Objective To gain insights into the biological characteristics of different populations of Culex tritaeniorhynchus within and around the Yellow Sea wetland from the perspective of the occurrence of resistance, we investigated the levels of resistance to deltamethrin and kdr gene mutation in the wetland and its peripheral areas. Methods Specimens were collected from Cx. tritaeniorhynchus populations at two monitoring sites in the Rare Bird National Nature Reserve and Tiaozi Ni Wetland Scenic Area, and also from two populations in Yancheng City and the Liuhe District of Nanjing, and the resistance of these mosquitoes to deltamethrin was determined using the CDC biotest bottle method. For each concentration of deltamethrin assessed, a random subset of exposed specimens was selected for amplification of the kdr gene fragment, followed by Sanger sequencing to identify and analyze resistance-associated mutations. Results The LC50 levels of deltamethrin among mosquitoes from the four populations in Luhe, Yancheng, the Rare Bird National Nature Reserve and the Tiaozi Ni Wetland Scenic Area were 2.048 5, 7.798 2, 3.473 3, and 17.695 5 mg/mL, respectively, with corresponding concentrations of deltamethrin ranging from 0.005 to 5.000,0.050 to 50.000,0.050 to 25.000 and 0.050 to 50.000 mg/mL, respectively. Furthermore, the ranges of the KT50 values were 11.76-107.43, 67.05-216.30,29.77-107.43 and 28.40-329.51 min; the 1-h knockdown rates were 34.58%-99.15%, 9.52%-43.80%, 55.09%-73.01%, and 10.09%-68.07%; and the 24-h mortality rates were 12.15%-67.52%,9.52%-79.56%,13.17%-82.21%, and 11.01%-78.99%, respectively. With respect to kdr gene mutation, we assayed a total of 63,70,59, and 57 mosquitoes for the four populations, for which we detected L1014F mutation frequencies of 14.29%, 35.00%, 20.34%, and 31.58%, respectively, with a majority of these mutations being heterozygous for resistance. In addition, five adult mosquitoes were identified has having synonymous mutations at site 1011[i. e. , AAT(asparagine)mutation to AAC(asparagine)]. Conclusions Our findings revealed the clear resistance of Cx. tritaeniorhynchus to deltamethrin in the Yancheng region of the Yellow Sea wetland, and the resistance phenotype and kdr frequency of Cx. tritaeniorhynchus in the wetland environment were comparable to those of Cx. tritaeniorhynchus in the wetland environment, thereby indicating that the resistance of different populations of Cx. tritaeniorhynchus was homogeneous under the pressure of different insecticide selection within and around the wetland. However, the underlying mechanisms need to be further studied.

Objective To investigate the setup error in patients with spinal bone metastasis who underwent radiotherapy under the guidance of kilovoltage cone-beam CT (KV-CBCT). Methods A total of 118 patients with spinal metastasis who underwent radiotherapy, including 17 cases of cervical spine, 62 cases of thoracic spine, and 39 cases of lumbar spine, were collected. KV-CBCT scans were performed using the linear accelerators from Elekta and Varian’s EDGE system. CBCT images were registered with reference CT images in the bone window mode. A total of 973 data were collected, and 3D linear errors were recorded. Results The patients with spinal bone metastasis were grouped by site, height, weight, and BMI. The P value of the patients grouped only by site was P<0.05, which was statistically significant. Conclusion When grouped by site in the 3D direction, the positioning effect of cervical spine is better than that of thoracic and lumbar spine. The positioning effect of the thoracic spine is better in the head and foot direction but worse in the left and right direction compared with that of the lumbar spine. Instead of extending or narrowing the margin according to the BMI of patients with spinal metastasis, the margin must be changed according to the site of spinal bone metastasis.

Objective:Acute kidney injury(AKI) is a common complication after cardiac surgery, and associated with increased risk of development of chronic kidney disease and mortality in the long term. Neutrophil percentage-to-albumin ratio(NPAR) is a new inflammatory marker that has been used to predict the poor prognosis of patients with cardiovascular disease or shock. However, the relationship between NPAR and AKI in patients with cardiac surgery has not been established. The aim was to evaluate the relationship between NPAR and AKI after cardiac surgery.Methods:Data of all adult patients underwent cardiac surgery with cardiopulmonary bypass from January 1, 2006 to December 31, 2018 were extracted from electronic medical record system of the Guangdong Provincial People's Hospital and retrospectively analyzed. The outcome of interest was AKI diagnosed by using the criteria of Kidney Disease Improving Global Outcomes. Logistic regression was used to assess the relationship between NPAR and postoperative AKI while adjust for potential confounders. In addition, restricted cubic spline(RCS) was utilized to provide a flexible description of the association of the preoperative NPAR and AKI. Results:Totally, 24 178 patients were analyzed. The incidence of AKI was 30.1%. Compared with patients without AKI, those with AKI were older and had higher rates of males, left ventricular ejection fraction(LVEF) less than or equal to 0.60, estimated glomerular filtration rate less than 90 ml·min -1·1.73 m -2, hypertension, diabetes, emergency surgery, preoperative critical illness, and reoperation. The baseline serum creatinine, serum uric acid, cardiopulmonary bypass time and postoperative mechanical ventilation time were higher or longer in AKI patients than those in none AKI patients. Then, patients were divided into four groups based on NPAR quartiles. After adjusting for confounding factors using logisitc regression, compared with patients with NPAR in group 3(1.551.97), respectively. The RCS showed a U-shaped nonlinear relationship( P for nonlinear less than 0.001) between NPAR and AKI after adjusting for potential confounding factors. RCS indicated the NPAR of 1.77 was the lowest risk for AKI. When NPAR less than 1.77, per 1-standard deviation(SD) increase in NPAR, the risk of AKI decreased by 23.2%( OR=0.768, 95% CI: 0.687, 0.859). Conversely, when NPAR above 1.77, per one SD increase in NPAR, the risk of AKI increased by 25.9%( OR=1.259, 95% CI: 1.166, 1.36). Conclusion:A U-shaped relationship between NPAR and AKI after cardiac surgery was shown. The appropriate value for NPAR might be 1.77. The risk of AKI might be increased, when less or above this value. NPAR might be used as an effective and economical tool to identify AKI risk among individuals with cardiac surgery, as well as to formulate individualized prevention and intervention strategy.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Central nervous system(CNS)degenerative disorders refer to a spectrum of pathological alterations triggered by struc-tural damage to cerebral neural tissues,clinically manifested as diverse neurological dysfunction syndromes,including multiple sclerosis(MS),neurodegenerative diseases(NDs),and ische-mic stroke.The hallmark pathological features of these disorders involve irreversible neuronal damage and decompensation of functional neural networks,ultimately leading to progressive neurological deficits.Notably,with the accelerating global popu-lation aging,the incidence of these diseases has surged signifi-cantly.According to WHO statistics,they now rank among the top three global causes of disability and mortality.Current re-search has confirmed that the pathogenesis of CNS degenerative disorders exhibits high heterogeneity,encompassing multifaceted pathophysiological processes such as genetic predisposition,oxi-dative stress,protein misfolding,and metabolic dysregulation.This intricate pathogenic network not only complicates clinical differential diagnosis but also poses substantial challenges to the development of precision therapeutic strategies.Importantly,re-cent studies have revealed that mitochondrial homeostasis disrup-tion-induced inflammatory cascades(termed mitochondrial in-flammation)play a pivotal regulatory role in neurodegenerative progression.Key molecular mechanisms include impaired mito-phagy,aberrant mitochondrial DNA(mtDNA)release and NL-RP3 inflammasome activation.This review systematically deci-phers the molecular regulatory network of mitochondrial inflam-mation,with a focus on its biological effects in critical pathologi-cal events such as blood-brain barrier disruption,microglial hy-peractivation and neuronal apoptosis.The overarching aim is to provide a theoretical foundation for developing innovative thera-peutic strategies targeting mitochondrial homeostasis restoration.

Objective:Acute kidney injury(AKI) is a common complication after cardiac surgery, and associated with increased risk of development of chronic kidney disease and mortality in the long term. Neutrophil percentage-to-albumin ratio(NPAR) is a new inflammatory marker that has been used to predict the poor prognosis of patients with cardiovascular disease or shock. However, the relationship between NPAR and AKI in patients with cardiac surgery has not been established. The aim was to evaluate the relationship between NPAR and AKI after cardiac surgery.Methods:Data of all adult patients underwent cardiac surgery with cardiopulmonary bypass from January 1, 2006 to December 31, 2018 were extracted from electronic medical record system of the Guangdong Provincial People's Hospital and retrospectively analyzed. The outcome of interest was AKI diagnosed by using the criteria of Kidney Disease Improving Global Outcomes. Logistic regression was used to assess the relationship between NPAR and postoperative AKI while adjust for potential confounders. In addition, restricted cubic spline(RCS) was utilized to provide a flexible description of the association of the preoperative NPAR and AKI. Results:Totally, 24 178 patients were analyzed. The incidence of AKI was 30.1%. Compared with patients without AKI, those with AKI were older and had higher rates of males, left ventricular ejection fraction(LVEF) less than or equal to 0.60, estimated glomerular filtration rate less than 90 ml·min -1·1.73 m -2, hypertension, diabetes, emergency surgery, preoperative critical illness, and reoperation. The baseline serum creatinine, serum uric acid, cardiopulmonary bypass time and postoperative mechanical ventilation time were higher or longer in AKI patients than those in none AKI patients. Then, patients were divided into four groups based on NPAR quartiles. After adjusting for confounding factors using logisitc regression, compared with patients with NPAR in group 3(1.551.97), respectively. The RCS showed a U-shaped nonlinear relationship( P for nonlinear less than 0.001) between NPAR and AKI after adjusting for potential confounding factors. RCS indicated the NPAR of 1.77 was the lowest risk for AKI. When NPAR less than 1.77, per 1-standard deviation(SD) increase in NPAR, the risk of AKI decreased by 23.2%( OR=0.768, 95% CI: 0.687, 0.859). Conversely, when NPAR above 1.77, per one SD increase in NPAR, the risk of AKI increased by 25.9%( OR=1.259, 95% CI: 1.166, 1.36). Conclusion:A U-shaped relationship between NPAR and AKI after cardiac surgery was shown. The appropriate value for NPAR might be 1.77. The risk of AKI might be increased, when less or above this value. NPAR might be used as an effective and economical tool to identify AKI risk among individuals with cardiac surgery, as well as to formulate individualized prevention and intervention strategy.

The aim of this study was to investigate the impact of overexpressing 70-kD heat shock pro-teins(Hsp70)on glycolysis in C2C12 cells during myogenesis and adipogenesis.Using C2C12 cells as the research material,adenovirus was used to overexpress the Hsp70 gene,and changes in the expression of glycolytic genes were detected using fluorescence quantitative PCR and Western blotting techniques.The study indicated that during C2C12 cell myogenic differentiation,the expression trend of the Hsp70 gene was consistent with that of Gsk3β,Pkm,Prkag3,Pfkm,and Hk-2 genes,suggesting a relationship between Hsp70 and the glycolytic pathway during myogenic differentiation.Overexpression of Hsp70 in the later stages of myogenic differentiation significantly upregulated the expression of Gsk3β,Pkm,Prk-ag3,and Pfkm genes(P＜0.05),with no significant impact on Hk-2 gene expression(P＞0.05).Dur-ing C2C12 cell adipogenic induction,the expression trend of the Hsp70 gene was similar to that of Gsk3β,Pkm,Prkag3,Pfkm,and Hk-2 genes,indicating a relationship between Hsp70 and the glycolytic path-way during adipogenic induction.Following Hsp70 overexpression,in the later stages of adipogenic in-duction,the number of lipid droplets was significantly higher compared to the control group,with a sig-nificant upregulation of Gsk3β,Pkm,Prkag3,and Pfkm gene expression(P＜0.05),while Hk-2 gene expression was not significantly affected(P＞0.05).In conclusion,Hsp70 in C2C12 cells in myogenic and adipogenic states promoted the breakdown of glycogen into 6-phospho-glucose,thereby enhancing the glycolytic pathway,providing insights into the functional role of the Hsp70 gene in glycolysis in C2C12 cells.

The pathogenesis of Alzheimer's disease(AD)is complex and unclear.Existing drugs can only alleviate its symp-toms,and there is an urgent need to develop effective therapeutic drugs.As the representative drugs of tonic and enlightening medicine,ginseng and acorus calamus have pharmacological effects to improve memory,improve learning ability and reduce cognitive impairment,which are commonly used in Chinese med-icine for the treatment of dementia.The combination of ginseng and acorus calamus can further promote the active ingredients in-to brain to exert their medicinal effects,and delay the process of AD through anti-inflammatory,anti-oxidative stress,modulation of neuronal-synaptic plasticity and other multiple pathways,with multi-level,multi-system and multi-target action characteristics.This paper attempts to summarize the existing research results and lay the foundation for further exploring the synergistic mech-anism of action of ginseng-acorus calamus combination and the dose-effect relationship of the combination,so as to provide a sci-entific basis for the development of innovative Chinese medicines for the prevention and treatment of AD.

Exosomes represent a class of nanoscale extracellular vesicles that facilitate the exchange of genetic information among various cells.Alzheimer's disease(AD)stands as a progressive neurodegenerative disorder characterized by its subtle and advan-cing onset,representing the foremost form of dementia lacking effective therapeutic interventions.Notably,investigations have illuminated the involvement of exosomes in the pathogenesis of AD,attributing diagnostic and therapeutic significance to their role,particularly concerning exosomal microRNAs(miRNA).The miRNAs carried by exosomes serve as potential biomarkers for AD,while also exhibiting potential benefits in ameliorating cognitive dysfunction in individuals afflicted by AD.This article aims to comprehensively review the origins of exosomes(encom-passing both mesenchymal cell-derived exosomes and brain-de-rived exosomes)and their potential as therapeutic agents targe-ting AD.

Panax notoginseng is the dried root and rhizome of Panax notoginseng(Burk.)F.H.Chen,a perennial erect herb of the genus Ginseng of the family Wujiaceae.As a traditional Chinese medicine in our country,Panax notoginseng has a good tonic effect,and the Dictionary of Traditional Chinese Medicines has the words that Panax notoginseng is used to tonify the blood,remove the blood stasis and damage,and stop epistaxis.It can also be used to pass the blood and tonify the blood with the best efficacy,and it is the most precious one of the prescription med-icines.Eaten raw,it removes blood stasis and generates new blood,subdues swelling and stabilizes pain,stops bleeding with-out leaving stasis,and promotes blood circulation without hurting the new blood;taken cooked,it can be used to replenish and strengthen the body.Notoginsenoside R1 is a characteristic com-pound in the total saponin of Panax ginseng.In recent years,China's aging has been increasing,and the incidence of neuro-logical disorders has been increasing year by year.Meanwhile,reports on notoginsenoside R1 in the treatment of neurological disorders are increasing,and its neuroprotective effects have been exerted with precise efficacy.The purpose of this paper is to review the treatment of neurological diseases and the mecha-nism of action of notoginsenoside R1,so as to provide a certain theoretical basis for clinical use and new drug development.