Acute hypoxic exposure can induce functional brain impairment, driven by molecular mechanisms including mitochondrial dysfunction, intracellular calcium overload, glial cell activation and inflammatory responses, blood-brain barrier disruption, and alterated cerebral blood flow. Acetazolamide, a broad-spectrum carbonic anhydrase inhibitor, is a standard clinical treatment and remains the only medication approved by the Food and Drug Administration for the prevention and treatment of acute mountain sickness. Substantial evidence confirms that under acute hypoxic exposure, acetazolamide exerts multi-level neuroprotective effects on brain tissue by inhibiting carbonic anhydrase VB and other isoforms. These protective mechanisms involve preserving mitochondrial integrity, regulating calcium homeostasis and pH balance, modulating glial cell activity to mitigate neuroinflammation, maintaining blood-brain barrier structure integrity, and improving cerebral perfusion through cerebrovascular regulation. This article reviewed the molecular pathological mechanisms of hypoxia-induced nervous system damage, summarized the pharmacological properties and neuroprotective effects of acetazolamide, and provided a theoretical basis for therapeutic interventions against high-altitude hypoxic neural injury.

Acute hypoxic exposure can induce functional brain impairment, driven by molecular mechanisms including mitochondrial dysfunction, intracellular calcium overload, glial cell activation and inflammatory responses, blood-brain barrier disruption, and alterated cerebral blood flow. Acetazolamide, a broad-spectrum carbonic anhydrase inhibitor, is a standard clinical treatment and remains the only medication approved by the Food and Drug Administration for the prevention and treatment of acute mountain sickness. Substantial evidence confirms that under acute hypoxic exposure, acetazolamide exerts multi-level neuroprotective effects on brain tissue by inhibiting carbonic anhydrase VB and other isoforms. These protective mechanisms involve preserving mitochondrial integrity, regulating calcium homeostasis and pH balance, modulating glial cell activity to mitigate neuroinflammation, maintaining blood-brain barrier structure integrity, and improving cerebral perfusion through cerebrovascular regulation. This article reviewed the molecular pathological mechanisms of hypoxia-induced nervous system damage, summarized the pharmacological properties and neuroprotective effects of acetazolamide, and provided a theoretical basis for therapeutic interventions against high-altitude hypoxic neural injury.

ObjectiveTo explore the possible mechanism of action of Lifei Xiaoji Pill （理肺消积丸， LXP） in the treatment of non small cell lung cancer based on the Warburg effect and the USP47/BACH1 pathway. MethodsFifty C57BL/6 mice were randomly divided into five groups， model group， LXP group， inhibitor group， LXP + inhibitor group， and cisplatin group， with 10 mice in each group. A lung cancer mouse model was established by subcutaneously injecting Lewis cells. On the next day， the model group mice were given 0.2 ml of saline by gavage daily， the LXP group given 240 mg/（kg·d） of LXP solution once a day by gavage， the inhibitor group intraperitoneally injected with P22077 at a dose of 10 mg/（kg·d） every day， the LXP + inhibitor group given both LXP by gavage and P22077 by intraperitoneal injection once a day， and the cisplatin group received 0.5 mg/（kg·d） cisplatin intraperitoneally every other day. All treatments lasted for 14 days. On the day after the last dose， tumor weight and volume were measured， tumor histopathology was examined by HE staining， apoptosis in tumor tissues was detected by TUNEL staining， and proliferation cell nuclear antigen （PCNA） protein levels were detected by immunohistochemistry. Warburg effect indicators， including glucose concentration， lactate content， and adenosine triphosphate （ATP） production in tumor tissues， were measured. Western Blot and qRT-PCR were used to detect the protein and mRNA expression levels of USP47， BACH1， hexokinase 2 （HK2）， and glyceraldehyde 3-phosphate dehydrogenase （GAPDH）. ResultsCompared with the model group， all drug intervention groups showed reduced tumor weight and volume， improved tumor pathology， decreased PCNA positive rate， increased apoptosis rate， and reduced expression levels of USP47， BACH1， and HK2 proteins and mRNA （P＜0.05 or P＜0.01）. Except for lactate content in the cisplatin group， the glucose concentration in tumor tissues of other drug intervention groups increased， while lactate content and ATP production decreased （P＜0.05 or P＜0.01）. Compared with the LXP group， the LXP + inhibitor group showed more significant improvements in these indicators （P＜0.05 or P＜0.01）. Compared with the cisplatin group， the LXP + inhibitor group had lower mRNA expression of HK2 and GAPDH， and lower protein levels of USP47 and HK2 （P＜0.05 or P＜0.01）. Compared with the inhibitor group， the cisplatin group had higher HK2 protein levels， while the LXP + inhibitor group showed lower mRNA expression of BACH1， HK2， and GAPDH （P＜0.05 or P＜0.01）. ConclusionLXP significantly inhibits tumor growth in lung cancer mice， and its mechanism of action may be related to inhibiting the Warburg effect via the USP47/BACH1 pathway.

Objective:To investigate the mediating effect of psychological flexibility between recurrence risk perception and health behavior in stroke patients.Methods:From July to December 2024, 233 stroke patients at the First Affiliated Hospital of Zhengzhou University were selected using convenience sampling. Electronic questionnaires were used to collect patients' general information, perception of stroke recurrence risk, health behavior, and psychological flexibility.Results:The scores for recurrence risk perception, psychological flexibility, and health behavior of 233 stroke patients were (39.75±4.39), (47.45±4.19), and (54.04±3.78), respectively. Health behavior were positively correlated with recurrence risk perception ( r=0.495, P<0.01), and negatively correlated with psychological flexibility ( r=-0.367, P<0.01). Psychological flexibility partially mediated the relationship between recurrence risk perception and health behavior, with an effect value of 0.080 and an effect proportion of 17.5% (0.080/0.458) . Conclusions:Recurrence risk perception not only directly predicts health behavior in stroke patients but also indirectly influences their health behavior through psychological flexibility. Healthcare providers should enhance recurrence risk perception among stroke patients and incorporate the improvement of psychological flexibility as part of intervention strategies to improve patients' health behavior.

To satisfy the growing healthcare demands of the public, it is essential to develop a public service platform for vaccination. This initiative aligns with national policies, optimizes resource allocation, innovates service models, enhances service efficiency, and reduces service costs. Drawing on relevant national policies and regulatory requirements, as well as the notable achievements and practical experiences gained through the exploration and innovation of vaccination service models across various regions, this paper proposes expert recommendations. It defines the essential components and functional specifications for public service platforms, focusing on public needs such as electronic vaccination record management, appointment management, the promotion of electronic vaccination certificates, vaccination certificate verification for school enrollment, vaccination site navigation, and science communication and public engagement. The recommendations aim to serve as a reference for the development of vaccination public service platforms nationwide.

Objective:To investigate the protective effect of PSD95 on neurobehavioral abnormalities and synaptic damage in cortex induced by hypoxia exposure in mice.Methods:The 3-week-old C57BL/6 male mice were injected with neuron-specific adeno-associated virus through stereotaxic brain after 7 days of normal environment adaptation.The mice were divided into normoxia group(AAV-NC-Nor),control hypoxia group(AAV-NC-Hyp),normal oxygen group with over-expression of postsynaptic density-95(PSD95)(AAV-PSD95-Nor),and hypoxia group with over-expression of PSD95(AAV-PSD95-Hyp).Using a hypobaric hypoxia chamber,PSD95-overexpressing mice were continuously ex-posed to hypoxic conditions for 14 days to establish a hypoxia exposure model.The open field,elevated cross maze and conditioned fear tests were used to detect the neurobehavioral activities of mice,and Golgi staining was used to observe the density of neuronal dendritic spines in cortex.The expression of PSD95,SYN1 and N-methyl-D-aspartate receptor subtype 2A(NMDAR2A)were detected by Western blot.Result:Compared with the normal oxygen group,the total distance and average speed of exercise in the open field experiment of mice in hypoxia group increased(P＜0.01),the rigidity time of mice in the conditioned fear box decreased(P＜0.01),and the density of dendritic spines in cortical region decreased(P＜0.05).The expressions of PSD95,SYN1 and NMDAR2A were decreased(P＜0.05).After the over-expression of PSD95,the autonomic activity of mice was reduced,the fear memory was relieved(P＜0.05),the dendrite density was reversed(P＜0.05),and the expression of synaptic related protein was increased(P＜0.05).Conclusion:Over-expression of PSD95 can alleviate neurobehavioral abnormalities and decline of fear memory induced under hypoxia exposure,protect neuronal dendritic spine injury in cortical region,and up-regulate the expression of syn-aptic protein.

Objective:To investigate the protective effect of PSD95 on neurobehavioral abnormalities and synaptic damage in cortex induced by hypoxia exposure in mice.Methods:The 3-week-old C57BL/6 male mice were injected with neuron-specific adeno-associated virus through stereotaxic brain after 7 days of normal environment adaptation.The mice were divided into normoxia group(AAV-NC-Nor),control hypoxia group(AAV-NC-Hyp),normal oxygen group with over-expression of postsynaptic density-95(PSD95)(AAV-PSD95-Nor),and hypoxia group with over-expression of PSD95(AAV-PSD95-Hyp).Using a hypobaric hypoxia chamber,PSD95-overexpressing mice were continuously ex-posed to hypoxic conditions for 14 days to establish a hypoxia exposure model.The open field,elevated cross maze and conditioned fear tests were used to detect the neurobehavioral activities of mice,and Golgi staining was used to observe the density of neuronal dendritic spines in cortex.The expression of PSD95,SYN1 and N-methyl-D-aspartate receptor subtype 2A(NMDAR2A)were detected by Western blot.Result:Compared with the normal oxygen group,the total distance and average speed of exercise in the open field experiment of mice in hypoxia group increased(P＜0.01),the rigidity time of mice in the conditioned fear box decreased(P＜0.01),and the density of dendritic spines in cortical region decreased(P＜0.05).The expressions of PSD95,SYN1 and NMDAR2A were decreased(P＜0.05).After the over-expression of PSD95,the autonomic activity of mice was reduced,the fear memory was relieved(P＜0.05),the dendrite density was reversed(P＜0.05),and the expression of synaptic related protein was increased(P＜0.05).Conclusion:Over-expression of PSD95 can alleviate neurobehavioral abnormalities and decline of fear memory induced under hypoxia exposure,protect neuronal dendritic spine injury in cortical region,and up-regulate the expression of syn-aptic protein.

To satisfy the growing healthcare demands of the public, it is essential to develop a public service platform for vaccination. This initiative aligns with national policies, optimizes resource allocation, innovates service models, enhances service efficiency, and reduces service costs. Drawing on relevant national policies and regulatory requirements, as well as the notable achievements and practical experiences gained through the exploration and innovation of vaccination service models across various regions, this paper proposes expert recommendations. It defines the essential components and functional specifications for public service platforms, focusing on public needs such as electronic vaccination record management, appointment management, the promotion of electronic vaccination certificates, vaccination certificate verification for school enrollment, vaccination site navigation, and science communication and public engagement. The recommendations aim to serve as a reference for the development of vaccination public service platforms nationwide.

Objective:To investigate the mediating effect of psychological flexibility between recurrence risk perception and health behavior in stroke patients.Methods:From July to December 2024, 233 stroke patients at the First Affiliated Hospital of Zhengzhou University were selected using convenience sampling. Electronic questionnaires were used to collect patients' general information, perception of stroke recurrence risk, health behavior, and psychological flexibility.Results:The scores for recurrence risk perception, psychological flexibility, and health behavior of 233 stroke patients were (39.75±4.39), (47.45±4.19), and (54.04±3.78), respectively. Health behavior were positively correlated with recurrence risk perception ( r=0.495, P<0.01), and negatively correlated with psychological flexibility ( r=-0.367, P<0.01). Psychological flexibility partially mediated the relationship between recurrence risk perception and health behavior, with an effect value of 0.080 and an effect proportion of 17.5% (0.080/0.458) . Conclusions:Recurrence risk perception not only directly predicts health behavior in stroke patients but also indirectly influences their health behavior through psychological flexibility. Healthcare providers should enhance recurrence risk perception among stroke patients and incorporate the improvement of psychological flexibility as part of intervention strategies to improve patients' health behavior.

In recent years, more and more researchers at home and abroad have realized that there is a certain relationship between allergic rhinitis(AR) and attention deficit hyperactivity disorder(ADHD) in children.Children with AR had higher ADHD related symptom scores than healthy children; ADHD children have a significantly increased risk of allergic diseases, such as asthma, eczema and atopic dermatitis.At present, it has been clear that they have the common characteristics of increasing prevalence year by year, genetic tendency, environmental and neuropsychological factors, and similar clinical manifestations.However, there is no final conclusion whether they are mutual cause and effect or comorbidities.This artide reviews the similarities between AR and ADHD in epidemiology, etiology, clinical manifestations and drug treatment, so as to further explore the correlation between AR and ADHD.