BACKGROUND:Currently,numerous experiments delve into the intricate anatomy and biomechanical behavior of distinct segments of the supraspinatus muscle.However,the impact of shoulder joint stress resulting from damage to various regions of this muscle remains a scarcely explored domain.Understanding the repercussions of supraspinatus muscle injuries across different regions on the stress distribution and magnitude of articular cartilage and the glenoid is crucial for providing some theoretical support for clinical diagnosis and treatment. OBJECTIVE:To ascertain the maximum stress values by simulating different degrees of supraspinatus muscle rupture on the humeral cartilage surface,glenoid lip,and glenoid cartilage joint surface using three-dimensional finite element software. METHODS:Normal and healthy shoulder joint CT or MRI scans were processed through Mimics and Geomagic to extract molds.Subsequently,models were constructed via Solidworks.Varying degrees of supraspinatus muscle damage were simulated for each model to mimic fractures in different regions.Finally,Ansys,mechanical software,was employed for three-dimensional finite element biomechanical analysis,calculating stress values for the humeral cartilage surface,glenoid lip,and glenoid cartilage joint surface. RESULTS AND CONCLUSION:(1)With worsening degrees of supraspinatus muscle injury,the stress on the shoulder joint cartilage surface and glenoid lip escalated.(2)Among various regions,the anterior part of the supraspinatus muscle exhibited paramount significance.(3)While supraspinatus muscle fractures of differing degrees impacted the magnitude of cartilage stress on the glenoid labial surface,the stress distribution remained constant.(4)It is indicated that during the initial stages of horizontal abduction of the shoulder joint,the anterior region assumes a pivotal role,followed by the posterior deep region.Injury to the anterior part of the supraspinatus muscle leads to a significant surge in stress within the shoulder joint's soft tissue,potentially causing damage to the top of the glenoid lip and the anterior part of the glenoid cartilage.

[摘 要] 目的：评估放疗作为原位疫苗的联合治疗模式在晚期软组织肉瘤（STS）患者中的有效性和安全性。方法：回顾性分析2020年12月至2024年9月期间在南京大学医学院附属鼓楼医院肿瘤中心接受联合治疗模式的12例晚期STS患者的临床资料。12例患者均接受了联合治疗。放疗主要以大分割为主。靶向治疗：安罗替尼10例、阿帕替尼2例。免疫治疗以PD-1抗体为主。主要研究终点为疾病控制率（DCR），次要研究终点为客观有效率（ORR）及安全性。结果：接受联合治疗的12例STS患者中有0例CR，4例PR，7例SD，1例PD。ORR为33%，DCR为91.7%，其中靶病灶的DCR为100%。12例患者中，9例出现Ⅰ~Ⅱ级不良反应。最常发生的血液学不良反应是贫血（6例）、肝功能检查结果异常（3例）。最常发生的非血液学不良反应是尿蛋白（5例）、高血压（4例）、甲状腺功能异常（3例）、厌食（3例）、恶心呕吐（2例）；仅2例发生Ⅲ级血液毒性，有1例发生Ⅲ级气胸。结论：放疗作为原位疫苗的联合治疗模式在晚期STS患者中展现出较高的DCR，且未出现严重不良反应。该联合治疗模式具有良好的有效性与安全性。

The sternalis muscle is a rare supernumerary muscle representing a normal anatomical variant in the anterior thoracic musculature. Due to wide variation in its morphology and relative unfamiliarity among radiologists, it has been implicated in the misdiagnosis of breast masses on mammography. A 23-year-old male with no significant medical history was referred to our institution for further management of painless bilateral breast enlargement since adolescence. Physical examination revealed breasts of slightly prominent size but there was no palpable breast lump. Mammography work-up found symmetrical, well-defined soft tissue masses projected over the posteromedial aspect of both breasts. Imaging findings were consistent with bilateral sternalis muscles, unusually hypertrophic in size due to intense upper body weight training by the patient. This case highlights the importance of recognizing the usual and unusual presentations of the sternalis muscles on mammography to avoid any unnecessary work-up.

The sternalis muscle is a rare supernumerary muscle representing a normal anatomical variant in the anterior thoracic musculature. Due to wide variation in its morphology and relative unfamiliarity among radiologists, it has been implicated in the misdiagnosis of breast masses on mammography. A 23-year-old male with no significant medical history was referred to our institution for further management of painless bilateral breast enlargement since adolescence. Physical examination revealed breasts of slightly prominent size but there was no palpable breast lump. Mammography work-up found symmetrical, well-defined soft tissue masses projected over the posteromedial aspect of both breasts. Imaging findings were consistent with bilateral sternalis muscles, unusually hypertrophic in size due to intense upper body weight training by the patient. This case highlights the importance of recognizing the usual and unusual presentations of the sternalis muscles on mammography to avoid any unnecessary work-up.

The sternalis muscle is a rare supernumerary muscle representing a normal anatomical variant in the anterior thoracic musculature. Due to wide variation in its morphology and relative unfamiliarity among radiologists, it has been implicated in the misdiagnosis of breast masses on mammography. A 23-year-old male with no significant medical history was referred to our institution for further management of painless bilateral breast enlargement since adolescence. Physical examination revealed breasts of slightly prominent size but there was no palpable breast lump. Mammography work-up found symmetrical, well-defined soft tissue masses projected over the posteromedial aspect of both breasts. Imaging findings were consistent with bilateral sternalis muscles, unusually hypertrophic in size due to intense upper body weight training by the patient. This case highlights the importance of recognizing the usual and unusual presentations of the sternalis muscles on mammography to avoid any unnecessary work-up.

Four novel β-galactoside prodrugs were designed and synthesized from anthraquinones HAQ-OH and AQ-OH in an attempt to use the prodrugs to selectively release superoxide anion (O2−) in cancer cells and to achieve selected anticancer activity by utilizing the Warburg effect and the elevated level of β-galactosidase in certain cancer cells. Cellular assays showed that the prodrugs Gal-HAQ and Gal-AQ selectively inhibited the proliferation and induced apoptosis of ovarian cancer OVCAR-3 cells overexpressing β-galactosidase. Using O2− fluorescent probe, it was found that in OVCAR-3 cells Gal-HAQ and Gal-AQ could time-dependently release O2−, which was essential for their anticancer activity. Furthermore, it was found that Gal-HAQ and Gal-AQ were effective senolytics toward senescent cells overexpressing β-galactosidase without affecting the viability of corresponding non-senescent cells, further confirming the β-galactosidase-dependent cytotoxicity of the prodrugs. In conclusion, Gal-HAQ and Gal-AQ, which release O2− in response to β-galactosidase, are expected to serve as candidate prodrugs targeting cancer cells.

[摘 要] 目的：探究三七总皂苷（PNS）通过JAK2/STAT3通路调控巨噬细胞极化对小鼠黑色素瘤B16-F10细胞的活力的影响。方法：常规培养B16-F10细胞和巨噬细胞RAW264.7，MTT法检测不同浓度PNS对RAW264.7或B16-F10细胞存活率的影响。实验分为空白组（仅B16-F10细胞）、对照组（B16-F10细胞与RAW264.7细胞共培养）、不同浓度（50、100、200 μg/mL）PNS组（B16-F10细胞与RAW 264.7细胞共培养）及200 μg/mL PNS + colivelin[（B16-F10细胞与RAW264.7细胞共培养，0.5 μmol/L colivelin JAK2/STAT3通路激活剂）]组，MTT法、流式细胞术检测各组共培养细胞的存活率和凋亡率，显微镜观察巨噬细胞形态变化；ELISA实验检测上清液中相关细胞因子TNF-α、IL-6、IL-1β的水平，qPCR法检测巨噬细胞极化相关基因诱导型一氧化氮合酶（iNOS）、IL-12、CD206、精氨酸酶-1（Arg-1）mRNA表达，WB法检测细胞中JAK2、STAT3蛋白磷酸化水平。结果：不同浓度PNS对单独培养的RAW264.7、B16-F10细胞的存活率均无明显影响（均P > 0.05）。与对照组相比，PNS呈浓度依赖性地促进共培养细胞凋亡、IL-6、TNF-α、IL-1β蛋白和IL-12、iNOS mRNA表达水平均显著增加（均P < 0.05），降低共培养细胞的存活率、JAK2与STAT3蛋白磷酸化水平（均P < 0.05），PNS对共培养细胞的作用部分被colivenlin抑制。结论：PNS通过抑制JAK2/STAT3通路促进M1巨噬细胞极化进而抑制小鼠黑色素瘤B16-F10细胞的活力。

OBJECTIVE: To investigate the effects of Danmu Extract Syrup (DMS) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and explore the mechanism. METHODS: Seventy-two male Balb/C mice were randomly divided into 6 groups according to a random number table (n=12), including control (normal saline), LPS (5 mg/kg), LPS+DMS 2.5 mL/kg, LPS+DMS 5 mL/kg, LPS+DMS 10 mL/kg, and LPS+Dexamethasone (DXM, 5 mg/kg) groups. After pretreatment with DMS and DXM, the ALI mice model was induced by LPS, and the bronchoalveolar lavage fluid (BALF) were collected to determine protein concentration, cell counts and inflammatory cytokines. The lung tissues of mice were stained with hematoxylin-eosin, and the wet/dry weight ratio (W/D) of lung tissue was calculated. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-1 β in BALF of mice were detected by enzyme linked immunosorbent assay. The expression levels of Claudin-5, vascular endothelial (VE)-cadherin, vascular endothelial growth factor (VEGF), phospho-protein kinase B (p-Akt) and Akt were detected by Western blot analysis. RESULTS: DMS pre-treatment significantly ameliorated lung histopathological changes. Compared with the LPS group, the W/D ratio and protein contents in BALF were obviously reduced after DMS pretreatment (P<0.05 or P<0.01). The number of cells in BALF and myeloperoxidase (MPO) activity decreased significantly after DMS pretreatment (P<0.05 or P<0.01). DMS pre-treatment decreased the levels of TNF-α, IL-6 and IL-1 β (P<0.01). Meanwhile, DMS activated the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway and reversed the expressions of Claudin-5, VE-cadherin and VEGF (P<0.01). CONCLUSIONS DMS attenuated LPS-induced ALI in mice through repairing endothelial barrier. It might be a potential therapeutic drug for LPS-induced lung injury.
Mice ; Male ; Animals ; Proto-Oncogene Proteins c-akt/metabolism* ; Lipopolysaccharides ; Phosphatidylinositol 3-Kinases/metabolism* ; Interleukin-1beta/metabolism* ; Vascular Endothelial Growth Factor A/metabolism* ; Tumor Necrosis Factor-alpha/metabolism* ; Claudin-5/metabolism* ; Acute Lung Injury/chemically induced* ; Lung/pathology* ; Interleukin-6/metabolism* ; Drugs, Chinese Herbal

Abnormal tumour cell adhesion is a key step in tumour metastasis， in which weakened homologous and enhanced heterologous adhesion of tumour cells is an important cause of tumour metastasis. Chronic stress can activate the sympathetic nervous system to link and regulate the homologous and heterologous adhesion of tumour cells and exacerbate tumour metastasis. Combining the understanding of traditional Chinese medicine （TCM） and Western medicine on tumour metastasis， it is believed that the mechanism of "qi constraint and stagnation， tumor toxin transmission and retention" in TCM theory is highly related to the abnormal adhesion of tumour cells triggered by chronic stress. Qi constraint and stagnation is closely related to chronic stress and its activation of the sympathetic nervous system， and transmission and retention of tumor toxin explained the mechanism of tumour metastasis due to abnormal adhesion of tumour cells from the perspective of TCM. By regulating the key link of sympathetic nervous system-tumour cell adhesion， application of the formulas of regulating qi and resolving toxin can improve chronic stress and inhibit tumour metastasis.

Objective: To investigate protective effects of nicotinamide mononucleotide (NMN) on ethanol-induced DNA damage in L02 cells, so as to provide the evidence for adjuvant therapy of NMN on alcoholic liver diseases. Methods: L02 cells were pretreated with different concentrations of NMN (0, 1, 2, 4 and 8 mmol/L) for 6 h, and then were exposed to 0.4% ethanol for 12 h. The treated cells were divided into the control group, 0.4% ethanol group and different concentrations of NMN groups. Cell viability was analyzed using trypan blue staining for determining the concentration of NMN as a protective agent. The effects of NMN on ethanol-induced DNA damage in L02 cells were evaluated using immunofluorescence detection and reactive oxygen species (ROS) assay. L02 cells were exposed to 0.4% ethanol for 12 h, cultured in a medium containing a protective concentration of NMN, and divided into PBS group and NMN group. Cell viability was detected at 0, 2, 4, 8, 16 and 32 h, and the effects of NMN on repairing ethanol-induced DNA damage were evaluated by alkaline comet assay. Results: The cell viability was lower in 0.4% ethanol group than than in the control group, and was higher in different concentrations of NMN groups than in 0.4% ethanol group (all P<0.05), with no significant difference in the cells viability between 4 mmol/L and higher concentrations of NMN groups and the control group (all P>0.05). Therefore, 4 mmol/L NMN was selected as a protective agent. The cell tail moments, relative immunofluorescence intensities of γH2AX and relative levels of ROS were higher in 0.4% ethanol group than in the control group, and lower in 4 mmol/L and higher concentrations of NMN groups than in 0.4% ethanol group (all P<0.05). The cell viability was increased and the cell tail moment was shortened with the increase of 4 mmol/L NMN intervention time; and the cell viability in 4 h and more of NMN groups were higher, and the cell tail moment were lower than that in PBS group (all P<0.05). Conclusions NMN attenuates DNA damage in a dose-dependent manner and promotes the repair of DNA damage in a time-dependent manner. NMN has a protective effect on ethanol-induced DNA damage in hepatocytes.