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 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.

Objective:To investigate the relationship between the virulence and the carbapenem resistance phenotype of Klebsiella pneumoniae from blood infection,and to identify carbapenem-resistant and hypervirulent Klebsiella pneumoniae(CR-HVKP)strains.Methods:A total of 192 Klebsiella pneumoniae strains were isolated from blood culture of patients with bloodstream infections from 2016 to 2019,of which 96 isolates were carbapenem-resistant Klebsiella pneumoniae(CRKP)and 96 were carbapenem-sensitive Klebsiella pneumoniae(CSKP).The drug susceptibility was detected by VITEK-2 automatic microbial analyzer;carbapenemase genes,virulence genes and capsule typing were detected by polymerase chain reaction;the high viscosity phenotype of strains was detected by string test,and the genome characteristics of CR-HVKP were detected by whole genome sequencing.Serum killing and biofilm formation test were used to further verify the virulence of CR-HVKP.Results:There were significant differences in drug resistance to common antibiotics,except for minocycline between CSKP and CRKP isolates(all P<0.05).92 out of 96 CRKP isolates carried carbapenemase genes,mainly blaKPC-2.The string tests were positive in 4 isolates of CRKP and 36 isolates of CSKP(P<0.05).The detection rates of virulence genes Kfu,aerobictin,iutA,ybtS,rmpA,magA,allS,and capsule antigen K1 and K2 in CSKP group were significantly higher than those in CRKP group(all P<0.05).One HVKP strain was detected in the CRKP group(CR-HVKP)and 36 HVKP was detected in the CSKP group(P<0.05).The CR-HVKP strain belonged to the MLST412,serotype K57,expressed iutA,entB,mrkD,fimH,and rmpA virulence genes,and showed strong biofilm formation and significantly increased serum resistance.Whole genome sequencing results showed that this CR-HVKP isolate carried blaSHV-145,blaTEM-1,blaCTX-M-3,fosA6,oqxA5,oqxB26,and aac(3)-Ⅱd resistance genes,accompanied by abnormalities in outer membrane protein K(OmpK)35 and OmpK36.Conclusions:The drug resistance of CRKP is significantly higher than that of CSKP,while CRKP carrying fewer virulence genes in both number and types compared to CSKP.A new MLST type of carbapenem-resistant and hypervirulent Klebsiella pneumoniae strain has been detected,which requires clinical awareness and epidemiological monitoring.

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.

By sorting out and analyzing the contents about pulse diagnosis in Tanksuqnameh, it was found that in terms of pulse theory, the book contains academic viewpoints of different periods and doctors about three portions and nine readings pulse method and nutritive qi operation law in Huang Di Nei Jing, the Cunkou pulse-taking method and the Cunguanchi theory in Nan Jing, the Renying and Qikou pulse-taking method and the three-region pulse-taking method in Mai Jing, and the seven superficies-indicating, eight interior-indicating and nine channels pulse of Mai Jue, etc.; in terms of pulse theory interpretation, multiple annotations from famous doctors are cited, and TCM basic theories and knowledge of astronomy and mathematics are applied, combined with the background of ancient Iranian medicine and local medical experience for explanation; in terms of pulse diagnosis techniques, pulse diagnosis techniques such as "three fingers determining three guan", "adjusting finger density", "floating and sinking pulse", "foot back pulse breaking life and death" were recorded in books of Nan Jing, Mai Jue, Lei Zheng Huo Ren Shu, etc.; in terms of influencing pulse factors, the male and female pulse, physical pulse, and four time pulse were recorded. Tanksuqnameh is a universal work of Persian Traditional Chinese Medicine, compiled by the author Rashid-ul-Din based on his research on Chinese culture and medical knowledge, combined with the unique customs, language and culture, and way of thinking in the Middle East region, to reorganize various pulse theories from before the Han Dynasty to the Tang and Song Dynasties in China. The publication of this book indicates that TCM pulse diagnosis had been promoted to the Middle East in the 14th century and provided valuable experience for local medical development. The author's sense of identification and research spirit towards different cultures provide a historical example for achieving cross-cultural communication between TCM and medicine in different regions. The preserved literature from the Tang and Song Dynasties in the book can provide clues for a deeper understanding of ancient pulse theory in TCM, but some details do not explain thoroughly or does not match the current clinical practice. Therefore, attention should be paid to distinguishing in research and application.