Objective: To explore whether the long-term and frequent use of citrate anticoagulants negatively affects the bone metabolism balance of female frequent plateletpheresis donors, so as to better protect their health. Methods: A total of 65 female plateletpheresis donors and 55 female whole-blood donors from Guangzhou Blood Center (May to December 2024) were enrolled as experimental and control groups respectively, stratified into age subgroups (18-39 years and 40-60 years). Serum levels of 25-hydroxyvitamin D [25(OH)D], procollagen type I N-terminal propeptide (PINP), osteocalcin (OC), and type I collagen carboxy-terminal telopeptide (CTX) were measured. Differences in bone metabolism markers between experimental and control groups across age subgroups were compared. ANOVA was used to analyze dose-response relationships between donation age, annual apheresis donation frequency, and biochemical indicators. Results: In the 40-60 age subgroup, 25(OH)D levels were significantly lower in the experimental group (P<0.05), exhibiting a linear increase with age and a linear decrease with annual donation frequency. No significant differences in CTX or PINP levels were observed between experimental and control groups in either age subgroup. Conclusion: High-frequency plateletpheresis donation does not disrupt bone metabolic balance in female donors. However, it is associated with reduced vitamin D levels in female donors aged >40 years, potentially increasing the risk of osteoporosis. Vitamin D supplementation is recommended for high-frequency female plateletpheresis donors in this age group.

ObjectiveTo prepare triptolide-Chuanxiong Rhizoma extract ethanol transfersomes（TP-CX@TESs）， conduct its quality evaluation， and investigate its in vitro anti-inflammatory efficacy and the underlying mechanisms. MethodsTP-CX@TESs was prepared via the ultrasonic injection method. With encapsulation efficiency and particle size as evaluation indicators， Box-Behnken design-response surface methodology（BBD-RSM） was employed to optimize the formulation process. The TP-CX@TESs prepared under the optimal process was characterized and evaluated for in vitro transdermal performance. A lipopolysaccharide（LPS）-induced RAW264.7 cell inflammation model was established. After 24 h of drug intervention， the levels of inflammatory factors such as nitric oxide（NO）， interleukin-6（IL-6）， and tumor necrosis factor-α（TNF-α） in the cell supernatant were detected. Western blot was used to determine the protein expression levels of Janus kinase 2（JAK2）， signal transducer and activator of transcription 3（STAT3）， and α7 nicotinic acetylcholine receptor（α7nAChR）， and real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） was applied to measure the mRNA expression levels of JAK2， STAT3， the encoding gene of α7nAChR（CHRNA7）， and nuclear transcription factor-κB（NF-κB）. ResultsResults of BBD-RSM showed that the optimal formulation for preparing TP-CX@TESs was as follows：egg yolk lecithin content of 2.3%， ethanol volume fraction of 30%， and ratio of polysorbate-80 to egg yolk lecithin of 2∶5. Microscopic characterization revealed that TP-CX@TESs exhibited a spherical-like structure with a particle size of （105.60±3.85） nm， a polydispersity index of 0.19±0.03， and a Zeta potential of （-15.89±0.98） mV. The encapsulation efficiencies of triptolide， ferulic acid， and ligustilide were （76.88±4.40）%， （78.84±4.40）%， and （65.88±0.06）%， respectively. Both in vitro release and transdermal penetration of triptolide， ferulic acid， and ligustilide in TP-CX@TESs all followed the first-order kinetic model， showing a certain sustained-release property. Experimental results in RAW264.7 cells indicated that TP-CX@TESs significantly inhibited the release of NO， TNF-α， and IL-6（P<0.01）， remarkably upregulated the protein expression levels of STAT3 and α7nAChR（P<0.01）， increased the mRNA expression level of CHRNA7， and significantly downregulated the mRNA expression level of NF-κB（P<0.05， P<0.01）. ConclusionThe optimized formulation process of TP-CX@TESs is simple and feasible， along with favorable in vitro release property， good transdermal permeability， and excellent in vitro anti-inflammatory activity， the mechanism is related to the inhibition of NF-κB.

ObjectiveTo prepare triptolide-Chuanxiong Rhizoma extract ethanol transfersomes（TP-CX@TESs）， conduct its quality evaluation， and investigate its in vitro anti-inflammatory efficacy and the underlying mechanisms. MethodsTP-CX@TESs was prepared via the ultrasonic injection method. With encapsulation efficiency and particle size as evaluation indicators， Box-Behnken design-response surface methodology（BBD-RSM） was employed to optimize the formulation process. The TP-CX@TESs prepared under the optimal process was characterized and evaluated for in vitro transdermal performance. A lipopolysaccharide（LPS）-induced RAW264.7 cell inflammation model was established. After 24 h of drug intervention， the levels of inflammatory factors such as nitric oxide（NO）， interleukin-6（IL-6）， and tumor necrosis factor-α（TNF-α） in the cell supernatant were detected. Western blot was used to determine the protein expression levels of Janus kinase 2（JAK2）， signal transducer and activator of transcription 3（STAT3）， and α7 nicotinic acetylcholine receptor（α7nAChR）， and real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） was applied to measure the mRNA expression levels of JAK2， STAT3， the encoding gene of α7nAChR（CHRNA7）， and nuclear transcription factor-κB（NF-κB）. ResultsResults of BBD-RSM showed that the optimal formulation for preparing TP-CX@TESs was as follows：egg yolk lecithin content of 2.3%， ethanol volume fraction of 30%， and ratio of polysorbate-80 to egg yolk lecithin of 2∶5. Microscopic characterization revealed that TP-CX@TESs exhibited a spherical-like structure with a particle size of （105.60±3.85） nm， a polydispersity index of 0.19±0.03， and a Zeta potential of （-15.89±0.98） mV. The encapsulation efficiencies of triptolide， ferulic acid， and ligustilide were （76.88±4.40）%， （78.84±4.40）%， and （65.88±0.06）%， respectively. Both in vitro release and transdermal penetration of triptolide， ferulic acid， and ligustilide in TP-CX@TESs all followed the first-order kinetic model， showing a certain sustained-release property. Experimental results in RAW264.7 cells indicated that TP-CX@TESs significantly inhibited the release of NO， TNF-α， and IL-6（P<0.01）， remarkably upregulated the protein expression levels of STAT3 and α7nAChR（P<0.01）， increased the mRNA expression level of CHRNA7， and significantly downregulated the mRNA expression level of NF-κB（P<0.05， P<0.01）. ConclusionThe optimized formulation process of TP-CX@TESs is simple and feasible， along with favorable in vitro release property， good transdermal permeability， and excellent in vitro anti-inflammatory activity， the mechanism is related to the inhibition of NF-κB.

Objective: To analyze the effects of maternal gestational weight gain and pre pregnancy body mass index (BMI) on the weight of preschool children,so as to provide scientific basis for prevention and treatment of overweight and obesity in children. Methods: Based on Jiangmen maternal and child health information platform, annual physical examination data of 3-6 years old preschool children from all nurseries and kindergartens in Jiangmen were collected from January to December 2024. A unique identification was made according to the mother s ID number and delivery date, and retrospective data collection was conducted on the platform to obtain pre pregnancy and pregnancy related information for 46 481 mothers. The Chi-square test,two way ordered variable analysis and Logistic regression analysis were used to compare the effects of maternal pre pregnancy BMI and gestational weight gain on overweight and obesity among preschool children. Results: A total of 5 168 (11.12%) children were overweight and obese, and the proportion of overweight and obesity in the 6 year old group was the highest (12.86%). There were significant differences in the detection rates of overweight and obesity between boys and girls ( χ 2=155.38), and there were also significant gender differences in the age groups of 4, 5 and 6 years ( χ 2=17.08, 96.97, 66.27)(all P <0.01). Through trend χ 2 test, the overall detection rates of overweight and obesity, as well as those for boys, increased with age ( χ 2 trend =49.36,60.54, both P <0.01). The BMI group of preschool children was correlated with the BMI group of their mothers before pregnancy and the weight gain group during pregnancy （χ 2= 1 250.64, 157.01, both P <0.01) and the proportion of children with higher BMI levels showed an upward trend with the improvement of their mothers pre-pregnancy BMI levels or gestational weight gain levels ( Gamma =0.13, 0.10, both P <0.01). Multiple Logistic regression analysis showed that pre pregnancy BMI groups as overweight ( OR =1.590, 1.922), obesity ( OR =2.100, 2.921 ), and male gender of the children ( OR =1.213, 1.763)，and newborns excessive birth weight( OR =1.001，1.001) increased the risks of overweight and obesity in preschool children; maternal gestational weight gain insufficiency ( OR =1.374) and advanced maternal age at the first prenatal visit ( OR =1.012) increased the risks of obesity in preschool children; maternal gestational weight gain deficiency or excess ( OR =1.324,1.118) increased the risk of overweight in preschool children (all P <0.01). Conclusions Maternal pre-pregnancy overweight and obesity and insufficient or excessive gestational weight gain increase the risk of overweight and obesity in preschool children. It is necessary to strengthen weight management before and during pregnancy to reduce the occurrence of childhood overweight and obesity.

Objective To utilize single-cell and peripheral blood transcriptomic data from 3D brain organoids,combined with machine learning,to analyze the role of mitochondrial autophagy genes in schizophrenia(SCZ).Methods By integrating two machine learning algorithms,we identified differentially expressed mitochondrial autophagy-related genes between schizophrenia patients and healthy controls using peripheral blood RNA sequencing data.The relationship between mitophagy gene,immune cells and inflammatory factors was further explored.Comprehensive single-cell analysis was used to explore the signaling pathways and specific transcription factors based on mitophagy genes.Results Using machine learning,seven key mitophagy genes expressed in schizophrenia patients were identified.Based on Mitoscore analysis,at the single-cell level,neurons with high mitochondrial autophagy activity(Mitohigh_Neuron)formed new interactions with endothelial cells via the SPP1 signaling pathway.Conclusion This study identified two subtypes of mitophagy and seven key mitophagy genes in schizophrenia,providing new insights into the pathogenesis of the disease.

Objective To develop an active monitoring model for adverse drug events(ADEs)related to antimicrobial use in children based on the China hospital pharmacovigilance system(CHPS).Methods Trigger items for the active monitoring model were initially drafted through a review of relevant literature,adverse reaction databases,and drug label warnings,and subsequently refined using the Delphi method.A retrospective analysis was performed on pediatric inpatients who received antibiotics at Anning First People's Hospital between January 1 and December 31,2024.The detection rate and positive predictive value(PPV)of the active monitoring model were calculated and compared with spontaneous ADE reports from the same period.Risk factors for ADEs were further analyzed using logistic regression.Results 25 trigger items were established for the active monitoring model.Among 1,784 cases,233 ADEs were identified,yielding a detection rate of 13.06%(233/1,784).The spontaneous reporting rate of adverse events during the same period was 1.85%(33/1,784).The difference between the two was statistically significant(P<0.001).There were 727 positive trigger events,with 299 cases of ADE detected,resulting in an overall PPV of 41.13%(299/727).Logistic regression revealed that antibiotic use exceeding 3 days(OR=1.454,95%CI:1.012-2.088)was significantly associated with ADE occurrence.Conclusion Compared with conventional spontaneous reporting,the active monitoring model can significantly improve the detection rate of ADEs of pediatric antimicrobial drugs and achieve active and real-time monitoring of drug adverse events.

Objective::To analyze fetal renal abnormality genetic features and the prenatal characteristics of the 17q12 microdeletion syndrome.Methods::This prospective cohort study examined prenatal ultrasound findings of renal abnormalities in pregnant women who underwent single nucleotide polymorphism (SNP) array or copy number variation sequencing (CNV-seq) testing on amniotic fluid or fetal tissue at Tianjin Central Obstetrics and Gynecology Hospital between January 2016 and August 2022. The study cohort comprised women with advanced maternal age, fetal ultrasound anomalies, high-risk non-invasive prenatal testing results, or suspected 17q12 microdeletion syndrome. Comprehensive clinical data, including maternal age, detailed ultrasound findings, and pregnancy outcomes, were systematically collected. SNP-array analysis was conducted using an Affymetrix CytoScan 750 K Array Chip to identify CNVs and loss of heterozygosity, while CNV-seq was performed on the Illumina HiSeq 2000 platform. Detected variants were classified according to the American College of Medical Genetics and Genomics guidelines. Statistical analyses were performed using SPSS version 27.0.Results::Abnormal renal development was identified in 141 patients, among whom 26 exhibited hyperechogenic kidneys (HCK). Of these, 12 cases were associated with 17q12 microdeletion syndrome, while the remaining 14 were linked to other chromosomal abnormalities. When excluding patients with HCK, those diagnosed with polycystic kidney disease demonstrated a higher prevalence of chromosomal abnormalities compared to those with multicystic dysplastic kidney and renal dysplasia. Although isolated conditions such as horseshoe kidney, hydronephrosis, ectopic kidney, and unilateral kidney typically presented with normal chromosomal findings, the incidence of chromosomal abnormalities increased when these conditions coexisted with other anomalies. A detailed analysis of the correlation between 17q12 microdeletion syndrome and HCK revealed that 12 out of the 14 patients diagnosed with 17q12 microdeletion syndrome exhibited HCK. Genetic testing confirmed the syndrome in seven patients, with five cases attributed to novel mutations and two cases resulting from inherited mutations.Conclusion::Fetal HCK was closely associated with the 17q12 microdeletion syndrome, and polycystic kidney disease showed a higher rate of chromosomal abnormalities. Chromosome test results were mostly normal in patients with other renal abnormalities, such as kidney dysplasia, horseshoe kidneys, hydronephrosis, kidney deficiency, and ectopic kidneys. Prenatal diagnosis is recommended, especially in cases of non-isolated fetal renal abnormalities. This study provides strong evidence supporting a link between fetal renal abnormalities and genetic syndromes.

Objective:To investigate the value of dual-energy CT parameters in the evaluation of pathological grade of pancreatic ductal adenocarcinoma.Methods:80 cases of pancreatic ductal adenocarcinoma confirmed by pathology were retrospectively analyzed and divided into high grade group (36 cases) and low grade group (44 cases) according to their differentiation degree. All 80 patients underwent SOMATOM Force DECT for arterial phase (AP) and pancreatic phase (PP) scanning, and measured dual-energy parameters including dual-phase iodine concentration (IC AP, IC PP) in tumors and normal pancreatic parenchyma, pancreatic phase and arterial phase iodine concentration difference (ICD PP-AP) in tumors, dual-phase iodine uptake ratio (IUR AP, IUR PP) , dual-phase tumor/normal pancreatic parenchyma fat fraction ratio, and dual-phase slope of energy spectrum curve. Differences between two groups were compared by two independent sample t-test or Mann-Whitney U test or chi-square test. The multivariate logistic regression model was used to analyze the influencing factors of pathological grading of PDAC. Results:There were statistically significant differences in gender, age, aspect ratio, positive lymph node, fat fraction ratio in pancreatic phase between the two groups ( P< 0.05) . The multivariate logistic regression analysis showed that fat fraction ratio in pancreatic phase ( OR=1.781, 95% CI 1.127-2.814, P=0.013) , positive lymph node ( OR=4.870, 95% CI 1.488-15.938, P=0.009) , aspect ratio ( OR=0.019, 95% CI 0.001-0.437, P=0.013) were independent factors influencing the pathologic grade of PDAC. Conclusion:Parameters of dual-energy CT are valuable in the evaluation of pathological grading of PDAC.

Approximately 60% of colorectal cancer (CRC) patients exhibit TP53 mutations, which are strongly associated with tumor progression, chemotherapy resistance, and an unfavorable prognosis. However, targeting p53 has historically been challenging, and currently, there are no approved p53-based therapeutics for clinical use worldwide. In this study, we discovered that ubiquitin carboxyl terminal hydrolase L3 (UCHL3) plays a crucial role in high-level glycolysis, enhanced stem-like properties, and 5-fluorouracil (5-FU) chemoresistance in TP53-mutant CRC by exerting its deubiquitinating enzyme activity to stabilize α-enolase (ENO1) protein. Notably, we identified a newly Food and Drug Administration (FDA)-approved drug, pacritinib, that potently suppresses UCHL3 expression by blocking the janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway in TP53-mutant CRC. Furthermore, Pacritinib was demonstrated to effectively inhibit glycolysis and improve the sensitivity to 5-FU chemotherapy in TP53-mutant CRC. Our findings suggest that targeting the JAK2-STAT3-UCHL3-ENO1 axis is a promising strategy to suppress glycolysis and enhance the efficacy of 5-FU chemotherapy in TP53-mutant CRC. Pacritinib shows potential for clinical application in the treatment of TP53-mutant CRC.

Inflammatory bowel disease (IBD) is a kind of complex, chronic digestive disease with unclear etiology. This article systematically reviews the evolution of IBD, from early clinical descriptions to advancements in diagnostic techniques and significant developments in treatments, outlining the progression of the IBD diagnosis and treatment framework and highlighting how optimized approaches have impacted patients' quality of life. In the future, emerging technologies such as targeted immune modulation, microbiome intervention, stem cell therapy, and artificial intelligence-assisted diagnosis and treatment are expected to provide new directions and strategies for precise, personalized IBD management.