Efficacy of cervical perivascular sympathectomy in improving upper limb motor function in children with cerebral palsy and construction of a predictive model.

BACKGROUND: The effectiveness of cervical perivascular sympathectomy (CPVS) in enhancing upper limb motor function in children with cerebral palsy is unclear, and the factors that influence the effectiveness of the surgery have not been documented. OBJECTIVE: To investigate the effectiveness of CPVS in enhancing upper limb motor function in children with cerebral palsy and develop a predictive chart for potential associated adverse outcomes METHODS: The study included 187 children with cerebral palsy who underwent CPVS at the Cerebral Palsy Center, Second Affiliated Hospital of Xinjiang Medical University, between January 2018 and January 2022. Patients were categorized into two groups based on prognostic outcomes: those with adverse and favorable prognoses. Demographic and laboratory data were collected and analyzed from both groups. To identify independent predictors of poor post-CPVS upper limb motor function outcomes, statistical techniques, including univariate analysis and binary logistic regression, were applied. Subsequently, these predictors were integrated to formulate a comprehensive predictive model. RESULTS: In this cohort of 187 children with cerebral palsy undergoing CPVS, 68 (36.36%) exhibited a favorable prognosis for upper limb motor function and 119 (63.64%) demonstrated an adverse prognosis. Age, motor function, and serum albumin levels were identified as significant prognostic factors via logistic regression analysis. To develop the model, we divided the sample into a training set (70%, n = 131) and a validation set (30%, n = 56). Employing motor function, serum albumin levels, and age as variables, we crafted a predictive model. The model's performance, reflected by the area under the curve was 0.813 (0.732, 0.894) in the training set and 0.770 (0.647, 0.892) in the validation set, demonstrating its robust predictive capability for post-CPVS adverse outcomes. Furthermore, the consistency curve and Hosmer-Lemeshow test (χ2 = 8.808, p = 0.359) illustrated a strong concordance between the model's predictions of poor prognosis and the actual incidence rate. CONCLUSION: CPVS has been shown to be effective in improving upper limb motor function in patients with cerebral palsy. Independent prognostic factors identified encompass motor function, age, and serum albumin levels. The composite predictive model shows potential for clinical applications.

Type 2 diabetes mellitus and characteristics of breast cancer in China.

Studies have showed an association between type 2 diabetes and breast cancer in Western countries. The association should be confirmed in an Asian population which has a lower incidence of breast cancer. Our study aimed to compare the clinicopathologic characteristics of breast cancers in women with and without type 2 diabetes mellitus in China. Each group included 143 cases, similar in parity, body mass index, family history, mode of diagnosis, menarche age and hormone receptors except for progesterone receptor (PR). The diabetic patients were older, with a mean age of 58.3±10 years and the percentage of postmenopausal patients was 52%, which was higher than non-diabetic patients. Significant differences were found in tumor stage, the amounts of lymph node and with metastasis, these persisting after adjustment for age. Furthermore, a positive association with higher TNM status and PR negative rate was noticed in premenopausal but not postmenopausal diabetic patients. Our results indicate that type 2 diabetes mellitus is a negative prognostic factor for breast cancer, especially in premenopausal women.

Positive regulation of migration and invasion by vasodilator-stimulated phosphoprotein via Rac1 pathway in human breast cancer cells.

This study aimed to investigate the role of the cytoskeleton-associated protein vasodilator-stimulated phosphoprotein (VASP) on the migration and invasion of human breast cancer cells and its relationship to Rac1 which is a member of the Rho family and has been found to be implicated in tumorigenesis, invasion and metastasis. We detected the mRNA and protein expression levels of VASP and Rac1 of the non-invasive breast cancer cell line MCF-7 as well as the invasive cell line MDA-MB-231 by RT-PCR and Western blotting. GST pull-down assay was used to examine the activity of Rac1. Accordingly, the cell invasive migration ability was analyzed in a wound-healing assay (2D) and transwell assays (3D migration and invasion). We then used VASP-siRNA to inhibit the expression of VASP in breast cancer cells in order to study the relationship between the VASP expression level and the invasive migration ability of breast cancer cells. Rac1-siRNA was used to decrease the expression of Rac1, and observe its effect on the VASP expression level together with the migration and invasion ability of MCF-7 and MDA-MB-231 cells. Our results revealed that the invasive breast cancer cell line MDA-MB-231 showed a higher Rac1 activity and VASP expression level compared with the non-invasive MCF-7. Inhibition of Rac1 or VASP by siRNA, respectively, decreased the migration and invasion ability of breast cancer cells and the transfection of Rac1 siRNA-mediated reduction of VASP expression at mRNA and protein levels. Collectively, our data showed that the higher expression level of VASP contributed to a higher invasive migration capacity of human breast cancer cells which was controlled by the Rac1 pathway.

[Abnormal expression of fragile histidine triad (FHIT) and Mut S homolog 2 (MSH2) proteins in human sporadic colorectal carcinoma and their clinical significance].

BACKGROUND & OBJECTIVE: Frequent loss of fragile histidine triad (FHIT) expression in human gastrointestinal tract carcinomas has been reported; however, there were divergent opinions regarding FHIT expression in colorectal carcinoma. Recent studies have suggested that FHIT inactivation can be a consequence of defects in mismatch repair proteins, particularly mut S homolog 2 (MSH2). This study was designed to investigate the expression and clinical significance of FHIT and MSH2 proteins in human sporadic colorectal carcinoma (SCC). METHODS: Immunohistochemistry SP method was used to determine the expression of FHIT and MSH2 in surgically resected specimens of 84 SCC and its corresponding paratumor normal colorectal tissues, and 23 cases of colonic adenomas. RESULTS: The positive expression rates of FHIT protein were 48.81%, 73.91%, and 100% in SCC, colonic adenomas, and adjacent normal colorectal tissues, respectively. The positive expression rates of FHIT protein showed increasing trend from SCC, colonic adenomas, to paratumor normal colorectal tissues; and the difference was statistically significant (P< 0.05). The expression levels of FHIT were not associated with age, gender, tumor site, and histological type (P >0.05), but were correlated with tumor invasive depth, differentiation degree, Dukes,stage, and lymph node metastasis (P< 0.05). The tumor tissues of deeper invade depth, lower differentiation degree, later Ducks,stage and with lymph node metastasis showed more reduction of FHIT protein expression. The expression level of MSH2 was only related to Dukes, stage (P< 0.05). FHIT expression was closely associated with MSH2 expression in SCC (r=0.3728,P< 0.01). CONCLUSION: (1) Loss or reduction of FHIT protein expression plays an important role in the development and progression of SCC. The expression levels of FHIT protein are related to the malignant degree of SCC and may be a valuable biological indicator for predicting the potent invasion and metastasis of SCC. (2) FHIT protein expression is in a positive correlation fashion with MSH2 protein expression in SCC.

Cyclooxygenase-2 expression and angiogenesis in colorectal cancer.

AIM: Cyclooxygenase-2 is involved in a variety of important cellular functions, including cell growth and differentiation, cancer cell motility and invasion, angiogenesis and immune function. However, the role of cyclooxygenase-2 as an angiogenic factor in colorectal cancer tissue is still unclear. We investigated the relationship between cyclooxygenase-2 and angiogenesis by analyzing the expression of cyclooxygenase-2 in colorectal cancer tissue, as well as its association with vascular endothelial growth factor (VEGF) and microvascular density (MVD). METHODS: The expression of cyclooxygenase-2, VEGF, as well as MVD was detected in 128 cases of colorectal cancer by immunohistochemical staining. The relationship between the cyclooxygenase-2 and VEGF expression and MVD was evaluated. Our objective was to determine the effect of cyclooxygenase-2 on the angiogenesis of colorectal cancer tissue. RESULTS: Among 128 cases of colorectal cancer, 87 were positive for cyclooxygenase-2 (67.9 %), and 49 for VEGF (38.3 %), respectively. The microvessel counts ranged from 23 to 142, with a mean of 51.7 (standard deviation, 19.8). The expression of cyclooxygenase-2 was correlated significantly with the depth of invasion, stage of disease, metastasis (lymph node and liver), VEGF expression and MVD. Patients in T3-T4, stage III-IV and with metastasis had much higher expression of cyclooxygenase-2 than patients in T1-T2, stage I-II and without metastasis (P<0.05). The positive expression rate of VEGF (81.6 %) in the cyclooxygenase-2 positive group was higher than that in the cyclooxygenase-2 negative group (18.4 %, P<0.05). Also, the microvessel count (56+/-16) in cyclooxygenase-2 positive group was significantly higher than that in cyclooxygenase-2 negative group (43+/-12, P<0.05). The microvessel count in tumors with positive cyclooxygenase-2 and VEGF was the highest (60+/-18, 41-142, P<0.05), whereas that in tumors with negative cyclooxygenase-2 and VEGF was the lowest (39+/-16, 23-68, P<0.05). CONCLUSION: Cyclooxygenase-2 may be associated with tumor progression by madulating the angiogenesis in colorectal cancer tissue and used as a possible biomarker.

Transforming growth factor-beta1 in invasion and metastasis in colorectal cancer.

AIM: To investigate the role of TGFbeta1 in invasion and metastasis in colorectal cancer by analysing TGFbeta1 correlated with depth of tumor invasion, stage and metastasis. METHODS: Serum TGFbeta1 levels were determined in 50 patients with colorectal cancer and 30 healthy volunteers using a TGFbeta1 enzyme-linked immunosorbent assay. TGFbeta1 expression in primary and lymph node metastatic lesions were detected in 98 cases of colorectal cancer by immunohistochemical staining and in situ hybridization. RESULTS: Serum levels of TGFbeta1 in patients with colorectal cancer(40+/-18 microg.L(-1)) were significantly higher than those in the healthy control group(19+/-8 microg.L(-1)), P<0.05. Elevated levels of serum TGFbeta1 were found in 60 % of patients with colorectal cancer when the mean +2 s was used as the upper limit of the normal range (35.1 microg.L(-1)). Increases in serum TGFbeta1 levels were significantly associated with Duke's stage (P<0.05), but there was no significant difference between Duke's stage B patients and Duke's stage C patients. In the cytoplasm of cancer cells, TGFbeta1 was immunostained in 37.8 % (37/98) of colorectal cancer, and this expression was confirmed by in situ hybridization. Among 35 cases of colorectal cancer with lymph node metastatic lesions, TGFbeta1 positive staining was found in 18 (51.4 %) cases of primary tumor, and 25 (71.4 %) cases with lymph node metastatic lesions, respectively. Of 17 cases w ith no staining in the primary lesion, 7 (41.2%) casesshowed TGFbeta1 staining in the metastatic lesion. Serum TGFbeta1 levels and TGFbeta1 expression in colorectal cancer tissues were correlated significantly with depth of tumor invasion, stage and metastasis. Patients in stage C-D,T3-T4 and with metastasis had significantly higher TGFbeta1 levels than patients in stage A-B,T1-T2 and without metastasis (P<0.05). CONCLUSION: These results suggest that transforming growth factor-beta1 is closely related to the invasion and metastasis of colorectal cancer. It increased the invasive and metastatic potential of tumor by altering a tumor microenvironment. TGFbeta1 may be used as a possible biomarker.

TGF beta1 expression and angiogenesis in colorectal cancer tissue.

AIM: Transforming growth factor TGF beta1 is involved in a variety of important cellular functions,including cell growth and differentiation, angiogenesis, immune function and extracellular matrix formation. However, the role of TGF beta(1) as an angiogenic factor in colorectal cancer is still unclear. We investigate the relationship between transforming growth factor beta(1) and angiogenesis by analyzing the expression of transforming growth factor TGF beta(1) in colorectal cancer, as well as its association with VEGF and MVD. METHODS: The expression of TGF beta(1),VEGF, as well as MVD were detected in 98 colorectal cancer by immunohistochemical staining. The relationship between the TGF beta(1) expression and VEGF expression,MVD was evaluated. To evaluate the effect of TGF beta(1) on the angiogenesis of colorectal cancers. RESULTS: Among 98 cases of colorectal cancer,37 were positive for TGF beta(1) 37.8% 36 for VEGF 36.7% respectively. The microvessel counts ranged from 19 to 139.8, with a mean of 48.7(standard deviation,21.8). The expression of TGF beta(1) was correlated significantly with the depth of invasion, stage of disease, lymph node metastasis, VEGF expression and MVD. Patients in T3-T4, stage III-IV and with lymph node metastasis had much higher expression of TGF beta(1) than patients in T1-T2, stage I-II and without lymph node metastasis (P<0.05). The positive expression rate of VEGF(58.3%) in the TGF-beta(1) positive group is higher than that in the TGF-beta(1) negative group(41.7%, P<0.05). Also, the microvessel count (54+/-18) in TGF-beta(1) positive group is significantly higher than that in TGF-beta(1) negative group(46+/-15, P<0.05). The microvessel count in tumors with both TGF-beta(1) and VEGF positive were the highest (58+/-20 36-140, P<0.05). Whereas that in tumors with both TGF-beta(1) and VEGF negative were the lowest (38+/-16, 19-60, P<0.05). CONCLUSION: TGF beta(1) might be associated with tumor progression by modulating the angiogenesis in colorectal cancer and TGF beta(1) may be used as a possible biomarker.