Doxorubicin (DOX)-induced cardiotoxicity and sepsis-induced myocardial injury (SIMI) represent significant clinical challenges in patients undergoing chemotherapy, sharing a common pathological basis of oxidative stress and mitochondrial dysfunction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently been shown to play a critical role in DOX-induced cardiotoxicity and lipopolysaccharide (LPS)-induced SIMI. This article systematically reviews the mechanisms underlying myocardial injury caused by DOX and sepsis, identifying ferroptosis as a central common pathway. DOX triggers a burst of reactive oxygen species within mitochondria and inhibits glutathione peroxidase 4 (GPX4) activity through redox cycling of its quinone group and high-affinity accumulation in mitochondrial cardiolipin. LPS, by activating pattern recognition receptors and related inflammatory signaling pathways, provokes a cytokine storm and mitochondrial dysfunction. Both can disrupt the core regulatory axis of cysteine-glutathione (GSH)-GPX4, synergistically promoting ferroptosis in cardiomyocytes. Moreover, epigenetic regulation plays a key role in DOX- and LPS-induced cardiomyocyte ferroptosis and may serve as a promising therapeutic target. A deeper understanding of the ferroptosis mechanism and its epigenetic regulatory network in the synergistic injury induced by DOX and sepsis is of great importance for developing novel strategies to mitigate chemotherapy-related cardiotoxicity and improve outcomes in cancer patients with concurrent infections.

To develop and validate a model for predicting intensive care unit (ICU) mortality risk in patients with malignant tumors complicated by acute respiratory failure (ARF) based on an explainable machine learning framework.

Gastric variceal rupture and bleeding and hepatic encephalopathy are common and life-threatening complications in decompensated cirrhosis. As a minimally invasive interventional technique， balloon-occluded retrograde transvenous obliteration （BRTO） has made significant progress in the clinical management of gastric varices and hepatic encephalopathy in recent years. This article systematically reviews the technical principles， indications （e.g.， isolated gastric varices and refractory hepatic encephalopathy）， clinical efficacy （an acute hemostasis rate of 85% — 95%， a 1-year rebleeding rate of <15%， and an improvement rate of 60% — 80% for hepatic encephalopathy）， and safety （including complications such as renal impairment and elevated portal vein pressure） of BRTO. Meanwhile， this article discusses the advantages and disadvantages of BRTO and conventional treatment modalities （e.g.， transjugular intrahepatic portosystemic shunt and endoscopic treatment） and reviews the latest technological improvements in recent years， such as coil-assisted retrograde transvenous obliteration and plug-assisted retrograde transvenous obliteration. Future research should focus on the precision of patient selection （e.g.， stratification based on hemodynamic parameters）， the optimization of embolic materials （e.g.， application of new biodegradable embolic agents）， and the development of individualized treatment regimens， so as to improve efficacy and reduce the risk of complications.

ObjectiveTo perform metabolic associated fatty liver disease （MAFLD） screening among individuals attending community health institutions， to identify the patients at a low， moderate or high risk of advanced liver fibrosis based on fibrosis-4 index （FIB-4） and liver stiffness measurement （LSM） measured by liver transient elastography， and to implement stratified management. MethodsA cross-sectional study was conducted among 630 individuals attending Beijing Baizhifang Community Health Service Center from January to July 2024， and they were divided into MAFLD group and non-MAFLD group. According to body mass index （BMI）， the MAFLD group was further divided into lean MAFLD group （BMI<23 kg/m²） and non-lean MAFLD group （BMI≥23 kg/m²）. The above groups were compared in terms of demographic features， laboratory markers， hepatic steatosis， and LSM. Fibrosis risk stratification was performed for MAFLD patients based on FIB-4 and LSM， and a closed-loop management system involving referral to tertiary hospitals and follow-up at community health institutions was implemented. The Mann-Whitney U test was used for comparison of non-normally distributed continuous data between two groups， and the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. ResultsThere were 445 individuals （70.6%） in the MAFLD group and 185 individuals （29.4%） in the non-MAFLD group. Compared with the non-MAFLD group， the MAFLD group had a significantly lower proportion of male individuals （χ²=4.299， P<0.05）， a significant reduction in the level of high-density lipoprotein cholesterol （Z=3.484， P<0.05）， and significant increases in body weight （Z=-7.366， P<0.05）， BMI （Z=-9.740， P<0.05）， waist circumference （Z=-6.397， P<0.05）， hip circumference （Z=-6.935， P<0.05）， alanine aminotransferase （ALT） （Z=-2.765， P<0.05）， fasting blood glucose （Z=-3.646， P<0.05）， triglyceride （TG） （Z=-6.569， P<0.05）， total cholesterol （Z=-2.033， P<0.05）， low-density lipoprotein cholesterol （Z=-2.935， P<0.05）， controlled attenuation parameter （CAP） （Z=-19.784， P<0.05）， and LSM （Z=-5.703， P<0.05）. Within the MAFLD group， there were 124 individuals （27.9%） in the lean MAFLD group and 321 individuals （72.1%） in the non-lean MAFLD group. Compared with the non-lean MAFLD group， the lean MAFLD group had significantly lower body weight （Z=-12.414， P<0.05）， BMI （Z=-16.363， P<0.05）， waist circumference （Z=-7.733， P<0.05）， hip circumference （Z=-8.595， P<0.05）， ALT （Z=-2.835， P<0.05）， aspartate aminotransferase （Z=-1.972， P<0.05）， TG （Z=-2.407， P<0.05）， CAP （Z=-4.429， P<0.05）， degree of steatosis （χ²=16.588， P<0.05）， and LSM （Z=-3.908， P<0.05）. Based on the results of FIB-4 and LSM， 76 patients at a moderate or high risk of liver fibrosis should be referred to a higher-level hospital for further management. ConclusionThe detection rate of MAFLD reaches 70.6% among the individuals attending community health institutions， among whom 76 （17.1%） should be referred to a higher-level hospital. Establishing a liver fibrosis risk stratification and management system based on FIB-4 and LSM among MAFLD individuals in communities provides a practical pathway for chronic disease management and referral system construction in community health institutions.

To analyze global trends and research hotspots in exercise intervention for overweight and obesity from 2010 to 2024, to provide novel perspectives for comprehensive management research on overweight and obesity.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Prostate cancer is a common malignant tumor in males.Androgen deprivation treatment(ADT)is the main therapeutic method for prostate cancer,which often leads to changes of body composition(BC)characterized by sarcopenia,centripetal fat redistribution and osteoporosis.Imaging techniques can accurately and conveniently assess changes of BC.The research progresses of imaging evaluation on BC changes in prostate cancer patients after ADT were reviewed in this article.

Objective:To translate the European organization for research and treatment of cancer quality of life questionnaire-head and neck 43(EORTC QLQ-H&N43) and to conduct cultural debugging and reliability and validity testing for the Chinese version of the scale.Methods:The Chinese version of EORTC QLQ-H&N43 was formed through literal translation, integration, back translation, group discussion, cultural adjustment, and pre-investigation of the English version of the scale. From March 2023 to December 2023, convenience sampling was used to investigate 254 patients with head and neck tumors at the Cancer Hospital of the Chinese Academy of Medical Sciences, including 197 males and 57 females, aged (55.6±13.6) years. SPSS 25.0 statistical software was used to analyze the performance of the scale.Results:The Chinese version of EORTC QLQ-H&N43 retained all 43 items. After evaluation by 5 experts, the content validity index (I-CVI) at the item level of the scale ranged from 0.80 to 1.00, and the average content validity index (S-CVI/Ave) at the scale level was 0.991. Through exploratory factor analysis, a total of 9 common factors were extracted, with a cumulative variance contribution rate of 68.158%; Cronbach′s α coefficient of the total scale was 0.943, and the half reliability was 0.896.Conclusion:The Chinese version of EORTC QLQ-H&N43 has good reliability and validity, which can be used as an effective tool to evaluate the quality of life of head and neck cancer patients in China.

Objective:To investigate effect of cordycepin on lung injury in rats with acute respiratory distress syndrome(ARDS)and its mechanism.Methods:Sixty Wistar rats were randomly divided into control group,lipopolysaccharide group(LPS),cordyce-pin low-dose group(5 mg/kg),cordycepin medium-dose group(15 mg/kg),cordycepin high-dose group(30 mg/kg),Compound C group(high-dose cordycepin 30 mg/kg+AMPK inhibitor 15 mg/kg),with 10 rats in each group.ARDS model of LPS rats was estab-lished,pathological changes of lung tissues were observed by HE staining and lung tissue pathological injury score was performed;wet/dry weight ratio(W/D)of rat lungs was measured;activity of myeloperoxidase(MPO)was detected;IL-6,IL-1β and TNF-α were measured by ELISA;malondialdehyde(MDA),superoxide dismutase(SOD)and glutathione peroxidase(GSH)were detected by kit;Western blot was used to detect expressions of AMP-activated protein kinase(AMPK),p-AMPK,mammalian target of rapamy-cin(mTOR),p-mTOR,P70 ribosomal protein S6 kinase(p70S6K)and p-p70S6K.Results:Compared with control group,rats in LPS group had obvious lung tissue damage,and a large number of inflammatory cells infiltration,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were increased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expres-sions were increased(P<0.05),SOD,GSH levels were decreased,p-AMPK/AMPK protein expression was decreased(P<0.05);after treatment with cordycepin,lung tissue damage was reduced,a small amount of inflammatory cells were infiltrated,lung W/D,pathological injury score of lung tissue,MPO activity,IL-6,IL-1β,TNF-α,MDA levels were decreased,p-mTOR/mTOR,p-p70S6K/p70S6K protein expressions were decreased(P<0.05),SOD,GSH levels were increased,p-AMPK/AMPK protein expressions were increased(P<0.05);AMPK inhibitor Compound C reversed improvement of cordycepin on lung injury in ARDS rats.Conclusion:Cordycepin can improve LPS induced lung injury of rats,reduce inflammatory and oxidative stress,whose mechanism may be related to regulation of AMPK/mTOR/p70S6K pathway.