Objective: To establish a real-time quality control scheme based on the median (MD-IC) of internal control cycle threshold value in negative samples (NEG-IC-CT), so as to monitor anomalies such as progressive drift in nucleic acid testing system not covered by conventional internal quality control (IQC) in blood center nucleic acid laboratories, and to verify its feasibility. Methods: The internal control CT values of 54 426 negative samples were retrospectively collected. These samples were from four reagent batches of the two new and old equipment sets during the operation of the Wantai nucleic acid testing system in our blood center. The daily median of NEG-IC-CT values was used as the research indicator. Control limits were calculated using median absolute deviation (MAD) to construct the Median-MAD quality control chart. The monitoring performance of this scheme for the operation status of the testing system was simultaneously evaluated. Results: Statistical analysis showed significant differences in NEG-IC-CT value distribution between the new and old equipment sets, as well as between the two different reagent batches of the old equipment (P<0.000 1). The NEG-IC-CT value performance of the two different reagent batches of the new equipment was no significant difference in distribution (P>0.05). This scheme identified three typies of distinct anomalies. The out-of-control events observed with the old equipment in both the O1 and O2 reagent batches suggested potential performance decay due to equipment aging. The unreported change of reagent batch in time of Phase B with new equipment caused a stepwise drift on the quality control chart. In the later stage of Phase A with the new equipment, an alert was triggered, indicating potential quality risks associated with practices such as the mixed use of the remaining reagents and extremely long operator working hours. Conclusion: The realtime quality control scheme based on NEG-IC-CT value established in this study has been preliminarily validated for its monitoring effectiveness in nucleic acid testing in our blood center. This scheme performed well in detecting differences among testing systems and reagent batches, serving as an effective supplement to routine internal quality control. It can provide an intuitive and effective evaluation method for monitoring the performance of the nucleic acid testing process at blood center.

ObjectiveTo observe the effect of Liuwei Dihuangwan on behavioral impairments in the rat model of autism spectrum disorder （ASD） and explore the mechanism of action. MethodsTwelve SD pregnant rats were intraperitoneally injected with valproic acid （VPA） （10 rats） or normal saline （2 rats）， and male offspring were selected to establish the model of ASD and the control rats. Rats were randomly assigned into model， low-dose （0.75 g·kg^-1） and high-dose （1.5 g·kg^-1） Liuwei Dihuangwan， vitamin D （positive drug， 3.7×10^-5 g·kg^-1）， and blank groups. Each group was administrated with the corresponding concentration of drugs or the same volume of normal saline by gavage for 2 weeks. After the intervention， the three-chamber social test was conducted to evaluate social interaction and social preference. The open field test was carried out to observe spontaneous behavior and anxiety state. Hematoxylin-eosin staining （HE） was used to observe the pathological changes of the prefrontal tissue. Transmission electron microscopy was employed to observe the ultrastructure of mitochondria in prefrontal neurons. Immunofluorescence was used to detect the expression of ionized calcium-binding adapter molecule-1 （Iba-1） in the prefrontal tissue. Enzyme-linked immunosorbent assay （ELISA） was adopted to measure the levels of tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6）. Western blot was employed to assess the expression differences of phosphorylated adenosine monophosphate-activated protein kinase （p-AMPK）， adenosine monophosphate-activated protein kinase （AMPK）， phosphorylated Unc-51-like autophagy-activating kinase 1 （p-ULK1）， Unc-51-like autophagy-activating kinase 1 （ULK1）， and FUN14 domain-containing protein 1 （FUNDC1）. ResultsCompared with the blank group， the model group spent less time sniffing stranger 1 and stranger 2 in the three-chamber social test （P<0.01） and showed reductions in the total distance traveled， average speed， distance traveled in the central area， and time spent in the central area in the open field test （P<0.01）. In addition， the model group showed extensive apoptosis of neurons， with shrunken nuclei and red-stained cytoplasm， and extensive necrosis of neurons in the prefrontal tissue， mitochondrial swelling， decreased matrix density， disrupted cristae， and autophagic lysosomes in neurons， increases in the rate of Iba-1 positive cells in the prefrontal area （P<0.01） and the levels of TNF-α and IL-6 （P<0.01）， and down-regulation in the expression of p-AMPK/AMPK， p-ULK1/ULK1， and FUNDC1 （P<0.01）. Compared with the model group， low-dose and high-dose Liuwei Dihuangwan and the vitamin D prolonged the time spent sniffing stranger 1 and stranger 2 in the three-chamber social test （P<0.05， P<0.01）， increased the total distance traveled， average speed， distance traveled in the central area， and time spent in the central area in the open field test （P<0.05， P<0.01）， restored the morphology of neurons in the prefrontal tissue， decreased the number of apoptotic cells， alleviated the swelling of mitochondria in neurons， increased the matrix density， mitigated the fragmentation and disorder of cristae， and increased the number of autophagosomes. Moreover， the drugs decreased the rate of Iba-1 positive cells in the prefrontal area （P<0.01）， lowered the levels of TNF-α and IL-6 （P<0.01）， and up-regulated the expression of p-AMPK/AMPK， p-ULK1/ULK1， and FUNDC1 （P<0.01）. ConclusionLiuwei Dihuangwan ameliorate autism-like behaviors and reduce neuronal apoptosis and neuroinflammatory damage in the rat model of ASD by promoting mitophagy mediated by the AMPK/ULK1/FUNDC1 pathway.

Neurocritical care involves complex pathophysiological mechanisms, and its incidence is higher, injuries are more severe, and treatment is more challenging in high-altitude environments. This consensus, based on the latest domestic and international evidence-based medical data, establishes a standardized, goal-oriented framework for neurocritical care management applicable in high-altitude regions and nationwide. The consensus was developed following international standards for evidence quality assessment and underwent two rounds of Delphi expert consultation, resulting in 32 recommendation statements covering three parts: management systems, monitoring and assessment, and core strategies. Key updates include: advocating for the establishment of independent neurocritical care units and implementing precise tiered diagnosis and treatment based on the "Five Differences in Critical Care" concept; constructing a "trinity" multimodal brain monitoring system centered on cerebral blood flow, cerebral oxygenation, and brain function, emphasizing routine bedside transcranial Doppler ultrasound, cerebral oximetry, and continuous electroencephalography monitoring; shifting management strategies from mild hypothermia therapy to targeted temperature management, and defining the "446" target management pathway for the supercritical stage; emphasizing the assessment of static and dynamic cerebrovascular autoregulation functions through multimodal methods to achieve individualized optimal mean arterial pressure management; elevating cerebrospinal fluid management goals to the level of "glymphatic system" function maintenance; implementing a multidisciplinary collaborative, whole-process management model focusing on patients' long-term neurological functional outcomes; de-escalation criteria include multidimensional indicators such as recovery of brain structure, restoration of cerebrovascular autoregulation, improvement in cerebrospinal fluid dynamics, and reduction in biomarker levels; and integrating cutting-edge technologies like artificial intelligence into post-critical care management and rehabilitation planning. This consensus systematically integrates the entire process of neurocritical care management, reflecting the modern connotation of goal-oriented, dynamic, and multimodal integration in neurocritical care medicine. It aims to adapt to new trends such as deepening understanding of pathophysiological mechanisms, the integration of medicine and engineering, and the empowerment of artificial intelligence, thereby further advancing the discipline of critical care medicine.

Objective: To investigate the status of condom use and its influencing factors among men who have sex with men (MSM), so as to provide a basis for improving condom utilization rates and AIDS prevention and control in this population. Methods: From May to October 2024, a snowball sampling method was employed to recruit MSM in Songjiang District, Shanghai Municipality. Self-administered questionnaires were used to collect data on demographic characteristics, AIDS-related knowledge, sexual behaviors, pre-exposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP), and condom use in the past six months. Multivariable logistic regression model was used to analyze the influencing factors for consistent condom use. Results: A total of 921 MSM were surveyed, with a median age of 29.00 (interquartile range, 9.00) years. Among them, 697 (75.68%) were aware of AIDS-related knowledge, 826 (89.69%) expressed willingness to use PrEP, and 835 (90.66%) were willing to use PEP. Additionally, 787 (85.45%) MSM reported their age at first homosexual intercourse as ≥18 years, while 519 (56.35%) reported consistent condom use in the past six months. Multivariable logistic regression analysis revealed that MSM who were aware of AIDS-related knowledge (OR=0.582, 95% CI: 0.423-0.801), willing to use PrEP (OR =0.611, 95% CI: 0.385-0.969), and whose age at first homosexual intercourse was <18 years (OR=0.480, 95% CI: 0.330-0.700) were less likely to consistent use condoms. Conclusion The proportion of consistent condom use among the MSM remains relatively low, which is primarily associated with AIDS-related knowledge, willingness to use PrEP, and the age at first homosexual intercourse.

Objective: To explore the experiences of obesity among junior high school students, and reveal its core themes and essential features, so as to provide evidence for health promotion. Methods: From March to August 2025, semi structured in depth interviews were conducted with 22 obese junior high school students (15 boys,7 girls) aged 13-16 years from two junior high schools in Beijing and one junior high school in Shenyang.Each interview lasted about 40 minutes, and the outline of the interview mainly involved three dimensions: obesity experience, obesity life experience, suggestions and future expectations. Data were analyzed using Moustakas phenomenological method. Results: A total of 4 core themes and 13 sub themes were identified: health experiences (external discipline, health conflicts, perceptual tension), exercise experiences (restricted activity, weight loss expectations, psychological catharsis, physical education test pressure), emotional experiences (appearance anxiety, self soothing, generalized impact), and social experiences (social devaluation, external support, covert suppression). Conclusions Obesity is a complex experience co-constructed by body awareness, physiological indicators, and sociocultural factors. Interventions should enhance students’ body awareness, facilitate a shift from external discipline to internal motivation, and form a collaborative health promotion pathway involving families, schools, and society.

[摘 要] 目的：探讨蟾毒灵（BU）对肿瘤相关巨噬细胞（TAM）介导的结直肠癌（CRC）细胞程序性死亡蛋白-配体1（PD-L1）表达的调控作用及其分子机制。方法：采用HCT116细胞与THP-1来源巨噬细胞构建体外共培养体系。佛波酯（PMA）诱导THP-1细胞分化为M0型巨噬细胞，进一步以HCT116细胞条件培养基（CM）刺激形成TAM样细胞。流式细胞术检测CD11b、CD206表达，以评价巨噬细胞极化水平；RT-qPCR及WB法检测TGF-β、IL-10、STAT3/p-STAT3及PD-L1表达变化；慢病毒转染构建STAT3敲低细胞系HCT116sh-STAT3，结合BU干预验证STAT3/PD-L1信号通路作用。结果：HCT116细胞CM可诱导巨噬细胞向M2表型极化，表现为CD11b⁺CD206⁺细胞比例升高（P < 0.01）及TGF-β、IL-10表达增加（均P < 0.001）。TAM条件培养基可显著促进HCT116细胞STAT3磷酸化（P < 0.001）并上调PD-L1 mRNA及蛋白表达水平（P < 0.001或P < 0.01）。BU干预后，TAM介导的STAT3磷酸化水平明显下降，PD-L1表达同步下调（均P < 0.01）。STAT3敲低可降低PD-L1表达，其作用趋势与BU一致。结论：BU可通过抑制TAM介导的STAT3信号激活，下调CRC细胞PD-L1表达，提示其在肿瘤免疫微环境调控中具有潜在的应用价值。

Objective To analyze the disease burden and trends of bladder cancer in China and globally from 1992 to 2021.  Methods Using the GBD 2021 database, the incidence, prevalence, mortality, and disability-adjusted life years (DALYs) rates of bladder cancer in China and globally from 1992–2021 were analyzed. Average annual percentage change (AAPC) was calculated using Joinpoint regression. Subgroup analyses by sex and age were conducted, and a Bayesian age-period-cohort (BAPC) model was used to predict trends in age-standardized incidence rate (ASIR) and age-standardized mortality rate (ASMR) for the next 15 years.  Results In 2021, China reported 106 000 new cases (ASIR: 5.14/100 000), 571 000 prevalent cases (age-standardized prevalence rate, ASPR: 26.61/100 000), 43 000 deaths (ASMR: 2.34/100 000), and a DALY rate of 45.31/100 000. From 1992–2021, China showed upward trends in ASIR and ASPR but declines in ASMR and DALYs, while global ASIR, ASMR, and DALYs decreased overall with slow ASPR growth. The peak cases in China and globally were both concentrated in the 65-79 age group, with a significantly higher burden on males than females. In China, smoking-related ASMR and ASDR exceeded global averages and rose, whereas high glucose-related indexes were lower and declined. Projections for 2021–2036 indicated that the global incidence and mortality rates would be rising, but ASIR/ASPR would be declining, while in China, the incidence rate would continue to rise, and the mortality rate will stabilize, with a significant increase in ASIR and a gradual decrease in ASPR.  Conclusion From 1992 to 2021, the incidence of bladder cancer in China has shown a continuous upward trend and is projected to persist in the future, with significant gender and age differences. Particular attention should be given to elderly males aged 85-89. The disease burden of bladder cancer attributable to smoking continues to rise, highlighting the urgent need to strengthen tobacco control policies.

ObjectiveThis study aims to investigate the effect of Liuwei Dihuangwan on the autophagy function in the hippocampus of senescence-accelerated mouse prone 8 （SAMP8） by regulating the expression of glycoprotein non-metastatic melanoma protein B （GPNMB）. Furthermore， it is designed to explore the mechanism of the method of tonifying the kidneys and replenishing essence in the treatment of Alzheimer's disease （AD）. MethodsIn experiment 1， 24 5-month-old SAMP8 mice were randomly and equally divided into the model group， and the low-， middle- and high-dose（0.59，1.18，2.36 g·kg^-1） Liuwei Dihuangwan groups. At the same time， six 5-month-old senescence accelerated mouse resistant 1 （SAMR1） mice were used as the control group. The learning and memory ability was evaluated through novel object recognition experiment. Serum cortisol （Cort）， adrenocorticotropic hormone （ACTH） and urine 17-hydroxycorticosteroid （17-OHCS） levels were detected by enzyme-linked immunosorbent assay （ELISA）. The ultrastructure of hippocampal neurons was observed by transmission electron microscope （TEM）， and the expression levels of hippocampal GPNMB， a disintegrin and metalloproteinase 10 （ADAM10） and autophagy-related proteins were detected by Western blot. In experiment 2， 18 SAMP8 mice were randomly and equally divided into the model group， vector control group （Vector）， and GPNMB overexpression group （GPNMB^OE）. Lentiviral vectors were stereotactically injected into the brain （2 μL per side in the GPNMB^OE group）. Western blot was used to detect the expression of the above target proteins in the hippocampus； In Experiment 3， 24 SAMP8 mice were randomly and equally divided into the model group， Liuwei Dihuangwan group， Liuwei Dihuangwan+negative control （NC） group， and Liuwei Dihuangwan+GPNMB silencing group （shGPNMB）. Before drug treatment， the Liuwei Dihuangwan+NC group and the Liuwei Dihuangwan+shGPNMB group were injected with negative control and GPNMB silencing lentivirus， respectively. Western blot was used to detect the expression of the above target proteins in the hippocampus. ResultsThe novel object discrimination index of mice in the model group was significantly lower than that of mice in the control group （P<0.01）. The novel object discrimination index of mice in the medium- and high-dose Liuwei Dihuangwan groups was significantly higher than that of mice in the model group （P<0.01）. Aggregated autolysosomes were observed in the normal hippocampus tissue by TEM. In the model group， mitochondria were dominant， and no typical characteristic autophagosomes were observed. In the low- and medium-dose Liuwei Dihuangwan groups， a small number of autolysosomes and autophagosomes with double-membrane structures were observed. In the high-dose Liuwei Dihuangwan group， the number of autophagosomes and autolysosomes was greater than that in the low- and medium-dose groups. The results of ELISA and Western blot showed that compared with the control group， the levels of serum Cort， ACTH， and urine 17-OHCS in the model group were substantially increased， while the expression of hippocampal ADAM10， Beclin1， and microtubule associated-protein light chain 3-Ⅱ/Ⅰ （LC3 Ⅱ/Ⅰ） was significantly decreased. The expression of GPNMB and ubiquitin binding protein p62 was significantly increased （P<0.05， P<0.01）. Compared with the model group， the serum Cort and ACTH levels in the low-， medium-， and high-dose Liuwei Dihuangwan groups were significantly reduced， while only the urine 17-OHCS level in the high-dose group was significantly reduced. The hippocampal GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ expression levels in the medium-， and high-dose groups of Liuwei Dihuangwan were significantly increased compared to the model group， whereas the expression of p62 was significantly reduced （P<0.01）. The above indicators showed a progressive trend among the three groups. Compared with the model group， the GPNMB^OE group showed a significant increase in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ expression， and a significant decrease in p62 expression （P<0.01）. Compared with the model group， the expression of GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ in the hippocampus of the Liuwei Dihuangwan group significantly increased， while the expression of p62 significantly decreased （P<0.01）. Compared with the Liuwei Dihuangwan group， the Liuwei Dihuangwan+shGPNMB group showed a significant decrease in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ， and a significant increase in p62 expression （P<0.01）. ConclusionLiuwei Dihuangwan can enhance hippocampal autophagy function and improve AD by upregulating GPNMB expression.

Objective: To summarize the best evidence for the management of patients with gastrointestinal graft-versushost disease after hematopoietic stem cell transplantation, and provide evidence-based references for clinical nursing work. Methods: A systematic search was conducted for relevant evidence on the management of patients with gastrointestinal graft-versus-host disease after hematopoietic stem cell transplantation from domestic and foreign databases, as well as websites of blood and bone marrow transplantation related societies. The search period was from the establishment of the database until February 2026. Results: After screening, a total of 19 articles were included, encompassing 3 clinical decisions, 1 recommended practice, 4 guidelines, 7 expert consensuses, and 4 evidence summaries. Twenty-five pieces of best evidence were summarized across 8 aspects: multidisciplinary collaboration, influencing factors, assessment and monitoring, diagnostic differentiation, symptom management, dietary nutrition, medication guidance, and health education. Conclusion: Summarizing the relevant evidence on the management of patients with gastrointestinal graft-versus-host disease after hematopoietic stem cell transplantation can provide evidence-based support for clinical medical staff, and it is recommended to apply it in combination with clinical practice and patient wishes.

ObjectiveTo investigate the role and mechanism of thymic stromal lymphopoietin （TSLP） in a mouse model of acetaminophen （APAP）-induced acute liver injury. MethodsA total of 16 wild-type （WT） male C57BL/6J mice were randomly divided into control group and APAP group， with 8 mice in each group， and the mice in the APAP group were given intraperitoneal injection of APAP solution at a dose of 400 mg/kg to establish an animal model， while those in the control group were given injection of an equal volume of normal saline， with samples collected after 6 hours. An automatic chemical analyzer was used to measure the serum levels of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）； quantitative real-time PCR was used to measure the mRNA expression levels of the inflammatory factors tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in liver tissue； the kit was used to measure the content of glutathione （GSH） in liver tissue homogenate； quantitative real-time PCR and Western blot were used to measure the transcriptional level and protein expression level of TSLP. Furthermore， 22 WT male C57BL/6J mice were randomly divided into control group with 8 mice， APAP group with 8 mice， and APAP+recombination TSLP （rTSLP） group with 6 mice； the mice in the APAP+rTSLP group were given intraperitoneal injection of rTSLP solution， while those in the control group and the APAP group were given injection of the solvent PBS； after 30 minutes， the mice in the APAP+rTSLP group and the APAP group were given injection of APAP solution， while those in the control group were given injection of an equal volume of normal saline. The serum levels of ALT and AST were measured； HE staining was used to observe the pathological changes of the liver； kits were used to measure the levels of the oxidative stress indices malondialdehyde （MDA） and superoxide dismutase （SOD） in liver tissue homogenate； Western blot was used to measure the expression levels of the autophagy-related proteins LC3‍Ⅰ/Ⅱ， Beclin1， and P62 and the molecules such as nuclear factor erythroid 2-related factor 2 （Nrf2）， protein kinase B （Akt）， phosphorylated Akt （p-Akt）， mammalian target of rapamycin （mTOR）， and phosphorylated mTOR （p-mTOR）. In addition， 16 WT male C57BL/6J mice and 16 TSLP receptor-silenced （TSLPR^-/-） mice were divided into WT mouse control group， WT mouse APAP group， TSLPR^-/- mouse control group， and TSLPR^-/- mouse APAP group， with 8 mice in each group； the mice in the WT mouse APAP group and the TSLPR^-/- mouse APAP group were used for modeling by intraperitoneal injection of APAP solution at a dose of 400 mg/kg， and those in the WT mouse control group and the TSLPR^-/- mouse control group were given injection of an equal volume of normal saline. The serum levels of ALT and AST and the content of MDA in liver tissue were measured for these four groups， and Western blot was used to measure the protein expression levels of LC3Ⅰ/Ⅱ， Akt， and p-Akt. The independent-samples t test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsAfter the mouse model of APAP-induced acute liver injury was established successfully， there were significant increases in the mRNA and protein expression levels of TSLP compared with the control group （both P<0.01）. In the study of rTSLP， compared with the control group， the APAP group had significant increases in ALT and AST （both P<0.001） and radial necrosis along the central vein observed by HE staining of liver tissue， as well as significant reductions in the protein expression levels of the oxidative stress indices SOD and Nrf2 and a significant increase in the level of MDA （all P<0.01）； compared with the APAP group， the APAP+rTSLP group had significant reductions in ALT and AST， a significant reduction in necrotic area of liver tissue， significant increases in the protein expression levels of SOD and Nrf2， and a significant reduction in MDA （all P<0.05）； there were significant differences in the protein expression levels of LC3Ⅰ/Ⅱ， Beclin1， P62， p-Akt， and p-mTOR between the APAP+rTSLP group and the control group （all P<0.01）. In the study of TSLPR^-/- mice， compared with the WT mice after modeling， the TSLPR^-/- mice had significant increases in the levels of ALT， AST， and MDA and significant reductions in the expression levels of LC3Ⅰ/Ⅱ and p-Akt （all P<0.05）. ConclusionTSLP can increase autophagy， reduce oxidative stress， and thus improve acute liver injury induced by APAP overdose， possibly by activating the PI3K/Akt signaling pathway and inhibiting mTOR.