Lung cancer is the leading cause of cancer-related deaths worldwide， and tumor metastasis is a key factor contributing to the mortality of most lung cancer patients. Aberrant activation of epithelial-mesenchymal transition （EMT） is a major driver of lung cancer progression and metastasis. EMT is characterized by the loss of apical-basal polarity and intercellular adhesion in highly differentiated， polarized， and organized epithelial cells， which acquire motility， migratory potential， and invasive properties. During this process， cells undergo cytoskeletal remodeling and transform into a mesenchymal phenotype， accompanied by associated changes in cellular markers. The EMT process is highly complex and is tightly regulated by intricate networks involving multiple transcription factors， post-translational controls， epigenetic modifications， and non-coding RNAs. Therefore， therapies targeting the mechanisms of malignant transformation and their associated pathways in lung cancer are of significant clinical importance. In recent years， EMT has attracted increasing attention as a potential target for cancer therapy. Chinese medicine， with its characteristics of multi-target action， low side effects， and good therapeutic efficacy， has demonstrated an important role in anticancer treatment. A series of studies have investigated the role of Chinese medicine in inhibiting EMT in lung cancer. Active ingredients of Chinese medicine， including flavonoids， glycosides， phenols， terpenoids， saccharides， and alkaloids， as well as Chinese medicine compound formulas， have shown significant regulatory effects on EMT. Their mechanisms mainly involve multiple pathways， targets， and links， including signaling pathways， exosomes， microRNAs （miRNAs）， and the tumor-associated immune microenvironment. This article summarizes the mechanisms by which EMT promotes malignant tumor progression and reviews the current research on how Chinese medicine active ingredients， monomers， and compound formulas inhibit EMT and suppress lung cancer cell migration and invasion. This study is expected to provide comprehensive theoretical information for basic and translational research on lung cancer.

Objective To explore the effects of 1 800 MHz electromagnetic radiation(EMR)on cognitive function of 3xTg-AD and 57C mice,providing a theoretical basis for the potential impacts of electromagnetic radiation on the human body.Methods A total of 12 3xTg-AD transgenic mice and 12 wild-type C57 mice were selected as research subjects.The one-month-old mice were divided into four groups:RF WT,Control WT,RF AD,and Control AD,with 6 mice in each group.The 1 800 MHz EMR exposure experiments were conducted from 20:00 to 8:00 the next day for a duration of 5 months.After the exposure,a water maze test was conducted to evaluate the effects of EMR on spatial learning and memory abilities of 3xTg AD mice,along with measurements of body weight,brain weight,and calculation of the brain-to-body ratio.Finally,Western Blot technique was used to measure the levels of APP,NR1,and NR2A in hippocampal tissue to analyze effects of 1 800 MHz EMR on the cognitive function of 3xTg AD mice.Results Under 1 800 MHz EMR exposure,there were no statistically significant differences in Morris water maze spatial learning ability among the four groups(P>0.05).However,longer escape time,greater swimming distances,and more crossings of target quadrant were exhibited in the RF AD group compared to the other groups(P<0.05).Western Blot results showed that the APP protein levels in 3xTg AD mice was higher than those in C57 mice(P<0.05).The expression levels of NR1 protein in the WT group was higher than those in the AD group(P<0.05);in the AD group,the RF AD group had higher levels than the Control WT group(P<0.05),and the NR2A protein levels in the Control WT group were higher than in the other groups(P<0.05).Conclusion Prolonged exposure to 1 800 MHz EMR can affect the learning and cognitive function of both 3xTg AD and C57 mice.

Objective To assess the prevalence and clinical features of nonalcoholic fatty liver disease(NAFLD)and its risk factors in patients with CHF,so as to provide the reference for early identification of NAFLD.Methods The data from 1120 CHF patients aged 14～89 was collected,including the general demographic information(age,gender,smoking status,height,weight,BMI,etc.),clinical diagnosis and treatment data(blood pressure,NYHA heart function classification,blood biochemical indicators,etc.),and medication use status.SPSS 27.0 was applied to analyze the clinical characteristics of CHF combined with NAFLD,and binary multivariate logistic regression was used to analyze the independent risk factors of CHF combined with NAFLD.Results Among the 1120 patients,634(56.6%)were male and 486(43.4%)were female.The prevalence of CHF patients with NAFLD was 25.0%.The results of univariate analysis showed that the weight of NAFLD patients BMI,systolic blood pressure,diastolic blood pressure,FPG,UA,left room expansion ratio,ALT,CHO,TG,obesity rate,hyperuricemia rate and β-blocker usage rate were all higher than those of non NAFLD patients.The age,BNP,HDL and ACEI/ARB/ARNI usage rate of NAFLD patients were lower than those of non NAFLD patients(all P<0.05).Logistic regression analysis showed that age(OR=0.988),FPG(OR=1.099),overweight(OR=3.497)and obesity(OR=9.193)were independent risk factors for CHF patients with NAFLD.Conclusion NAFLD may be a common complication in CHF patients,especially those who are young,have high FPG,overweight and obese.In the clinical practice,NAFLD screening,evaluation and management should be focused on CHF patients who are young,have high fasting blood sugar,overweight,and obese.

Objectives To identify key clinical factors influencing recurrence in osteosarcoma patients,to construct and validate a Nomogram-based recurrence risk prediction model,thereby providing a quantitative tool for clinical decision-making and recurrence prevention/control.Methods Clinical data of 469 osteosarcoma patients admitted to Yunnan Cancer Hospital between 2013～2022 were retrospectively collected.Statistical analysis was performed using R software(version 4.3.2).Potential influencing factors were initially screened via univariate analysis and LASSO regression analysis.Independent predictors of osteosarcoma recurrence were then identified using multivariate logistic regression analysis.Based on the identified independent factors,a Nomogram prediction model for recurrence risk was constructed.The area under the receiver operating characteristic curve(AUC)was used to evaluate the model's discriminative ability.Results Among the entire cohort,68 patients experienced recurrence,yielding a recurrence rate of 14.50%.Multivariate analysis identified the following as independent predictors of recurrence:Primary Tumor Location:Tibial lesions(P=0.009)were associated with a significantly lower recurrence risk compared to femoral lesions(OR=0.297),while lesions in"Other Bones"(P=0.008)carried a significantly higher risk(OR=3.294).Biopsy Method:Needle biopsy(P=0.033)was associated with a significantly lower recurrence risk compared to open biopsy(OR=0.461).Lung Metastasis Status:Patients with lung metastasis(P<0.001)had a significantly higher recurrence risk than those without(OR=11.873).Lymphocyte Count:A higher lymphocyte count(P=0.001)was a protective factor,associated with a lower recurrence risk(OR=0.450).The constructed Nomogram prediction model demonstrated excellent performance:Validation results showed an AUC=0.842(95%CI:0.806～0.875),indicating outstanding discriminative ability.Conclusions This study successfully constructed and validated a Nomogram prediction model for osteosarcoma recurrence risk integrating key clinical factors.The model demonstrates superior discriminative ability and can accurately and quantitatively assess the recurrence risk for individual patients.This tool thus provides critical reference for guiding clinical treatment decisions.

Hereditary spastic paraplegia type 58 is rare, caused by pathogenic variations in KIF1C gene. Here, a case diagnosed in Qilu Hospital, Shandong University, was reported. The 15-year-old female suffered tremor in bilateral upper limbs which was aggravated gradually since age 8. Cerebellar ataxia, positive pyramidal tract sign and dystonic tremor were prominent on physical examination. The brain magnetic resonance imaging showed T 2-hyperintense signals in bilateral pyramidal tracts, optic radiations and superior cerebellar peduncles, with mild cerebellar atrophy. Whole exon sequencing revealed the unreported homozygous c.425_426delTG (p.V142Gfs*10) mutation which was presumed pathogenic.

BACKGROUND: Excessive exposure to fluoride can reduce intelligence. Methylenetetrahydrofolate dehydrogenase, cyclohydrolase, and formyltetrahydrofolate synthetase 1 ( MTHFD1 ) polymorphisms have important roles in neurodevelopment. However, the association of MTHFD1 polymorphisms with children's intelligence changes in endemic fluorosis areas has been rarely explored. METHODS: A cross-sectional study was conducted in four randomly selected primary schools in Tongxu County, Henan Province, from April to May in 2017. A total of 694 children aged 8 to 12 years were included in the study with the recruitment by the cluster sampling method. Urinary fluoride (UF) and urinary creatinine were separately determined using the fluoride ion-selective electrode and creatinine assay kit. Children were classified as the high fluoride group and control group according to the median of urinary creatinine-adjusted urinary fluoride (UF Cr ) level. Four loci of MTHFD1 were genotyped, and the Combined Raven's Test was used to evaluate children's intelligence quotient (IQ). Generalized linear model and multinomial logistic regression model were performed to analyze the associations between children's UF Cr level, MTHFD1 polymorphisms, and intelligence. The general linear model was used to explore the effects of gene-environment and gene-gene interaction on intelligence. RESULTS: In the high fluoride group, children's IQ scores decreased by 2.502 when the UF Cr level increased by 1.0 mg/L (β = -2.502, 95% confidence interval [CI]:-4.411, -0.593), and the possibility for having "excellent" intelligence decreased by 46.3% (odds ratio = 0.537, 95% CI: 0.290, 0.994). Children with the GG genotype showed increased IQ scores than those with the AA genotype of rs11627387 locus in the high fluoride group ( P   <  0.05). Interactions between fluoride exposure and MTHFD1 polymorphisms on intelligence were observed (Pinteraction < 0.05). CONCLUSION Our findings suggest that excessive fluoride exposure may have adverse effects on children's intelligence, and changes in children's intelligence may be associated with the interaction between fluoride and MTHFD1 polymorphisms.
Child ; Creatinine ; Cross-Sectional Studies ; Fluorides/urine* ; Formate-Tetrahydrofolate Ligase ; Humans ; Intelligence/genetics* ; Methylenetetrahydrofolate Dehydrogenase (NADP) ; Methylenetetrahydrofolate Reductase (NADPH2)

Objective:To evaluate the intervention effect of various drugs on glutathione (GSH) and superoxide dismutase (SOD) enzyme activity of rats kidney with acute nickel carbonyl poisoning.Methods:In January 2019, The 250 SPF male SD rats were randomly divided into normal control group ( n=10) , poisoned group ( n=40) and treatment groups ( n=200) according to the random number table method. And the treatment groups were divided into methylprednisolone group (20 mg/kg) , DDC group (100 mg/kg) , sodium selenite group (10 μmol/kg) , Shenfu huiyang decoction group (0.25 ml) and methylprednisolone combined with DDC group (100 mg/kg) , with 40 mice in each group. Except for the normal control group, rats in the other groups were exposed to nickel carbonyl for 30 min, at 4 h and 30 h after exposure, the rats in each treatment group were intraperitoneally injected with corresponding drugs, and kidney tissues were collected 3 d and 7 d after administration, with 10 mice in each group. The activities of GSH and SOD in kidney were measured by enzyme-linked immunosorbent assay, and using electron microscopy observe ultrastructure changes. Results:Compared to the control group, the activities of GSH and SOD enzyme of poisoned group were significantly decreased at 3 d or 7 d after 4 h or 30 h exposure, and the difference was statistically significant ( P=0.000, 0.031, 0.001, 0.033) , the epithelial nuclei of proximal convoluted tubules were pyknosis and lysosome hyperplasia in the cytoplasm. And compared to poisoned group, the activities of GSH and SOD enzyme of methylprednisolone+DDC group were significantly increased at treatment with 7 d after 4 h exposure, the difference was statistically significant ( P=0.022, 0.000) , and the activities of GSH and SOD enzyme of methylprednisolone and enzyme of methylprednisolone+DDC group were significantly higher at 7 days than at 3 days, the difference was statistically significant ( P=0.020, 0.017, 0.018, 0.033) . The results of electron microscopy showed that the cell nuclei and cytoplasmic organelles of proximal convolute tubule were almost restored to normal tissue level of both methylprednisolone group and methylprednisolone+DDC group. Conclusion:The methylprednisolone and methylprednisolone+DDC have obvious repair effect on renal enzyme activity level of rats with acute nickel carbonyl poisoning, and the treatment effect is better for a long time of medication.

Objective:To evaluate the intervention effect of various drugs on glutathione (GSH) and superoxide dismutase (SOD) enzyme activity of rats kidney with acute nickel carbonyl poisoning.Methods:In January 2019, The 250 SPF male SD rats were randomly divided into normal control group ( n=10) , poisoned group ( n=40) and treatment groups ( n=200) according to the random number table method. And the treatment groups were divided into methylprednisolone group (20 mg/kg) , DDC group (100 mg/kg) , sodium selenite group (10 μmol/kg) , Shenfu huiyang decoction group (0.25 ml) and methylprednisolone combined with DDC group (100 mg/kg) , with 40 mice in each group. Except for the normal control group, rats in the other groups were exposed to nickel carbonyl for 30 min, at 4 h and 30 h after exposure, the rats in each treatment group were intraperitoneally injected with corresponding drugs, and kidney tissues were collected 3 d and 7 d after administration, with 10 mice in each group. The activities of GSH and SOD in kidney were measured by enzyme-linked immunosorbent assay, and using electron microscopy observe ultrastructure changes. Results:Compared to the control group, the activities of GSH and SOD enzyme of poisoned group were significantly decreased at 3 d or 7 d after 4 h or 30 h exposure, and the difference was statistically significant ( P=0.000, 0.031, 0.001, 0.033) , the epithelial nuclei of proximal convoluted tubules were pyknosis and lysosome hyperplasia in the cytoplasm. And compared to poisoned group, the activities of GSH and SOD enzyme of methylprednisolone+DDC group were significantly increased at treatment with 7 d after 4 h exposure, the difference was statistically significant ( P=0.022, 0.000) , and the activities of GSH and SOD enzyme of methylprednisolone and enzyme of methylprednisolone+DDC group were significantly higher at 7 days than at 3 days, the difference was statistically significant ( P=0.020, 0.017, 0.018, 0.033) . The results of electron microscopy showed that the cell nuclei and cytoplasmic organelles of proximal convolute tubule were almost restored to normal tissue level of both methylprednisolone group and methylprednisolone+DDC group. Conclusion:The methylprednisolone and methylprednisolone+DDC have obvious repair effect on renal enzyme activity level of rats with acute nickel carbonyl poisoning, and the treatment effect is better for a long time of medication.

Antibodies, Neutralizing/immunology* ; Antibodies, Viral/immunology* ; COVID-19/virology* ; COVID-19 Vaccines/immunology* ; Humans ; SARS-CoV-2/pathogenicity* ; Spike Glycoprotein, Coronavirus/immunology* ; Vaccines, Inactivated/immunology*

Objective:To explore the factors affecting bone mineral density (BMD) in adult males with low-to-moderate fluoride exposure in Henan Province.Methods:Adult male villagers from low-to-moderate fluoride exposure areas in Tongxu County, Kaifeng City, Henan Province were recruited from April to May 2017 based on cluster random sampling. Questionnaire survey, physical measurements and urinary samples collection were conducted respectively. Urinary fluoride (UF) was determined by fluoride ion-selective electrode. Ultrasound bone densitometer was used to measure BMD (T-score). Partial correlation analysis and multiple linear regression were used to analyze the influence factors of BMD.Results:A total of 439 adult males were included in this study. Age, body mass index (BMI), UF content, and T-score of the participants were (47.99 ± 8.49) years, (25.77 ± 3.23) kg/m 2, (1.34 ± 0.74) mg/L, and-1.79 ± 0.79, respectively. Partial correlation analysis showed a significantly positive correlation between BMI and T-score after age adjustment ( r = 0.194, P < 0.05). Multiple linear regression showed that T-score decreased by 0.015 (95% CI:-0.024 -- 0.005, P < 0.05) for each 1-year increase in age and T-score increased by 0.034 (95% CI: 0.009-0.059, P < 0.05) for each 1.0 kg/m 2 increase in BMI. Interaction analysis showed that T-score was closely related to the interaction between overweight (≥24.0 kg/m 2), non-smoking, tea drinking and UF [ β (95% CI): 0.134 (0.001-0.269), 0.163 (- 0.015-0.337), 0.215 (- 0.006-0.436), P < 0.10]. Conclusions:Our findings reveal a negative correlation between age and BMD, and a positive correlation between BMI and BMD in adult males with low-to-moderate fluoride exposure in Henan Province. In addition, low-to-moderate fluoride exposure is more likely to damage the BMD of smokers.