Esophageal cancer is a prevalent malignant tumor of the digestive tract in China, and radical surgery remains the cornerstone of its comprehensive treatment. However, multifactorial challenges such as postoperative gastrointestinal tract reconstruction, traumatic stress, and tumor-related metabolic disturbances render esophageal cancer patients highly susceptible to malnutrition. Perioperative nutritional support therapy plays a crucial role in enhancing surgical safety, improving clinical outcomes, and elevating patients' quality of life by regulating metabolic homeostasis, preserving organ function, and optimizing the immune microenvironment. This article reviews the mechanisms underlying malnutrition in esophageal cancer, methods for nutritional status assessment, and precision intervention pathways based on multi-omics evaluations. The aim is to strengthen clinicians' awareness of standardized perioperative nutritional management for esophageal cancer patients and promote its clinical implementation, thereby facilitating postoperative recovery and improving long-term quality of life.

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 explore the therapeutic efficacy and mechanism of oridonin （ORI） against obesity-related glomerulopathy （ORG） based on the liver X receptor α （LXRα） signaling pathway. METHODS Kidney tissues of LXRα wild-type homozygous （LXRα+/+） mice and LXRα homozygous knockout （LXRα－/－） mice were subjected to high-throughput renal transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis to predict key pathways and targets regulated by LXRα， followed by verification via Western blot assay. An ORG mouse model was established by feeding a high-fat diet. The LXRα agonist GW3965 （30 mg/kg） was set as the positive control. After intragastric administration of 50 mg/kg and 100 mg/kg ORI once daily for 4 consecutive weeks， the body weight， renal weight， renal histopathological alterations， serum renal function indicators， blood lipid levels and inflammatory factor levels in renal tissue of mice were detected and observed to evaluate the efficacy of ORI in alleviating ORG. Meanwhile， the mRNA and protein expression levels of LXRα and its downstream targets in mouse renal tissues were detected to validate the mechanism by which ORI relieves ORG. RESULTS Compared with LXRα+/+ mice， the upregulated differentially expressed genes in renal tissues of LXRα－/－ mice were significantly enriched in the arachidonic acid（AA） metabolic pathway， and the expression level of Cyp4a12 was markedly elevated （adjusted P＜0.05）. Western blot results verified that cytochrome P450 family 4 subfamily A member 12（CYP4A12）protein expression was significantly increased in the kidneys of LXRα－/－ mice （P＜0.05）. Pharmacodynamic results showed that both 50 mg/kg and 100 mg/kg ORI notably improved renal pathological lesions in ORG mice； these two doses reduced body weight， renal weight， serum creatinine， blood urea nitrogen， blood lipid levels as well as renal interleukin-6 （IL-6） and IL-1β levels （P＜0.05）. In addition， ORI significantly upregulated the mRNA and protein expression of renal nuclear LXRα and ABCA1， and downregulated the mRNA and protein expression of CYP4A12（P＜0.05）. CONCLUSIONS ORI may exert an ameliorative effect on ORG by activating the LXRα signaling pathway， downregulating CYP4A12 expression， and inhibiting AA-induced inflammatory metabolism.

Hepatocellular carcinoma (HCC) imposes a major health and economic burden worldwide, with disproportionate effects in low- and middle-income countries (LMICs). Surveillance in high-risk populations, typically using semiannual ultrasound and alpha-fetoprotein testing, has been shown to be cost-effective by enabling earlier detection and improving survival. Yet, its overall value is reduced by poor adherence and the limited sensitivity of ultrasound, particularly in patients with metabolic-associated steatotic liver disease. Emerging approaches—including abbreviated magnetic resonance imaging, multi-biomarker models (e.g., gender, age, AFP, AFP-L3, and DCP), and liquid biopsy assays such as methylated DNA markers—demonstrate greater diagnostic accuracy and potential economic advantages compared with conventional methods. Integration of artificial intelligence into imaging may further enhance efficiency and reduce downstream costs. Moving toward precision surveillance, guided by individualized risk stratification that incorporates etiology, fibrosis stage, and molecular profiles, can optimize allocation of resources and maximize cost-effectiveness at the population level. Interventions to improve adherence, including mailed outreach and behavioral economic incentives, have shown both clinical benefit and cost savings, underscoring the role of implementation science. Because socioeconomic disparities influence both access and outcomes, economic models must explicitly address equity to achieve sustainable impact. Future research should prioritize prospective trials that evaluate not only clinical performance but also the real-world cost-effectiveness of novel technologies and stratified surveillance strategies. For LMICs, adapting proven models into affordable, context-appropriate programs is essential. By combining prevention, precision risk assessment, innovative technologies, and equitable implementation, HCC surveillance can deliver both clinical and economic value, reducing the global burden of disease.

ObjectiveTo explore the clinical potential of magnetic resonance elastography （MRE） for assessing the stiffness of common intracranial tumors. MethodsA retrospective analysis was conducted on 47 patients with brain tumors who underwent surgical treatment at The First Affiliated Hospital of Sun Yat-sen University between April 2023 and September 2024. The cohort included 10 cases of glioma， 12 cases of vestibular schwannoma， and 25 cases of meningioma. All patients underwent multiparameter MRI and MRE preoperatively. After co-registering MRE images with contrast-enhanced 3D T1-weighted images， three regions of interest （ROIs） were placed in the areas of maximum and minimum tumor stiffness respectively to measure the shear stiffness values， and the mean was calculated as the average shear stiffness. Additionally， one ROI was placed in the white matter and one in the grey matter of the posterior horn of the lateral ventricle at the basal ganglia level to obtain normal reference values. A neurosurgeon， blind to the MRE results， graded the intraoperative tumor stiffness based on surgical videos using a 5-point scale （1： soft； 5： hard）. Intraclass correlation coefficient （ICC） was used to assess inter-observer consistency. Analysis of variance （ANOVA） and nonparametric tests were employed to compare the differences of shear stiffness values between groups. Spearman correlation analysis was used to examine the correlation between elasticity values and clinicopathological parameters. The discriminatory efficacy of shear stiffness values for tumor types was evaluated with receiver operating characteristic （ROC） curves. ResultsThe ICCs for elasticity values measured by two physicians in the hardest and softest tumor areas were 0.868 and 0.831， respectively （both P＜ 0.01）. The maximum， minimum， and average shear stiffness values of meningiomas［（1.91±0.28） m/s， （1.66±0.25） m/s， （1.78±0.26） m/s， respectively］ were significantly higher than those of gliomas［（1.59±0.23） m/s， （1.42±0.23） m/s， （1.50±0.22） m/s， respectively （P＜0.05）］. The shear stiffness values of vestibular schwannomas［（1.70±0.30） m/s， （1.51±0.23） m/s， （1.61±0.26） m/s， respectively） were lower than those of meningiomas and higher than those of gliomas， but these differences were not statistically significant （both P＞0.05）. The shear stiffness values of white matter were significantly higher than that of grey matter［（1.63±0.08） m/s vs. （1.39±0.12） m/s， P＜0.05）］. In the overall sample， the maximum， minimum， and average shear stiffness values were significantly positively correlated with the intraoperative hardness grade （r_s = 0.591， r_s = 0.541， r_s = 0.571， respectively； all P＜0.001）， negatively correlated with WHO grade （r_s = -0.458， r_s = -0.458， r_s = -0.480， respectively； all P＜0.01）， but showed no correlation with Ki-67 （all P＞0.05）. ConclusionMRE can be used to assess the stiffness of intracranial tumors and to some extent differentiate between tumor types， which aids in formulating more individualized preoperative surgical plans.

ObjectiveTo characterize the features of etomidate-related criminal cases in Guangxi after its formal scheduling as a controlled substance in China. MethodsWe collected judicial documents of etomidate-related criminal cases in Guangxi， published on China Judgments Online from October 2023 to July 2025. Demographic， criminological， and forensic toxicological characteristics were extracted. We analyzed the differences in demographic characteristics between the offenders and the baseline of the general population in Guangxi， and examined the associations of age， educational attainment， prior criminal conviction， and employment status with offense types. ResultsA total of 51 adjudicated cases were included， involving 174 individuals. The offenders were predominantly male， young adults， with low educational attainment， prior criminal convictions， and unemployed status. Statistically significant differences were observed between the offenders and the baseline of the general population in Guangxi across four dimensions： gender， age， educational attainment， and employment status （all P values＜0.01）. The primary offense types were the crime of providing shelter for others to use drugs and drug trafficking offenses. The majority of cases involved joint offenses committed by multiple perpetrators， with e-cigarettes and related products as the main drug delivery vehicles. Forensic toxicological testing confirmed concurrent polydrug use of etomidate and ketamine among the involved individuals. Prior criminal conviction status was statistically associated with the choice of offense type （Fisher's P = 0.006）. Offenders with prior convictions predominantly committed single-type offenses， while those without prior convictions accounted for a significantly higher proportion of multiple concurrent offenses relative to the former group. ConclusionAfter the scheduling of etomidate， the offender population in etomidate-related criminal cases in Guangxi is characterized by low educational attainment， low employment rate， and high prevalence of prior criminal convictions. The offenses exhibited covert modus operandi， group-based offending patterns， and a growing trend of polydrug use. We recommend strengthening the monitoring of high-risk populations and upgrading the technical system of forensic toxicological testing to address the challenges posed by emerging illicit drugs.

ObjectiveTo investigate the clinicopathological features， molecular profile， treatment response， and prognosis of SMARCA4 （BRG-1） and SMARCB1 （INI-1）-deficient undifferentiated tumors of the digestive system， aiming to enhance the understanding of this rare and highly aggressive molecular subtype. MethodsThis study is a single-center retrospective analysis. We included 9 cases of malignant digestive system tumors with loss of BRG-1 expression and 3 cases with loss of INI-1 expression， all pathologically confirmed at Sun Yat-sen University Cancer Center between April 2022 and December 2025. By reviewing clinical data， histological morphology，immunohistochemistry and next-generation sequencing （NGS） results from partial cases， we systematically summarized their clinicopathological and molecular characteristics， treatment strategies， and survival outcomes. Results​ Among the 12 patients， 6 were male and 6 were female， with a median age of 62 （44-70） years. 9 cases exhibited SMARCA4 deficiency， and 3 cases exhibited SMARCB1 deficiency. Tumors originated in the stomach （5 cases）， colon （3 cases）， pancreas （1 case）， with the primary site unknown in 3 cases. The histology predominantly showed undifferentiated carcinoma， with 1 case of poorly differentiated carcinoma. The tumor cells were epithelioid with significant atypia. Epithelial markers （e.g. CKpan） were often lost or markedly decreased， while vimentin could be positive. All 9 cases tested for MMR status were mismatch repair proficient （pMMR）， and the Ki-67 proliferation index was high ［median 80% （60%-90%）］. A discordance was observed between IHC findings and NGS results in the 6 sequenced cases. The NGS profiling revealed frequent co-occurring mutations， including TP53， KRAS， and NRAS， with no germline mutations identified.The median follow-up time was 277 （55-867） days. 9 of the 12 patients presented with stage Ⅳ disease at the time of initial diagnosis. Among 3 newly diagnosed patients without metastasis who received treatment， 2 achieved prolonged recurrence-free survival. Patients with advanced disease at initial diagnosis primarily underwent platinum-based chemotherapy or combination regimens， yet their prognosis was generally poor， with a median overall survival of 60 （45-541） days， ranging from 16 to 867 days. Notably， several patients who received chemotherapy combined with targeted therapy and immunotherapy achieved extended survival. ConclusionSMARCA4/SMARCB1-deficient undifferentiated tumor of the digestive system is a distinct molecular subtype characterized by high aggressiveness and poor prognosis， predominantly affecting middle-aged and elderly individuals. Diagnosis relies on the immunohistochemical loss of BRG-1 or INI-1 proteins. While no standard of care currently exists， treatment often refers to regimens for adenocarcinoma of the primary site. Combined immunotherapy and targeted therapy may offer potential benefits， warranting further validation in large-scale prospective studies.

ObjectiveTo investigate whether photoreceptor-specific knockout of lanosterol synthase （Lss） induces age-related retinal degeneration and to elucidate the underlying molecular mechanisms. MethodsPhotoreceptor-specific Lss knockout mice （Lss^flox/flox； Rho-Cre， CKO） models were established. Retinal structure and function were assessed at 1， 4， and 8 months of age using fundus photography， optical coherence tomography （OCT）， scotopic electroretinogram （ERG） and hematoxylin and eosin （HE） staining. The mouse photoreceptor cell line 661W served as an in vitro model. Lss was knocked down via siRNA， followed by analyses including Seahorse XF mitochondrial stress test， JC-1， MitoSOX Red and DCFH-DA probes to evaluate mitochondrial function and oxidative stress， glycolytic rate assay for glycolysis ability， RT-qPCR for inflammatory factors， γH2AX immunofluorescence for double-strand DNA damage detection， and transcriptome sequencing to identify differentially expressed genes and enriched pathways. ResultsCompared with controls， 1-month-old CKO mice showed no abnormalities. Mild fundus lesions appeared at 4 months. By 8 months， CKO mice exhibited significant thinning of the outer nuclear layer， disorganization of the inner/outer segment structure， and markedly reduced amplitudes of the dark-adapted ERG a- and b-waves （P<0.05）. Transcriptome analysis revealed 1 842 differentially expressed genes （826 up-regulated， 1 016 down-regulated）， with Lss being the most significantly downregulated gene； these genes significantly enriched in sterol biosynthesis， oxidative phosphorylation， aerobic electron transport chain， and ATP synthesis （P<0.05）. In 661W cells， knockdown of Lss significantly reduced mitochondrial basal respiration （P=0.006）， ATP production （P=0.015）， maximal respiration （P<0.001）， and spare respiratory capacity （P<0.001）， while basal glycolysis （P=0.005） and compensatory glycolysis （P=0.028） were increased. These changes were accompanied by mitochondrial membrane potential depolarization （P<0.001）， elevated mitochondrial reactive oxygen species （ROS） levels （P<0.001）， and increased total ROS levels （P=0.013）. Additionally， the mRNA expression of inflammatory factors， including Ccl2 （P=0.004）， Ccl5 （P=0.012）， Cxcl1 （P<0.001）， Cxcl5 （P<0.000 1）， Tgfb （P=0.008）， Hgf （P<0.000 1） and Mmp3 （P=0.003） was significantly upregulated. Moreover， γH2AX fluorescence intensity was increased （P=0.002）. ConclusionsPhotoreceptor-specific Lss deficiency induces mitochondrial dysfunction， oxidative stress and cellular inflammation， ultimately leading to age-dependent retinal degeneration. This study provides novel mechanistic insights and potential therapeutic targets for hereditary and age-related retinal degenerative diseases.

ObjectiveTo investigate the inhibitory effect of tauroursodeoxycholic acid （TUDCA） on neurogenic heterotopic ossification （NHO） after spinal cord injury and its potential mechanism. MethodsSPF-grade male C57BL/6 mice were used to establish an NHO model. The mice were randomly divided into three groups： sham operation group （laminectomy only）， NHO model group （spinal cord injury + intramuscular injection of cardiotoxin）， and TUDCA treatment group （NHO model + daily intragastric administration of TUDCA at 200 mg/kg for 4 consecutive weeks）. The area and maturity of heterotopic ossification were quantitatively assessed by micro-computed tomography（micro-CT） and hematoxylin-eosin（H&E） staining. Flow cytometry was used to quantify the interleukin（IL）-1β secretion level of M2 macrophages. RAW264.7 macrophages were cultured in vitro and divided into control， tumor necrosis factor（TNF）α， and TNFα+TUDCA （200 μmol/L） groups to detect the expression level of the polarization marker CD206. Additionally， macrophages were divided into control， TUDCA 200 μmol/L， and TUDCA 400 μmol/L groups to assess the IL-1β secretion level. ResultsCompared with the NHO group， the bone volume in the TUDCA-treated group was significantly reduced （12.69±1.13 vs. 7.647±1.19， P=0.003）. Compared with the TNFα group， qPCR results showed that the expression of the M2 macrophage marker CD206 was significantly upregulated in the TNFα+TUDCA group （0.55±0.019，1.11±0.023， P＜0.001）. Compared with the control group， ELISA results showed that TUDCA stimulation of macrophages significantly upregulated IL-1β secretion （404.7±24.38 vs. 652.8±32.61， P=0.003 7）. TUDCA administration upregulated IL-1β secretion by local muscle macrophages and inhibited heterotopic ossification formation. ConclusionsTUDCA might participate in inhibiting NHO formation by inducing M2 macrophage polarization and upregulating IL-1β secretion， thereby alleviating the development and progression of neurogenic heterotopic ossification after spinal cord injury. This finding provides experimental evidence for expanding the application of TUDCA in the treatment of complications following spinal cord injury.