Long-term chronic stress is an important factor in the poor prognosis of cancer patients. Chronic stress reduces the tissue infiltration of immune cells in the tumor microenvironment (TME) by continuously activating the adrenergic signaling, inhibits antitumor immune response and tumor cell apoptosis while also inducing epithelial-mesenchymal transition (EMT) and tumor angiogenesis, promoting tumor invasion and metastasis. This review first summarizes how adrenergic signaling activates intracellular signaling by binding different adrenergic receptor (AR) heterodimers. Then, we focused on reviewing adrenergic signaling to regulate multiple functions of immune cells, including cell differentiation, migration, and cytokine secretion. In addition, the article discusses the mechanisms by which adrenergic signaling exerts pro-tumorigenic effects by acting directly on the tumor itself. It also highlights the use of adrenergic receptor modulators in cancer therapy, with particular emphasis on their potential role in immunotherapy. Finally, the article reviews the beneficial effects of stress intervention measures on cancer treatment. We think that enhancing the body's antitumor response by adjusting adrenergic signaling can enhance the efficacy of cancer treatment.

In the current research context of precision treatment of malignant tumors, the advantages of immunotherapy are unmatched by conventional antitumor therapy, which can prolong progression-free survival and overall survival. The search for new targets and novel combination therapies can improve the efficacy of immunotherapy and reduce adverse effects. Since current research targets for immunotherapy mainly focus on lymphocytes, little research has been done on erythrocytes. Nucleated erythroid precursor stem cells have been discovered to play an essential role in tumor progression. Researchers are exploring new targets and therapeutic approaches for immunotherapy from the perspective of erythroid progenitor cells (EPCs). Recent studies have shown that different subtypes of EPCs have specific surface markers and distinct biological roles in tumor immunity. CD45⁺ EPCs are potent myeloid-derived suppressor cell-like immunosuppressants that reduce the patient’s antitumor immune response. CD45⁻ EPCs promote tumor invasion and metastasis by secreting artemin. A specific type of EPC also promotes angiogenesis and provides radiation protection. Therefore, EPCs may be involved in tumor growth, infiltration, and metastasis. It may also be an important cause of anti-angiogenesis and immunotherapy resistance. This review summarizes recent research advances in erythropoiesis, EPC features, and their impacts and processes on tumors.

Lung cancer (LC) and tuberculosis (TB) are two major global public health problems, and the incidence of LC-TB is currently on the rise. Therefore effective clinical interventions are crucial for LC-TB. The aim of this review is to provide up-to-date information on the immunological profile and therapeutic biomarkers in patients with LC-TB. We discuss the immune mechanisms involved, including the immune checkpoints that play an important role in the treatment of patients with LC-TB. In addition, we explore the susceptibility of patients with LC to TB and summarise the latest research on LC-TB. Finally, we discuss future prospects in this field, including the identification of potential targets for immune intervention. In conclusion, this review provides important insights into the complex relationship between LC and TB and highlights new advances in the detection and treatment of both diseases.

S: Idiopathic pulmonary fibrosis (IPF) is a chronic disease of unknown etiology that lacks a specific treatment. In IPF, macrophages play a key regulatory role as a major component of the lung immune system, especially during inflammation and fibrosis. However, our understanding of the cellular heterogeneity and molecular characterization of macrophages in IPF, as well as their relevance in the clinical setting, is relatively limited. In this study, we analyzed in-depth single-cell transcriptome sequencing (scRNA-seq) data from lung tissues of IPF patients, identified macrophage subpopulations in IPF, and probed their molecular characteristics and biological functions. hdWGCNA identified co-expressed gene modules of a subpopulation of IPF-associated macrophages (IPF-MΦ), and probed the IPF-MΦ by a machine-learning approach. hdWGCNA identified a subpopulation of IPF-associated macrophage subpopulations and probed the IPF-MΦ signature gene (IRMG) for its prognostic value, and a prediction model was developed on this basis. In addition, IPF-MΦ was obtained after recluster analysis of macrophages in IPF lung tissues. Coexpressed gene modules of IPF-MΦ were identified by hdWGCNA. Then, a machine learning approach was utilized to reveal the characteristic genes of IPF-MΦ, and a prediction model was built on this basis. In addition, we discovered a type of macrophage unique to IPF lung tissue named ATP5-MΦ. Its characteristic gene encodes a subunit of the mitochondrial ATP synthase complex, which is closely related to oxidative phosphorylation and proton transmembrane transport, suggesting that ATP5-MΦ may have higher ATP synthesis capacity in IPF lung tissue. This study provides new insights into the pathogenesis of IPF and provides a basis for evaluating disease prognosis and predictive medicine in IPF patients. Graphical Abstract

To observe the curative effect of Zishengukang Pill () on delayed union of fracture. Sixty-four patients with delayed union of fracture were randomly divided into a control group of 32 cases treated with Western medicine and a treatment group of 32 cases treated with Western medicine and Zishengukang Pill. After 3 courses of treatment with 30 days as a course, the curative effects in the two groups were evaluated and their clinical symptoms, union rate and union time of fracture were compared. The treatment resulted in cure in 25 cases, improvement in 6 cases and ineffectiveness in 1 case with the effective rate at 96.8% in the treatment group, higher than 81.3% in the control group (P < 0.05). The union rate of fracture in the treatment group was higher than that in the control group (34.3% vs. 12.5%, P < 0.05). The union time of fracture in the treatment group was shorter than that in the control group ((4.0±1.7) months vs. (5.0±1.4) months, P < 0.05). Zishengukang Pill with obvious curative effect in the treatment of delayed union of fracture is worth popularizing.