Objective: To detect the different proteomic characteristics of microvesicles (MVs) and exosomes (EXOs) released from apheresis platelets during storage, and to explore their role in mediating platelet storage damage lesion (PSL). Methods: Apheresis platelets were collected from the retention bag on the third day of storage. MVs and EXOs were isolated using differential centrifugation. Platelet, MVs and EXOs protein samples were extracted respectively, and the differentially expressed proteins were detected by quantitative proteomics technology. Further, the co-incubation model of MVs, EXOs and fresh platelets was adopted to evaluate the effect of extracellular vesicles on PSL. The aggregation response of platelets to collagen agonizers and the changes in ATP release rate were evaluated by optical turbidimetry. Flow cytometry was used to evaluate the changes of platelet early activation indicators (P-selectin and PAC-1) and mitochondrial membrane potentia. Western blot was used to detect the changes in the expression of key proteins for platelet activation and apoptosis (P-selectin, Integrin β3 and Bcl-xl). Results: Proteomic analysis revealed a significantly separation in protein expression profiles of platelet, MVs and EXOs samples within the latent variable space. Energy metabolization-related proteins such as mitochondrial respiratory chain complex and oxidative phosphorylation were enriched specifically, in MVs while EXOs were enriched with inflammation-related proteins. Co-incubation experiments confirmed that extracellular vesicles could significantly induce platelet responses to agonists (the maximum aggregation rate in the MVs group increased by 187.36%, P<0.001; 71.26%, in the EXOs group P=0.002). The maximum ATP release rate of platelets also increased (275.44% in the MVs group, P<0.001; 70.18% in the EXOs group, P=0.015). The expression of P-selectin increased (119.33% in the MVs group, P<0.001; 25.61% in the EXOs group, P=0.013), as detected by flow cytometry. The binding rate of PAC-1 increased (132.18% in MVs group, P<0.001; 21.41% in EXOs group, P=0.043), and the mitochondrial membrane potential decreased (20.49% in MVs group, P<0.001; 9.73% in EXOs group, P=0.044). In the MVs group, platelet P-selectin and Integrin β3 expression were significantly increased (100.83% and 395.64%, P<0.001), while Bcl-xl expression was lower than that in the control group (83.94%, P<0.001). Compared with the control group, P-selectin and Integrin β3 expression were also increased (27.89% and 181.91%, P=0.007和P=0.002), while Bcl-xl was decreased in the EXOs group (36.52%, P<0.001). Conclusion: MVs and EXOs derived from stored platelets show different proteomic characteristics. Compared with EXOs, MVs exhibits a stronger effect in inducing mitochondrial dysfunction. Mvs also promots PSL responses including platelet activation and apoptosis.

Sarcopenia is highly prevalent in old patients with cancer, forcing a vicious circle.Sarcopenia increases the incidence of tumor treatment-related side effects and even mortality risk in the elderly.The progression and certain treatments of cancer can lead to an increased risk or severity of sarcopenia, which exacerbate in older adults, accompanied by aggravated physical function impairment.Except for patients with terminal malignant tumors undergoing palliative therapy, screening for sarcopenia is recommended for older patients at the time of diagnosis of malignancy and before initiation of tumor-related treatment, and a more comprehensive geriatric assessment should be conducted, if necessary, to improve the detection rate of sarcopenia and identify the risk factors of sarcopenia.A clear treatment plan should be tailored to meet the needs of tumor treatment at each stage, and the benefits and risks should be weighed in consideration of the intervention goals and physical function status.It is a promising intervention that holistic care including individualized nutrition therapy and progressive resistance training, in collaboration with the multi-disciplinary team, to maintain or improve skeletal muscle mass, strength and physical function, and improve the prognosis and outcome of cancer among elderly patients with sarcopenia.

Background/Aims: Metabolic dysfunction-associated steatohepatitis (MASH) is a significant risk factor for gallstone formation, but mechanisms underlying MASH-related gallstone formation remain unclear. Golgi membrane protein 1 (GOLM1) participates in hepatic cholesterol metabolism and is upregulated in MASH. Here, we aimed to explore the role of GOLM1 in MASH-related gallstone formation. Methods: The UK Biobank cohort was used for etiological analysis. GOLM1 knockout (GOLM1-/-) and wild-type (WT) mice were fed with a high-fat diet (HFD). Livers were excised for histology and immunohistochemistry analysis. Gallbladders were collected to calculate incidence of cholesterol gallstones (CGSs). Biles were collected for biliary lipid analysis. HepG2 cells were used to explore underlying mechanisms. Human liver samples were used for clinical validation. Results: MASH patients had a greater risk of cholelithiasis. All HFD-fed mice developed MASH, and the incidence of gallstones was 16.7% and 75.0% in GOLM1-/- and WT mice, respectively. GOLM1-/- decreased biliary cholesterol concentration and output. In vivo and in vitro assays confirmed that GOLM1 facilitated cholesterol efflux through upregulating ATP binding cassette transporter subfamily G member 5 (ABCG5). Mechanistically, GOLM1 translocated into nucleus to promote osteopontin (OPN) transcription, thus stimulating ABCG5-mediated cholesterol efflux. Moreover, GOLM1 was upregulated by interleukin-1β (IL-1β) in a dose-dependent manner. Finally, we confirmed that IL-1β, GOLM1, OPN, and ABCG5 were enhanced in livers of MASH patients with CGSs. Conclusions In MASH livers, upregulation of GOLM1 by IL-1β increases ABCG5-mediated cholesterol efflux in an OPN-dependent manner, promoting CGS formation. GOLM1 has the potential to be a molecular hub interconnecting MASH and CGSs.

Background/Aims: Metabolic dysfunction-associated steatohepatitis (MASH) is a significant risk factor for gallstone formation, but mechanisms underlying MASH-related gallstone formation remain unclear. Golgi membrane protein 1 (GOLM1) participates in hepatic cholesterol metabolism and is upregulated in MASH. Here, we aimed to explore the role of GOLM1 in MASH-related gallstone formation. Methods: The UK Biobank cohort was used for etiological analysis. GOLM1 knockout (GOLM1-/-) and wild-type (WT) mice were fed with a high-fat diet (HFD). Livers were excised for histology and immunohistochemistry analysis. Gallbladders were collected to calculate incidence of cholesterol gallstones (CGSs). Biles were collected for biliary lipid analysis. HepG2 cells were used to explore underlying mechanisms. Human liver samples were used for clinical validation. Results: MASH patients had a greater risk of cholelithiasis. All HFD-fed mice developed MASH, and the incidence of gallstones was 16.7% and 75.0% in GOLM1-/- and WT mice, respectively. GOLM1-/- decreased biliary cholesterol concentration and output. In vivo and in vitro assays confirmed that GOLM1 facilitated cholesterol efflux through upregulating ATP binding cassette transporter subfamily G member 5 (ABCG5). Mechanistically, GOLM1 translocated into nucleus to promote osteopontin (OPN) transcription, thus stimulating ABCG5-mediated cholesterol efflux. Moreover, GOLM1 was upregulated by interleukin-1β (IL-1β) in a dose-dependent manner. Finally, we confirmed that IL-1β, GOLM1, OPN, and ABCG5 were enhanced in livers of MASH patients with CGSs. Conclusions In MASH livers, upregulation of GOLM1 by IL-1β increases ABCG5-mediated cholesterol efflux in an OPN-dependent manner, promoting CGS formation. GOLM1 has the potential to be a molecular hub interconnecting MASH and CGSs.

Traditional Chinese medicine (TCM) is a well-accepted therapy for atopic dermatitis (AD). However, there are currently no evidence-based guidelines integrating TCM and Western medicine for the treatment of AD, limiting the clinical application of such combined approaches. Therefore, the China Association of Chinese Medicine initiated the development of the current guideline, focusing on key issues related to the use of TCM in the treatment of AD. This guideline was developed in accordance with the principles of the guideline formulation manual published by the World Health Organization. A comprehensive review of the literature on the combined use of TCM and Western medicine to treat AD was conducted. The findings were extensively discussed by experts in dermatology and pharmacy with expertise in both TCM and Western medicine. This guideline comprises 23 recommendations across seven major areas, including TCM syndrome differentiation and classification of AD, principles and application scenarios of TCM combined with Western medicine for treating AD, outcome indicators for evaluating clinical efficacy of AD treatment, integration of TCM pattern classification and Western medicine across disease stages, daily management of AD, the use of internal TCM therapies and proprietary Chinese medicines, and TCM external treatments. Please cite this article as: Du XR, Wu MY, Tao MC, Lin Y, Gu CY, Wu MF, Cao Y, Chen DC, Li W, Wang HW, Wang Y, Wang Y, Lu HZ, Liu X, Su XF, Li FL. Clinical practice guidelines for the diagnosis and treatment of atopic dermatitis with integrative traditional Chinese and Western medicine. J Integr Med. 2025; 23(6):641-653.
Dermatitis, Atopic/drug therapy* ; Humans ; Medicine, Chinese Traditional/methods* ; Integrative Medicine ; Drugs, Chinese Herbal/therapeutic use* ; Practice Guidelines as Topic