The neurophysiological mechanisms by which exercise improves cognitive function have not been fully elucidated. A comprehensive and systematic review of current domestic and international neurophysiological evidence on exercise improving cognitive function was conducted from multiple perspectives. At the molecular level, exercise promotes nerve cell regeneration and synaptogenesis and maintains cellular development and homeostasis through the modulation of a variety of neurotrophic factors, receptor activity, neuropeptides, and monoamine neurotransmitters, and by decreasing the levels of inflammatory factors and other modulators of neuroplasticity. At the cellular level, exercise enhances neural activation and control and improves brain structure through nerve regeneration, synaptogenesis, improved glial cell function and angiogenesis. At the structural level of the brain, exercise promotes cognitive function by affecting white and gray matter volumes, neural activation and brain region connectivity, as well as increasing cerebral blood flow. This review elucidates how exercise improves the internal environment at the molecular level, promotes cell regeneration and functional differentiation, and enhances the brain structure and neural efficiency. It provides a comprehensive, multi-dimensional explanation of the neurophysiological mechanisms through which exercise promotes cognitive function.
Animals ; Humans ; Brain/physiology* ; Cognition/physiology* ; Exercise/physiology* ; Nerve Regeneration/physiology* ; Neuronal Plasticity/physiology*

Cervical spine health issues not only seriously affect patients' quality of life but also impose a heavy burden on the social healthcare system. Existing guidelines lack sufficient clinical guidance on lifestyle and work habits, such as exercise, posture, daily routine, and diet, making it difficult to meet practical needs. To address this, relying on the China Association of Chinese Medicine, Wangjing Hospital of China Academy of Chinese Medical Sciences took the lead and joined hands with more than ten institutions to form a multidisciplinary guideline development group. For the first time, the group developed the Guidelines for Cervical Spine Health Intervention based on evidence-based medicine methods, strictly following the standardized procedures outlined in the World Health Organization Handbook for Guideline Development and the Guiding Principles for the Formulation/Revision of Clinical Practice Guidelines in China (2022 Edition). This proposal systematically explains the methods and steps for developing the guideline, aiming to make the guideline development process scientific, standardized, and transparent.
Humans ; Practice Guidelines as Topic/standards* ; Cervical Vertebrae ; China

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

An innovative on-site real-time avian influenza virus(AIV)detection method was estab-lished by integratingrecombinase-aided amplification(RAA)with the clustered regularly inter-spaced short palindromic repeats(CRISPR)/CRISPR-associated protein(Cas)system.After analy-zing 120 sequences of the M gene of avian influenza viruses of different subtypes publicly available on NCBI,the RAA primers and crRNA were designed based on the identified highly conserved segment and used for RAA nucleic acid amplification.After the amplified products were transferred to a CRISPR/Cas13a detection system,the fluorescence values were monitored throughout the re-action process to indicate the results.The sensitivity and specificity of the RAA-CRISPR/Cas13a method were validated using gradient dilutions(106-100 copies/μL)of positive plasmids and sev-en other avian viruses.Fifty clinical samples were tested using this method and compared with the national standard fluorescence RT-PCR method.The results indicated that the detection limit for RAA-CRISPR/Cas13a method was 102 copies/μL,a two-fold improvement over the standard RAA.Specificity assay showed the established method only detected AIV with no cross-reactivity with other seven avian viruses.Compared to the national standard fluorescence RT-PCR method,this method exhibited 100％specificity,95.24％accuracy,and 98.00％consistency in detection of clinical samples.In conclusion,a universal and rapid RAA-CRISPR/Cas13a for detection of AIV was established with the capacity of achieving detection within 60 minutes at 37 ℃,which provides a rapid,sensitive,and specific on-site detection method for AIV.

Objective To detect the expression levels of tumor necrosis factor alpha induced protein 3(TN-FAIP3)and LINC00887 in clear cell renal cell carcinoma(ccRCC)tissue,and to study their relationship with clinical pathological parameters and prognosis.Methods A total of 101 ccRCC patients admitted to the hospi-tal from January 2013 to October 2018 were selected.The expression levels of TNFAIP3 and LINC00887 were detected in ccRCC cancer tissue and paired adjacent tissues,respectively.The relationship between TNFAIP3 and LINC00887 expression and clinical pathological parameters and prognosis of ccRCC patients was analyzed,and the influencing factors of poor prognosis in ccRCC patients were also analyzed.Spearman correlation coef-ficient was used to analyze the correlation between TNFAIP3 and LINC00887 expression.Results The posi-tive rate of TNFAIP3 expression in ccRCC(37.62％)was significantly lower than that in adjacent tissues(52.48％),and the difference was statistically significant(X2=4.500,P=0.034).The expression level of LINC00887 in ccRCC(1.38±0.61)was significantly higher than that in adjacent tissues(1.03±0.43),and the difference was statistically significant(t=5.396,P＜0.001).The positive rates of TNFAIP3 protein in pa-tients with maximum tumor diameter ≥4.5 cm and TNM stage Ⅲ-Ⅳ were lower than those in patients with maximum tumor diameter＜4.5 cm and TNM stage Ⅰ-Ⅱ,and the differences were statistically significant(P＜0.05).The positive rates of LINC00887 in patients with maximum tumor diameter ≥ 4.5 cm,pathologi-cal grading Ⅲ-Ⅳ,and TNM stage Ⅲ-Ⅳ were higher than those in patients with maximum tumor diameter＜4.5 cm,pathological grading Ⅰ-Ⅱ,and TNM stage Ⅰ-Ⅱ,and the differences were statistically signifi-cant(P＜0.05).Compared with the TNFAIP3 high expression group,the TNFAIP3 low expression group had a poorer prognosis,and the difference was statistically significant(x2=5.118,P=0.024).Compared with the LINC00887 low expression group of,the LINC00887 high expression group had a poorer prognosis,and the difference was statistically significant(x2=4.638,P=0.031).Low expression of TNFAIP3,high expres-sion of LINC00887,pathological grade Ⅲ-Ⅳ,and TNM stage Ⅲ-Ⅳ were risk factors for poor prognosis in ccRCC patients(P＜0.05).Spearman rank correlation analysis showed that there was a negative correlation between TNFAIP3 and LINC00887 expression in ccRCC tissue(r=-0.638,P=0.012).Conclusion TN-FAIP3 expression is down-regulated and L1NC00887 expression is up-regulated in ccRCC tissue,and there is a negative correlation.They may jointly regulate the occurrence and development of ccRCC,and have the poten-tial to become tumor markers for evaluating the prognosis of ccRCC patients.

Objective To observe the therapeutic effect of allogeneic hematopoietic stem cell transplantation (allo-HSCT) on acute myeloid leukemia (AML) and analyze the influencing factors of survival prognosis. Methods The clinical data of 32 AML patients who underwent allo-HSCT treatment were retrospectively analyzed. The hematopoietic reconstitution, occurrence of graft-versus-host disease (GVHD), survival status, recurrence, and transplantation-related mortality (TRM) of patients were observed, and the influencing factors of survival prognosis were analyzed. Results All 32 AML patients who underwent allo-HSCT achieved granulocyte reconstitution, with a time range of 10 to 26 days and a median time of 11.0 days. Granulocyte-macrophage lineage reconstitution was achieved in 30 patients, with a time range of 10 to 54 days and a median time of 13.5 days. Among the 30 evaluable patients, 10 developed acute GVHD (with incidence rate of 33.33%) and 10 developed chronic GVHD (incidence rate of 33.33%). Up to May 31, 2023, the follow-up time ranged from 2 to 28 months, with a median follow-up time of 14.5 months. Of the 30 patients, 28 survived (25 patients were in disease-free survival status), and 2 died. Multivariate Cox regression analysis showed that age>35 years (P=0.035, HR=2.021) and recurrence after transplantation (P=0.021, HR=2.546) were independent risk factors of patients' survival prognosis. Among 30 patients, 5 relapsed, with a time range of 6 to 24 months and a median time of 9.0 months. Of 5 relapsed patients, 2 died (non-TRM). Conclusion Allo-HSCT is an effective treatment for AML. Age>35 years and recurrence after transplantation are independent risk factors of patients' survival prognosis.

This study aimed to investigate the mechanism by which Shegan Mahuang Decoction(SGMH) and its bitter Chinese herbs(BCHs) regulated the lung-gut axis through the bitter taste receptor 14(TAS2R14)/secretory immunoglobulin A(SIgA)/thymic stromal lymphopoietin(TSLP) to intervene in the epithelial cell barrier of cold asthma rats. Fifty SD rats were randomly divided into the following five groups: normal group, model group, dexamethasone group, SGMH group, and BCHs group. A 10% ovalbumin(OVA) solution was used to sensitize the rats via subcutaneous injection on both sides of the abdomen and groin, combined with 2% OVA atomization and cold(2-4 ℃) stimulation to induce a cold asthma model in rats. The SGMH, BCHs, and dexamethasone groups were given corresponding treatments by gavage and nebulization, while the normal and model groups received normal saline by gavage and nebulization. After the final stimulation, pathological changes in the lung and intestine tissues were observed using hematoxylin-eosin(HE) and periodic acid-Schiff(PAS) staining. Lung function was assessed by measuring the ratio of forced expiratory volume in the first second to forced vital capacity(FEV1/FVC), the ratio of the average flow rate at 25%-75% of forced vital capacity to foned vital capacity(FEV25%-75%/FVC), the peak expiratory flow(PEF), and pulmonary resistance(RL). The levels of IL-4, IL-5, IL-13, and TNF-α in serum, and sIgA in serum, intestinal, and bronchial mucosa were detected by enzyme-linked immunosorbent assay(ELISA). The expression of TAS2R14 protein in lung tissue was detected by Western blot(WB). The content of short-chain fatty acids(SCFAs) in rat feces was determined by gas chromatography-mass spectrometry(GC-MS). The effect of TAS2R14/TSLP on lipopolysaccharide(LPS)-induced inflammation in epithelial cells in the BCHs group was observed, and the expression of TAS2R14 and TSLP in cells was detected by WB. Compared with the normal group, the model group showed reduced water intake, diet, and body weight, increased infiltration of inflammatory cells in the lung and intestinal tissues, goblet cell hyperplasia, significantly decreased FEV1/FVC, FEV25%-75%/FVC, and PEF, and significantly increased RL. Moreover, serum levels of IL-4, IL-5, IL-13, and TNF-α were elevated, and sIgA levels in serum, intestine, and bronchial mucosa were significantly decreased. TAS2R14 expression in lung tissues was inhibited, and the content of acetic acid, propionic acid, and butyric acid in feces was significantly reduced. In the LPS group, TSLP expression increased, and TAS2R14 expression decreased. Compared with the model group, the general condition of rats in the SGMH and BCHs groups improved, with reduced infiltration of inflammatory cells and goblet cell hyperplasia in the lung and intestinal tissues. FEV1/FVC, FEV25%-75%/FVC, and PEF significantly increased, and RL significantly decreased. Serum levels of IL-4, IL-5, IL-13, and TNF-α decreased, while sIgA levels in serum, intestine, and bronchial mucosa significantly increased, and TAS2R14 expression was activated in lung and intestinal tissues. The content of acetic acid, propionic acid, and butyric acid in feces significantly increased. Compared with the model group, the BCHs group and the agonist group showed inhibited TSLP expression and increased TAS2R14 expression. The results showed that both SGMH and BCHs could reduce lung and intestinal inflammatory reactions, improve lung function, and regulate the content of intestinal SCFAs in asthmatic rats. There was no significant difference in TAS2R14 protein expression between the SGMH and BCHs groups, indicating that the clinical efficacy of BCHs may be related to the activation of the bitter receptor TAS2R14 and the regulation of immune inflammatory mediators in lung and intestinal epithelial cells.
Animals ; Drugs, Chinese Herbal/administration & dosage* ; Rats ; Rats, Sprague-Dawley ; Lung/metabolism* ; Asthma/metabolism* ; Cytokines/immunology* ; Male ; Receptors, G-Protein-Coupled/immunology* ; Epithelial Cells/metabolism* ; Thymic Stromal Lymphopoietin ; Immunoglobulin A, Secretory/genetics* ; Humans ; Cold Temperature

The study investigated the effect of casticin on the proliferation of non-small cell lung cancer(NSCLC) H322 cells and explored its molecular mechanism. Firstly, the cell counting kit-8(CCK-8) assay, colony formation assay, and EdU assay were used to detect the effect of casticin on the proliferation capacity of H322 cells under different concentrations and treatment durations. Then, glucose uptake, lactate production, extracellular pH, and oxygen consumption of H322 cells were measured before and after casticin treatment to analyze its impact on glycolysis in NSCLC H322 cells. Finally, real-time fluorescence quantitative PCR(RT-qPCR) and Western blot assays were performed to explore glycolysis-related molecules affected by casticin. The experiments showed that casticin inhibited the proliferation of NSCLC H322 cells in a dose-and time-dependent manner, with half-maximal inhibitory concentrations(IC_(50)) of 28.64 and 19.41 μmol·L~(-1) after 48 and 72 hours of treatment, respectively. Casticin also inhibited glucose uptake and lactate production in H322 cells, while increasing extracellular pH and oxygen consumption. Further investigation revealed that casticin inhibited the expression of glycolysis-related molecules, including glucose transporter 1(GLUT1), hexokinase 2(HK2), aldolase A(ALDOA), pyruvate kinase M2(PKM2), and hypoxia-inducible factor-1α(HIF-1α). Overexpression of HIF-1α was found to reverse the inhibitory effects of casticin on H322 cell proliferation and glycolysis. These findings suggest that casticin may regulate cellular glycolysis by inhibiting the expression of HIF-1α, thereby inhibiting the proliferation of NSCLC H322 cells. This study identifies a potential drug for the treatment of NSCLC and provides a direction for further research.
Humans ; Cell Proliferation/drug effects* ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics* ; Carcinoma, Non-Small-Cell Lung/physiopathology* ; Lung Neoplasms/drug therapy* ; Glucose/metabolism* ; Cell Line, Tumor ; Glycolysis/drug effects*

Cardiovascular disease (CVD) is a major contributor to patient deaths worldwide, and its pathogenesis is complex and mortality rates are increasing every year. Numerous researches have shown that the gut microbiota and its metabolites were closely associated with the development of CVD, and gut microbiota was expected to be a potential new target for the treatment of CVD. Traditional Chinese medicine (TCM), characterized by its multi-component, multi-target and integrity, can play a therapeutic role in CVD by regulating the gut microbiota, which has obvious advantages in stabilizing the disease, improving heart function and enhancing quality of life, and is an ideal intestinal microecological regulator. Therefore, this review will mainly discuss the intimate association of gut microbiota and its metabolites with CVD, and the therapeutic strategies of TCM targeting gut microbiota to improve CVD, including regulating the composition of gut microbiota, protecting the intestinal mucosal barrier, influencing the intestinal immune function and modulating the metabolites of gut microbiota, in order to provide a reference for the research of TCM targeting gut microbiota for CVD.

Chromodomain-helicase-DNA-binding protein 1 (CHD1) deletion is among the most common mutations in prostate cancer (PCa), but its role remains unclear. In this study, RNA sequencing was conducted in PCa cells after clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 (Cas9)-based CHD1 knockout. Gene set enrichment analysis (GSEA) indicated upregulation of hypoxia-related pathways. A subsequent study confirmed that CHD1 deletion significantly upregulated hypoxia-inducible factor 1α (HIF1α) expression. Mechanistic investigation revealed that CHD1 deletion upregulated HIF1α by transcriptionally downregulating prolyl hydroxylase domain protein 2 (PHD2), a prolyl hydroxylase catalyzing the hydroxylation of HIF1α and thus promoting its degradation by the E3 ligase von Hippel-Lindau tumor suppressor (VHL). Functional analysis showed that CHD1 deletion promoted angiogenesis and glycolysis, possibly through HIF1α target genes. Taken together, these findings indicate that CHD1 deletion enhances HIF1α expression through PHD2 downregulation and therefore promotes angiogenesis and metabolic reprogramming in PCa.
Male ; Humans ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism* ; DNA-Binding Proteins/metabolism* ; Prolyl Hydroxylases/metabolism* ; Hypoxia ; Prostatic Neoplasms/pathology* ; Glycolysis ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Cell Line, Tumor ; DNA Helicases/metabolism*