ObjectiveThis study aimed to investigate the anti-Mycoplasma pneumoniae (MP) activity of luteolin and elucidate its underlying mechanisms. MethodsLuteolin was identified as the primary active compound from the polyphenol extract ofF. diotrys using network pharmacology. Its efficacy was evaluated against two MP strains: the standard strain M129 and the multidrug-resistant strain M19. A modified culture medium with visual characteristics was employed to determine the minimum inhibitory concentration (MIC) of luteolin. The expression of key proteins involved in MP growth and pathogenicity was assessed by qRT-PCR following luteolin treatment. Additionally, the viability of A549 cells infected with MP was compared between luteolin-treated and untreated groups. In vivo anti-MP activity was evaluated using a mouse model, and the expression of inflammatory cytokines in lung tissues was analyzed. ResultsLuteolin effectively inhibited both MP strains, with MIC₉₀ values of 100 mg/L for M19 and M129. Treatment with luteolin significantly downregulated the expression of adhesion proteins P1 and P30 in both strains. However, the expression of P65, HMW3, TrmB, and CARDS TX was reduced only in the M19 strain following luteolin intervention. Luteolin also enhanced the growth and viability of A549 cells infected with MP. In the mouse model, luteolin treatment resulted in steady weight gain and was well tolerated. The bacteriostatic rate of luteolin in lung tissues was 50.7%, significantly higher than the 25.2% observed in the roxithromycin group. Furthermore, luteolin reduced the expression of inflammatory factors, including IL-6, TNF-α, and HMGB1, in MP-infected mice. ConclusionLuteolin effectively and safely inhibits the proliferation and pathogenicity of MP, particularly the drug-resistant M19 strain, by downregulating the expression of toxicity-associated proteins (P1, P30, P65, HMW3, TrmB, CARDS TX) and modulating host inflammatory responses. These findings suggest that luteolin may offer a novel therapeutic strategy for treating MP infections, especially those caused by drug-resistant strains.

Objective To explore the prevalence of depressive symptoms in postoperative patients with ovarian cancer and to analyze its influencing factors from multiple dimensions, including clinical characteristics, psychological factors, and laboratory indicators. Methods A cross-sectional study was conducted, which enrolled 235 postoperative patients with ovarian cancer. Depressive status was assessed using the patient health questionnaire, and the demographic, pathological, and medical record data of the patients were collected using the generalized anxiety disorder scale, Pittsburgh sleep quality index, European organization for research and treatment of cancer quality of life questionnaire core 30, and ECOG performance status score. Peripheral blood tumor marker (CA125), routine blood test, lymphocyte subsets, and serum cytokine levels were measured. Univariate and multivariate binary logistic regression analysis were used for statistical analysis. Results The prevalence of depression in postoperative patients with ovarian cancer was 39.15% (92/235). Univariate analysis showed that ECOG score ≥ 2 points, pain, anxiety, poor sleep quality, low quality of life, low life satisfaction, tumor recurrence, six or more cycles of chemotherapy, as well as higher levels of CA125, NLR, and NAR, and lower hemoglobin levels were significantly associated with depression (all P<0.05). Multivariate binary Logistic regression analysis showed that anxiety (OR=1.975, 95%CI: 1.231-3.170), sleep efficiency (OR=4.181, 95%CI: 1.211-14.43), sleep latency (OR=34.806, 95%CI: 4.258-284.542), ECOG performance status score, cognitive function (OR=0.918, 95%CI: 0.868-0.97), and life satisfaction were independent risk factors for depression (all P<0.05). Laboratory indicators were not independent influencing factors in the multivariate Logistic regression model. Conclusion Depression in postoperative patients with ovarian cancer is influenced by physiological, psychological, and social factors. Clinical management should focus on patients with anxiety, sleep disorders, poor physical condition, and low life satisfaction, and a comprehensive prevention and treatment strategy centered on psychological intervention and taking into account symptom management and social support should be implemented.

ObjectiveThis study aimed to investigate the anti-Mycoplasma pneumoniae (MP) activity of luteolin and elucidate its underlying mechanisms. MethodsLuteolin was identified as the primary active compound from the polyphenol extract ofF. diotrys using network pharmacology. Its efficacy was evaluated against two MP strains: the standard strain M129 and the multidrug-resistant strain M19. A modified culture medium with visual characteristics was employed to determine the minimum inhibitory concentration (MIC) of luteolin. The expression of key proteins involved in MP growth and pathogenicity was assessed by qRT-PCR following luteolin treatment. Additionally, the viability of A549 cells infected with MP was compared between luteolin-treated and untreated groups. In vivo anti-MP activity was evaluated using a mouse model, and the expression of inflammatory cytokines in lung tissues was analyzed. ResultsLuteolin effectively inhibited both MP strains, with MIC₉₀ values of 100 mg/L for M19 and M129. Treatment with luteolin significantly downregulated the expression of adhesion proteins P1 and P30 in both strains. However, the expression of P65, HMW3, TrmB, and CARDS TX was reduced only in the M19 strain following luteolin intervention. Luteolin also enhanced the growth and viability of A549 cells infected with MP. In the mouse model, luteolin treatment resulted in steady weight gain and was well tolerated. The bacteriostatic rate of luteolin in lung tissues was 50.7%, significantly higher than the 25.2% observed in the roxithromycin group. Furthermore, luteolin reduced the expression of inflammatory factors, including IL-6, TNF-α, and HMGB1, in MP-infected mice. ConclusionLuteolin effectively and safely inhibits the proliferation and pathogenicity of MP, particularly the drug-resistant M19 strain, by downregulating the expression of toxicity-associated proteins (P1, P30, P65, HMW3, TrmB, CARDS TX) and modulating host inflammatory responses. These findings suggest that luteolin may offer a novel therapeutic strategy for treating MP infections, especially those caused by drug-resistant strains.

OBJECTIVE To analyze the distribution characteristics of mirtazapine steady-state trough concentration and concentration-to-dose ratio （ C / D ）， and to investigate the influence of clinical and genetic factors on C / D . METHODS A retrospective study was conducted on hospitalized patients with depression who received mirtazapine treatment and underwent therapeutic drug monitoring at the First Hospital of Hebei Medical University from May 2022 to May 2025. The collected data included patients’ gender， age， body mass index， daily dose， steady-state trough concentration， smoking status， history of liver disease， drug type， concomitant medications， and CYP2D6 metabolic phenotype. The C / D was calculated. Spearman rank correlation was used to analyze the relationship between mirtazapine steady-state trough concentration and daily dose. Univariate analysis and multiple linear regression model were employed to screen the factors potentially influencing the C / D of mirtazapine. RESULTS A total of 226 patients were included. The daily dose of mirtazapine was 25.00 （24.82， 30.00） mg/d， the steady-state trough concentration was 44.46 （20.00， 70.00） ng/mL， and the C / D was 1.83 （1.00， 2.00） （ng·d）/（mL·mg）. Steady-state trough concentrations were within the reference range （30-80 ng/mL） in 121 patients （53.54%）， below the lower limit in 80 patients （35.40%）， and above the upper limit in 25 patients （11.06%）. A positive correlation was observed between mirtazapine steady-state trough concentration and daily dose （coefficient of determination was 0.320 8， P ＜0.001）. Gender， smoking status， and CYP2D6 metabolic phenotype were significantly associated with the mirtazapine C / D （ P ＜0.05）. CONCLUSIONS Significant interindividual variability exists in mirtazapine steady-state trough concentrations. Gender， smoking status， and CYP2D6 metabolic phenotype are identified as independent influencing factors for the mirtazapine C / D ， with higher C / D ratios observed in females， non-smokers， and intermediate metabolizers.

AIM: To investigate variation patterns of corneal biomechanical parameters and binocular symmetry among children of different genders aged 8-16 years.METHODS:A retrospective study was conducted, and children who underwent optometric examinations at the ophthalmology department of our hospital were enrolled between January 2022 and December 2024. Measurements included the flat keratometry(K1), steep keratometry(K2), and mean curvature(Km)of the anterior corneal surface, horizontal visible iris diameter(HVID), central corneal thickness(CCT), corneal endothelial cell density(CECD), average cell size(ACS), coefficient of variation(CV), and hexagonality(HEX). Corneal parameters and binocular differences were compared between genders and across age groups.RESULTS:A total of 621 children(1 242 eyes)were enrolled in this study, including 284 males(568 eyes), 337 females(674 eyes), 528 children aged 8-12 years(1 056 eyes), and 93 children aged 13-16 years(186 eyes). In children aged 8-16 years, the K1, K2, Km and CV of both eyes, as well as the interocular CCT differences in boys were significantly lower than those in girls(all P<0.05), while the HVID and HEX of both eyes, as well as the CCT of the left eye in boys were significantly higher than those in girls(all P<0.05). Children aged 8-12 years had significantly higher K1, Km, CECD and HEX in both eyes, and significantly lower ACS in both eyes than those aged 13-16 years(all P<0.05). K1, K2, Km, CECD and HEX in both eyes were negatively correlated with age(P<0.05); ACS in both eyes was positively correlated with age(P<0.001); K1 and Km of the right eye were positively correlated with the CECD of the right eye(P<0.05), and K1 and CCT of the left eye were positively correlated with the CECD of the left eye(P<0.05).CONCLUSION:Significant gender differences exist in corneal parameters among children aged 8 to 16 years, while binocular symmetry remained stable.

OBJECTIVE To systematically evaluate the influencing factors affecting the poor prognosis of drug-induced liver injury （DILI） in the Chinese population， and to provide evidence-based support for early identification and interventions of DILI. METHODS Retrieved from PubMed， Medline， Embase， the Cochrane Library， CNKI， Wanfang database， China biomedical medicine database （CBM） and VIP， clinical studies （case-control studies， cohort studies） related to influencing factors for poor prognosis of DILI were collected from inception to May 31， 2025. After literature screening， data extraction and quality evaluation of included studies， meta-analysis was carried out by using RevMan 5.4 software. RESULTS A total of 17 literature were included， involving 4 078 DILI patients， of whom 673 were in the poor prognosis group and 3 405 were in the favorable prognosis group. Meta-analysis showed that history of liver disease （OR＝2.47， 95%CI was 1.61-3.78， P ＜0.001）， alcohol drinking history （OR＝1.77， 95%CI was 1.22-2.56， P ＝0.003）， Chinese herbal medicine/Chinese patent medicine （OR＝1.87， 95%CI was 1.30-2.70， P ＜0.001）， non-hepatocellular injury type （OR＝1.70， 95%CI was 1.37-2.10， P ＜0.001）， international normalized ratio （INR） elevated （OR＝2.51， 95%CI was 1.97-3.19， P ＜0.001）， and alanine transamine （ALT） elevated （OR＝1.27， 95%CI was 1.14-1.41， P ＜0.001） were risk factors of poor prognosis in DILI. Higher albumin （ALB） level （OR＝0.47， 95%CI was 0.39-0.57， P ＜0.001）， elevated prothrombin activity （PTA） （OR＝0.88， 95%CI was 0.85-0.91， P ＜0.001） and more than 2 kinds of hepatoprotective drugs （OR＝0.62， 95%CI was 0.41-0.95， P ＝0.030） were protective factors for poor prognosis of DILI. CONCLUSIONS Patients with alcohol drinking history， history of liver disease， elevated INR， elevated ALT， taking Chinese herbal medicine/Chinese patent medicine， and non-hepatocellular injury type of DILI have a greater risk of poor prognosis， and higher ALB level， higher PTA and more than 2 kinds of hepatoprotective drugs can reduce the risk of poor prognosis of DILI.

Objective To investigate the protective effect and underlying mechanisms of HydroMg, a novel sustained-release hydrogen donor, in a model of doxorubicin (DOX)-induced chronic cardiotoxicity. Methods H9C2 cells were treated with 1 μmol/L DOX and/or 1 μg/mL HydroMg, and mitochondrial membrane potential, reactive oxygen species (ROS) levels, and apoptosis were measured. In the animal experiment, mice were divided into control, HydroMg, DOX, and DOX＋HydroMg groups. The HydroMg group received intraperitoneal injection of HydroMg (100 mg/kg). Chronic cardiotoxicity was established by intraperitoneal injection of DOX (5 mg/kg every week) for four consecutive weeks; In the DOX＋HydroMg group, HydroMg (100 mg/kg) was administered intraperitoneally 4–5 h prior to each DOX injection. Cardiac function and remodeling were evaluated by echocardiography and heart weight index (HWI). The long-term survival of mice were analyzed. Subsequently, transcriptome sequencing was performed on myocardial tissues from the DOX group to identify key molecular alterations compared with controls. Results At the cellular level, HydroMg treatment effectively reversed DOX-induced mitochondrial dysfunction and oxidative stress, as evidenced by restored membrane potential, reductions in total ROS and mitochondrial superoxide levels by approximately 30% and 9%, respectively, and a decrease in the apoptosis rate from 34.13% to 18.27%. In the animal model, compared with the DOX group, HydroMg intervention increased left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) by 9.62% and 5.82%, respectively, attenuated the reduction in HWI (4.41 mg/mm vs 3.53 mg/mm), and improved the 4-week survival rate (80% vs 60%). Transcriptomic analysis revealed that the core molecular features of DOX-induced cardiotoxicity, including widespread suppression of oxidative phosphorylation and antioxidant pathways. Conclusions HydroMg protects against DOX-induced chronic cardiotoxicity by alleviating oxidative stress and improving mitochondrial function, and provides a potential therapeutic strategy against DOX-related cardiotoxicity.

ObjectiveTo investigate the intervention effect of modified Xiangsha Liujunzitang （M-XSLJZ） on insulin resistance-regulated fatty acid synthesis via Lon protease 1 （Lonp1） in the liver of spleen-deficiency hyperlipidemia rats. MethodsA total of 70 male SD rats were randomly allocated into seven groups （n=10）： blank control group， high-fat diet （HFD） group， spleen-deficiency hyperlipidemia （PX-HFD） model group， low-， medium-， and high-dose Modified Xiangsha Liujunzitang （JW-L， JW-M， JW-H）， and rosuvastatin group. The spleen-deficiency model was induced in the PX-HFD， JW-L， JW-M， JW-H， and rosuvastatin groups by irregular diet combined with exhaustive swimming. Except for the control group， all groups were fed an HFD for 10 weeks to establish a hyperlipidemia rat model. Following modeling， the rats in the JW-L， JW-M， and JW-H groups received the decoction by gavage at 3.51， 7.02， 14.04 g·kg^-1， respectively， while the rosuvastatin group received 9×10^-4 g·kg^-1. After 8 weeks of administration， samples were collected. D-xylose excretion rate was quantified using the phloroglucinol method. Serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， and low-density lipoprotein cholesterol （LDL-C） were measured by an automatic biochemical analyzer. Hepatic TG content was quantified by the glycerol phosphate oxidase-peroxidase anti-peroxidase （GPO-PAP） method. Serum insulin （INS）， fasting blood glucose （FBG）， hepatic reactive oxygen species （ROS） levels， and mitochondrial complex Ⅰ activity were assessed by enzyme-linked immunosorbent assay （ELISA）. The mRNA levels of Lonp1， and acetyl-CoA carboxylase 1 （ACC1） were determined by real-time quantitative PCR （Real-time PCR）. Protein expression levels of Lonp1， c-Jun N-terminal kinase （JNK）， phosphorylated （p）-JNK， insulin receptor substrate 1 （IRS1）， p-IRS1， and ACC1 in liver tissues were analyzed by Western blot. ResultsCompared with the control group， the HFD group showed a significant increase in body weight （P<0.01）. The PX-HFD group showed a significant decrease in D-xylose excretion rate （P<0.01）. Both the HFD and PX-HFD groups exhibited significantly elevated serum levels of TC， TG， HDL-C， LDL-C， FBG， INS， and HOMA-IR （P<0.01）， along with increased orange-red lipid droplets， prominent fatty vacuoles， and significantly elevated hepatic TG level （P<0.01）. Mitochondrial complex Ⅰ activity significantly decreased （P<0.05）， while ROS level， Lonp1 mRNA and protein expression， and ACC1 mRNA and protein expression significantly increased （P<0.05， P<0.01）. The p-IRS1/IRS1 protein expression ratio significantly decreased （P<0.01）， whereas the p-JNK/JNK protein expression ratio significantly increased （P<0.01）. Compared with the HFD group， the PX-HFD group showed significantly reduced D-xylose excretion rate and serum HDL-C level （P<0.01）， significantly decreased hepatic TG level （P<0.05）， and significantly increased HOMA‑IR index （P<0.01）. Hepatic Lonp1 mRNA and protein expression significantly decreased （P<0.05， P<0.01）， p‑IRS1/IRS1 protein expression ratio was significantly decreased （P<0.01）， while ACC1 mRNA and protein expression and p‑JNK/JNK protein expression ratio were significantly increased （P<0.01）. Compared with the PX-HFD group， all treatment groups showed significantly reduced serum TC， TG， LDL-C levels， and HOMA-IR index （P<0.05， P<0.01）， with ameliorated orange‑red lipid droplet deposition and significantly reduced hepatic TG and ROS levels （P<0.05， P<0.01）. The JW-M， JW-H， and rosuvastatin groups exhibited significantly decreased body weight （P<0.05， P<0.01）， significantly increased D‑xylose excretion rate （P<0.01）， significantly decreased HDL‑C level （P<0.05， P<0.01）， significantly increased mitochondrial complex I activity， Lonp1 mRNA and protein expression， and p-IRS1/IRS1 protein expression ratio （P<0.05， P<0.01）， as well as significantly decreased p-JNK/JNK protein expression ratio （P<0.01）. ConclusionM-XSLJZ may exert its lipid‑lowering effect by regulating Lonp1 expression in rat liver， thereby improving insulin resistance and subsequently inhibiting hepatic lipid synthesis.

The patient is a 63-year-old man with a history of chronic illness, presenting with intermittent low-grade fever, recurrent dry cough, and shortness of breath upon exertion. Lung CT showed a nodule in the left lung and a large mass in the right lung with liquefactive necrosis and an air-fluid level accompanied by pleural effusion. Laboratory findings showed significantly increasedf immunoglobulin G (IgG), IgG4, and total immunoglobulin E, along with a mild increase in eosinophils, and moderate elevations in erythrocyte sedimentation rate and high-sensitivity C-reactive protein. Malignant tumors, immunological, and hematological diseases were ruled out. Various antibiotic treatments were ineffective and the condition was recurrent. Conventional methods failed to identify the pathogen. Metagenomic next-generation sequencing (mNGS) technology was used to detect Mycobacterium monacense from lung tissue. Targeted antibiotic treatment was effective with no further episodes of low-grade fever and alleviation of dry cough symptoms. This case underscores the clinical significance of mNGS technology for the diagnosis and treatment of unexplained pulmonary infections, providing a useful reference for clinical diagnostic and treatment.

This study investigated the association between a proximal promoter polymorphism of IFNGR1 (interferon-γ receptor α chain, IFNGR-α) and breast cancer susceptibility, as well as the prognostic value of its expression variation in breast cancer patients. A case-control study was conducted at the Sixth Medical Center of PLA General Hospital from June 2020 to June 2022. The study included 182 pathologically confirmed breast cancer patients as the breast cancer group, 177 non-tumor patients with benign breast lesions as the benign breast lesions group, and 229 healthy individuals as the normal control group. 2-3 ml EDTA anticoagulant whole blood samples were collected from all participants, and genomic DNA was extracted and stored for further analysis. Basic patient information was retrieved from the hospital′s electronic medical records by patients′ ID number. The proximal promoter sequence of IFNGR1 was obtained from NCBI, and sequencing primers were designed using Primer Premier 6.0. Sanger sequencing was employed to analyze the IFNGR1 promoter sequence in the three groups, and the results were compared with the Eukaryotic Promoter Database (EPD) sequence using Bioedit software. Statistical analysis was performed on single nucleotide polymorphisms (SNPs) in the IFNGR1 promoter. The TCGA database was utilized to assess the relationship between IFNGR1 expression levels and breast cancer patient survival. The findings revealed that the -56 TG genotype of the IFNGR1 promoter was significantly associated with increased breast cancer risk ( Z=2.73, P<0.05). Notably, IFNGR1 expression was lower in breast cancer group compared to normal control group ( P<0.05). Analysis of the TCGA database indicated that patients with high IFNGR1 expression had longer survival times than those with low expression ( HR=0.87, 95% CI:0.77-0.98, P<0.05). In summary, the IFNGR1 -56 TG genotype is associated with an increased risk of breast cancer, and there is a positive correlation between IFNGR1 expression levels and the survival of breast cancer patients.