Chronic obstructive pulmonary disease(COPD) is a common lung disease characterized by persistent airflow limitation, and diaphragmatic dysfunction is particularly prominent among the multiple extrapulmonary effects caused by COPD. Diaphragm, as the main respiratory muscle, whose dysfunction directly affects the ventilation efficiency of patients, is one of the key pathological mechanisms leading to the progressive exacerbation of COPD and respiratory failure, and is closely related to the mortality of the disease. Although COPD-associated diaphragm dysfunction has received increasing attention in recent years with the in-depth study of this pathology by clinicians and the continuous progress and innovation of diagnostic and therapeutic techniques, there is a lack of uniform and standardized treatment protocols at present. The purpose of this article is to review the pathogenesis of COPD-associated diaphragmatic dysfunction and its therapeutic strategies.

Metabolic-associated fatty liver disease(MAFLD) is a chronic liver disease associated with metabolic dysfunction, and its onset is mostly correlated with obesity, insulin resistance and lipid metabolism disorders. However, the specific pathogenesis has not been fully elucidated. Tryptophan hydroxylase 1(TPH1) belongs to hydroxylase, which participates in the key step in tryptophan metabolism and thus plays biological function. In recent years, studies have found that TPH1 and its synthesized 5-hydroxytryptamine(5-HT) are correlated with the occurrence and development of MAFLD. The synthesis of 5-HT by TPH1 can inhibit mitochondrial autophagy, induce liver lipid aggregation, oxidative stress and inflammation aggravation, and thus promote MAFLD. Therefore, inhibiting TPH1 may be a potential therapeutic target for MAFLD. This research will review action mechanism of TPH1 in MAFLD, emphatically analyze its influences on mitochondrial autophagy and explore therapeutic prospects of TPH1 inhibitors in MAFLD so as to develop personalized treatment strategies for MAFLD.

Breast cancer is the most common cancer in women. Bone metastasis is the most common complication in patients with advanced breast cancer, which seriously affects the quality of life and overall survival of patients. In current clinical treatment, complete cure remains a very difficult issue. However, through medication, the bone pain symptoms of patients can be effectively alleviated, and the occurrence of complications such as fractures can be reduced, making it a crucial treatment method. This article provides a review of the therapeutic effects and side effects of the mainstream drugs currently used in the treatment of breast cancer bone metastasis. It focuses on the latest clinical advancements in bone-targeted drugs, targeted drug delivery systems(DDS) and artificial intelligence in drug research.

Polatuzumab Vedotin(Pola), the inaugural antibody-drug conjugate(ADC) targeting CD79b, received approval in China in January 2023 for use in combination with rituximab, cyclophosphamide, doxorubicin, and prednisone(Pola-R-CHP) as a frontline regimen for adult patients with untreated diffuse large B-cell lymphoma(DLBCL). Leveraging the cytotoxic properties of Pola and its impact on signaling pathways implicated in the pathogenesis of DLBCL, numerous studies have explored combination therapies with Pola in recent years. These studies have demonstrated favorable efficacy and safety profiles, particularly in patients with relapsed or refractory DLBCL. The findings have paved the way for further research into the efficacy of Pola-based regimens in specific patient subgroups, such as the elderly and those with double/triple-hit DLBCL.