BACKGROUND:Autophagy,as a key regulatory mechanism of cell development,plays an important role in different stages of embryonic development.The mechanism of how autophagy regulates embryonic development through histone modifications is currently unclear.OBJECTIVE:To investigate the effect of autophagy on trimethylation of lysine 4 on histone H3(H3K4me3)modification in embryos and its effect on embryonic development.METHODS:Mouse fertilized eggs were divided into control and autophagy inhibitor-treated groups(chloroquine phosphate-treated group and 3-methyladenine-treated group),and cultured in vitro to different periods of time,and were then classified as early 2-cell embryos,middle 2-cell embryos,late 2-cell embryos,4-cell embryos,8-cell embryos,morula stage,and blastocyst stage.Levels of reactive oxygen species,autophagy marker proteins LC3B and P62,DNA loss marker γH2AX,and H3K4me3 were analyzed by immunofluorescence assay in late 2-cell embryos of each group.Changes in H3K4me3 modification in late 2-cell embryos of each group were detected by CUT&Tag.RESULTS AND CONCLUSION:(1)Autophagy inhibition caused embryo development arrest.(2)There was no significant difference in reactive oxygen species and γH2AX between the autophagy inhibitor-treated groups and control group.(3)H3K4me3 levels were significantly elevated in the autophagy inhibitor-treated group compared with the control group.(4)CUT&Tag results showed a significantly increased H3K4me3 peaks on the proximal promoter region of the genes after autophagy inhibition and an increase of H3K4me3-specific modification genes.These findings suggest that autophagy may affect embryonic development by regulating the level of H3K4me3 modification.

Objective: To explore the barriers to physical activity behavior among overweight and obese children and adolescents, so as to provide evidence for developing physical activity intervention programs. Methods: From March to April 2025, 13 overweight or obese children and adolescents from one primary school and one secondary school in Nanjing were selected by purposive sampling for semi structured interviews. Guided by the capability, opportunity and motivation-behavior model, data were coded, categorized and analyzed using content analysis. Results: A total of 13 interviews were completed, with a cumulative duration of 358 minutes. Three themes and eight subthemes were identified:capability factors, including physical discomfort and limited physical fitness, weak exercise skills and insufficient behavioral regulation ability, and insufficient psychological capability; opportunity factors, including insufficient family support and negative influence, pressure from school and peer environments, and limited time resources and exercise conditions; and motivation factors, including low self efficacy and situations prone to giving up, and insufficient positive feedback and lack of attractiveness of exercise forms. Conclusions Barriers to physical activity among overweight and obese children and adolescents result from the combined effects of capability, opportunity and motivation. It is necessary to lower the threshold for initiating exercise, strengthen positive experiences and feedback, and build integrate family-school support environments to promote the initiation and maintenance of physical activity behaviors in children and adolescents.

Objective: To systematically evaluate the performance of machine learning (ML) models in predicting non suicidal self injury (NSSI) behavior among adolescents, providing an evidence based foundation for the development of clinically applicable risk assessment tools. Methods: A comprehensive search was conducted in PubMed, Embase, Web of Science, CNKI, and Wanfang databases for relevant studies from their inception to July 21, 2025. The Prediction Model Risk of Bias Assessment Tool (PROBAST) was used to evaluate the methodological quality of the included studies. Stata 18 software was used to calculate the area under the receiver operating characteristic curve (AUC) of the models, and publication bias assessment, sensitivity analysis, and Egger s test were performed. Results: The total of 12 studies (42 prediction models) involving 58 070 adolescents were included. There were 15 machine learning algorithms in total, among which Random Forest, Logistic Regression, XGBoost, and Support Vector Machines were the most frequently utilized. The most common predictors were gender (female), family function, depression, emotion regulation, and age. All 12 included studies exhibited a high risk of bias. The pooled AUC was 0.80 (95% CI =0.78-0.82), although heterogeneity was substantial ( I 2=95.8%, P <0.01). Sensitivity analysis confirmed the robustness of these findings (no overlap in 95% CI ), while Egger s test indicated the presence of publication bias ( P <0.05). Conclusions Machine learning demonstrates potential in the risk prediction of adolescent NSSI, but existing models have a high risk of bias. Future research should focus on improving methodological quality and optimizing model reliability through rigorous external validation.

Objective To investigate the clinical features of glial fibrillary acidic protein immunoglobulin G （GFAP-IgG）-associated myelitis， to compare the differences in clinical features between GFAP-IgG-associated myelitis and aquaporin-4 immunoglobulin G （AQP4-IgG）-associated myelitis/myelin oligodendrocyte glycoprotein immunoglobulin G （MOG-IgG）-associated myelitis， and to provide help for early diagnosis and treatment. Methods A retrospective analysis was performed for the clinical data of 34 patients who were diagnosed with GFAP-IgG-associated myelitis in The First Affiliated Hospital of Zhengzhou University and Henan Children Hospital from May 2018 to May 2023， and their demographic features， clinical features， serological parameters，cerebrospinal fluid （CSF） parameters， imaging features， and prognosis were systematically analyzed. In addition， 30 patients diagnosed with AQP4-IgG-associated myelitis and 42 patients diagnosed with MOG-IgG-associated myelitis during the same period of time were enrolled as control groups， and the mean clinical features were compared between the three groups. Results Among the 34 patients with GFAP-IgG-associated myelitis， there were 15 female patients and 12 children. The median age of onset was 28.5 years， and more than half of the patients had prodromal symptoms. More than half of the patients had the symptoms of pyrexia （29/34， 85%）， headache （19/34，56%）， nausea/vomiting （20/34，59%），and limb weakness （27/34，79%） during the course of the disease， with 19 patients（19/34，56%） admitted to the intensive care unit （ICU）.Imaging examination showed gadolinium-enhancing spinal cord lesions and longitudinally extensive sagittal T2 hyperintensity， i.e.，longitudinally extensive transverse myelitis.Compared with the AQP4-IgG-associated myelitis group and the MOG-IgG-associated myelitis group，the GFAP-IgG-associated myelitis group had a significantly higher proportion of patients with pyrexia （85% vs 10%， P1<0.01； 85% vs 38%，P2<0.01）， neck stiffness （41% vs 7%， P1<0.01； 41% vs 12%， P2<0.01）， admission to the ICU （56% vs 10%， P1<0.01； 56% vs 17%， P2<0.01）， or mechanical ventilation （38% vs 3%， P1<0.01； 38% vs 0%， P2<0.01） and a significant increase in serum monocyte-to-lymphocyte ratio [0.43（0.24，0.71） vs 0.23 （0.18，0.32）， P1<0.01； 0.43 （0.24，0.71） vs 0.21 （0.14，0.30），P2<0.01]， as well as a significantly higher proportion of patients with hyponatremia （45% vs 13%，P1<0.01； 45% vs 7%，P2<0.01）， an increase in leukocyte count in CSF（68% vs 14%， P1<0.01； 68% vs 34%， P2<0.01）， an increase in total protein in CSF （82% vs 31%， P1<0.01； 82% vs 20%， P2<0.01）， a reduction in glucose level in CSF （26% vs 3%，P1=0.03； 26% vs 2%， P2<0.01）， or the presence of central canal enhancement （29% vs 0%， P1=0.02；29% vs 0%， P2=0.01）. Compared with the AQP4-IgG-associated myelitis group， the GFAP-IgG-associated myelitis group had a significantly higher number of the diseased segments of spinal cord [13（5.8，18） vs 6（3，12.5），P=0.01]. Compared with the MOG-IgG-associated myelitis group， the GFAP-IgG-associated myelitis group had a significantly higher EDSS score at discharge [4（3，6） vs 1（0，3），P2=0.01] and at last follow-up [0（0，2.8） vs 0（0，1），P2=0.047]. Conclusion There are differences in clinical features， serological/CSF profiles， and imaging features among the three groups of patients with myelitis，which may help with the differential diagnosis of the different subtypes of myelitis.
Myelitis

Deep medullary vein （DMV） lesions refer to the structural and functional abnormalities of the small venous system within the deep white matter under pathological conditions. Under normal physiological circumstances， DMV are responsible for venous drainage of deep white matter and clearance of metabolic waste. The pathogenesis of DMV lesions mainly involves luminal stenosis caused by collagen deposition in the venous wall， hemodynamic disturbances due to elevated venous pressure， functional impairment of the venous wall induced by inflammatory responses and cytokines， and microcirculatory disturbance caused by ischemia and hypoxia. Studies have shown that DMV lesions are extensively observed in various neurological disorders， including acute ischemic stroke， cerebral small vessel disease， multiple sclerosis， and Sturge-Weber syndrome， and are closely associated with the imaging manifestations， clinical progression， and prognosis of these diseases. However， despite the continuous improvement in the capability for DMV detection， the specific role of DMV in the pathogenesis of different diseases remains unclear. Further studies are needed to explore the role of DMV in pathophysiological processes and assess its clinical value as a target for early diagnosis and intervention， so as to facilitate the development of precision medicine.

[摘 要] 目的：探讨乙醛脱氢酶1A1（ALDH1A1）mRNA负载树突状细胞（DC）疫苗体外诱导抗鼻咽癌干细胞免疫反应的能力。方法：体外转录ALDH1A1 mRNA并电转染至人外周血DC，构建ALDH1A1-DC疫苗，转染EGFP mRNA为对照。流式细胞术检测DC表型、淋巴细胞亚群、细胞毒性T 淋巴细胞（CTL）增殖和细胞因子分泌。分选ALDH+和ALDH- C666-1细胞，检测干细胞标志物（CD24、CD133）和干性基因（OCT4、SOX2、Nanog）的表达水平，采用CCK-8法评估ALDH1A1-DC疫苗诱导的特异性免疫杀伤能力。结果：EGFP-DC荧光表达率显著高于未转染DC（P < 0.000 1），ALDH1A1-DC抗原提呈分子HLA-ABC、共刺激分子CD86、CD40和CCR7表达与未转染DC相比显著增强（P = 0.001 3、P = 0.005 9、P = 0.000 4及P = 0.001 9）。与单独淋巴细胞组（T）及空载DC诱导的淋巴细胞组（DC-T）相比，ALDH1A1-DC诱导的CTL比例最高（均P < 0.000 1），分裂指数最高（P = 0.000 2、P = 0.000 3），且CD8+CD69+（P = 0.000 5、P < 0.000 1）和CD8+ IFN-γ+（P = 0.012 6、P = 0.001 9）细胞亚群比例均显著提高。ALDH1A1-DC-T细胞对ALDH+C666-1悬浮细胞球的杀伤效果显著优于ALDH-细胞球（P = 0.001 0），且与其他各组淋巴细胞相比表现出较强的抗ALDH+C666-1悬浮细胞球的免疫效应（P = 0.001 0，P < 0.000 1）。然而，HLA-ABC阻断后其对ALDH+C666-1细胞的特异性杀伤效应显著降低（P < 0.000 1）。结论：mRNA转染DC后可翻译蛋白并促进DC成熟，增强其诱导特异性CTL免疫反应的能力。

[摘 要] 目的：探究雌激素受体（ER）阳性乳腺癌患者新辅助内分泌治疗后病理完全缓解（pCR）的疗效影响因素，构建并验证预测模型。方法：回顾性选取2020年1月至2024年1月河北医科大学第四医院收治的715例接受新辅助内分泌治疗及手术治疗的ER阳性乳腺癌患者，根据术后病理结果分为pCR组（72例）和未达pCR组（643例）。按7∶3比例随机分为训练集和测试集，收集患者临床病理资料及实验室指标。通过单因素和多因素Logistic回归分析筛选未达pCR的独立危险因素，并构建预测模型。利用训练集和测试集的受试者工作特征（ROC）曲线、校准曲线及决策曲线分析（DCA）评估模型性能。结果：训练集与测试集患者临床资料比较无显著差异。训练集中，pCR组与未达pCR组在肿瘤增殖标志蛋白Ki-67指数、治疗前血清癌抗原15-3（CA15-3）水平、治疗前雌激素受体1（ESR1）基因突变状态、治疗前miR-1-3p表达水平、治疗前性别决定区Y框蛋白9（SOX9）表达水平、临床分期、淋巴结转移等方面存在差异（P < 0.05）。多因素Logistic回归分析显示，Ki-67指数、治疗前血清CA15-3水平、治疗前ESR1基因突变状态、治疗前miR-1-3p表达水平、临床分期为ER阳性乳腺癌患者新辅助内分泌治疗后未达pCR的独立影响因素（P < 0.05）。基于上述因素构建列线图预测模型，并通过ROC曲线、校准曲线及DCA验证模型具有较好的区分度、预测准确性和临床实用性。结论：基于Ki-67指数、血清CA15-3水平、ESR1基因突变状态等因素构建的列线图预测模型，对ER阳性乳腺癌患者新辅助内分泌治疗后未达到pCR风险具有良好预测效能，可为临床决策提供参考。

Objective To study the mini-character and microscopic features of Plantago asiatica from different populations and summarize the exclusive features to provide a reference for the effective identification of Plantago asiatica. Methods Stereomicroscope and optical microscope were used to identify 30 batches of Plantago asiatica from different populations.The similarities and differences in mini-character and microscopic features of Plantago asiatica among different populations were identified. Results The differences in mini character between the Plantago asiatica from different populations were mainly reflected in whether there was fluff on the surface of leaves, inflorescence peduncles, and persistent sepals, as well as whether the epidermis of fibrous roots was flaky. The differences in microscopic characteristics between the Plantago asiatica from different populations were mainly reflected in the number of non-glandular hairs on the leaf surface, the shape of the petiole endothelial layer cells, and the number of large vascular bundles, and the number of layers of mesophyll palisade tissue cells, etc. Conclusion Plantago asiatica from different populations can be identified through mini-character and microscopic; by comparing the relevant identification features, which can provide a basis for revising and improving the standards of Plantago asiatica.

Objective To analyze the effect of Helicobacter pylori (Hp) infection on serum pepsinogen (PG) I, PGII and gastrin-17 (G-17) levels in elderly patients with chronic atrophic gastritis (CAG). Methods A total of 122 elderly patients with CAG and 85 elderly patients with CSG in the hospital were selected. According to Hp infection status, elderly patients with CAG were divided into CAG Hp (+) group (n=75) and CAG Hp (-) group (n=47). Another 122 healthy subjects with physical examination were enrolled as healthy group. The clinical data and levels of serum PGI, PGII and G-17 were compared among the three groups, and the risk factors affecting CAG with Hp infection were analyzed. Results There were significant differences in the proportion of Hp family infection history, the proportion of often spicy diet, the proportion of frequent dining out and levels of serum PGI, PGII and G-17 among CAG, CSG and healthy groups (P<0.05). Serum PGI and PGII in CAG Hp (+) group were lower than those in CAG Hp (-) group while G-17 level was higher (P<0.05). Binary logistic regression analysis showed that Hp family infection history, frequent dining out, serum PGI, PGII and G-17 levels were independent risk factors for Hp infection in elderly CAG (P<0.05). Conclusion Hp infection in elderly CAG patients is related to family aggregation, route of transmission and eating habits. Serum PGI, PGII and G-17 levels are influencing factors for elderly CAG with Hp infection.

Objective Magnetoreception, the remarkable ability of diverse animals to sense and utilize the geomagnetic field for orientation and navigation, remains a molecularly unresolved mystery in sensory biology. The putative magnetoreceptor (MagR, previously known as IscA1) is a highly conserved iron-sulfur protein implicated in both magnetoreception and iron metabolism; however, the functional diversity among its cross-species homologs remains poorly understood. Cellular morphology is a key genetically determined trait that can be altered through genetic or environmental modifications—a process known as cell morphology engineering. Constructing engineered cells with specific morphological features and magnetic sensitivity to achieve remote, non-invasive magnetic modulation represents a crucial goal in this field with significant application potential. Therefore, this study aims to systematically investigate the effects of MagR heterologous expression on bacterial morphology and magnetic sensing capabilities, screen for MagR-based magnetically sensitive morphology engineering pathways, and reveal the underlying molecular mechanisms. Methods We systematically screened 28 MagR homologous genes from diverse prokaryotic and animal taxa to evaluate their expression and corresponding phenotypic effects in Escherichia coli (E. coli). To compare the differential magnetic responses among bacteria expressing various recombinant MagR proteins, we utilized high-throughput automated bright-field microscopic imaging and scanning electron microscopy (SEM). Furthermore, comprehensive biochemical and biophysical characterizations of iron and iron-sulfur cluster binding were performed using Ferrozine colorimetric assays, electron paramagnetic resonance (EPR) spectroscopy, ultraviolet-visible (UV-Vis) absorption, and circular dichroism (CD) spectroscopy. Additionally, 100 mT static magnetic field (SMF) exposure experiments were conducted to assess magnetically tunable phenotypes, while the intrinsic magnetic properties of purified MagR proteins were directly measured using a superconducting quantum interference device (SQUID) magnetometer. Results Our results demonstrated that the heterologous expression of MagR homologs induced varying degrees of bacterial filamentation. From this comprehensive screen, two distinct morphological patterns were identified: hydra (Hydra vulgaris) MagR (hyMagR) promoted uniform cell elongation and filamentation, exhibiting robust magnetic sensitivity manifested as significantly enhanced filamentation under the 100 mT SMF. In contrast, pigeon (Columba livia) MagR (clMagR) induced only low-frequency, extreme filamentation (sporadically exceeding 80 μm) with a relatively weaker magnetic morphological response. Mechanistically, our data unambiguously proved that these phenotypic differences are primarily driven by distinct iron redox preferences rather than total cellular iron accumulation. Specifically, hyMagR preferentially binds ferrous iron (Fe²⁺), whereas clMagR favors ferric iron (Fe³⁺) and forms more stable iron-sulfur clusters. Intriguingly, although SQUID magnetometry showed that purified clMagR exhibited approximately five-fold higher mass magnetic susceptibility than hyMagR, its cellular magnetic response was weaker. We hypothesize that the Fe²⁺-preferred intracellular environment associated with hyMagR overexpression primes the cell for enhanced generation of reactive oxygen species (ROS) via the Fenton reaction. Exposure to an SMF synergizes with this primed redox state, triggering the bacterial SOS response and upregulating cell division inhibitors to efficiently induce uniform filamentation. Conclusion Our findings identify the Fe²⁺/Fe³⁺ redox state as a critical determinant of MagR-mediated morphological remodeling and magnetic responsiveness. This discovery suggests a potential strategy for engineering magnetically responsive cellular systems for synthetic biology applications, and provides a plausible framework, which potentially combines intrinsic protein magnetism with redox-state modulation, for further investigating the evolutionary mechanisms of MagR-mediated magnetoreception.