ObjectiveThis study aims to systematically analyze the blood-absorbed components and metabolic profiles of Xiebaisan（XBS） in normal and chronic bronchitis （CB） mice using ultra performance liquid chromatography-quadrupole-electrostatic field orbitrap high resolution mass spectrometry（UPLC-Q-Exactive Orbitrap MS）， while comparing differences between the two states. MethodsThirty female BABL/c mice were randomly divided into the normal group， the normal drug administration group， the CB group， the CB drug administration group and the dexamethasone group， with 6 mice in each group. The CB mouse model was established by inducing with ovalbumin （OVA）. The mice in the normal drug administration group and the CB drug administration group started to be gavaged with XBS（13.2 g·kg^-1） from the 21^st day， and the dexamethasone group mice were simultaneously gavaged with dexamethasone （0.5 mg·kg^-1） until the end of the 35^th day of the experiment. Subsequently， serum samples were collected and evaluated for their efficacy， based on the pharmacological evaluation indicators， to determine the efficacy of XBS in treating CB. Then the UPLC-Q-Exactive Orbitrap MS was employed to identify and analyze the chemical constituents， blood-absorbed components， and metabolites of XBS. Chemometric analysis was conducted to reveal metabolic profile differences under "dual states". Concurrently， Real-time PCR technology was utilized to detect the expression levels of key liver metabolic enzymes CYP2E1， CYP3A1， UGT1A1， and UGT1A6. ResultsA total of 28 prototype components and 158 metabolites （including 48 phase Ⅰ metabolites and 110 phase Ⅱ metabolites） of XBS were unambiguously identified in the serum of normal mice. Additionally， a comprehensive characterization was performed on a total of 32 prototype components and 178 metabolites （including 50 phase Ⅰ metabolites and 128 phase Ⅱ metabolites） of XBS in the serum of CB mice. Among them， 27 prototype components were detected in both states， including 12 flavonoids， 2 alkaloids， 3 triterpenes， 4 organic acids， 3 amides， 1 stilbene and 2 other compounds. The chemometrics analysis revealed no significant difference in the prototype components and metabolites of XBS between normal and CB mice； however， there was a significant increase in the in-vivo exposure of XBS in CB mice. Compared to normal mice， the levels of phase Ⅰ metabolites such as oxidation， reduction and methylation of blood components of XBS as well as phase Ⅱ metabolites of glucuronidation showed significant changes in CB mice. Real-time PCR further confirmed that these alterations were attributed to the upregulation of CYP2E1 （P<0.05）， CYP3A1 （P>0.05）， UGT1A1 （P<0.01） and UGT1A6 （P<0.01） enzymes expression in the liver of CB mice. ConclusionThis study elucidated the disparities in the levels of the blood-absorbed components and metabolic profiles of XBS in normal and CB mice， especially in oxidation， reduction， methylation in phase Ⅰ metabolism and glucoaldehyde acidification in phase Ⅱ metabolism. And there are related to the differences in the expression levels of phase Ⅰ and phase Ⅱ metabolic enzymes CYP2E1， CYP3A1， UGT1A1 and UGT1A6 in the liver.

ObjectiveTaking the cuproptosis/oxidative stress pathway as the entry point， this study investigated the effect and mechanism of Liangyi Paste on hepatic lipid deposition in naturally aged mice fed with a high-fat diet. MethodsAfter adaptive feeding， 80 ten-week-old male C57BL/6 mice were used. Thirty of them were randomly divided into three groups （10 mice per group）： The 12-month-old control group （12MCON）， the 15-month-old control group （15MCON）， and the 15-month-old group with a high-fat diet （15MHFD）. The 12MCON and 15MCON groups were continuously fed a standard diet， while the 15MHFD group started receiving a high-fat diet at 12 months of age. Tissue samples were collected at the corresponding time points for each group. The remaining 50 mice were randomly divided into five groups （10 mice per group）： the 20-month-old control group （20MCON）， the model group， and the low-， medium-， and high-dose Liangyi Paste groups （2.91 ， 5.82 ， 11.64 g·kg^-1·d^-1， respectively）. The 20MCON group was continuously fed a standard diet， while the other groups started receiving a high-fat diet at 15 months of age. At 18 months of age， the Liangyi Paste groups were administered the corresponding doses of Liangyi Paste by gavage， while the 20MCON and model groups were given an equal volume of saline by gavage. After 8 weeks of continuous gavage （when the mice reached 20 months of age）， tissue samples were collected. Hepatic TG levels were measured using assay kits； liver histology and lipid deposition were observed via hematoxylin-eosin （HE） and oil red O staining； reactive oxygen species （ROS） were detected by enzyme-linked immunosorbent assay （ELISA）； Cu²⁺， superoxide dismutase （SOD）， and malondialdehyde （MDA） levels were measured by colorimetry； mRNA and protein expression of genes related to cuproptosis and oxidative stress pathways were analyzed by Real-time polymerase chain reaction（Real-time PCR） and Wes automated protein expression system. ResultsCompared with 12MCON， the 15MCON group showed significantly increased hepatic TG， Cu²⁺， ROS， and MDA levels （P<0.01）， decreased SOD （P<0.01）， hepatocyte swelling， and disordered arrangement. The mRNA and protein levels of ferredoxin 1 （FDX1）， dihydrolipoamide S-acetyltransferase （DLAT）， heat shock protein 70 （HSP70）， dihydrolipoamide dehydrogenase （DLD）， pyruvate dehydrogenase E1 subunit-β （PDHB）， nuclear factor erythroid 2-related factor 2 （Nrf2）， and peroxisome proliferator-activated receptor γ （PPARγ） were significantly elevated （P<0.05， P<0.01）. Compared with 15MCON group， the 15MHFD and 20MCON groups exhibited further increases in TG， Cu²⁺， ROS， and MDA （P<0.01）， reduced SOD （P<0.01）， and aggravated hepatocyte swelling and disorder. There were increased lipid droplets with mild vacuolization in the 15MHFD group， and no significant lipid deposition was observed in the 20MCON group. FDX1， DLAT， HSP70， DLD， PDHB， Nrf2， and PPARγ mRNA and protein levels were significantly increased （P<0.05， P<0.01）. Compared with 20MCON group， the model group demonstrated markedly elevated TG， Cu²⁺， ROS， and MDA （P<0.01）， reduced SOD （P<0.01）， severe hepatic steatosis， and upregulated expression of FDX1， DLAT， HSP70， DLD， PDHB， Nrf2， and PPARγ mRNA and proteins （P<0.05， P<0.01）. All abnormalities were significantly reversed after Liangyi Paste treatment. ConclusionLiangyi paste can ameliorate hepatic lipid deposition in naturally aged mice with a high-fat diet by modulating the cuproptosis/oxidative stress pathway.

ObjectiveTo systematically synthesize the illness experiences and unmet needs of patients with stroke during the rehabilitation phase. MethodsQualitative studies focusing on the illness experiences and needs of stroke patients in the rehabilitation period were retrieved from the databases of Cochrane Library, PubMed, Embase, Web of Science, CINAHL, CNKI, CBM, Wanfang data and VIP. The search timeframe was from database inception to December, 2024. Methodological quality was evaluated using the Joanna Briggs Institute Qualitative Assessment and Review Instrument. A meta-synthesis method was adopted to categorize and integrate the findings. ResultsA total of ten studies were included. Forty-nine themes were extracted and further grouped into ten categories, which were finally integrated into three overarching themes: negative illness perceptions, multifaceted rehabilitation motivations and unmet multidimensional needs. ConclusionPatients with stroke undergo complex physical and psychological experiences during rehabilitation and present diverse and multidimensional needs.

ObjectiveTo systematically synthesize the illness experiences and unmet needs of patients with stroke during the rehabilitation phase. MethodsQualitative studies focusing on the illness experiences and needs of stroke patients in the rehabilitation period were retrieved from the databases of Cochrane Library, PubMed, Embase, Web of Science, CINAHL, CNKI, CBM, Wanfang data and VIP. The search timeframe was from database inception to December, 2024. Methodological quality was evaluated using the Joanna Briggs Institute Qualitative Assessment and Review Instrument. A meta-synthesis method was adopted to categorize and integrate the findings. ResultsA total of ten studies were included. Forty-nine themes were extracted and further grouped into ten categories, which were finally integrated into three overarching themes: negative illness perceptions, multifaceted rehabilitation motivations and unmet multidimensional needs. ConclusionPatients with stroke undergo complex physical and psychological experiences during rehabilitation and present diverse and multidimensional needs.

ObjectiveTo systematically synthesize the illness experiences and unmet needs of patients with stroke during the rehabilitation phase. MethodsQualitative studies focusing on the illness experiences and needs of stroke patients in the rehabilitation period were retrieved from the databases of Cochrane Library, PubMed, Embase, Web of Science, CINAHL, CNKI, CBM, Wanfang data and VIP. The search timeframe was from database inception to December, 2024. Methodological quality was evaluated using the Joanna Briggs Institute Qualitative Assessment and Review Instrument. A meta-synthesis method was adopted to categorize and integrate the findings. ResultsA total of ten studies were included. Forty-nine themes were extracted and further grouped into ten categories, which were finally integrated into three overarching themes: negative illness perceptions, multifaceted rehabilitation motivations and unmet multidimensional needs. ConclusionPatients with stroke undergo complex physical and psychological experiences during rehabilitation and present diverse and multidimensional needs.

Objective To explore the characteristics and temporal trends of renal cancer burden among Chinese adolescents and young adults(AYA), and predict its future epidemic situation, so as to provide evidence for formulating public health policies and reducing the disease burden.Methods Epidemiological data of renal cancer in Chinese AYA(15-39 years)from 1990 to 2021 were obtained from the Global Burden of Disease(GBD)2021 database. The current status and trends of renal cancer in this population were analyzed. The incidence and mortality trends of renal cancer in AYA over the next 15 years was predicted with ARIMA model. The impacts of smoking and body mass index(BMI)on the disease burden were evaluated. Results In 2021, the incidence(1.12/100000), prevalence(8.61/100000), mortality(0.19/100000), and disability-adjusted life years(DALYs)(11.37/100000 person-years)of renal cancer in Chinese AYA were significantly higher than those in 1990 and above the global average. All burden indicators and their increases were higher in males than in females, and the burden accelerated after 30 years of age. The incidence rose steadily from 2003 to 2021(APC=3.95), while the mortality increased significantly from 2013 to 2021(APC=2.40). The burden attributed to high BMI continued to rise, and the smoking-attributable fraction in males first increased then decreased. ARIMA predicted that the incidence of renal cancer in Chinese AYA males would accelerate, while the mortality in both genders would stabilize. Conclusion The burden of renal cancer in Chinese AYA shows a significant upward trend. Males and people over 30 years old are key targets for prevention and control. Strengthening the management of risk factors(smoking, high BMI)and promoting early diagnosis and treatment are essential to reduce the disease burden.

Objective To screen the aging-related genes associated with prognosis in clear cell renal cell carcinoma (ccRCC), construct a prognostic model to optimize risk stratification, explore the underlying mechanisms, and provide reference for individualized diagnosis and treatment of this disease.Methods RNA sequencing data, clinical data, and aging-related genes of ccRCC were obtained from databases.After differentially expressed genes were screened, a prognostic model was constructed using Cox regression.The performance of the model was evaluated with Kaplan-Meier curves and receiver operating characteristic (ROC) curves, and validated with clinical features.Key genes were verified with immunohistochemistry.Results A total of 70 differentially expressed genes were identified, including IFI16, PECAM1, and ABCB1 as key genes, and a model formula was constructed.Internal and external validations showed that the survival rate of the high-risk group was significantly lower, with the area under the ROC curve (AUC)＞0.6.The risk score was correlated with clinical features.IFI16 was highly expressed in cancer tissues and associated with poor prognosis.Conclusion The prognostic model constructed in this study has good performance.Integrating clinical features, it can improve the accuracy of prognosis assessment of ccRCC.

Objective To describe the clinical characteristics and nutritional management status of hospitalized elderly patients with multimorbidity in a tertiary hospital's geriatric center in 2024, and to analyze the correlation between nutritional status and hospitalization outcomes, thereby providing a basis for optimizing nutritional management pathways for this population. Methods A retrospective study was conducted, including 2 937 elderly patients with multimorbidity. Data on general information, clinical indicators, nutritional risk screening and assessment, nutritional therapy, and costs were collected for descriptive analysis. The relationship between nutritional status (based on BMI and serum albumin levels) and hospitalization outcomes was explored. Results The average age of the patients was (77.45±10.70) years, with 57.17% being male. The average number of chronic diseases diagnosed was (11.56±5.08) per patient, and 26.01% were critically ill. The nutritional risk screening rate was 80.40%, with a screening positivity rate of 33.44%. The nutritional assessment rate was 31.63%, and the malnutrition prevalence was 23.08%. The low BMI group had the longest median hospital stay [15 (9.75, 22) days] and the highest hospitalization costs [15 057.2 (8 980.48, 28 160.46) CNY]. Serum albumin levels were negatively correlated with hospital stay duration (rs=-0.276, P< 0.01) and hospitalization costs (rs=-0.276, P<0.01). Conclusion Hospitalized elderly patients with multimorbidity are characterized by multiple comorbidities and high healthcare resource consumption. While the nutritional risk screening rate is relatively high, there remains room for improvement in nutritional assessment and therapy. It is necessary to strengthen standardized management throughout the entire process. Nutritional status is a significant variable affecting hospital stay duration and costs, with poorer nutritional status significantly associated with prolonged hospitalization and higher costs, suggesting that it may be an important factor influencing hospitalization outcomes.

BACKGROUND:Mitochond rial biogenesis in skeletal muscle and its regulatory mechanisms during exercise have become focal points of research.Pathways such as AMP-activated protein kinase,peroxisome proliferator-activated receptory coactivator 1α,mitogen-activated protein kinase,calcium-regulated signaling play profound roles in exercise-induced mitochondrial biogenesis,impacting muscle metabolic optimization,enhanced athletic performance,and the prevention of metabolic diseases.However,the interactions among these pathways,their regulatory mechanisms,and their comprehensive effects on exercise-induced mitochondrial biogenesis in skeletal muscle remain unclear.OBJECTIVE:To explore the signaling pathways related to mitochondrial biogenesis in skeletal muscle,precisely analyze the induction and regulatory details of exercise within these pathways,and clearly elucidate the principles by which exercise-activated signaling pathways promote mitochondrial generation and functional enhancement.This will establish a theoretical foundation for improving muscle metabolism,enhancing exercise efficiency,and preventing metabolic diseases.METHODS:An extensive literature search was conducted using China National Knowledge Infrastructure(CNKI),WanFang,VIP,PubMed,and Web of Science.The latest publications related to mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms were collected from inception to August 2024.By integrating findings from multiple signaling pathways,the regulatory mechanisms of exercise on mitochondrial biogenesis were systematically reviewed,with a focus on the interactions and synergistic mechanisms of AMP-activated protein kinase,peroxisome proliferator-activated receptor y coactivator 1α,protein kinase A,mitogen-activated protein kinase,calcium-regulated signaling pathways.RESULTS AND CONCLUSION:(1)Mitochondrial biogenesis in skeletal muscle is a complex biological process involving the coordinated regulation of multiple signaling pathways.This process aims to optimize the metabolic capacity,fatigue resistance,and overall athletic performance of skeletal muscle in response to changes in energy demand and external stress.The core mechanisms include the interactions and regulation of key factors such as AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator 1α,and mitogen-activated protein kinase.(2)AMP-activated protein kinase senses the cellular energy status and activates peroxisome proliferator-activated receptor gamma coactivator 1α,thereby promoting mitochondrial biogenesis.Peroxisome proliferator-activated receptor gamma coactivator 1α,as the main regulator of mitochondrial biogenesis in skeletal muscle,can modulate the synthesis of mitochondrial proteins and DNA,enhance the antioxidant stress response,and improve mitochondrial function.(3)The mitogen-activated protein kinase signaling pathway,particularly p38 mitogen-activated protein kinase,further promotes mitochondrial generation by activating peroxisome proliferator-activated receptor gamma coactivator 1α during stress responses.(4)Additionally,calcium signaling and protein kinase A pathways play significant roles in the metabolic regulation of skeletal muscle.(5)Exercise can significantly enhance mitochondrial biogenesis capacity in skeletal muscle by activating these multiple signaling pathways,optimizing cellular metabolic efficiency,increasing muscle endurance,and improving athletic performance.(6)Future research should focus on in-depth exploration of the interaction mechanisms among AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator1α,mitogen-activated protein kinases,and calcium signaling under different exercise intensities and modalities;strengthen studies across diverse age groups,genders,and health conditions;validate the universality and population-specificity of research findings;investigate the intricate mechanisms of emerging regulatory factors such as FNIP1 and PERM1 and their potential in exercise interventions;and promote the translation of exercise health research outcomes into clinical applications.

BACKGROUND:Mitochond rial biogenesis in skeletal muscle and its regulatory mechanisms during exercise have become focal points of research.Pathways such as AMP-activated protein kinase,peroxisome proliferator-activated receptory coactivator 1α,mitogen-activated protein kinase,calcium-regulated signaling play profound roles in exercise-induced mitochondrial biogenesis,impacting muscle metabolic optimization,enhanced athletic performance,and the prevention of metabolic diseases.However,the interactions among these pathways,their regulatory mechanisms,and their comprehensive effects on exercise-induced mitochondrial biogenesis in skeletal muscle remain unclear.OBJECTIVE:To explore the signaling pathways related to mitochondrial biogenesis in skeletal muscle,precisely analyze the induction and regulatory details of exercise within these pathways,and clearly elucidate the principles by which exercise-activated signaling pathways promote mitochondrial generation and functional enhancement.This will establish a theoretical foundation for improving muscle metabolism,enhancing exercise efficiency,and preventing metabolic diseases.METHODS:An extensive literature search was conducted using China National Knowledge Infrastructure(CNKI),WanFang,VIP,PubMed,and Web of Science.The latest publications related to mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms were collected from inception to August 2024.By integrating findings from multiple signaling pathways,the regulatory mechanisms of exercise on mitochondrial biogenesis were systematically reviewed,with a focus on the interactions and synergistic mechanisms of AMP-activated protein kinase,peroxisome proliferator-activated receptor y coactivator 1α,protein kinase A,mitogen-activated protein kinase,calcium-regulated signaling pathways.RESULTS AND CONCLUSION:(1)Mitochondrial biogenesis in skeletal muscle is a complex biological process involving the coordinated regulation of multiple signaling pathways.This process aims to optimize the metabolic capacity,fatigue resistance,and overall athletic performance of skeletal muscle in response to changes in energy demand and external stress.The core mechanisms include the interactions and regulation of key factors such as AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator 1α,and mitogen-activated protein kinase.(2)AMP-activated protein kinase senses the cellular energy status and activates peroxisome proliferator-activated receptor gamma coactivator 1α,thereby promoting mitochondrial biogenesis.Peroxisome proliferator-activated receptor gamma coactivator 1α,as the main regulator of mitochondrial biogenesis in skeletal muscle,can modulate the synthesis of mitochondrial proteins and DNA,enhance the antioxidant stress response,and improve mitochondrial function.(3)The mitogen-activated protein kinase signaling pathway,particularly p38 mitogen-activated protein kinase,further promotes mitochondrial generation by activating peroxisome proliferator-activated receptor gamma coactivator 1α during stress responses.(4)Additionally,calcium signaling and protein kinase A pathways play significant roles in the metabolic regulation of skeletal muscle.(5)Exercise can significantly enhance mitochondrial biogenesis capacity in skeletal muscle by activating these multiple signaling pathways,optimizing cellular metabolic efficiency,increasing muscle endurance,and improving athletic performance.(6)Future research should focus on in-depth exploration of the interaction mechanisms among AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator1α,mitogen-activated protein kinases,and calcium signaling under different exercise intensities and modalities;strengthen studies across diverse age groups,genders,and health conditions;validate the universality and population-specificity of research findings;investigate the intricate mechanisms of emerging regulatory factors such as FNIP1 and PERM1 and their potential in exercise interventions;and promote the translation of exercise health research outcomes into clinical applications.