Annals of translational medicine最新文献

[This corrects the article DOI: 10.21037/atm-21-601.].

Background: β-hydroxy-β-methylbutyrate (HMB) is a metabolite of the essential amino acid leucine that promotes muscle protein synthesis and inhibits muscle cell degradation. This study aimed to clarify the effects of HMB on skeletal muscle mass loss using a mouse model of esophageal squamous cell carcinoma (ESCC).

Methods: ESCC cells (TE-8) (5×10⁶ cells/body) were subcutaneously transplanted into 10 nude mice to generate a mouse model of ESCC. Thirteen mice were divided into three groups: (I) non-tumor group (n=3), non-ESCC mice fed a normal diet; (II) ESCC + HMB group (n=5), ESCC-bearing mice fed HMB; (III) ESCC control group (n=5), ESCC-bearing mice fed a normal diet. A powdered Ca-HMB product was used as the HMB source. Body weight, grip strength, and gastrocnemius muscle weight of the three groups of mice were measured and compared.

Results: Body weight did not differ between the ESCC + HMB and ESCC control groups. Grip strength and gastrocnemius muscle weight were significantly higher in the ESCC + HMB group than those in the ESCC control group (grip strength, P=0.03; gastrocnemius muscle weight, P<0.01). No significant difference in grip strength or gastrocnemius muscle weight was observed between the ESCC + HMB and non-tumor groups (grip strength, P=0.94; gastrocnemius muscle weight, P=0.65). No difference in grip strength or gastrocnemius muscle weight was observed between non-tumor mice and ESCC mice (grip strength: P=0.35, gastrocnemius muscle weight: P=0.37).

Conclusions: HMB administration to ESCC-bearing mice maintained grip strength and gastrocnemius muscle weight at levels comparable to those of non-transplanted (non-ESCC) mice. Future studies should elucidate the mechanisms by which HMB counteracts cachexia and confirm these physiological findings with molecular biological evidence.

Background and objective: Panax notoginseng (P. notoginseng) has traditionally been used to support circulatory health. Its higher ginsenoside content and the presence of notoginsenoside R1 distinguish it from Panax ginseng and contribute to broader therapeutic potential. This review summarizes the anti-inflammatory mechanisms of P. notoginseng and their relevance to cardiovascular, hepatic, and metabolic disorders.

Methods: A structured search of PubMed, Web of Science, Scopus, and Google Scholar was performed on December 20, 2024, covering January 2010 to July 2024. Studies published in English that provided mechanistic insights into anti-inflammatory activity in relation to P. notoginseng were included. Commentaries and studies without mechanistic detail were excluded. Screening was conducted independently by two authors.

Key content and findings: P. notoginseng modulates key inflammatory pathways-including nuclear factor-κB (NF-κB), modulating mitogen-activated protein kinase (MAPK), cytokine regulation, oxidative stress, and endothelial function-supporting its benefits in vascular injury, liver inflammation, metabolic dysfunction, and gut-liver axis imbalance. Its unique phytochemical profile explains its stronger cardiovascular and hepatoprotective actions compared to P. ginseng.

Conclusions: The broad pharmacological activities of P. notoginseng are largely driven by its anti-inflammatory mechanisms. These findings provide a framework for its clinical relevance and highlight the need for further translational and integrative research.

Background and objective: Although the global incidence of hematologic malignancies is decreasing, the risk of developing these cancers is increasing due to increased lifespan and modern treatments including targeted therapy, chemotherapy, and radiation. Intrathoracic manifestations of hematologic malignancies may be the presenting sign leading to diagnosis or result from various treatment toxicity. The most common respiratory manifestation of hematologic malignancies is infectious, but up to half of pulmonary findings are from non-infectious etiologies. We aim to summarize the current literature on non-infectious intrathoracic manifestations of hematologic malignancies and their treatment.

Methods: We performed a literature review using PubMed Central and Google Scholar for articles published between January 1^st, 2014, and January 1^st, 2024. We used medical subject heading terms to search titles, abstracts, and diagnoses. We reviewed textbook chapters, literature reviews, practice guidelines, randomized controlled trials, and retrospective articles.

Key content and findings: There are many pulmonary manifestations of hematologic malignancies. Lymphadenopathy and disease of serosal membranes are common. Pleural effusions can be malignant or related to treatment, and interventions include serial thoracentesis or indwelling pleural catheters (IPCs). Parenchymal diseases consist of primary pulmonary lymphoma, leukemic pulmonary infiltration, myeloid sarcoma, pulmonary alveolar proteinosis, and leukemic cell lysis pneumopathy. Endobronchial disease is rare. Pulmonary vascular disorders involve leukostasis, thromboembolic disease, pulmonary hypertension (PH), superior vena cava (SVC) syndrome, and pseudohypoxemia. Therapy-related sequelae may also occur.

Conclusions: Intrathoracic manifestations of hematologic malignancies should be considered in the differential diagnosis at the time of presentation since their management differs substantively.

Background and objective: Extranodal marginal zone B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) are indolent non-Hodgkin lymphomas (NHLs) that can arise in various extranodal organs, often due to chronic inflammation. Gastric MALT lymphomas are well characterized; however, MALT lymphomas may occur in diverse sites such as the ocular adnexa, salivary glands, thyroid, lung, skin, and the small intestine. These site-specific MALT lymphomas have distinct etiologic associations, clinical presentation, and management considerations. This review provides an updated, site-specific overview to guide the diagnostic and therapeutic approach to non-gastric MALT lymphoma in adults.

Methods: We reviewed peer-reviewed articles [2015-2025] on non-gastric MALT lymphomas, focusing on pathophysiology/etiology, diagnostic workup, and treatment strategies for each site. Key sources include recent reviews and guidelines from high-impact journals.

Key content and findings: Chronic antigenic stimulation is a unifying theme in MALT lymphoma genesis, either through infectious etiologies or autoimmune conditions. Ocular adnexal MALT lymphoma (OAML) is linked to Chlamydia psittaci (C. psittaci) infection in certain regions; salivary MALT lymphoma is related to Sjogren's syndrome (SS); thyroid MALT lymphoma develops in the background of Hashimoto's thyroiditis; pulmonary MALT lymphoma can be linked to chronic airway inflammation due to Achromobacter xylosoxidans (A. xylosoxidans); small intestinal MALT lymphoma can be associated with Campylobacter jejuni (C. jejuni) infection; and cutaneous MALT lymphoma can be linked to Borrelia burgdorferi (B. burgdorferi) infection. Diagnostic evaluation requires adequate tissue biopsy for histopathology and immunohistochemistry. MALT lymphomas exhibit an immunophenotype consistent with CD20⁺, CD79a⁺, IgM⁺ with light chain restriction, BCL2⁺, and negative for CD5, CD10, and cyclin D1. Staging for OAML and cutaneous lymphomas is tumor-node-metastasis (TNM)-based, while the others utilize an Ann Arbor staging system. Computed tomography (CT)/magnetic resonance imaging (MRI) and positron emission tomography (PET)/CT are used to determine the staging and spread of tumors. Treatments are not standardized but consist of therapy with radiotherapy and surgical excision for localized disease, and chemotherapy/for disseminated disease. Intestinal MALT lymphoma differs, as first-line treatment consists of antibiotics and then chemotherapy/immunotherapy.

Conclusions: The non-gastric MALT lymphomas have an excellent prognosis as a whole; relapses are common but manageable, and disseminated disease is rare. Long-term follow-up is recommended in all cases.

Background: Chronic myocardial infarction (CMI) is a leading cause of heart failure and is increasingly recognized as a systemic condition involving multi-organ dysfunction, particularly impaired gut health due to systemic inflammation and metabolic disturbances. Dapagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, exerts cardioprotective effects beyond glycemic control, but its role in CMI-induced gut dysbiosis and barrier dysfunction remains unclear. This study aimed to determine whether dapagliflozin mitigates CMI-induced gut dysbiosis and intestinal barrier dysfunction-alongside systemic inflammation and metabolic disturbances-and whether these changes are associated with improved cardiac function.

Methods: Thirty-nine male Wistar rats underwent left anterior descending (LAD) coronary artery ligation (CMI, n=26) or sham surgery (n=13). One-week post-surgery, CMI rats with anterior wall akinesia and left ventricular ejection fraction (LVEF) <50% were randomized to receive vehicle (distilled water; n=13) or dapagliflozin (1 mg/kg/day, oral; n=13) for 10 weeks. Outcomes measured included cardiac function, gut microbiota composition, gut barrier integrity, intestinal apoptosis, inflammatory cytokines, and levels of plasma microbial metabolites-short-chain fatty acids (SCFAs) and trimethylamine-N-oxide (TMAO).

Results: Dapagliflozin improved cardiac function and attenuated CMI-induced gut dysbiosis by restoring microbial diversity, enriching beneficial bacteria (UCG-007, Bacillus), and reducing harmful taxa (Holdemania). Gut barrier integrity was preserved through upregulation of tight junction proteins (TJPs) and suppression of intestinal apoptosis and inflammation. Metabolically, dapagliflozin increased butyrate production while lowering plasma TMAO levels, indicating a favorable microbial metabolic shift.

Conclusions: In this CMI rat model, dapagliflozin was associated with changes in the gut-heart axis that may relate to its observed cardioprotective effects. Further studies are required to determine causality and the relative contribution of these pathways.