Objective To investigate the association between physical activity levels and blood lipids among college freshmen, and to provide scientific evidence for the health management of college freshmen. Methods An electronic questionnaire survey on physical activity was conducted on freshmen of a university, and fasting blood biochemical indicators were detected. The International Physical Activity Questionnaire (IPAQ) short form was used to evaluate the physical activity levels of the participants. Dyslipidemia was defined as an abnormality in any one of the following serum lipid parameters: total cholesterol, triglycerides, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), or non-high-density lipoprotein cholesterol. Binary logistic regression and stratified analyses were employed to explore the relationship between physical activity and blood lipids. Results A total of 3 401 participants were included, with an average age of 18.45 ± 0.92 years, and 60.5% were female. The prevalence of dyslipidemia was 17.7%, with a higher rate among males (22.1%) than females (14.8%). After adjusting for confounding factors related to blood lipids, high-intensity physical activity was negatively associated with the risk of elevated LDL-C among males (OR = 0.36, 95% CI: 0.13–0.99, P = 0.049). Conclusion Among freshmen at a medical college in Hubei Province, high-intensity physical activity is negatively associated with the risk of elevated LDL-C in males, but this association needs to be further confirmed by larger prospective cohort studies.

ObjectiveTo investigate the fluctuations in serum uteroglobin-related protein 1（UGRP1） levels in Hashimoto’s thyroiditis （HT） patients before and after pregnancy， and to analyze the influencing factors. MethodsTen healthy individuals and ten HT patients were enrolled. Thyroid fine needle aspiration cytology combined with immunohistochemistry was used to detect the expression of UGRP1 protein in thyroid cells between the two groups. A total of 30 healthy women were enrolled as the control group， and 149 HT patients were recruited， including 36 non-pregnant HT patients， 77 pregnant HT patients and 36 post-partum HT patients. According to levothyroxine sodium （L-T4） administration status， the pregnant HT group was further subdivided into the non-L-T4 subgroup （n=36） and the L-T4 subgroup （n=41）. Kruskal-Wallis H test was used to compare the general clinical data， thyroid-related indicators and serum UGRP1 levels among groups. Spearman correlation analysis and univariate linear regression analysis were performed to explore the influencing factors of serum UGRP1 levels in HT patients. ResultsUGRP1 expression was negative in thyroid cells of all healthy individuals， while 80% of HT patients exhibited positive expression. The serum UGRP1 levels in the control group， non-pregnant HT group， pregnant HT group， and post-partum HT group were 359.52 （297.84， 440.60）， 695.77 （518.55， 865.04）， 207.96 （173.82， 264.91）， and 582.08 （280.83， 735.87） pg/mL， respectively， with statistically significant differences among groups （P<0.001）. Correlation analysis showed no significant correlation between serum UGRP1 levels and thyroid-related indicators or gestational age in pregnant HT patients. Univariate linear regression analysis revealed that pregnancy status was negatively correlated with serum UGRP1 levels in HT patients （β= -424.457， P<0.001）， while L-T4 administration had no statistically significant effect on serum UGRP1 levels in pregnant HT patients （P=0.890）. ConclusionSerum UGRP1 levels are significantly higher in HT patients than in healthy individuals. Pregnancy is an important factor affecting serum UGRP1 levels in HT patients， which can lead to a decrease in UGRP1 levels， while L-T4 administration has no significant effect on serum UGRP1 levels.

ObjectiveTo investigate the risk factors for plastic bronchitis （PB） in children with Mycoplasma pneumoniae pneumonia （MPP） and to construct a predictive model. MethodsPropensity score matching （1∶4 nearest neighbor matching） was used to balance baseline data between the two groups. Univariate and multivariate Logistic regression analyses were performed to identify independent risk factors. Various machine learning algorithms were applied to build predictive models， and model performance was evaluated using receiver operating characteristic curves， decision curves， and calibration curves. SHapley Additive exPlanations （SHAP） method was used for model interpretation. ResultsAfter matching， baseline characteristics were comparable between the two groups. Compared with the non-PB group， the PB group had significantly longer fever duration， higher incidence of pleural effusion and right upper lobe involvement， and higher levels of procalcitonin （PCT）， D-dimer， lactate dehydrogenase （LDH）， alanine aminotransferase （ALT）， aspartate aminotransferase （AST）， immunoglobulin E （IgE）， and red blood cell count in bronchoalveolar lavage fluid （BALF） （all P<0.05）， while lymphocyte and eosinophil counts in blood were significantly lower （P<0.05）. Multivariate Logistic regression showed that PCT>0.207 μg/L， LDH>386.25 U/L， right upper lobe involvement， and red blood cell count in BALF>1 500×10⁶ were independent risk factors. Among machine learning models， the gradient boosting machine （GBM） model achieved an area under the curve of 0.786 in the validation set， demonstrating the best generalization ability. SHAP analysis validated the importance of the above variables. ConclusionThe four indicators above have independent predictive value for PB occurrence， and the GBM model shows certain clinical risk stratification capability.

OBJECTIVE: To explore the genetic characteristics of a Chinese pedigree with rare mosaic 11q partial duplication and its pathogenetic mechanisms. METHODS: A pedigree which underwent prenatal diagnosis at Wenzhou Central Hospital between September 25, 2015 and November 30, 2023 was selected for the study. Clinical data were collected from the pedigree. Peripheral blood samples from the parents, amniotic fluid from the fetus, and peripheral blood sample from the neonate were obtained. Genetic testing was carried out by using G-banded chromosomal karyotyping and single nucleotide polymorphism array (SNP-array) technology. Relevant literature was searched in the CNKI, Wanfang Data Knowledge Service Platform, and PubMed databases to summarize the clinical phenotypes of patients with 11q partial duplication. This study was approved by the Medical Ethics Committee of Wenzhou Central Hospital (Ethics No. L2024-07-080). RESULTS: The pregnant woman (G₃) had a history of adverse pregnancy outcomes. During her first pregnancy (G₁), prenatal ultrasound indicated intrauterine growth restriction and a Dandy-Walker variant. Follow-up at 8 years of age showed developmental delays and mild intellectual disability. During her second pregnancy (G₂), prenatal ultrasound revealed nasal bone hypoplasia, and the pregnancy was terminated at 23rd gestational week. During her third pregnancy (G₃), all prenatal tests were normal, and the neonate showed normal growth and development at 4 months of age. The karyotype of amniotic fluid of her first pregnancy was 46,X?, and the SNP-array analysis of neonatal peripheral blood showed arr[GRCh37/hg19]11q13.4q25(70432450_134607121)×2~3, with a mosaicism rate being approximately 40%. The karyotype for her second pregnancy was 46,X?,rec(11)dup(11q)inv(11)(p15q13)dmat[6]/46,X?[27], and the SNP-array result was arr[GRCh38]11q13.4q25(71406636_135067522)×2~3, with a mosaicism rate being approximately 75%. The karyotype for her third pregnancy was 46,X?,inv(11)(p15q13)mat, and the SNP-array result was arr(XN)×1,(1~22)×2. The karyotype of the woman was 46,XX,inv(11)(p15q13), and that of her husband was 46,XY. A review of 12 similar cases (including G₁) from the literature revealed that the common clinical phenotypes of 11q partial duplication included intellectual disability (12/12), developmental delay (12/12), ear abnormalities (12/12), microcephaly (10/12), seizures (8/12), hypotonia (8/12), and congenital heart malformations (7/12). CONCLUSION Mosaic partial duplication of 11q may underlie the genetic etiology of this pedigree. The pregnant woman is a carrier of an inversion on chromosome 11, which might have formed the mosaic 11q partial duplication through meiotic errors and mitotic trisomy rescue mechanisms during reproduction.
Adult ; Female ; Humans ; Male ; Pregnancy ; China ; Chromosome Duplication ; Chromosomes, Human, Pair 11/genetics* ; East Asian People/genetics* ; Karyotyping ; Mosaicism ; Pedigree ; Polymorphism, Single Nucleotide ; Prenatal Diagnosis

Objective:To examine the longitudinal relationships between perceived social support,life satis-faction and acceptance by others among relocated residents for poverty alleviation.Methods:A two-wave longitudi-nal survey was conducted with 383 relocated residents from 39 resettlement communities in Guizhou Province,with a six-month interval.Participants completed the Perceived Social Support Scale(PSSS),the Acceptance by Others Scale of the Acceptance of others Scale(AOS),and the Satisfaction With Life Scale(SWLS).Results:T1 PSSS scores positively predicted T2 acceptance by others scores(β=0.20,P＜0.001).T2 acceptance by others scores positively predicted T2 SMLS scores(β=0.45,P＜0.001).Perceived acceptance by others fully mediated the lon-gitudinal relationship between perceived social support and life satisfaction(effect=0.09,95％CI:0.03-0.18).Conclusion:Perceived social support predicts life satisfaction of relocated residents for poverty alleviation through perceived acceptance by others.

Stem-leaf saponins from Panax notoginseng (SLSP) comprise numerous PPD-type saponins with diverse pharmacological properties; however, their role in Parkinson's disease (PD), characterized by microglia-mediated neuroinflammation, remains unclear. This study evaluated the effects of SLSP on suppressing microglia-driven neuroinflammation in experimental PD models, including the 1-methyl-4-phenylpyridinium (MPTP)-induced mouse model and lipopolysaccharide (LPS)-stimulated BV-2 microglia. Our findings revealed that SLSP mitigated behavioral impairments and excessive microglial activation in models of PD, including MPTP-treated mice. Additionally, SLSP inhibited the upregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX2) and attenuated the phosphorylation of PI3K, protein kinase B (AKT), nuclear factor-κB (NFκB), and inhibitor of NFκB protein α (IκBα) both in vivo and in vitro. Moreover, SLSP suppressed the production of inflammatory markers such as interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α) in LPS-stimulated BV-2 cells. Notably, the P2Y2R agonist partially reversed the inhibitory effects of SLSP in LPS-treated BV-2 cells. These results suggest that SLSP inhibit microglia-mediated neuroinflammation in experimental PD models, likely through the P2Y2R/PI3K/AKT/NFκB signaling pathway. These novel findings indicate that SLSP may offer therapeutic potential for PD by attenuating microglia-mediated neuroinflammation.
Animals ; Panax notoginseng/chemistry* ; Saponins/pharmacology* ; Microglia/immunology* ; Mice ; NF-kappa B/immunology* ; Signal Transduction/drug effects* ; Proto-Oncogene Proteins c-akt/immunology* ; Phosphatidylinositol 3-Kinases/genetics* ; Male ; Parkinson Disease/immunology* ; Mice, Inbred C57BL ; Disease Models, Animal ; Plant Leaves/chemistry* ; Neuroinflammatory Diseases/drug therapy* ; Humans

Objective:To explore the genetic characteristics of a Chinese pedigree with rare mosaic 11q partial duplication and its pathogenetic mechanisms.Methods:A pedigree which underwent prenatal diagnosis at Wenzhou Central Hospital between September 25, 2015 and November 30, 2023 was selected for the study. Clinical data were collected from the pedigree. Peripheral blood samples from the parents, amniotic fluid from the fetus, and peripheral blood sample from the neonate were obtained. Genetic testing was carried out by using G-banded chromosomal karyotyping and single nucleotide polymorphism array (SNP-array) technology. Relevant literature was searched in the CNKI, Wanfang Data Knowledge Service Platform, and PubMed databases to summarize the clinical phenotypes of patients with 11q partial duplication. This study was approved by the Medical Ethics Committee of Wenzhou Central Hospital (Ethics No. L2024-07-080).Results:The pregnant woman (G 3) had a history of adverse pregnancy outcomes. During her first pregnancy (G 1), prenatal ultrasound indicated intrauterine growth restriction and a Dandy-Walker variant. Follow-up at 8 years of age showed developmental delays and mild intellectual disability. During her second pregnancy (G 2), prenatal ultrasound revealed nasal bone hypoplasia, and the pregnancy was terminated at 23rd gestational week. During her third pregnancy (G 3), all prenatal tests were normal, and the neonate showed normal growth and development at 4 months of age. The karyotype of amniotic fluid of her first pregnancy was 46, X? , and the SNP-array analysis of neonatal peripheral blood showed arr[GRCh37/hg19]11q13.4q25(70432450_134607121)×2~3, with a mosaicism rate being approximately 40%. The karyotype for her second pregnancy was 46, X? , rec(11)dup(11q)inv(11)(p15q13)dmat[6]/46, X? [27], and the SNP-array result was arr[GRCh38]11q13.4q25(71406636_135067522)×2~3, with a mosaicism rate being approximately 75%. The karyotype for her third pregnancy was 46, X? , inv(11)(p15q13)mat, and the SNP-array result was arr(XN)×1, (1~22)×2. The karyotype of the woman was 46, XX, inv(11)(p15q13), and that of her husband was 46, XY. A review of 12 similar cases (including G 1) from the literature revealed that the common clinical phenotypes of 11q partial duplication included intellectual disability (12/12), developmental delay (12/12), ear abnormalities (12/12), microcephaly (10/12), seizures (8/12), hypotonia (8/12), and congenital heart malformations (7/12). Conclusion:Mosaic partial duplication of 11q may underlie the genetic etiology of this pedigree. The pregnant woman is a carrier of an inversion on chromosome 11, which might have formed the mosaic 11q partial duplication through meiotic errors and mitotic trisomy rescue mechanisms during reproduction.

To establish a rapid Akabane virus(AKAV)antibody detection method in animals,the re-combination AKAV N protein was expressed by the expression system of Escherichia coli,puri-fied from the supernatant,and used to immunized New Zealand White rabbits.The polyclonal anti-body against AKAV N protein had a titer of 1∶8.192×107 and showed good reactivity.After opti-mizing the reaction conditions,an AKAV double antigen sandwich ELISA antibody detection method was established.This method can detect AKAV antibody in a variety of animals including cattles,sheep and goats.The method had no cross-reactivity with the positive serum of BTV,EHDV,BEV and PRV with the intra-and inter-batch coefficients of variation less than 10％.Com-pared with the AKAV blocking ELISA kit,the sensibility of the method was increased by 8-16 folds with a compliance rate of 93.33％and the κ value of 0.864.These results showed that the double antigen sandwich ELISA displayed strong specificity,high sensitivity and repeatability,which could provide technical suport for detection,the prevention and control of AKAV.

Liver cancer has high prevalence and mortality rates around the world， and its development and progression are closely associated with the interaction between the tumor microenvironment and tumor-associated macrophages （TAMs）. TAMs play a significant role in immune suppression， immune escape， cell proliferation， invasion， metastasis， and drug resistance in liver cancer. Traditional Chinese medicine （TCM）， with its unique therapeutic concepts and methods， has shown great potential in regulating TAMs and improving the prognosis of liver cancer. This article reviews the role and molecular mechanisms of TCM in regulating TAMs for the treatment of liver cancer， discusses the key role of TAMs in the progression of liver cancer， and analyzes the impact of Chinese medicinal components on the recruitment， polarization， and activity of TAMs and the expression of related factors based on TCM theory. Studies have shown that TCM can regulate the polarization state of TAMs， promote the formation of M1-type antitumor macrophages， and inhibit the activity of M2-type tumor macrophages， thereby playing a role in inhibiting the proliferation of liver cancer cells， promoting apoptosis， inhibiting angiogenesis， and enhancing immune response. In addition， this article also summarizes the molecular targets and mechanisms of action of TCM monomers， compound prescriptions， and novel preparations in the treatment of liver cancer， such as inhibiting the secretion of cytokines by TAMs， regulating signaling pathways， and affecting metabolic pathways， in order to provide a scientific basis for the application of TCM in liver cancer treatment and offer new ideas for immunotherapy for liver cancer.

Objective:To conduct clinical analysis and genetic variant detection in patients with congenital hypothyroidism, and to explore the role of paired box 8(PAX8) gene variants in the pathogenic mechanism of congenital hypothyroidism, thereby providing insights for its diagnosis and management.Methods:This study was a retrospective analysis based on previously collected clinical and genetic data. Clinical information from 763 children with congenital hypothyroidism and some of their family members was collected between 2014 and 2025. Peripheral blood samples were obtained for genomic DNA extraction. Next-generation sequencing was performed to detect pathogenic variants in the patients. The identified pathogenic PAX8 variants were confirmed by Sanger sequencing and pedigree analysis. Functional analysis of the variant was then performed using bioinformatics tools.Results:Five PAX8 variants were identified among 763 children with congenital hypothyroidism. One proband was identified through neonatal screening and subsequently confirmed to have congenital hypothyroidism. Thyroid ultrasound revealed a small thyroid gland. A heterozygous missense variant in the PAX8 gene, NM_003466.3: c.91C>T: p.R31C, was identified in this proband, resulting in the substitution of arginine with cysteine at Codon 31 of the PAX8 protein. Sanger sequencing confirmed that this was a de novo variant, as it was absent in the proband′s parents. Multiple bioinformatic programs consistently predicted the variant to be deleterious. According to the American College of Medical Genetics and Genomics(ACMG) guidelines, the variant was classified as pathogenic. Conclusions:A de novo PAX8 variant, p. R31C, was identified in a patient with congenital hypothyroidism. This variant is located within the paired domain of the PAX8 protein and may impair the protein′s function by disrupting its binding to DNA.