This paper summarizes Professor SHI Zaixiang's clinical experience in treating high fever caused by sepsis using Chaihu Guizhi Ganjiang Decoction （柴胡桂枝干姜汤）. He holds that the key pathogenesis of sepsis involves constrained heat in the shaoyang and internal accumulation of water and fluids. The clinical manifestations such as high fever， chills， and alternating sensations of cold and heat are attributed to pathogenic heat constrained in the shaoyang. Meanwhile， soft tissue edema and serous cavity effusions are due to shaoyang dysfunction and internal water retention. In clinical practice， treating sepsis-related high fever requires addressing both the shaoyang-constrained heat and the associated edema and effusions. The therapeutic approach focuses on harmonizing the shaoyang and resolving internal fluids， using Chaihu Guizhi Ganjiang Decoction as the base formula with flexible modifications. Professor SHI emphasizes that this formula shows a rapid antipyretic effect， particularly in cases where multiple anti-infective treatments have failed.

At present, there is no effective drug treatment for obstructive sleep apnea hypopnea syndrome (OSAHS). It is usually treated by mechanical ventilation through a ventilator. In this paper, a non-invasive bi-level breathing therapy system suitable for home scenarios is developed. The system supports single-level and bi-level positive airway pressure therapies, and introduces the function of inspiratory synchronous trigger based on flow monitoring to enhance the synchrony of patient-ventilator synchronization. The test results show that the performance indicators of the system meet expectations. Each ventilation mode can operate normally and can meet the requirements for the use of home non-invasive ventilators.
Humans ; Sleep Apnea, Obstructive/therapy* ; Equipment Design ; Noninvasive Ventilation/instrumentation* ; Respiration, Artificial

OBJECTIVE To discuss the effect mechanism of atractylodin （ATR） on lung injury and airway inflammation in rats with acute exacerbation of chronic obstructive pulmonary disease （AECOPD）. METHODS AECOPD model was established using smoke exposure and intratracheal injection of lipopolysaccharide. Rats were randomly grouped into model group， ATR low-， medium- and high-dose groups （25， 50 and 100 mg/kg）， as well as high-dose ATR+anisomycin [ANS， c-Jun N-terminal kinase （JNK） activator] group （100 mg/kg ATR+5 mg/kg ANS）. Additionally， a non-modeled control group was set up， with 12 rats in each group. Rats in each group were intraperitoneally injected with the corresponding drug solution/normal saline once daily for 14 consecutive days. After the last medication， lung function [peak expiratory flow （PEF）， the ratio of forced expiratory volume （FEV） to forced vital capacity （FVC）， arterial partial pressure of oxygen （PaO2）]， as well as the number of inflammatory cells and the levels of inflammatory cytokines [interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and IL-1β] in bronchoalveolar lavage fluid （BALF）， were measured. The pathological morphology of lung tissue in rats was observed. 163.com The apoptosis of lung epithelial cells was detected， and the expression levels of proteins related to the JNK/p38 mitogen-activated protein kinase （p38 MAPK） signaling pathway in rat lung tissues were detected. RESULTS Compared with control group， PEF， FEV/FVC and PaO2 of model group were slowed or decreased significantly （P＜0.05）. The number of white blood cells， neutrophils， lymphocytes and macrophages， as well as the levels of IL-1β， TNF-α and IL-6 in BALF， along with the pathological score， the apoptosis rate of lung epithelial cells， and the phosphorylation levels of JNK and p38 MAPK proteins in lung tissues， were all increased or raised significantly （P＜0.05）； lung tissue exhibited severe damage， with disordered cell arrangement and marked infiltration of inflammatory cells. Compared with model group， the levels of above quantitative indicators in rats from all ATR dosage groups showed significant improvement in a dose-dependent manner （P＜0.05）； moreover， the pathological damage in lung tissue was alleviated， with cells arranged in a regular and orderly fashion. Compared with ATR high-dose group， the levels of the above quantitative indicators in rats from the high-dose ATR+ANS group were significantly reversed （P＜0.05）， and the pathological damage in lung tissue was exacerbated. CONCLUSIONS ATR inhibits airway inflammation by suppressing the activity of the JNK/p38 MAPK signaling pathway， thereby improving lung tissue damage in AECOPD rats.

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.

Objective To investigate the impact of phase Ⅱ cardiac rehabilitation on the rehabilitation needs and physical activity status of patients after coronary heart disease intervention.Methods A total of 90 patients with coronary heart disease who underwent percutaneous coronary intervention(PCI)in the Coronary Heart Disease Center of the hospital from August 2023 to August 2024 were selected as the research subjects.They were subjected to a 12-week standardized phase Ⅱ cardiac rehabilitation training.General data survey forms,cardiac rehabilitation scales,and the International Physical Activity Questionnaire were used for scale surveys to understand the patients' needs before and after rehabilitation and their weekly physical activity en-ergy expenditure.The cardiopulmonary exercise test gold standard,which reflects exercise capacity through three indicators-maximum oxygen uptake(VO2 max),anaerobic threshold(AT),and metabolic equivalents(MET),were used to compare the physical activity status before and after cardiac rehabilitation.Results Compared with before the implementation,after the implementation of cardiac rehabilitation,the autonomy score in-creased(21.36±1.85 vs.16.73±3.28),the process anxiety(12.60±3.87 vs.14.27±2.12)and outcome anxiety scores(2.31±1.76 vs.4.56±3.56)decreased,the level of low-intensity physical activity decreased[(2 711.62±1 487.09)min/week vs.(3 845.97±2 083.71)min/week],the levels of moderate-intensity[(1 314.67±783.54)min/week vs.(686.22±126.79)min/week],high-intensity[(1 861.33±798.27)min/week vs.(112.00±40.77)min/week],and total physical activity increased[(5 887.62±2 843.54)min/week vs.(4 644.19±2 287.16)min/week].The levels of VO2 max[(28.11±14.28)mL·min-1·kg-1 vs.(23.82±12.34)mL·min-1·kg-1],AT[(16.06±5.41)mL·min-1·kg-1 vs.(13.53±4.56)mL·min-1·kg-1],and MET[(6.89±1.59)mL·min-1·kg-1 vs.(5.78±1.21)mL·min-1·kg-1]all in-creased,with statistically significant differences(P＜0.05).Conclusion Phase Ⅱ rehabilitation after PCI can effectively improve patients' physical activity levels.

Objective:To analyze the epidemiological characteristics of wasting, spinal curvature abnormalities and multimorbidity among children and adolescents aged 6-18 in Inner Mongolia and explore the related factors of these two health problems.Methods:In September 2022, a stratified random cluster sampling method was employed to select 188 635 children and adolescents aged 6-18 in Inner Mongolia for physical examinations and questionnaire surveys. Data on height, weight, as well as dietary behavior, physical activity, classroom environment, academic tasks, writing posture, and screen behavior were collected. The epidemiological characteristics of wasting, spinal curvature abnormalities and multimorbidity were analyzed. Additionally, a multivariate logistic regression model was used to analyze the factors associated with wasting, spinal curvature abnormalities and multimorbidity.Results:A total of 188 635 children and adolescents aged 6-18 years participated in this study, including 95 393 boys (50.6%) with an average age of (11.53±3.32) years. The detection rate of wasting was 3.79%, with a higher detection rate in boys (4.18%) than in girls (3.38%) ( P<0.001). The detection rate of spinal curvature abnormalities was 3.64%, with a higher detection rate in girls (4.04%) than in boys (3.25%) ( P<0.001). The detection rate of multimorbidity between wasting and spinal curvature abnormalities was 0.17%, and there was no statistically significant difference between genders ( P>0.05). The detection rates of wasting, spinal curvature abnormalities, and multimorbidity all increased with age ( P t<0.001). The multivariate logistic regression analysis showed that, after adjusting for gender, age, urban/rural status, and school grade, compared to children and adolescents who exercised ≥1 hour of moderate-to-vigorous physical activity (MVPA) for at least 5 days per week and had daily screen time <2 hours, those who exercised <5 days per week ( OR=1.28, 95% CI: 1.19-1.37) and had daily screen time ≥2 hours ( OR=1.11, 95% CI: 1.03-1.19) had a higher risk of wasting. Compared to children and adolescents who had ≥5 physical education (PE) classes per week, adjusted desk and chair height,<1 hour of after-school study/writing time, and whose parents or teachers rarely or never reminded them about posture, those with <5 PE classes per week ( OR=1.11, 95% CI: 1.02-1.21), unadjusted desk and chair height ( OR=1.08, 95% CI: 1.01-1.15),≥1 hour of after-school study/writing time ( OR=1.15, 95% CI: 1.07-1.24), frequent reminders from parents ( OR=1.16, 95% CI: 1.09-1.23), and frequent reminders from teachers ( OR=1.10, 95% CI: 1.04-1.16) had a higher risk of spinal curvature abnormalities. Compared to children and adolescents who did not consume sugary drinks daily, exercised ≥1 hour of MVPA for at least 5 days per week, and whose teachers rarely or never reminded them about posture, those who consumed sugary drinks daily ( OR=1.61, 95% CI: 1.00-2.46), exercised <5 days per week ( OR=1.33, 95% CI: 1.01-1.79), and had teachers who frequently reminded them about posture ( OR=1.35, 95% CI: 1.05-1.75) had a higher risk of multimorbidity between wasting and spinal curvature abnormalities. Conclusion:The detection rates of wasting, spinal curvature abnormalities and multimorbidity among children and adolescents aged 6-18 in Inner Mongolia are generally low, with an increasing trend observed with age. Both lifestyle and school environmental factors are associated with wasting, spinal curvature abnormalities and multimorbidity.

Objective:To report the clinical, imaging, and pathological features of a case of MYH7 gene-related scapuloperoneal myosin storage myopathy. Methods:Clinical data were collected from a patient with MYH7 gene-related scapuloperoneal myosin storage myopathy who presented to Peking University First Hospital in February 2025. The patient was evaluated with muscle magnetic resonance imaging, muscle biopsy, and whole-exome sequencing. Results:The patient was a 52-year-old female, with a 12-year history of progressive difficulty in foot dorsiflexion, exercise-induced fatigue, and lower limb pain. Over the past 3 years, she developed proximal upper limb weakness and post-exertional myalgia. Physical examination revealed scapuloperoneal weakness distribution accompanied by sensorineural hearing loss. Electromyography demonstrated myogenic changes in the deltoid and tibialis anterior muscles. Serum creatine kinase levels were within normal limits. Lower limb magnetic resonance imaging showed mild atrophy of the thigh muscles and significant fatty infiltration in the tibialis anterior, extensor hallucis longus, and extensor digitorum longus. Tibialis anterior muscle biopsy revealed dystrophic-like changes with sub-sarcolemmal hyaline bodies containing abundant granulofilamentous material. Whole exome sequencing identified a heterozygous pathogenic variant of c.5352_5354del(p.K1784del) in the MYH7 gene. Conclusions:This patient is the first reported one in China with MYH7 gene-related scapuloperoneal myosin storage myopathy, exhibiting characteristic scapuloperoneal weakness, selective fatty infiltration of the anterior lower leg muscles on imaging and sub-sarcolemmal hyaline body pathological changes. The diagnosis of this disease relies on characteristic pathological findings and genetic test results.

Objective:To explore the phenotypic heterogeneity among patients harboring identical pathogenic variants in the dystrophin ( DMD) gene by analyzing clinical and imaging data from 7 pairs of male twins with dystrophinopathy. Methods:Clinical and laboratory data of 14 (7 pairs) male twins diagnosed with dystrophinopathy through genetic testing among 1 767 patients at Peking University First Hospital from January 2017 to October 2024 were collected. Eleven patients underwent thigh muscle magnetic resonance imaging (MRI), and muscle biopsies were performed in at least 1 case of each pair.Results:Among the 7 pairs of twin patients, 2 pairs had Duchenne muscular dystrophy, and 5 pairs had Becker muscular dystrophy. In terms of variant types, 4 pairs had in-frame deletions, while the remaining 3 pairs had duplication variants, frameshift variants, and nonsense variants, respectively. Clinically, 6 individuals had asymptomatic hypercreatine kinasemia, and 8 had varying degrees of limb weakness. Among the 5 pairs of symptomatic twins, there were differences in the degree of limb weakness. Four individuals showed no significant abnormalities in thigh muscle MRI, 7 showed fat infiltration mainly in the bilateral gluteus maximus and adductor magnus muscles, and 2 pairs of twins had obvious differences in the degree of fat infiltration in muscle MRI. Muscle biopsies revealed dystrophic or mild myopathic pathological changes, with 2 individuals showing severe loss of dystrophin, while the others had partial loss.Conclusions:Dystrophinopathy exhibits significant individual differences. Even among individuals with highly similar genetic background, clinical and imaging manifestations caused by the same pathogenic variant also vary.