Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

Purpose: Cancer has become a significant major public health concern, making the discovery of new cancer markers or therapeutic targets exceptionally important. Elevated expression of tumor necrosis factor receptor superfamily member 12A (TNFRSF12A) expression has been observed in certain types of cancer. This project aims to investigate the function of TNFRSF12A in tumors and the underlying mechanisms. Materials and Methods: Various websites were utilized for conducting the bioinformatics analysis. Tumor cell lines with stable knockdown or overexpression of TNFRSF12A were established for cell phenotyping experiments and subcutaneous tumorigenesis in BALB/c mice. RNA-seq was employed to investigate the mechanism of TNFRSF12A. Results: TNFRSF12A was upregulated in the majority of cancers and associated with a poor prognosis. Knockdown TNFRSF12A hindered the colorectal cancer progression, while overexpression facilitated malignancy both in vitro and in vivo. TNFRSF12A overexpression led to increased nuclear factor кB (NF-κB) signaling and significant upregulation of baculoviral IAP repeat containing 3 (BIRC3), a transcription target of the NF-κB member RELA, and it was experimentally confirmed to be a critical downstream factor of TNFRSF12A. Therefore, we speculated the existence of a TNFRSF12A/RELA/BIRC3 regulatory axis in colorectal cancer. Conclusion TNFRSF12A is upregulated in various cancer types and associated with a poor prognosis. In colorectal cancer, elevated TNFRSF12A expression promotes tumor growth, potentially through the TNFRSF12A/RELA/BIRC3 regulatory axis.

OBJECTIVES: This retrospective study aimed to investigate factors influencing positional changes of the condyle and temporomandibular joint (TMJ) following mandibular defect reconstruction with bone flaps, and to evaluate the biomechanical impacts of flap reconstruction on condylar positioning, thereby providing evidence for optimizing surgical protocols and TMJ functional rehabilitation. METHODS: A retrospective study was conducted on 90 patients undergoing mandibular segmental resection with immediate bone flap reconstruction at Guizhou Medical University Affiliated Stomatological Hospital (June 2019 to May 2024). After strict screening, 50 cases with complete data were analyzed. Clinical parameters (defect size, location, reconstruction method) and craniofacial CT scans at four timepoints [preoperative (T0), 7-10 days (T1), 3 months (T2), and 6 months (T3) postoperatively] were collected. Mimics 20 software facilitated 3D reconstruction for measuring TMJ anterior/posterior/superior joint spaces (Kamelchuk method) and calculating condylar position via the Pullinger index [Ln (posterior/anterior space)]. Vitral and Krisjane methods quantified mandibular linear parameters (ramus length, condylar pole distances to the sagittal plane, angulation) and glenoid fossa morphology. Statistical analyses were performed using SPSS 21.0. RESULTS: Mandibular defect size and location were significant factors influencing postoperative condylar position changes (P<0.05). Compared to preoperative measurements, postoperative condylar anterior, posterior, and superior joint spaces were significantly increased (P<0.001). The most pronounced anterior condylar displacement occurred within 7-10 days postoperatively (P<0.05). In patients with condyle resection, postoperative joint space and angle changes were significant; in patients with condyle preservation, only superior and anterior joint space changes were statistically significant (P<0.05). Additionally, from T1 to T2, the changes in condylar medial-lateral distance, superior joint space, and anterior joint space were negatively correlated with the preoperative condylar position. Compared with preoperative,in the T0-T1 period, condylar medial-lateral distance, posterior joint space, and articular tubercle angle changes were significantly negatively correlated with time (P<0.05). Notably, the angle between the condylar long axis and the coronal axis showed a sustained negative trend from T1 to T3 (P<0.05). CONCLUSIONS Condylar position changes after mandibular defect repair with bone flap reconstruction are associated with the size and location of the defect. Additionally, adaptive remodeling of the temporomandibular joint (TMJ) joint space occurs postoperatively. The phenomenon of anterior displacement of the condyle in the early postoperative period (7-10 days) shows a trend of reduction with prolonged follow-up time, and further sample size research is needed.
Humans ; Retrospective Studies ; Temporomandibular Joint/surgery* ; Mandibular Condyle/surgery* ; Male ; Female ; Adult ; Middle Aged ; Mandibular Reconstruction/methods* ; Mandible/surgery* ; Surgical Flaps ; Tomography, X-Ray Computed ; Young Adult ; Biomechanical Phenomena ; Aged ; Adolescent ; Imaging, Three-Dimensional

Objective To analyze the predictive value of serum inflammatory factors in multidrug-re-sistant pulmonary tuberculosis.Methods A total of 151 newly treated pulmonary tuberculosis patients admit-ted to Quzhou Hospital Affiliated to Wenzhou Medical University from February 2021 to February 2023 were enrolled for standardized treatment.Based on whether multidrug resistance developed after treatment,patients were divided into multidrug-resistant group and non-multidrug-resistant group.Pretreatment serum levels of inflammatory factors were measured and compared between groups,including hypersensitive C-reactive pro-tein(hs-CRP),procalcitonin(PCT),IL-1α,IL-1β,IL-1 receptor antagonist(IL-1RA),IL-2,IL-4,IL-5,IL-6,IL-8,IL-9,IL-10,IL-12,IL-13,IL-15,IL-17,IL-18,IL-22,IL-35,tumor necrosis factor-α(TNF-α),TNF-γ,and CD40 ligand(CD40L).Logistic regression identified influencing factors for multidrug-resistant pulmonary tu-berculosis.Receiver operating characteristic(ROC)curves evaluated the predictive value of these indicators.Results The incidence of multidrug-resistant pulmonary tuberculosis was 21.85%(33/151).The levels of se-rum inflammatory factors in the drug-resistant group were higher than those in the non-drug-resistant group before treatment(P<0.05).History of alcohol consumption,presence of cavities,severe illness,adherence to treatment,and pre-treatment serum hs-CRP,PCT,IL-6,IL-18,TNF-α levels were all influencing factors for multidrug resistance in pulmonary tuberculosis patients(P<0.05).The sensitivity and area under curve(AUC)of the combined prediction of serum hs-CRP,PCT,IL-6,IL-18,TNF-α levels before treatment for multidrug-resistant pulmonary tuberculosis were higher than those of individual predictions.Conclusion The levels of serum inflammatory factors are related to multidrug resistance in pulmonary tuberculosis,and the combina-tion of serum hs-CRP,PCT,IL-6,IL-18,TNF-α can predict multidrug resistance in pulmonary tuberculosis.

Head and neck squamous cell carcinoma (HNSCC) is the most common type of heterogeneous malignant tumor. Over 60% of HNSCC patients are at locally advanced stage at the time of diagnosis. Despite the emergence of advanced diagnosis and treatment measures, the prognosis of patients with recurrent or metastatic HNSCC remains poor. The Period (PER) gene family is an important member of the circadian clock genes, with family members PER1, PER2, and PER3 showing differential expression in HNSCC, participating in biological processes such as proliferation, apoptosis, invasion, or metastasis of tumor cells. In most studies, they exhibit anti-cancer effects and are closely related to the tumor microenvironment, immunotherapy, chronotherapy, etc., making them potential biomarkers. A comprehensive analysis of the expression of PER gene family in HNSCC, its biological role in the occurrence and development of tumor and the corresponding molecular biological mechanism is helpful to explore its potential application value in the diagnosis and treatment of HNSCC.

BACKGROUND:Mesenchymal stem cells are susceptible to senescence during in vitro expansion,which greatly hinders their application in vivo and in vitro.How to improve the replicative senescence of mesenchymal stem cells is an urgent problem to be solved in tissue engineering. OBJECTIVE:To determine whether vascular endothelial growth factor combined with basic fibroblast growth factor can improve the aging of bone marrow mesenchymal stem cells caused by replicative passage. METHODS:Rat bone marrow mesenchymal stem cells were extracted by whole bone marrow adhesion method.Passage 2 cells were selected as normal control group.Passage 7 and later algebraic cells were selected as aging model group.Vascular endothelial growth factor(50 μg/L),basic fibroblast growth factor(10 μg/L),and their combination were administered.Cell proliferation was detected by CCK-8 assay.Cell senescence was observed by β-galactosidase activity staining.Cytoskeleton size and colony formation ability were observed by phalloidine staining and Giemsa staining,respectively,and the levels of senescence-related genes P16,P21,and P53 were detected by qRT-PCR.Gene expression levels of P16,P21,and P53 were tested by qRT-PCR. RESULTS AND CONCLUSION:(1)Vascular endothelial growth factor combined with basic fibroblast growth factor could promote the proliferation of aged bone marrow mesenchymal stem cells,which began to enter the plateau stage on day 9,and the absorbance value of the combined intervention group was significantly higher than that of the model group on day 9(P<0.05).(2)The phenotypic markers of the cells in the combined intervention group did not change,and the cell morphology changed from broad to slender.(3)Compared with the model group,the positive rate of β-galactosidase was significantly decreased(P<0.01);the number of nuclei increased(P<0.001);the total area of cytoskeleton increased(P<0.01);colony formation ability was enhanced(P<0.05);expression level of P16 was decreased(P<0.01)in the combined intervention group.These results indicate that vascular endothelial growth factor combined with basic fibroblast growth factor can improve the senescence of bone marrow mesenchymal stem cells caused by replicative passage without changing the cell phenotype.

Objective:To explore the differences in bacterial community structure between proximal colon cancer (PC), distal colon cancer (DC), and rectal cancer (RC), and the values of featured microbiota in differentiating PC with tumor markers.Methods:This case-control study enrolled 85 newly diagnosed colorectal cancer patients, including 22 PC, 15 DC and 48 RC patients, and 8 colorectal adenoma patients from May 2019 to July 2022 at the Department of General Surgery, Anyang Oncology Hospital. The blood and fecal samples were collected before surgery and then subjected to biochemical tests for tumor markers and 16S rDNA tests, respectively. SPSS (27.0.1) was applied to perform the t-test, one-way ANOVA, Mann-Whitney U test, Kruskal-Wallis H test, and Chi-Squared Test. Also, the receiver operating characteristic curve (ROC) was plotted on tumor markers and/or f_Bacteroidaceae with SPSS software .Results:All groups had significant differences in the CA125 ( F=3.543, P<0.05), CA72-4 ( F=3.596, P<0.05), and serum tumor-associated materials (TAM) levels ( F=5.787, P<0.01). In PC group, the levels of CA125 [PC vs RC, (36.84±6.30) kU/L vs (12.73±4.21) kU/L, P<0.01] and CA72-4 [PC vs RC, (45.56±10.86) kU/L vs (3.30±7.63) kU/L, P<0.01] were significantly higher than that of the RC group, while the level of TAM was remarkably elevated in PC group than in RC group [PC vs RC, (124.84±5.19) U/ml vs (102.44±3.63) U/ml, P<0.001] and CRA group [PC vs CRA, (124.84±5.19) U/ml vs (95.39±8.42) U/ml, P<0.01]. The LEfSe analysis showed that the featured microbiota in the PC group included f_Bacteroidaceae, f_Neisseriaceae, f_Clostridiaceae_1, f_Spirochaetaceae, and so on. The largest area under the ROC belonged to the combination of TAM and f_Bacteroidaceae, which reached 0.845 (95% CI 0.747-0.944), with sensitivity being 0.857 and specificity being 0.815. Conclusions:There is heterogeneity in gut microbiota composition among PC, DC, RC, and CRA. The combination of gut microbiota and tumor biomarkers demonstrated good differentiating effects in proximal colon cancers.