BACKGROUND: The transcription factor POU2F1 regulates the expression levels of microRNAs in neoplasia. However, the miR-29b1/a cluster modulated by POU2F1 in gastric cancer (GC) remains unknown. METHODS: Gene expression in GC cells was evaluated using reverse-transcription polymerase chain reaction (PCR), western blotting, immunohistochemistry, and RNA in situ hybridization. Co-immunoprecipitation was performed to evaluate protein interactions. Transwell migration and invasion assays were performed to investigate the biological behavior of GC cells. MiR-29b1/a cluster promoter analysis and luciferase activity assay for the 3'-UTR study were performed in GC cells. In vivo tumor metastasis was evaluated in nude mice. RESULTS: POU2F1 is overexpressed in GC cell lines and binds to the miR-29b1/a cluster promoter. POU2F1 is upregulated, whereas mature miR-29b-3p and miR-29a-3p are downregulated in GC tissues. POU2F1 promotes GC metastasis by inhibiting miR-29b-3p or miR-29a-3p expression in vitro and in vivo . Furthermore, PIK3R1 and/or PIK3R3 are direct targets of miR-29b-3p and/or miR-29a-3p , and the ectopic expression of PIK3R1 or PIK3R3 reverses the suppressive effect of mature miR-29b-3p and/or miR-29a-3p on GC cell metastasis and invasion. Additionally, the interaction of PIK3R1 with PIK3R3 promotes migration and invasion, and miR-29b-3p , miR-29a-3p , PIK3R1 , and PIK3R3 regulate migration and invasion via the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway in GC cells. In addition, POU2F1 , PIK3R1 , and PIK3R3 expression levels negatively correlated with miR-29b-3p and miR-29a-3p expression levels in GC tissue samples. CONCLUSIONS The POU2F1 - miR-29b-3p / miR-29a-3p-PIK3R1 / PIK3R1 signaling axis regulates tumor progression and may be a promising therapeutic target for GC.
MicroRNAs/metabolism* ; Humans ; Stomach Neoplasms/pathology* ; Cell Line, Tumor ; Cell Movement/physiology* ; Phosphatidylinositol 3-Kinases/metabolism* ; Animals ; Mice ; Octamer Transcription Factor-1/metabolism* ; Mice, Nude ; Class Ia Phosphatidylinositol 3-Kinase/metabolism* ; Neoplasm Invasiveness ; Gene Expression Regulation, Neoplastic/genetics* ; Male ; Immunohistochemistry ; Female

Objective:To analyze the epidemic trend of influenza-like illness（ILI）cases，etiological detection results，and the evolution of the hemagglutinin（HA）gene of the predominant strains in Hanzhong City，Shaanxi Province during the 2018-2024 influenza seasons.Methods:ILI sentinel surveillance data and network laboratory test results during the 2018-2024 influenza seasons in Hanzhong City，Shaanxi Province were collected for descriptive analysis. The HA gene sequences of 25 predominant strains were obtained through whole-genome deep sequencing method，and then compared with the vaccine strains recommended by the World Health Organization in the same period to analyze the evolution of the virus.Results:A total of 37 770 cases of ILI were reported in Hanzhong City during the 2018-2024 influenza seasons，and the proportion of total ILI cases（ILI%）was 2.87%（37 770/1 316 009）. The epidemic trend of ILI showed an obvious epidemic peak in winter and spring（from December of the current year to March of the following year）. The specimens with the highest positive rate were of type A（H3N2）（39.12%，365/933），and the predominant epidemic strains in each influenza season alternated among A（H1N1）pdm09（in the 2018-2019 and 2022-2023 influenza seasons），A（H3N2）（in the 2019-2020 and 2023-2024 influenza seasons）and B（Victoria）（in the 2021-2022 influenza season）. The phylogenetic relationship gradually became more distant over time across different influenza seasons. Among them，the epidemic strains of A（H1N1）pdm09 belonged to the 6B.1 clade，and the evolution mainly occurred in the Sa and Sb regions of the HA epitope. Meanwhile，the epidemic strains of A（H3N2）belonged to the 3C clade，and the evolution mainly took place in the A，B and C regions of the HA epitope. The strains of the B（Victoria）lineage belonged to the V1a.3a.2 clade，and the evolution mainly occurred in the 120-loop，150-loop，and 190-helix regions of the HA epitope.Conclusions:The influenza epidemic in Hanzhong City has obvious seasonality，and the amino acids of the epidemic strains have shown a certain degree of variation over the years. In future prevention and control work，influenza surveillance should be continuously strengthened，and the change trend of the predominant circulating strains should be closely monitored.

Objective:To analyze the clinical features and diagnostic process of ring chromosome syndrome.Methods:Clinical data of 9 children with ring chromosome syndrome who were treated at the Children′s Medical Center of Peking University First Hospital from September 2009 to May 2025, were summarized and analyzed in a case series study. The data included clinical manifestations, types of epileptic seizures, genetic testing, treatment outcomes, and follow-up results, et al.Results:Among the 9 children with ring chromosome syndrome, there were 6 girls and 3 boys, including 4 children with ring chromosome 20 syndrome, 3 children with ring chromosome 14 syndrome, and 1 child each with ring chromosome 13 and 17 syndrome. All 9 children had de novo chromosomal variations. Among them, 3 children of ring chromosome 20 syndrome were mosaic, and the remaining 6 children were non-mosaic. All 9 children exhibited diverse clinical features, especially those with ring chromosome 20 syndrome, which presented with specific manifestations. The 4 children with ring chromosome 20 syndrome all had acute epileptic seizures as the initial symptom, with onset ages of 67, 39, 17, and 96 months, and all had focal seizures. One child with ring chromosome 20 syndrome had non-convulsive status epilepticus. Development of all 4 children with ring chromosome 20 syndrome was normal before seizure onset, but 3 children showed regression after onset. No physical deformities were observed in 4 children with ring chromosome 20 syndrome, and 2 children were misdiagnosed, 3 children underwent whole exome sequencing and copy number variation analysis in their families, with no abnormalities detected. All 4 children with ring chromosome 20 syndrome were diagnosed through chromosomal karyotype analysis, the intervals between onset and diagnosis were 2, 81, 19 and 13 months, respectively. Follow-up showed that epileptic seizures were not controlled in all 4 children with ring chromosome 20 syndrome. The other 5 children were characterized by developmental delay as the initial symptom, followed by epileptic seizures between 3 and 24 months of age. Developmental regression of the other 5 children did not occur after onset, 2 of them had microcephaly, and 3 had wide-set eyes. No misdiagnoses were reported in these 5 children, and the intervals between onset and diagnosis were 7, 3, 55, 3, and 106 months, respectively. Follow-up showed that epileptic seizures were controlled in these 5 children. Conclusions:Ring chromosome 20 syndrome typically manifest with epilepsy as the initial symptom and are refractory to drug treatment, their early development is entirely normal. Ring chromosome 13, 14, and 17 syndrome are characterized by developmental delay from an early age, followed by the onset of epileptic seizures, which are easily controlled. Conventional whole exome sequencing and copy number variation analysis in families rarely detect ring chromosome abnormalities. Early chromosomal karyotype analysis is essential for the diagnosis of ring chromosome syndrome.

OBJECTIVE To explore the clinical characteristics of bronchial asthma with secondary pulmonary infec-tions in children and compare the expressions of transcriptomes in peripheral blood between the bronchial asthma with secondary pulmonary infections and the bronchial asthma without the secondary pulmonary infections.METHODS The clinical data were collected from 425 children with bronchial asthma who were treated in respirato-ry medicine department of Children's Hospital of Anhui Province from Apr.2022 to Feb.2025 and were retrospec-tively analyzed.The enrolled children were divided into the infection group with 60 cases and the non-infection group with 365 cases according to the status of complication with pulmonary infections.The clinical characteristics were compared between the infection group and the non-infection group.The gene expression profile sequencing was carried out for peripheral blood mononuclear cells by transcriptome high throughput technology,and the bio-logical information was analyzed.RESULTS There were significant differences in course of asthma,frequencies times of acute attack,complication with nasosinusitis or allergic rhinitis,standardized use of antibiotics and intra-venous use of glucocorticoids between the two groups of children(P＜0.05).Totally 60 children had secondary pulmonary infections,with the infection rate 14.12％.Totally 73 strains of pathogens were isolated,43.84％of which were gram-positive bacteria,and 56.16％were gram-negative bacteria.As compared with the non-infection group,there were 1578 genes with the changed expression in the infection group,and the expressions of the genes such as nuclear factor κB were upregulated.The differentially expressed genes were primarily enriched in immuno-regulation-related pathways,including proinflammatory factor signal transduction,interacted networks of cyto-kines and its receptors,T lymphocyte activation signal transduction and other biological processes.CONCLUSION The specific clinical characteristics and abnormal immune pathways may jointly result in the pulmonary infec-tions in children with the asthma and provide theoretical bases for early identification of the children at high risk of pneumonia and targeted intervention.

Objective:To investigate the clinical manifestations and genetic characteristics of a child with glycogen storage disease type Ⅲ (GSD-Ⅲ) complicated with Guillain-Barré syndrome (GBS) caused by AGL gene variants, and to analyze the pathogenesis, potential correlation, treatment and prognosis of the two diseases. Methods:A child with GSD-Ⅲ who visited the General Hospital of Ningxia Medical University due to " limb weakness for more than ten days" in July 2024 was selected as the study subject. Clinical data of the child were collected. Peripheral blood samples of the child and his parents were collected for whole exome sequencing and Sanger sequencing. Candidate variants were verified, and pathogenicity analysis was conducted for the variant sites. This study was approved by the Medical Ethics Committee of General Hospital of Ningxia Medical University (Ethics No.: KYLL-2025-1984).Results:The child has presented with inability to stand or walk independently, difficulty in grasping, accompanied by numbness and pain at the distal end, choking when drinking water, occasional non-projectile vomiting, and enlargement of liver and spleen. Laboratory tests showed abnormal liver function and a significant increase in creatine kinase. Color Doppler ultrasound of the heart showed an enlarged left atrium and mild regurgitation of mitral and tricuspid valves. Genetic testing confirmed that he has harbored compound heterozygous variants of the AGL gene, namely c. 1611G>A (p.E537E) and c. 579del (p.W194Gfs*7), which were inherited from his father and mother, respectively. According to the guidelines from the American Collage for Medical Genetics and Genomics (ACMG), the two variants were respectively predicted as variant of unknown significance (PM2_Supporting+ PM3+ PP3_Supporting) and likely pathogenic (PVS1+ PM2_Supporting). Electrophysiological examination confirmed that the child had severe damage to the motor and sensory nerves accompanied by axonal injury, which was consistent with the axonal variant type of GBS -acute motor and sensory axonal neuropathy. After a clear diagnosis, the child was treated with intravenous human immunoglobulin. His condition deteriorated progressively, presenting with breathing difficulties, liver failure, and gastrointestinal bleeding, and eventually deceased due to multiple organ failures. Conclusion:The etiology of GSD-Ⅲ and GBS involves multiple aspects such as genetics, metabolism and immunity. In clinical practice, it should be noted that similar clinical manifestations may occur in both conditions. Close attention should be paid to the patients′ blood glucose, blood gas, coagulation function and liver function, etc. Clinical intervention should be carried out as early as possible to improve the prognosis.

Chaihu Guizhi Ganjiangtang （CGG）is a classic prescription in the Treatise on Cold Damage，which has the effects of clearing and relieving stagnation heat in Shaoyang，warming and dissolving water drink，and relieving the pivot mechanism. It is a classic prescription for treating spleen deficiency and liver depression and stopping internal stagnation caused by water drink. The formula is exquisite and well-matched and is often modified and used by ancient and modern medical practitioners to treat various miscellaneous diseases of internal and external medicine，with significant therapeutic effects. In recent years，with the rapid development of modern pharmacology，research on the micro mechanism of CGG has been continuously developed and deepened，providing new ideas for the treatment of diseases with CGG. Therefore，the authors systematically searched databases such as China National Knowledge Infrastructure，Wanfang Data Knowledge Service Platform，VIP Database， and PubMed for literature on the clinical application and pharmacological mechanism of CGG published by Chinese and foreign scholars in recent years. This article summarized the literature from two aspects：the modern clinical application and mechanism of action of CGG and elaborated on the diseases treated by CGG in modern literature，involving digestive system，respiratory system，nervous system，endocrine system，circulatory system，urinary system，gynecology，as well as its application in reducing the side effects of radiotherapy and chemotherapy， gynecology， dermatology， ophthalmology， and orthopedics. At the same time，the mechanism of CGG in treating diseases may be related to anti-inflammatory，anti-oxidative stress， regulation of immunity， anti-fibrosis， anti-tumor， improvement of gastrointestinal flora and motility， protection of liver tissue， reduction of blood lipids and blood sugar， and regulation of hormone levels.

Triple-negative breast cancer (TNBC) remains a refractory subtype of breast cancer due to its resistance to various therapeutic strategies. In this study, we introduce a "brake-release and accelerator-pressing" approach to engineer a microneedle patch embedded with copper-doped Prussian blue nanoparticles (Cu-PB) and the ferroptosis inducer sorafenib (SRF) for raised chemodynamic (CDT)/photothermal (PTT) combination therapy against TNBC. Upon transdermal insertion, the dissolving microneedles swiftly disintegrate and facilitate the release of SRF. Under gentle external light exposure, copper ions (Cu²⁺) and iron ions (Fe³⁺) were liberated from Cu-PB. The direct chelation of Cu²⁺ and the indirect suppression by SRF, collectively attenuate glutathione peroxidase 4 (GPX4) enzymatic function, destabilizing the cellular redox equilibrium (referred to as the "brake-release" strategy). The release of Cu²⁺ and Fe³⁺ ions instigates a Fenton/Fenton-like reaction within tumor cells, further yielding hydroxyl radicals and elevating reactive oxygen species (ROS) concentrations (referred to as the "accelerator-pressing" strategy). This overwhelming ROS accumulation, coupled with the impaired clearance of resultant lipid peroxides (LPO), ultimately triggers a robust ferroptosis cell death response. In summary, this study presents an innovative combinatorial therapeutic strategy based on dual-ferroptosis induction for TNBC, implying a promising therapeutic platform for developing ferroptosis-centered treatments for this aggressive breast cancer subtype.

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Objective To investigate the relationships of the expression of Calponin 1 and tumor ubiquitin-specific protease 1(OTUB1)with clinicopathological features in gastric cancer tissues as well as their prognostic values.Methods A total of 98 patients with gastric cancer were enrolled in this study.The qPCR was used to detect the expression levels of Calponin 1 mRNA and OTUB1 mRNA in gastric cancer tissues;the immunohistochemical staining was performed to detect the protein expres-sion levels of Calponin 1 and OTUB1;the Kaplan-Meier curve was plotted to compare the survival differences among gastric cancer patients with different expression levels of Calponin 1 and OTUB1;the Cox regression model was used to screen the influencing factors of prognosis in gastric cancer.Results Compared with adjacent tissues,the expression levels of Calponin 1 mRNA and OTUB1 mRNA in gastric cancer tissues were significantly higher(P＜0.05).The positive expression rates of Calponin 1 and OTUB1 protein in gastric cancer tissues were 63.27％and 65.31％respectively,which were significantly higher than 6.12％and 8.16％in adjacent tissues(P＜0.001).The expression levels of Calponin 1 and OTUB1 proteins were increased significantly in gastric cancer tissues of cases with stage Ⅲ ofTNM staging and lymph node metastasis(P＜0.05).The 3-year overall survival rate was 45.16％(28/62)in the Calponin 1-positive group,which was significantly lower than 83.33％(30/36)in the Calponin 1-negative group(Log-rank x2=12.990,P＜0.001).The 3-year overall survival rate was 45.31％(29/64)in the OTUB1-positive group,which was significantly lower than 85.29％(29/34)in the OTUB1-negative group(Log-rank x2=14.880,P＜0.001).The results of multivariate Cox regression showed that Calponin 1 positivity,OTUB1 positivity,stage Ⅲ ofTNM staging,and lymph node metastasis were risk factors for death in gastric cancer patients(P＜0.001).Conclusion The expressions of Calponin 1 and OTUB1 are upregulated in gastric cancer tissues and are related to TNM staging and lymph node metastasis.

OBJECTIVE: To investigate the clinical manifestations and genetic characteristics of a child with glycogen storage disease type III (GSD-III) complicated with Guillain-Barré syndrome (GBS) caused by AGL gene variants, and to analyze the pathogenesis, potential correlation, treatment and prognosis of the two diseases. METHODS: A child with GSD-III who visited the General Hospital of Ningxia Medical University due to "limb weakness for more than ten days" in July 2024 was selected as the study subject. Clinical data of the child were collected. Peripheral blood samples of the child and his parents were collected for whole exome sequencing and Sanger sequencing. Candidate variants were verified, and pathogenicity analysis was conducted for the variant sites. This study was approved by the Medical Ethics Committee of General Hospital of Ningxia Medical University (Ethics No.: KYLL-2025-1984). RESULTS: The child has presented with inability to stand or walk independently, difficulty in grasping, accompanied by numbness and pain at the distal end, choking when drinking water, occasional non-projectile vomiting, and enlargement of liver and spleen. Laboratory tests showed abnormal liver function and a significant increase in creatine kinase. Color Doppler ultrasound of the heart showed an enlarged left atrium and mild regurgitation of mitral and tricuspid valves. Genetic testing confirmed that he has harbored compound heterozygous variants of the AGL gene, namely c.1611G>A (p.E537E) and c.579del (p.W194Gfs*7), which were inherited from his father and mother, respectively. According to the guidelines from the American Collage for Medical Genetics and Genomics (ACMG), the two variants were respectively predicted as variant of unknown significance (PM2_Supporting+PM3+PP3_Supporting) and likely pathogenic (PVS1+PM2_Supporting). Electrophysiological examination confirmed that the child had severe damage to the motor and sensory nerves accompanied by axonal injury, which was consistent with the axonal variant type of GBS -acute motor and sensory axonal neuropathy. After a clear diagnosis, the child was treated with intravenous human immunoglobulin. His condition deteriorated progressively, presenting with breathing difficulties, liver failure, and gastrointestinal bleeding, and eventually deceased due to multiple organ failures. CONCLUSION The etiology of GSD-III and GBS involves multiple aspects such as genetics, metabolism and immunity. In clinical practice, it should be noted that similar clinical manifestations may occur in both conditions. Close attention should be paid to the patients' blood glucose, blood gas, coagulation function and liver function, etc. Clinical intervention should be carried out as early as possible to improve the prognosis.
Humans ; Male ; Guillain-Barre Syndrome/complications* ; Glycogen Storage Disease Type III/complications* ; Mutation ; Child