotics. The minimum inhibitory concentrations (MICs) of 94 non repetitive tigecycline-non-susceptible A. baumannii from 20 hospitals in 12 cities of China were determined by agar dilution method and broth microdilution method. The molecular epidemiology was studied by Multilocus sequence typing (MLST) and eBURST software. PCR and sequencing techniques were used to analyze the resistance genes (blaOXA-40-like, blaOXA-58-like, blaOXA-23-like, blaOXA-51-like, blaNDM-1), ISAba1, and the mutation sites of adeR, adeS, and trm. The activity of polymyxin B and minocyclinem against tigecycline-non-susceptible A. baumannii were 100% and 25.5%, respectively. The sensitivities of other antibiotics were less than 3.5%, and the sensitivities of imipenem and meropenem totigecycline-nonsusceptible A. baumannii were only 1.1%. A total of 12 ST types were identified, including ST195 (45, 47.9%), ST208 (19, 20.2%) and ST457 (10, 10.6%). EBURST analysis found that 8 of the ST types belonged to the clone complex 92 (Clonal Complex 92, CC92). The blaOXA-23-like type carbapenem gene was identiefied in 93 strains (99% positive); and none of the strains contained the blaNDM-1 gene. The detection rates of adeR and adeS were 73.4% and 91.5% respectively and high frequency mutation sites were located in adeR (Asp26Asn) and adeS (Ala97Glu); The ISAba1 located upstream of the adeS gene was detected in 12 strains of A. baumannii, mainly from the northern region of China. The 240 nucleotide deletion of the trm gene caused a frameshift leading to a premature stop. So the tigecycline-non-susceptible A. baumannii showed high resistance against most antibiotics except polymyxin B. The deletion and mutation of adeR, adeS and trm were the main resistant mechanisms in tigecycline-non-susceptible A. baumannii in China.

To dynamically investigate the distribution and antimicrobial resistance profiles of bacteremia pathogens isolated from different regions in China in 2011, 2013 and 2016. Non-repetitive isolates from nosocomial bloodstream infections were retrospectively collected and detected for antimicrobial susceptibility tests (AST) by agar dilution or microbroth dilution methods. Whonet 5.6 was used to analyze the AST data. Among 2 248 isolates, 1 657 (73.7%) were Gram-negative bacilli and 591 (26.3%) were Gram-positive cocci. The top five bacteremia pathogens were as follows, Escherichia coli (32.6%, 733/2 248), Klebsiella pneumoniae (14.5%, 327/2 248), Staphylococcus aureus (10.0%, 225/2 248), Acinetobacter baumannii (8.7%, 196/2 248) and Pseudomonas aeruginosa (6.2%, 140/2 248). Colistin (96.5%, 1 525/1 581, excluding innate resistant organisms), tigecycline (95.6%, 1 375/1 438, excluding innate resistant organisms), ceftazidine/clavulanate acid (89.2%, 1 112 /1 246), amikacin (86.4%, 1 382/1 599) and meropenem (85.7%, 1 376/1 605) showed relatively high susceptibility against Gram-negative bacilli. While tigecycline, teicoplanin and daptomycin (the susceptibility rates were 100.0%), vancomycin and linezolid (the susceptibility rates were 99.7%) demonstrated high susceptibility against Gram-positive cocci. The prevalence of extended-spectrum β-lactamases (ESBLs)-producing Enterobacteriaceae were 50.6% (206/407), 49.8% (136/273) and 38.9% (167/429) in 2011, 2013 and 2016 respectively; carbapenem-non-susceptible Enterobacteriaceae were 2.2% (9/408), 4.0% (16/402) and 3.9% (17/439) in 2011, 2013 and 2016 respectively; The prevalence of multidrug-resistant A. baumannii (MDRA) was 76.4% (55/72) in 2011, 82.7% (43/52) in 2013 and 87.5% (63/72) in 2016, respectively. The prevalence of multidrug-resistant P. aeruginosa (MDRP) was 9.8% (5/51) in 2011, 20.0% (7/35) in 2013 and 13.0% (7/54) in 2016, respectively. The prevalence of methicillin-resistant S. aureus (MRSA) was 51.9% (41/79) in 2011, 29.7% (19/64) in 2013 and 31.7% (26/82) in 2016, respectively. The prevalence of high level gentamicin resistance (HLGR) of Enterococcus faecium and Enterococcus faecalis were 43.2% (48/111) and 40.9% (27/66), respectively. The predominant organism of carbapenem-non-susceptible Enterobacteriaceae was K. pneumoniae with its proportion of 57.1% (24/42). Among 30 tigecycline-non-susceptible Enterobacteriaceae, K. pneumoniae was the most popular organism with 76.7% (23/30). Among 39 colistin-resistant Enterobacteriaceae, E. coli, Enterobacter cloacae and K. pneumoniae were constituted with the percent of 43.6 (17/39), 35.9 (14/39) and 15.4 (6/39), respectively. The Gram-negative bacilli (E. coli and K. pneumoniae were the major organisms) were the major pathogens of nosocomial bacteremia, to which tigecycline, colistin and carbapenems kept with highly in vitro susceptibility. Whereas, among the Gram-positive cocci, S. aureus was the top 1 isolated organism, followed by E. faecium, to which tigecycline, daptomycin, linezolid, vancomycin and teicoplanin kept with highly in vitro susceptibility. Isolation of colistin-resistant Enterobacteriaceae, tigecycline-non-susceptible Enterobacteriaceae, linezolid- or vancomycin-non-susceptible Gram-positive cocci suggests more attention should be paid to these resistant organisms and dynamic surveillance was essential.

To meet the need of accurate positioning for biopsy gun in the breast biopsy operation, a new stereotactic biopsy guide device have been developed to adapt to the domestic mammary machine, which can help physician to carry out biopsy operation more accurately and effectively. The guide device has the motion model, measurement model and display model and can realize linear motion and display real-time displacement values in X, Y and Z direction. The experimental results showed that the guide device could be well fixed in the domestic mammary machine, and achieved good accuracy and repeatability in each direction. Depending on the displacement values, physician can change the space of biopsy gun accurately.
Biopsy, Needle ; instrumentation ; methods ; Breast ; pathology ; Equipment Design ; Female ; Humans ; Stereotaxic Techniques ; instrumentation