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.

Objective:To investigate the efficacy of radiotherapy in patients with advanced esophageal cancer receiving first-line chemoimmunotherapy.Methods:A retrospective analysis was conducted on the data of 137 patients with Stage Ⅳ esophageal squamous cell carcinoma (ESCC) treated at our hospital from January 2018 to May 2023. These patients were divided into two groups: a group treated with first-line chemoimmunotherapy combined with radiotherapy (chemoimmunotherapy + radiotherapy group, n = 43) and a group treated with only chemoimmunotherapy ( n = 94). Inverse probability of treatment weighting (IPTW) was applied to balance baseline characteristics between the groups. With overall survival (OS) and progression-free survival (PFS) as study endpoints, the survival data were analyzed using the Kaplan-Meier method, the log-rank test, and the Cox regression method. Results:Before calibration, the chemoimmunotherapy + radiotherapy group significantly outperformed the sole chemoimmunotherapy group in median PFS (13.6 months vs. 7.0 months; HR: 0.501, 95% CI: 0.309-0.811, P = 0.005). After calibration using the COX proportional-hazards model for age, gender, Eastern Cooperative Oncology Group (ECOG) performance status, smoking history, T/N/M stage, and tumor location, the chemoimmunotherapy + radiotherapy group still had significant advantages in PFS (14.7 months vs. 7.0 months; HR: 0.441, 95% CI: 0.261-0.745, P = 0.002). IPTW analysis further confirmed this trend (13.9 months vs. 7.0 months; HR: 0.492, 95% CI: 0.304-0.795, P < 0.001). Specifically, the median OS of the chemoimmunotherapy + radiotherapy group demonstrated significant improvement in all analyses: pre-calibration (29.5 months vs. 18.0 months; HR: 0.507, 95% CI: 0.297-0.867, P = 0.013), after calibration using the Cox model (27.5 months vs. 16.7 months; HR: 0.470, 95% CI: 0.266-0.830, P = 0.009), and after calibration using IPTW (29.5 months vs. 16.9 months; HR: 0.448, 95% CI: 0.262-0.764, P < 0.001). Conclusions:The combination of radiotherapy and first-line chemoimmunotherapy can significantly improve survival outcomes of patients with advanced ESCC, suggesting its potential as a standard treatment strategy.

Objective:Comprehensive characterization of B-cell phenotypes and spatial distribution in oral lichen planus (OLP) and related oral lichenoid lesions (OLL)(OLP/OLL), with an emphasis on transcriptomic profiling and functional analysis, to uncover the epigenetic mechanisms underlying B cell-mediated immune regulation within the oral mucosal microenvironment.Methods:Single-cell RNA sequencing raw data were sourced from the GSE211630 database, encompassing samples from 2 cases of erosive OLP (EOLP), 3 cases of non-erosive OLP (NEOLP) and 1 healthy control (NORMAL). Following stringent quality control, the data underwent normalization, selection of highly variable genes and batch effect correction. Subsequent analyses included dimensionality reduction and unsupervised clustering to identify distinct cell populations. This study collected pathological specimens from 3 OLP/OLL patients and 3 healthy controls who were treated at the Department of Oral Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine from January 2021 to December 2023. Using 10X Genomics Visium HD spatial transcriptomics technology, tissue sections were processed through dewaxing, staining and histological imaging, enabling the reconstruction of nucleic acid structures and the capture of gene expression profiles. Data analysis included quality assessment, gene quantification, normalization, dimensionality reduction and clustering. Furthermore, cell type deconvolution was performed using the robust cell type decomposition algorithm, integrating single-cell transcriptomic data to accurately predict and spatially resolve cell type distributions within the tissue microenvironment.Results:After integrating single-cell data from EOLP, NEOLP and NORMAL, cells were classified into seven major categories: B/plasma cells, endothelial cells, epithelial cells, fibroblasts, myeloid cells, smooth muscle cells and T/natural killer cells. The proportion of B/plasma cells varied significantly among the three groups, accounting for 10.7% (1 693/15 815), 3.8% (833/21 653) and 0.4% (47/11 556) of the total cells respectively. Further clustering analysis of B/plasma cells identified four distinct subpopulations: naive B cells, activated B cells, memory B cells and plasma cells. In the EOLP group, these subpopulations constituted 25.9% (348/1 344), 45.9% (617/1 344), 3.3% (45/1 344) and 24.9% (334/1 344) of the B/plasma cells respectively. In the NEOLP group, they represented 31.6% (195/617), 59.6% (368/617), 0.2% (1/617) and 8.6% (53/617). Howerer, only plasma cells were detected in the NORMAL group. Spatial analysis revealed that B cells were actively involved in the formation of tertiary lymphoid structures (TLS) at various stages in OLP/OLL samples, with a prominent structural organization observed in secondary follicle-like TLS. Within these structures, the expressions of T cells marker gene CD3E and B cells marker gene MS4A1 were significantly elevated. Additionally, in secondary follicle-like TLS, the gene encoding follicular dendritic cell secreted protein, germinal center marker gene B cell lymphoma 6 and the gene for activation induced cytidine deaminase also showed strong expression. In OLP/OLL samples, plasma cell marker gene CD38, immunoglobulin (IGH) G3, IGHG1, IGHM, IGHD, IGHE, imunoglobulin Kappa constant, immunoglobulin alpha 1, immunoglobulin Lambda constant 1 and complement gene C3 all exhibited high levels of expression.Conclusions:Compared to normal mucosa, extensive B-cell infiltration is observed in both OLP and OLL, accompanied by significant differences in B-cell phenotypes and proportions. B cells appear to play a central role in local immune responses, primarily through the formation of TLS. However, the precise functional mechanisms underlying their involvement require further investigation.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

HR-positive HER2-low breast cancer is a new hotspot therapeutic subtype, accounting for approximately 53.7% of all breast cancers. Patients with this type of cancer tend to have a high rate of lymph node metastasis and poor sensitivity to neoadjuvant chemotherapy and conventional anti-HER2 therapy, and exploring therapeutic strategies for this subtype of patient is a current clinical challenge. Therapeutic strategies for HR-positive HER2-low breast cancer are constantly being updated, including CDK4/6 inhibitors across the lines of therapy, and next-generation antibody-drug conjugates such as T-DXd. With the accumulation of high-level evidence-based evidence for HR-positive HER2-low breast cancer in the future, the research data will provide more practical support for precise diagnosis and treatment, thereby improving the prognosis of patients with HR-positive HER2-low breast cancer.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Guided by the cancer toxin theory of TCM master Professor Zhou Zhongying,and absorbing the thoughts of academician Tong Xiaolin's theory of state-target,the pathogenesis of multiple myeloma is summarized as deficiency of healthy qi,bone erosion and marrow damage,cancer toxin accumulation,phlegm and stasis mingling,the combat between healthy qi and evil qi,and dynamic evo-lution;a full-cycle anti-cancer and detoxification prevention and treatment strategy for multiple myeloma is proposed that incorporates the ideas of nourishing deficiency and strengthening healthy qi,preventing cancer and detoxification,resolving phlegm and removing stasis throughout the entire treatment process.The scientific connotation of the pathogenesis theory of"healthy qi deficiency and cancer toxin"in multiple myeloma is explained from multiple aspects such as protein overload and tumor microenvironment,and a prescrip-tion-drug medicine system with Xuanbi Xiaoliu Formula as the core is constructed,which provides new ideas and scientific basis for the clinical diagnosis and treatment plan and full-cycle prevention and control model of multiple myeloma combining Chinese and West-ern medicine.