Objective: To understand the allocation and use of safety seats for preschool children and explore its related factors, so as to provide a scientific reference for promoting the usage of safety seats. Methods: A stratified random cluster sampling method was used to select 3 143 parents of preschool children aged 3 to 6 from six kindergartens in Shunyi District, Beijing from January 3 to 10, 2022. An online questionnaire survey was conducted to collect and evaluate the equipment and use of child safety seats in different characteristics of preschool children, as well as their scores of health beliefs. Multiple factor Logistic regression analysis was used to investigated the related factors of safety seat configuration and use. Results: The equipping rate and usage rate of safety seats for preschool children were 66.56% and 58.45%, respectively. The proportion of equipped and used safety seats for preschool children in core families (69.52%, 62.23%) were higher than that in large families (64.35%, 55.62%), only child families ( 72.39 %, 64.87%) were higher than non only child families (61.49%, 52.86%), and urban families (71.63%, 63.04%) were higher than rural families (52.31%, 45.51%) ( χ 2=9.23, 13.86; 41.72, 46.44; 101.96 ,76.97,all P <0.05) . As the educational level of parents ( χ 2 trend =154.23,98.76) and annual income of the family ( χ 2 trend =155.78,127.69) rised, the reporting rates of the equipped and used child safety seats in the family also increased(all P <0.05 ). There were statistically significant differences in the scores of different dimensions of health beliefs for the provision ( t =-20.22-18.16) and use ( t =24.32-24.17) of safety seats for preschool children(all P <0.05). After adjusting for child sex, child age, family annual income, parental education level, family type, whether the child was an only child, and place of residence，multivariate Logistic regression analysis showed that preschool children with higher perceived susceptibility score( OR =1.11, 1.08), higher self efficacy score( OR =1.23, 1.33), and higher suggestive factors score( OR =1.08, 1.12) were more likely to have and use safety seats in their families, while preschool children with higher perceived impairments score( OR =0.82, 0.80) were less likely to have and use safety seats in their families (all P <0.05). Conclusions The installation rate of child safety seats needs to be improved, and there is also a certain gap in their use after installation. Parents of preschool children should improve susceptibility and self efficacy to safety seat equipment and use, and perceptual barriers should be reduced.

Infection is an important trigger for the initiation of pancreatic islet autoimmunity in type 1 diabetes mellitus （T1DM）. From the perspective of latent pathogen and dryness disorder， this study analyzes the core pathogenesis and dynamic evolution of T1DM in the subclinical and clinical stages. Combined with the T1DM "constraint， heat， deficiency， damage" state and target differentiation and treatment theory， the course of infection-induced T1DM is divided into three stages， including latent dryness， dry-heat and collateral damage. The "latent dryness" stage corresponds to the subclinical phase of T1DM， while the "dry-heat" stage corresponds to the clinical phase， and the "collateral damage" stage corresponds to the phase in which chronic complications develop. Treatment principles include supplementing deficiency and dispelling pathogen during the "latent dryness" stage， clearing heat and moistening dryness in the "dry-heat" stage， and dissolving stasis and unblocking collaterals in the "collateral damage" stage. Furthermore， syndrome-targeted and target-directed therapeutic modifications were made according to T1DM-related autoimmune activity， metabolic comorbidities， and vascular comorbidities， providing a reference for clinical management of T1DM.

ObjectiveTo investigate the therapeutic effects of direct-acting antiviral agents (DAAs) combined regimens for hepatitis C virus (HCV) patients in Dehong Prefecture, Yunnan Province from 2022 to 2024, to analyze the characteristics of treatment failure patients, so as to provide a basis for discovering more effective treatment regimens in the future. MethodsData on HCV prevention and treatment in Dehong Prefecture was extracted from the China Disease Control and Prevention Information System. A total of 617 patients with HCV antiviral therapy were included, and the differences in variable characteristics among patients with different genotypes were analyzed using comparative statistical tests, including basic socio-demographic characteristics, biochemical testing indicators, and information on previous treatment and current treatment. In addition, the cure rate of HCV patients with diverse characteristics was compared, and the potential causes of treatment failure were explored simultaneously. ResultsThe cure rate of HCV was 96.8%, and statistically significant differences were observed in aspartate transaminase (AST) and alanine transaminase (ALT) levels, previous antiviral therapy history and initial treatment regimens among patients with different HCV genotypes (all P<0.05). Among the multi-type combination regimens, the cure rate of sofosbuvir (SOF)-containing regimens was 97.00%, that of velpatasvir (VEL)-containing regimens was 95.45%, and the cure rate of other treatment regimens, including the regimens with ribavirin (RIB) intervention, was 93.10%. Among the patients with treatment failure, 45.00% had genotype 3, 40.00% had abnormal abdominal ultrasound results, and all presented with elevated baseline AST test levels. ConclusionThe clinical treatment of HCV patients should consider the differences in genotype and biochemical test results. DAAs combined regimens for HCV have achieved a high cure rate in Dehong Prefecture and are applicable to HCV patients with diverse clinical characteristics, providing research evidence for wider application.

This paper summarizes Professor ZHAO Jiping's acupuncture diagnostic and therapeutic approach for tic disorders (TD). Focusing on the pathological characteristics of tic disorder (TD), this study analyzes TD's multilayered disease localization. Based on disease-based differentiation, it is proposed that the fundamental pathological location lie in the liver and brain, while the manifestation is in the sinew meridians. The core pathogenesis is characterized as "internal stirring of wind due to liver hyperactivity, upward disturbance of the mind in the brain, and external disharmony of the sinews", based on which the fundamental therapeutic principles are established as calming the liver and extinguishing wind, tranquilizing the mind and awakening the brain, and dredging and regulating the sinews. In clinical practice, attention is paid to meridian and acupoint examination, integrating the four diagnostic methods to assess the deficiency or excess of the liver, the state of the mind, and the condition of the sinews. Acupoint selection emphasizes three regulatory strategies: (1) liver regulation: Taichong (LR3), Hegu (LI4) are selected to soothe the liver and regulate qi; (2) brain regulation: Baihui (GV20), Shenting (GV24), Yintang (GV24⁺), Fengchi (GB20) are selected to calm the mind and stabilize the spirit; (3) sinew regulation: Yanglingquan (GB34), Zusanli (ST36), Quchi (LI11) are selected to regulate qi and blood and relax the sinews. Manipulation techniques, as well as various acupuncture and moxibustion methods, are also emphasized. A differential treatment framework of "layered disease localization-corresponding pathogenesis-precise acupoint selection and technique" has been established to provide a clinical guide for the diagnosis and treatment of TD.
Humans ; Acupuncture Therapy/history* ; Tic Disorders/diagnosis* ; Acupuncture Points ; Meridians ; Diagnosis, Differential ; China

Objective: To analyze the serological characteristics of anti-Mur antibodies and investigate the distribution frequency of the Mur antigen among voluntary blood donors in Shiyan, thereby providing a basis for guiding clinical transfusion and establishing a Mur blood type database. Methods: ABO blood grouping of donors and patients was performed using an automated blood typing analyzer and the gel card method, respectively. Unexpected antibody screening and identification were performed using the saline, tube anti-human globulin, and polybrene methods. The specificity of anti-Mur antibodies was confirmed using Fisher's exact probability test. Plasma treated with 2-mercaptoethanol was used to distinguish IgM and IgG antibodies. IgM and IgG anti-Mur titers were determined by the saline tube method and the anti-human globulin tube method, respectively, at 4℃, room temperature, and 37℃. A total of 1 659 donor red blood cell samples were initially screened for the Mur antigen phenotype using three samples of human-derived anti-Mur plasma by the micro-tube method. Donors who tested positive for Mur antigen were further tested by the direct antiglobulin test (DAT); those with negative results were confirmed for Mur antigen by the gel card and polybrene methods. Results: Three blood samples were identified to contain mixed IgG and IgM anti-Mur antibodies. The titers of both IgM and IgG anti-Mur antibodies were highest at 4℃, intermediate at room temperature, and lowest at 37℃. The positive frequency of the Mur antigen among voluntary blood donors in Shiyan was 1.99% (33/1 659). Conclusion: anti-Mur antibodies were detected in both blood donors and patients in our region. The Mur antigen shows a certain distribution frequency among voluntary blood donors in Shiyan. Screening for the Mur blood type and establishing a corresponding database could enhance transfusion safety.

This study investigated the role of the nuclear factor of activated T cells c3 (NFATc3) in vascular smooth muscle cells (VSMCs) during aortic aneurysm and dissection (AAD) progression and the underlying molecular mechanisms. Cytoplasmic and nuclear NFATc3 levels were elevated in human and mouse AAD. VSMC-NFATc3 deletion reduced thoracic AAD (TAAD) and abdominal aortic aneurysm (AAA) progression in mice, contrary to VSMC-NFATc3 overexpression. VSMC-NFATc3 deletion reduced extracellular matrix (ECM) degradation and maintained the VSMC contractile phenotype. Nuclear NFATc3 targeted and transcriptionally upregulated matrix metalloproteinase 9 (MMP9) and MMP2, promoting ECM degradation and AAD development. NFATc3 promoted VSMC phenotypic switching by binding to eukaryotic elongation factor 2 (eEF2) and inhibiting its phosphorylation in the VSMC cytoplasm. Restoring eEF2 reversed the beneficial effects in VSMC-specific NFATc3-knockout mice. Cabamiquine-targets eEF2 and inhibits protein synthesis-inhibited AAD development and progression in VSMC-NFATc3-overexpressing mice. VSMC-NFATc3 promoted VSMC switch and ECM degradation while exacerbating AAD development, making it a novel potential therapeutic target for preventing and treating AAD.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

According to zang-fu （脏腑） wind-damp theory， it is believed that wind， cold， and dampness are internal pathogenic factors that， when stagnated， transform into heat and invade the zang-fu organs， leading to chronic conditions. Heat is seen as a manifestation， while cold is considered the root cause. When external factors trigger these latent pathogens， the disease of the zang-fu organs exacerbates or relapses， often presenting with a complex syndrome of cold and heat. Based on this theory， the viewpoint of "for complex syndrome of cold and heat， cold is the root" is proposed. It suggests that for diseases with a complex cold-heat syndrome， external invasion of wind， cold， and dampness are the initiating factors. During the acute phase， treatment should focus on dispelling and eliminating the pathogens to promote the expulsion of the latent wind， cold， and dampness. During the remission phase， the focus shifts to reinforcing the healthy qi and tonifying the root， allowing the cold and dampness to be cleared. Internal dampness originates from the spleen； therefore， regulating the spleen and stomach， and dispersing cold and removing dampness is the key to treating wind-damp disorders of zang-fu organs. Cold and dampness are both yin pathogens， which damage yang qi， and repeated invasions of wind， cold， and dampness obstruct the qi flow of the zang-fu organs， progressively weakening yang qi. Hence， it is necessary to protect yang qi， and thereafter dispelling cold and dampness by warming yang. The theory that "for complex syndrome of cold and heat， cold is the root" provides guidance for the clinical application and the treatment of complex and difficult diseases in traditional Chinese medicine.