The lung collaterals form a network that branches from the lung meridian, traversing the lung system and extending across the body′s surface. Lung collateral disease refers to the structural alterations or dysfunction in these collaterals caused by external or internal pathogens. Research into the structural and physiological functions of children′s lung collaterals, as well as the pathogenesis and syndrome differentiation for treating lung collateral diseases in children, holds significant value in guiding the prevention and treatment of pediatric respiratory conditions. Drawing on the theory of collateral disease, the clinical insights of both historical and contemporary physicians, and modern research findings—while considering the unique physiological and pathological characteristics of children′s respiratory systems—this study provides a foundational summary of the morphology and spatial distribution of children′s lung collaterals. The characteristics of these collaterals are highlighted as thin, sparse, short, narrow, brittle, and tender. From this structural understanding, the unique physiological functions of children′s lung collaterals are analyzed. The study further explores the interactions between pathogenic factors and lung collaterals, elucidating the pathogenesis and progression of children′s lung collateral diseases. It proposes treatment principles centered on "seeking treatment in the collaterals and employing the method of unblocking collaterals, "which align with the unique features of pediatric lung collaterals. Common treatment approaches, and relevant prescriptions for managing these diseases are summarized. This paper lays the foundation for a theoretical system encompassing the structure, function, pathogenesis, and syndrome differentiation for treating children′s lung collateral diseases. It offers valuable insights for the clinical diagnosis and management of pediatric respiratory diseases linked to collateral dysfunction and serves as a reference for the systematic development of a broader theoretical framework for children′s collateral diseases.

It is considered that the fundamental pathogenesis of pediatric pertussis lies in the dysfunction of lung qi， and it is advocated to treat the disease with the method of regulating qi and relieving cough. Clinically， the disease is divided into three stages for syndrome differentiation and treatment， initial coughing stage， spasmodic coughing stage， and prolonged coughing stage. In the initial coughing stage， the pathogenesis involves invasion by external pathogens and failure of lung qi to disperse； the treatment principle is to release the exterior， expel pathogens， ventilate the lungs， and relieve cough. For cold patterns， modified San'ao Decoction （三拗汤） is prescribed； for heat type， a self-formulated Qingqi Xuanfei Decoction （清气宣肺汤） is used. In the spasmodic coughing stage， the pathogenesis is the congealing of phlegm and fire with impaired lung purification； the treatment focuses on eliminating phlegm， dredging the meridians， purging the lungs， and relieving cough. Mild cases are treated with a self-formulated Tongluo Xiefei Decoction （通络泻肺汤）， while severe cases are treated with a modified combination of Maxing Shigan Decoction （麻杏石甘汤） and Qianjin Weijing Decoction （千金苇茎汤）. In the prolonged coughing stage， the pathogenesis involves the depletion of qi and yin and latent pathogens in a weakened lung； the treatment aims to tonify qi， nourish yin， moisten the lungs， and eliminate residual pathogens. For lung yin deficiency， modified Shashen Maidong Decoction （沙参麦冬汤） is used； for lung-spleen qi deficiency， a self-formulated Jianpi Gufei Decoction （健脾固肺汤） is prescribed.

Objective: To investigate the assocation of sedentary behavior among college students on psychological health issues, such as depressive, anxiety, and stress symptoms, and to analyze the moderating role of takeaway consumption behavior in the context, in order to provide a scientific basis for reducing emotional symptoms among college students. Methods: A stratified cluster sampling method was employed to conduct a questionnaire on 3 427 first year students of a higher education institution in Hefei of Anhui Province from May to June 2021. The study variables included demographic characteristics, sedentary time, takeaway consumption behavior, and emotional (symptoms depressive, anxiety, and stress symptoms). The Spearman correlation analysis was used to analyze the association between variables, and linear regression analysis was used to analyze the association between takeaway consumption behavior and depressive, anxiety and stress symptoms among college students with sedentary time. Results: Both sedentary time and takeaway consumption behavior were positively correlated with depressive, anxiety and stress symptoms among college students ( r =0.10, 0.10, 0.10; 0.10, 0.11, 0.11, all P <0.05). The results of linear regression analysis showed that the interaction term between takeaway consumption behavior and sedentary time was positively correlated with symptoms of depressive, anxiety, and stress symptoms among college students (depression: β =0.04, anxiety: β =0.04, stress: β =0.04, all P <0.05). The results of the simple slope test demonstrated that regardless of the level of takeaway consumption behavior, sedentary time was positively correlated with the depressive symptoms of college students; compared with low takeaway consumption behavior, high takeaway consumption behavior ( β=0.77, P <0.01) enhanced the association between sedentary time and depressive symptoms among college students. In addition, under the condition of high takeaway consumption behavior, sedentary time was positively correlated with the anxiety and stress symptoms of college students (anxiety: β =0.64; stress: β =0.71, both P <0.01); while under the condition of low takeaway consumption behavior, sedentary time was not related to the anxiety and stress symptoms of college students ( β =0.17, 0.22, both P >0.05). Conclusions Sedentary behavior is related to a the emotional symptoms of depressive, anxiety, and stress among college students. Takeaway consumption behavior may exacerbate this impact.

Debates persist regarding the efficacy and safety of azvudine, particularly its real-world outcomes. This study involved patients aged ≥60 years who were admitted to 25 hospitals in mainland China with confirmed SARS-CoV-2 infection between December 1, 2022, and February 28, 2023. Efficacy outcomes were all-cause mortality during hospitalization, the proportion of patients discharged with recovery, time to nucleic acid-negative conversion (T _NANC), time to symptom improvement (T _SI), and time of hospital stay (T _HS). Safety was also assessed. Among the 5884 participants identified, 1999 received azvudine, and 1999 matched controls were included after exclusion and propensity score matching. Azvudine recipients exhibited lower all-cause mortality compared with controls in the overall population (13.3% vs. 17.1%, RR, 0.78; 95% CI, 0.67-0.90; P = 0.001) and in the severe subgroup (25.7% vs. 33.7%; RR, 0.76; 95% CI, 0.66-0.88; P < 0.001). A higher proportion of patients discharged with recovery, and a shorter T _NANC were associated with azvudine recipients, especially in the severe subgroup. The incidence of adverse events in azvudine recipients was comparable to that in the control group (2.3% vs. 1.7%, P = 0.170). In conclusion, azvudine showed efficacy and safety in older patients hospitalized with COVID-19 during the SARS-CoV-2 omicron wave in China.

Myocardial fibrosis is a serious cause of heart failure and even sudden cardiac death. However, the mechanisms underlying myocardial ischemia-induced cardiac fibrosis remain unclear. Here, we identified that the expression of sterile alpha and TIR motif containing 1 (SARM1), was increased significantly in the ischemic cardiomyopathy patients, dilated cardiomyopathy patients (GSE116250) and fibrotic heart tissues of mice. Additionally, inhibition or knockdown of SARM1 can improve myocardial fibrosis and cardiac function of myocardial infarction (MI) mice. Moreover, SARM1 fibroblasts-specific knock-in mice had increased deposition of extracellular matrix and impaired cardiac function. Mechanically, elevated expression of SARM1 promotes the deposition of extracellular matrix by directly modulating P4HA1. Notably, by using the Click-iT reaction, we identified that the increased expression of ZDHHC17 promotes the palmitoylation levels of SARM1, thereby accelerating the fibrosis process. Based on the fibrosis-promoting effect of SARM1, we screened several drugs with anti-myocardial fibrosis activity. In conclusion, we have unveiled that palmitoylated SARM1 targeting P4HA1 promotes collagen deposition and myocardial fibrosis. Inhibition of SARM1 is a potential strategy for the treatment of myocardial fibrosis. The sites where SARM1 interacts with P4HA1 and the palmitoylation modification sites of SARM1 may be the active targets for anti-fibrosis drugs.

Perimenopause raises the risk and incidence of depression, whereas the underlying molecular mechanism remains unclear. Disturbed glucose regulation has been widely documented in depressive disorders, which renders the brain susceptible to various stresses such as estrogen depletion. However, whether and how glucose dysfunction regulates depression-like behaviors and neuronal damage in perimenopausal transition remains unexplored. Here, a prominent depressive phenotype was found in perimenopausal mice induced by the ovarian toxin 4-vinylcyclohexene diepoxide (VCD). The VCD depression susceptible group (VCD^SS) and the VCD depression resilient group (VCD^RES) were determined using a ROC-based behavioral screening approach. We found that the hippocampus, a crucial region linked to depression, had hyperglycemia and mitochondrial abnormalities. Interestingly, oral administration of the SGLT2 inhibitor empagliflozin (EMPA) and intrahippocampal glucose infusion suggest a close relationship between hyperglycemia in the hippocampus and the susceptibility to depression. We verified that cytochrome c oxidase 7c (COX7C) downregulation is a potential cause of the high glucose-induced neuronal injury using proteomic screening and biochemical validations. High glucose causes COX7C to be ubiquitinated in a S-phase kinase associated protein 1 (SKP1)-dependent manner. According to these results, SKP1/COX7C represents a unique therapeutic target and a novel molecular route for treating perimenopausal depression.

Objective To investigate the correlations microRNA-203a-3p(miR-203a-3p)and paired allographic box protein 2B(PHOX2B)expression levels in glioma tissues with clinical features and prognosis.Methods Ninety-six glioma patients admitted to our hospital from June 2017 to April 2020 were included in the study.The resected glioma tissues and corresponding paracancerous tissues from the patients were collected intraop-eratively.qRT-PCR and immunohistochemistry were conducted to detect the expression of miR-203a-3p and PHOX2B mRNA in glioma tissues and paracancerous groups.Pearson's method was used to analyze the correlation between miR-203a-3p and PHOX2B mRNA.Kaplan-Meier survival curves were used to analyze the correlations of miR-203a-3p and PHOX2B mRNA with the prognosis of glioma patients.COX regression was used to analyze the risk factors affecting the prognosis of glioma patients.Results The miR-203a-3p level and positive expression rate of glioma tissues were significantly lower than that of paracancerous tissues(P<0.05),and the PHOX2B mRNA level and positive expression rate were significantly higher than that of paracancerous tissues(P<0.05).By Pearson correlation analysis,the miR-203a-3p and PHOX2B mRNA levels of glioma patients were negatively correlated(P<0.05).miR-203a-3p and PHOX2B were associated with KPS score,tumor tissue necrosis,and WHO grading(P<0.05).Kaplan-Meier curve analysis yielded the results that the survival rate of the miR-203a-3p highly expressed group was significantly higher than that of the lowly expressed group(P<0.05),and the survival rate of the PHOX2B mRNA highly expressed group was significantly lower than that of the lowly expressed group(P<0.05).COX regression analysis showed that miR-203a-3p,PHOX2B mRNA,tumor tissue necrosis,and WHO grading were the risk factors affecting the prognosis of glioma patients(P<0.05).Conclusion The expression level of miR-203a-3p is obviously reduced and the expression level of PHOX2B mRNA is obviously increased in glioma,both showing close correlation with clinical characteristics and prognosis.

In order to promote the development of grassroots hospitals through targeted assistance,ZhuJiang Hospital of Southern Medical University took the lead in responding in Guangdong Province and established a tight-ly-knit specialty alliance belonging to Zhujiang.It introduces the construction content,principles and measures of Zhujiang Tightly-Knit Specialty Alliance,and proposes a dual-promotion management model for the tightly-knit Spe-cialty Alliance.A comprehensive comparison of the changes in specialized technical capabilities and medical quality of Guangning County People's Hospital before and after aid shows that the close specialist alliance has achieved initial results in effectively promoting the sinking of resources and improving the medical technology capabilities and quality of member units.It is of great practical significance for further promoting the development of specialist alliances and filling the shortcomings of primary medical institutions.

Platelet elevation is a rare manifestation in the peripheral blood of patients with chronic myeloid leukemia (CML). In this paper, we report for the first time a case of CML combined with cerebral hemorrhage manifested by abnormally elevated platelets. The patient had elevated platelets in the peripheral blood, showed normal coagulation function, and underwent intracranial hematoma removal due to cerebral hemorrhage. After the operation, bleeding from the operated area and other systems occurred, and the patient was diagnosed as having accelerated CML after combining bone marrow biopsy and genetic testing. His condition was controlled after administration of flumatinib through a jejunal tube. Based on this patient's experience, the feasibility ofadministering flumatinib via a jejunostomy tube was determined, which is the first report of its kind in China and abroad.This article summarizes the diagnosis and treatment process of this patient, with the aim of providing a warning and reference for clinicians.

Objective:To study the clinicopathological features of Sjogren′s syndrome (SS) with liver injury and to improve the understanding of this disease.Methods:Forty-nine patients with SS complicated with liver injury were collected from Beijing Ditan Hospital, Capital Medical University from October 2008 to January 2022. All patients underwent ultrasound-guided liver biopsy, and all specimens were stained with HE. The histopathologic characteristics were observed and the pathologic indexes were graded. Immunohistochemical stains for CK7, CK19, CD38, MUM1 and CD10 were performed by EnVision method; and special histochemical stains for reticulin, Masson′s trichrome, Rhodanine, Prussian blue, periodic acid Schiff (PAS) and D-PAS stains were conducted .Results:The age of patients ranged from 31 to 66 years, including 3 males and 46 females. SS combined with drug-induced liver injury was the most common (22 cases, 44.9%), followed by autoimmune liver disease (13 cases, 26.5%, including primary biliary cholangitis in eight cases, autoimmune hepatitis in 3 cases, and PBC-AIH overlap syndrome in 2 cases), non-alcoholic fatty liver disease (NAFLD, 9 cases, 18.4%) and other lesions (5 cases, 10.2%; including 3 cases of nonspecific liver inflammation, 1 case of liver amyloidosis, and 1 case of porto-sinusoidal vascular disease). Among them, 28 cases (57.1%) were associated with obvious interlobular bile duct injury, mainly in SS combined with PBC group and drug-induced liver injury group. Twenty-three cases (46.9%) were associated with hepatocyte steatosis of varying degrees. In SS with autoimmune liver disease group, ISHAK score, degree of fibrosis bile duct injury, bile duct remodeling, lymphocyte infiltration of portal area, and plasma cell infiltration, MUM1 and CD38 expression; serum ALP and GGT, IgM; elevated globulin; positive AMA, proportion of AMA-M2 positive and IgM positive were all significantly higher than those in other groups(all P<0.05). Serum ALT, direct bilirubin and SSA positive ratio in SS combined with drug liver group were significantly higher than those in other groups(all P<0.05). The serum total cholesterol level in SS combined with PBC group ( P=0.006) and NALFD group ( P=0.011) were significantly higher than those in other groups ( P<0.05). Conclusions:The pathologic manifestations of SS patients with liver injury are varied. The inflammatory lesions of SS patients with autoimmune liver disease are the most serious, and the inflammatory lesions of SS patients with non-alcoholic fatty liver disease and non-specific inflammation are mild. Comprehensive analysis of liver histopathologic changes and laboratory findings is helpful for the diagnosis of SS complicated with different types of liver injury.