ObjectiveTo examine the effects of Chaihu Jia Longgu Muli Tang （CLMT）-containing serum on Neuro-2A cell damage when exposed to conditioned medium from lipopolysaccharide （LPS）-stimulated microglia （BV-2） and explore the underlying mechanism. MethodsBV-2 cells were activated by LPS at a concentration of 1 mg·L^-1 to generate conditioned medium. Concurrently， a blank control group， a model group and groups treated with varying concentrations of CLMT （5%， 10%， and 15%）， dexamethasone （2.5 μmol·L^-1）， stimulator of interferon genes （STING） agonist （MSA-2， 10 μmol·L^-1）， and STING inhibitor （STING-IN-4， 4 μmol·L^-1） were established. Neuro-2A cells were subsequently cultured in the conditioned medium from each treatment group. The viability of BV-2 cells following interventions was assessed by the cell counting kit-8 （CCK-8） assay. The levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in the supernatant of Neuro-2A cells from each group were measured through enzyme linked immunosorbent assay （ELISA）. Additionally， the expression of tyrosine hydroxylase （TH） in Neuro-2A cells was evaluated through immunohistochemistry （IHC）， while the expression of phosphorylated alpha-synuclein （p-α-Syn） was assessed by immunofluorescence （IF） assay. The expression levels of STING， interferon regulatory factor 3 （IRF3）， phosphorylated interferon regulatory factor 3 （p-IRF3）， nuclear transcription factor-kappa B p65 （NF-κB p65）， and phosphorylated nuclear transcription factor-kappa B p65 （p-NF-κB p65） in Neuro-2A cells were determined by Western blot. ResultsIn comparison to the control group， both the model group and the MSA-2 group exhibited reduced viability of Neuro-2A cells （P<0.01）， elevated concentrations of TNF-α， IL-1β， and IL-6 in the cell supernatant （P<0.01）， reduced expression of TH （P<0.01）， increased expression of p-α-Syn （P<0.01）， and upregulated relative protein levels of STING， p-IRF3， and p-NF-κB p65 （P<0.01）. Compared with the model group， medium- and high-dose CLMT enhanced the viability of Neuro-2A cells （P<0.01）， lowered the levels of TNF-α， IL-1β， and IL-6 （P<0.01）， promoted TH expression， and suppressed p-α-Syn expression （P<0.01）. In the dexamethasone group， the levels of IL-6， TNF-α， and IL-1β were reduced （P<0.05， P<0.01）. In the STING-IN-4 group， the levels of TNF-α and IL-1β were decreased （P<0.01）. The expression of TH was increased in both the dexamethasone group and the STING-IN-4 group （P<0.01）， while the expression of p-α-Syn was reduced （P<0.01）. The relative protein levels of p-IRF3， STING， and p-NF-κB p65 were reduced in medium- and high-dose CLMT groups （P<0.05， P<0.01）. Similarly， the dexamethasone group exhibited decreases in the expression levels of STING， p-IRF3， and p-NF-κB p65 （P<0.01）. In the STING-IN-4 group， the expression levels of p-NF-κB p65， STING， and p-IRF3 were also diminished （P<0.05， P<0.01）. However， no statistically significant differences were observed in the expression of IRF3 or NF-κB p65 across the groups. ConclusionCLMT has the potential to suppress the activation of BV-2 microglial cells， consequently mitigating the inflammatory response induced by LPS and further preventing inflammation-mediated damage to Neuro-2A cells. The underlying mechanism is likely associated with the modulation of the STING/NF-κB signaling pathway， which results in reduced inflammation and confers neuroprotective effects.

By integrating existing research,this paper systematically analyzes the impact of exercise training in low-temperature environments on immune regulation and infection defense,in order to explore its potential benefits and risks.Strictly following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses:2020(PRISMA 2020)guidelines,multiple databases were systematically reviewed,to include original studies on the impact of exercise training in low-temperature environments on immune regulation and infection defense,and to evaluate the quality of the studies.The 25 included literature indicated that moderate-intensity exercise training in low-temperature environments could cause an increase in white blood cell count,neutrophils and natural killer cells,changes in both pro-inflammatory and anti-inflammatory factors,and predominant upregulation of most mucosal immunity level,as well as accelerated infection recovery in several studies.High-intensity exercise training in low-temperature environments has shown an immunosuppressive trend in individual studies,and physiological indicators such as body temperature,heart rate and metabolism have also been affected to varying degrees.This suggests that moderate-intensity exercise training in a low-temperature environment is conducive to enhancing immunity and preventing infection,which is of great significance for health management and occupational protection in cold climates.Reasonable control of exercise intensity and duration in a low-temperature environment is crucial for preventing immunosuppression.

By integrating existing research,this paper systematically analyzes the impact of exercise training in low-temperature environments on immune regulation and infection defense,in order to explore its potential benefits and risks.Strictly following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses:2020(PRISMA 2020)guidelines,multiple databases were systematically reviewed,to include original studies on the impact of exercise training in low-temperature environments on immune regulation and infection defense,and to evaluate the quality of the studies.The 25 included literature indicated that moderate-intensity exercise training in low-temperature environments could cause an increase in white blood cell count,neutrophils and natural killer cells,changes in both pro-inflammatory and anti-inflammatory factors,and predominant upregulation of most mucosal immunity level,as well as accelerated infection recovery in several studies.High-intensity exercise training in low-temperature environments has shown an immunosuppressive trend in individual studies,and physiological indicators such as body temperature,heart rate and metabolism have also been affected to varying degrees.This suggests that moderate-intensity exercise training in a low-temperature environment is conducive to enhancing immunity and preventing infection,which is of great significance for health management and occupational protection in cold climates.Reasonable control of exercise intensity and duration in a low-temperature environment is crucial for preventing immunosuppression.

BACKGROUND:Circadian rhythms are closely related to the life activities of most mammals and insects.Timless gene plays a crucial role in the generation of circadian rhythms as key components encoding the Timeless/Period gene complex.However,its specific mechanism in circadian rhythms is still unclear.OBJECTIVE:To study the relationship between Timless protein gene,Period gene,circadian rhythm,environment and cryptochrome gene,so as to have a more comprehensive understanding of the nucleation and accumulation mechanism of circadian cycle and the influence of environment on circadian rhythm.METHODS:Literature retrieval was conducted in the Web of science Core Collection database,PubMed and CNKI,and the relevant literature was searched,consulted and screened after the keyword was set as"Timless,Period,circadian rhythm,environment"in English and Chinese.Non-relevant literature was progressively excluded through full-text reading,and 126 papers were finally included for the review.RESULTS AND CONCLUSION:In the circadian clock,the circadian spontaneous output of the cyclins kaput and CYCLE activate the Timeless/Period gene,Timeless gene regulates the nucleation mechanism and stability of Period gene,and Period gene can also be nucleated individually by a number of mechanisms.Casein kinase 2,Shaggy protein kinase and double time genes can regulate circadian rhythms and participate in transcription by phosphorylating Timeless gene/Period gene.Cryptochrome gene-mediated degradation of Timeless gene has a very important role in transcriptional integrity.External factors such as environmental factors and dietary patterns can influence circadian rhythms through the Timeless gene/Period gene.Interestingly,time-restricted eating can be used as an effective way to improve circadian rhythm disturbances.

BACKGROUND:Circadian rhythms are closely related to the life activities of most mammals and insects.Timless gene plays a crucial role in the generation of circadian rhythms as key components encoding the Timeless/Period gene complex.However,its specific mechanism in circadian rhythms is still unclear.OBJECTIVE:To study the relationship between Timless protein gene,Period gene,circadian rhythm,environment and cryptochrome gene,so as to have a more comprehensive understanding of the nucleation and accumulation mechanism of circadian cycle and the influence of environment on circadian rhythm.METHODS:Literature retrieval was conducted in the Web of science Core Collection database,PubMed and CNKI,and the relevant literature was searched,consulted and screened after the keyword was set as"Timless,Period,circadian rhythm,environment"in English and Chinese.Non-relevant literature was progressively excluded through full-text reading,and 126 papers were finally included for the review.RESULTS AND CONCLUSION:In the circadian clock,the circadian spontaneous output of the cyclins kaput and CYCLE activate the Timeless/Period gene,Timeless gene regulates the nucleation mechanism and stability of Period gene,and Period gene can also be nucleated individually by a number of mechanisms.Casein kinase 2,Shaggy protein kinase and double time genes can regulate circadian rhythms and participate in transcription by phosphorylating Timeless gene/Period gene.Cryptochrome gene-mediated degradation of Timeless gene has a very important role in transcriptional integrity.External factors such as environmental factors and dietary patterns can influence circadian rhythms through the Timeless gene/Period gene.Interestingly,time-restricted eating can be used as an effective way to improve circadian rhythm disturbances.

BACKGROUND:Exercise as a viable non-pharmacological treatment has the potential to reverse skeletal muscle aging that deteriorates with age.The role of autophagy in the skeletal muscle aging process is indispensable.During skeletal muscle aging,Atg genes involved in regulating autophagy regulate the autophagic process in either a facilitative or inhibitory manner to improve the physiological morphology of skeletal muscle.However the specific molecular mechanisms of autophagy in the exercise regulation of skeletal muscle aging remain puzzling. OBJECTIVE:To search for general patterns of the effects of autophagic mechanisms on skeletal muscle aging during exercise through a review of articles in this field. METHODS:(1)CNKI and Web of Science were searched,reviewed,and screened for relevant literature using the keywords of"Atg genes(proteins),autophagy,exercise,and skeletal muscle aging"to lay the theoretical foundation for the full-text analysis.(2)The comparative analysis method was used to compare the similarities and differences among the included documents to provide reasonable theoretical support for the arguments.By the further comparative analysis of the literature,the relationship between relevant indicators was clarified,to provide the ideas for the full-text analysis. RESULTS AND CONCLUSION:Atg family-mediated autophagy is indispensable for delaying skeletal muscle aging.Atg genes involved in regulating autophagy regulate the autophagic process in either a facilitative or inhibitory manner to improve the physiological morphology and function of skeletal muscle.Different exercise patterns,such as age,time,or intensity at initiation,may have heterogeneous effects on the expression of autophagy-related proteins,but long-term aerobic exercise regulates Atg-related proteins,induces skeletal muscle autophagy,and delays the loss of muscle mass.

BACKGROUND:Aging is an irreversible process that is characterized by genes,diet and environment.As a central regulator of growth and development,mammalian target of rapamycin(mTor)can regulate the negative effects caused by aging,exercise and poor diet,which are correlated with the activity of mTor and its complexes.However,the relationship between these factors,such as mTor and the effect of exercise on aging,is still unclear. OBJECTIVE:To study the relationship between exercise,high fat/high salt diet and mTor in aging,so as to have a more comprehensive understanding of the prevention and treatment mechanism of aging. METHODS:(1)Literature retrieval was conducted in the core database of Web of Science and CNKI,using the keywords of"mTor gene,exercise,high fat/high salt diet,aging,"thereby providing theoretical support for this review.(2)Comparative analysis provided a theoretical basis for this thesis by carefully reading the obtained effective literature and comparing the differences among various literatures.(3)Through the comparative analysis of similarities and differences between the included articles,we could define each index and their relationship,so as to clarify the ideas of this review. RESULTS AND CONCLUSION:mTor is closely related to aging.Through the literature analysis,we believe that two complexes of mTor,mTorC1 and mTorC2,play important roles in aging,exercise and skeletal muscle growth and development.In addition,mTor-mediated S6K1,Akt,FOXO,and 4E-BP1 signaling pathways are strongly associated with exercise,high-fat diet,high-salt diet,and skeletal muscle/heart aging.

Objective:To investigate the association between body composition and coronary artery calcification in patients with chronic kidney disease (CKD).Methods:This cross-sectional study enrolled patients with CKD hospitalized from May 2019 to April 2022 at Sun Yat-sen Memorial Hospital, Guangzhou, China. Skeletal muscle mass index and visceral fat area were measured by bioelectrical impedance analysis. Coronary artery calcification was assessed by computed tomography. Patients were divided into coronary artery calcification group and non-coronary artery calcification group according to the incidence of coronary artery calcification. Patients were categorized into tertile groups according to their skeletal muscle mass index and visceral fat area levels ranging from the lowest to the highest levels (T1 to T3). We defined skeletal muscle mass index≤30.4% as low muscle mass and visceral fat area≥80.6 cm 2 as high visceral fat based on the results of the restricted cubic spline graph. All individuals were divided into 4 phenotypes: normal body composition, low muscle mass, high visceral fat, and low muscle mass with high visceral fat. Spearman correlation analysis and logistic regression analysis were used to assess the association between skeletal muscle mass index, visceral fat area and coronary artery calcification. Results:A total of 107 patients with CKD were enrolled, with an age of (60.0±14.1) years, including 41 female patients (38.3%). Patients of coronary artery calcification group had lower skeletal muscle mass index ((32.0±4.8) vs. (34.3±4.8), P=0.016) and higher visceral fat area ((70.8±32.6) cm 2 vs. (47.9±23.8) cm 2, P<0.001) than those of non-coronary artery calcification group. Patients in the T3 group of skeletal muscle mass index had a lower prevalence of coronary artery calcification (17 (48.6%) vs. 28 (77.8%)) and a lower coronary artery calcification score (0.5 (0, 124.0) vs. 12.0 (0.3, 131.0)) than those in the T1 group ( P<0.05). Similarly, patients in the T1 group of visceral fat area had a lower prevalence of coronary artery calcification (14 (40.0%) vs. 29 (80.6%)) and a lower coronary artery calcification score (0 (0, 3.0) vs. 37.0 (2.0, 131.0)) than those in the T3 group ( P<0.05). Likewise, patients with both low muscle mass and low muscle mass with high visceral fat had a higher prevalence of coronary artery calcification (11(78.6%) vs. 33 (47.8%); 15 (83.3%) vs. 33 (47.8%)) and a higher coronary artery calcification score (31.1 (0.8, 175.8) vs. 0 (0, 16.4); 27.6 (6.4, 211.4) vs. 0 (0, 16.4)) than those with normal body composition ( P<0.05). Spearman correlation analysis showed that skeletal muscle mass index was inversely correlated with coronary artery calcification score ( r=-0.212, P=0.028), and visceral fat area was positively correlated with coronary artery calcification score ( r=0.408, P<0.001). Multivariate logistic regression analysis showed that increased skeletal muscle mass index was inversely associated with coronary artery calcification prevalence (T2: OR=0.208, 95% CI: 0.056-0.770, P=0.019; T3: OR=0.195, 95% CI: 0.043-0.887, P=0.034), and reduced visceral fat area was inversely associated with coronary artery calcification prevalence (T1: OR=0.256, 95% CI: 0.071-0.923, P=0.037; T2: OR=0.263, 95% CI: 0.078-0.888, P=0.031). Consistently, both low muscle mass and low muscle mass with high visceral fat were associated with coronary artery calcification prevalence ( OR=6.616, 95% CI: 1.383-31.656, P=0.018; OR=5.548, 95% CI: 1.062-28.973, P=0.042). Conclusion:Reduced skeletal muscle mass index and increased visceral fat area are significantly associated with both the prevalence and severity of coronary artery calcification in patients with CKD.

Background: Feline panleukopenia virus (FPV) is a widespread and highly infectious pathogen in cats with a high mortality rate. Although Yanji has a developed cat breeding industry, the variation of FPV locally is still unclear. Objectives: This study aimed to isolate and investigate the epidemiology of FPV in Yanji between 2021 and 2022. Methods: A strain of FPV was isolated from F81 cells. Cats suspected of FPV infection (n = 80) between 2021 and 2022 from Yanji were enrolled in this study. The capsid protein 2 (VP2) of FPV was amplified. It was cloned into the pMD-19T vector and transformed into a competent Escherichia coli strain. The positive colonies were analyzed via VP2 Sanger sequencing. A phylogenetic analysis based on a VP2 coding sequence was performed to identify the genetic relationships between the strains. Results: An FPV strain named YBYJ-1 was successfully isolated. The virus diameter was approximately 20–24 nm, 50% tissue culture infectious dose = 1 × 10 −4.94 /mL, which caused cytopathic effect in F81 cells. The epidemiological survey from 2021 to 2022 showed that 27 of the 80 samples were FPV-positive. Additionally, three strains positive for CPV-2c were unexpectedly found. Phylogenetic analysis showed that most of the 27 FPV strains belonged to the same group, and no mutations were found in the critical amino acids. Conclusions A local FPV strain named YBYJ-1 was successfully isolated. There was no critical mutation in FPV in Yanji, but some cases with CPV-2c infected cats were identified.

Objective:To characterize the histopathological subtypes and their clinicopathological parameters of gender and onset age by common, rare and sparse primary esophageal malignant tumors (PEMT).Methods:A total of 272 437 patients with PEMT were enrolled in this study, and all of the patients were received radical surgery. The clinicopathological information of the patients was obtained from the database established by the State Key Laboratory of Esophageal Cancer Prevention & Treatment from September 1973 to December 2020, which included the clinical treatment, pathological diagnosis and follow-up information of esophagus and gastric cardia cancers. All patients were diagnosed and classified by the criteria of esophageal tumor histopathological diagnosis and classification (2019) of the World Health Organization (WHO). The esophageal tumors, which were not included in the WHO classification, were analyzed separately according to the postoperative pathological diagnosis. The χ 2 test was performed by the SPSS 25.0 software on count data, and the test standard α=0.05. Results:A total of 32 histopathological types were identified in the enrolled PEMT patients, of which 10 subtypes were not included in the WHO classification. According to the frequency, PEMT were divided into common (esophageal squamous cell carcinoma, ESCC, accounting for 97.1%), rare (esophageal adenocarcinoma, EAC, accounting for 2.3%) and sparse (mainly esophageal small cell carcinoma, malignant melanoma, etc., accounting for 0.6%). All the common, rare, and sparse types occurred predominantly in male patients, and the gender difference of rare type was most significant (EAC, male∶ female, 2.67∶1), followed with common type (ESCC, male∶ female, 1.78∶1) and sparse type (male∶ female, 1.71∶1). The common type (ESCC) mainly occurred in the middle thoracic segment (65.2%), while the rare type (EAC) mainly occurred in the lower thoracic segment (56.8%). Among the sparse type, malignant melanoma and malignant fibrous histiocytoma were both predominantly located in the lower thoracic segment (51.7%, 66.7%), and the others were mainly in the middle thoracic segment.Conclusion:ESCC is the most common type among the 32 histopathological types of PEMT, followed by EAC as the rare type, and esophageal small cell carcinoma and malignant melanoma as the major sparse type, and all of which are mainly occur in male patients. The common type of ESCC mainly occur in the middle thoracic segment, while the rare type of EAC mainly in the lower thoracic segment. The mainly sparse type of malignant melanoma and malignant fibrous histiocytoma predominately occur in the lower thoracic segment, and the remaining sparse types mainly occur in the middle thoracic segment.