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OBJECTIVE@#To investigate short-term effectiveness and clinical application advantages of orthopedic robot-assisted resection for osteoid osteoma compared with traditional open surgery.@*METHODS@#A retrospective analysis was conducted on clinical data of 48 osteoid osteoma patients who met the selection criteria between July 2022 and April 2023. Among them, 23 patients underwent orthopedic robot-assisted resection (robot-assisted surgery group), and 25 patients received traditional open surgery (traditional surgery group). There was no significant difference ( P>0.05) in gender, age, disease duration, lesion location and size, and preoperative visual analogue scale (VAS) score, and musculoskeletal tumor society (MSTS) score between the two groups. The surgical time, intraoperative blood loss, intraoperative lesion localization time, initial localization success rate, infection, and recurrence were recorded and compared. VAS scores before surgery and at 24 hours, 1, 3, 6, and 9 months after surgery and MSTS score before surgery and at 3 months after surgery were assessed.@*RESULTS@#All patients completed the surgery successfully, with no significant difference in surgical time between the two groups ( P>0.05). Compared to the traditional surgery group, the robot-assisted surgery group had less intraoperative blood loss, shorter lesion localization time, and shorter hospitalization time, with significant differences ( P<0.05). The initial localization success rate was higher in the robot-assisted surgery group than in the traditional surgery group, but the difference between the two groups was not significant ( P>0.05). All patients in both groups were followed up, with the follow-up time of 3-12 months in the robot-assisted surgery group (median, 6 months) and 3-14 months in the traditional surgery group (median, 6 months). The postoperative MSTS scores of both groups improved significantly when compared to those before surgery ( P<0.05), but there was no significant difference in the changes in MSTS scores between the two groups ( P>0.05). The postoperative VAS scores of both groups showed a gradually decreasing trend over time ( P<0.05), but there was no significant difference between the two groups after surgery ( P>0.05). During follow-up, except for 1 case of postoperative infection in the traditional surgery group, there was no infections or recurrences in other cases. There was no significant difference in the incidence of postoperative infection between the two groups ( P>0.05).@*CONCLUSION@#Orthopedic robot-assisted osteoid osteoma resection achieves similar short-term effectiveness when compared to traditional open surgery, with shorter lesion localization time.
الموضوعات
Humans , Robotics , Blood Loss, Surgical , Osteoma, Osteoid/surgery , Retrospective Studies , Treatment Outcome , Postoperative Complications , Bone Neoplasms/surgeryالملخص
Molecular targeted therapy has become an emerging promising strategy in cancer treatment, and screening the agents targeting at cancer cell specific targets is very desirable for cancer treatment. Our previous study firstly found that a secretory peroxidase of class III derived from foxtail millet bran (FMBP) exhibited excellent targeting anti-colorectal cancer (CRC) activity in vivo and in vitro, whereas its underlying target remains unclear. The highlight of present study focuses on the finding that cell surface glucose-regulated protein 78 (csGRP78) abnormally located on CRC is positively correlated with the anti-CRC effects of FMBP, indicating it serves as a potential target of FMBP against CRC. Further, we demonstrated that the combination of FMBP with the nucleotide binding domain (NBD) of csGRP78 interfered with the downstream activation of signal transducer and activator of transcription 3 (STAT3) in CRC cells, thus promoting the intracellular accumulation of reactive oxygen species (ROS) and cell grown inhibition. These phenomena were further confirmed in nude mice tumor model. Collectively, our study highlights csGRP78 acts as an underlying target of FMBP against CRC, uncovering the clinical potential of FMBP as a targeted agent for CRC in the future.
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OBJECTIVE To explore the effect of clofenotane (DDT) on epithelial-mesenchymal transition (EMT) and the relevant molecular mechanism in human colorectal cancer cells. METHODS Human colorectal cancer cells DLD1 were treated with DDT 0.01, 0.1, 1.0, 10.0 and 100.0 nmol·L-1 for 48 h. Then, the morphology of DLD1 cells was observed. mRNA levels of E-cadherin, N-cadherin, vimentin and Snail1 were detected by real-time PCR. Protein expression of STAT3 signaling pathway of proteins STAT3 and p-STAT3 was detected by Western blotting. STAT3 inhibitor WP1006 (5μmol · L-1) was added to determine its impact on DDT-induced alternation of STAT3/Snail1 signaling and EMT-related molecules. Protein expression of STAT3 and p-STAT3 was detected by Western blotting and mRNA levels of E-cadherin, N-cadherin, Vimentin and Snail1 were detected by real-time PCR. RESULTS DLD1 cell morphology was changed after exposure to DDT 0.01-100.0 nmol · L- 1. Meanwhile, real-time PCR showed that the mRNA level of E-cadherin was significantly decreased compared with normal cell control (P<0.01), which was 42.4±2.8%of that in the normal control group. The mRNA levels of N-cadherin, Vimentin and Snail1 were significantly increased (P<0.01), which were 1.91±0.1, 1.5±0.2 and 1.5±0.1 times that of the normal control group. DDT 0.1, 1.0 and 10.0 nmol · L-1 exposure induced up-regulation of STAT3 and p-STAT3 protein levels (P<0.01), which were 2.1 and 1.8 times that of the normal control group. The addition of STAT3 inhibitor WP1066 (5 μmol · L-1) prevented STAT3 from phosphorylation as well as the up-regulation of Snail1(P<0.01), which was (56.3 ± 0.9)% that of the DDT 1.0 nmol · L-1 treat?ment group. Compared with DDT treatment alone, the mRNA levels of EMT-related molecules were remarkably reversed by WP1066 (5 μmol · L- 1) co-treatment, increasing E-cadherin but decreasing N-cadherin and vimentin in DLD1 cells(P<0.01), which were 50.2±2.9%and 61.6±6.1%of those in the DDT 1.0 nmol · L- 1 treatment group, respectively. CONCLUSION DDT alters the expressions of EMT-related molecules including E-cadherin, N-cadherin and vimentin via STAT3/Snail1 signaling, thus promoting the EMT process in human colorectal cancer cells. This progress may be closely related to DDT-induced colorectal cancer development.
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Objective To discuss the value of serum thymidine kinase 1 and DNA ploidy for the diagnosis of patients with acute myeloid lecukemia.Methods Determined TK1 and DI in 20 healthy people,6 patients with benign proliferate in hematological system and 66 patients with acute myeloid lecukemia by chemiluminescence detection technique and flow cytometry.Nonparametric comparisons among three group were done by rank sum test.ROC curve was used to determine the AUC and the diagnosis value serum thymidine kinase 1 and DNA.Results As showed by peripheral blood results,the TK1 (x2 =36.877,P<0.001) and DI (x2=4.040,P<0.05) had statistically difference among healthy people group,patients with benign proliferate in hematological system group and AML group.The normal control group compared with the AML group,TK1 (Z=-6.073,P<0.001)and DI (Z=-2.012,P =0.044) had statistically difference;The normal control group compared with the benign proliferate patients,TK1 (Z=-1.234,P =0.169) and DI (Z=-1.084,P =0.278) had no statistically difference.The benign proliferate patients and that with AML patients,TK1 (Z=2.177,P=0.036) had statistically difference,but DI (Z=-1.801,P=0.061) had no statistically difference.The TK1 and DI area under the ROC curve were 0.950 (P<0.001) and 0.638 (P=0.063),best cut-off were 1.73 pmol/L and 0.98,sensitivity were 0.95,0.78,and specifity were 0.88,0.39.Conclusion Serum TK1 and DI is a important diagnostic marker of early for AML patients,TK1 have a better diagnostic performance than DI significantly.
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OBJECTIVE To investigate the effects and mechanism of PCB118 on cell-matrix and cel-cel adhesion in human hepatocel ular carcinoma cel s. METHODS Human hepatocel ular carcinoma cel s BEL-7402 were treated with PCB118 0.1,1.0 and 10.0 nmol · L-1 for 4 or 6 d,respectively. Then the cell-matrix adhesion assay and cell aggregation experiments were conducted to study the effect of PCB118 on cell-matrix adhesion and cell-cell adhesion in BEL-7402 cells. Quantitative real-time PCR and Western blotting methods were employed to assess the expression of key cytokines CD29,N-cadherin and E-cadherin. RESULTS The results showed that the cell-matrix adhesion ability of human hepato?cellular carcinoma cells BEL-7402 were significantly increased(P<0.05)after treatment with PCB118 0.1,1.0 and 10.0 nmol·L-1 for 6 d,whereas the cell-cell adhesion ability was significantly reduced(P<0.05). Exposure to PCB118(0.1,1.0 and 10.0 nmol·L-1)for 6 d induced significant upregulation of the mRNA expression levels of CD29 and N-cadherin along with the downregulation of E-cadherin(P<0.05). Western blotting analysis revealed that PCB118 exposure significantly increased protein expressions of CD29 and N-cadherin but reduced E-cadherin protein level(P<0.01). CONCLUSION PCB118 exposure affects the expression of CD29,N-cadherin and E-cadherin, which may be involved in PCB118-induced alteration of cell adhesion of hepatocellular carcinoma cell line BEL-7402.
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The developing vascular network is grown on the surface of chick embryo chorioallantoic membrane [CAM], so CAM is widely used as an in vivo model to study the angiogenesis. Because the CAM is hindered or wrinkled by the vehicle, the drug effect is difficult to be observed. In the present study, we firstly introduced the pluronic F127 aquogel to deliver drugs for the CAM model. The biocompatibility and advantage of this vehicle was shown by applied ranibizumab-pluronic F127 mix on the CAM. The results were showed that, the growth of blood vessels was not impaired by pluronic F127 gel, and the gel was almost imperceptible on the CAM, at the same time, the degradation of blood capillaries caused by ranibizumab was clearly visible. In conclusion, pluronic F127 was a good vehicle for angiogenesis research
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The trypsin inhibitor is a kind of substance that can inhibit trypsin activity.It shares extensive physiological roles.The trypsin inhibitor not only inhibits the activities of many enzymes,but also has significant anti-cancer effects by suppressing cell invasion and promoting cell apoptosis.Wnt signaling pathway involves in the regulation of cell growth,proliferation and apoptosis.It also plays an important role in tumor development.This review focuses on the impacts of trypsin inhibitors on Wnt signaling pathway and tumor cell apoptosis.