Objective To investigate changes of surface electromyogr8phic(sEM G)signal of pelvic floor muscles in complete spinal cord injury(cSCI)patients with neurogenic bowel dysfunction.Methods Fifteen hospitalized patients with cSCI(observation group)and fifteen normal subjects(control group)were involved in this study.The root mean square(RMS)of sEMG signals were collected at pelvic floor muscles with rectal surface electrode when subjects'pelvic floor muscles were rest(10 s),fleetly contract(2 s×3),continually contract(10 s).Both groups'data of different contracting states of pelvic floor muscles were analyzed and compared.Results The max RMS and average RMS(16.61±2.83,13.52±2.22)at pelvic floor muscles'rest in observation group were higher than that in control group(8.41±5.55,3.45±1.53).There was statistical difference between two groups(P<0.01).In the subjects of observation group max RMS and average RMS(20.24±13.99,13.36±2.39)at continual contraction and average RMS(13.40±2.31)at fleet contraction were nearly the same as RMS value at pelvic floor muscles'rest.There was no statistical difference between these two states(P>0.05).Conclusion The sEMG could be a quantitative index in assessing function of pelvic floor muscles and the neurogenic bowel dysfunction after cSCI.It can supply some clinical value in framing the training of pelvic floor muscles and improving the bowel dysfunction.

Objective To explore the correlation between ITGA6 gene (rs12621278, G), MSMB gene (rs10993994, T), chromosome 8q24 (rs10086908, T) and prostate cancer (PCa) in Beijing residents, and to explore the correlation between genotype and phenotype in PCa patients. Methods PCa patient phenotypes were collected including clinical, genetic, dietary habits, hobbies and blood samples. ITGA6 gene (rs12621278, G), chromosome 8q24 (rs10086908, T) and MSMB gene (rs10993994, T) compared the allele distribution between 112 PCa and 91 healthy control age matched patients. The genotype and phenotype analysis was conducted in the 2 groups. Results Between the case and control groups, only rs10993994, T of MSMB gene (case 56.4%,control 46.2%) was significantly different (P=0.001; OR=1.97, 95%CI:1.28-3.04). The rs10086908, T of 8q24 (case 83.5%, control 79.2%) and rs12621278, G of ITGA6 gene (case 27.2%, control 27.0%) were not significantly associated with PCa in the study sample (P>0.05). Quantitative trait analysis showed that the disease duration of ITGA6 risk genotypes (G/G,1.40±0.55 years) in PCa patients was significantly shorter (P=0.003) than the other genotype carriers (A/G, 4.38±3.10 years; A/A, 2.37±1.84 years). Conclusion The genetic variation in MSMB is possibly associated with PCa susceptibility, suggesting that MSMB genes might be associated with PCa in a Chinese population.

BACKGROUND: Bladder cancer, characterized by a high potential of tumor recurrence, has high lifelong monitoring and treatment costs. To date, tumor cells with intrinsic softness have been identified to function as cancer stem cells in several cancer types. Nonetheless, the existence of soft tumor cells in bladder tumors remains elusive. Thus, our study aimed to develop a micro-barrier microfluidic chip to efficiently isolate deformable tumor cells from distinct types of bladder cancer cells. METHODS: The stiffness of bladder cancer cells was determined by atomic force microscopy (AFM). The modified microfluidic chip was utilized to separate soft cells, and the 3D Matrigel culture system was to maintain the softness of tumor cells. Expression patterns of integrin β8 (ITGB8), protein kinase B (AKT), and mammalian target of rapamycin (mTOR) were determined by Western blotting. Double immunostaining was conducted to examine the interaction between F-actin and tripartite motif containing 59 (TRIM59). The stem-cell-like characteristics of soft cells were explored by colony formation assay and in vivo studies upon xenografted tumor models. RESULTS: Using our newly designed microfluidic approach, we identified a small fraction of soft tumor cells in bladder cancer cells. More importantly, the existence of soft tumor cells was confirmed in clinical human bladder cancer specimens, in which the number of soft tumor cells was associated with tumor relapse. Furthermore, we demonstrated that the biomechanical stimuli arising from 3D Matrigel activated the F-actin/ITGB8/TRIM59/AKT/mTOR/glycolysis pathways to enhance the softness and tumorigenic capacity of tumor cells. Simultaneously, we detected a remarkable up-regulation in ITGB8, TRIM59, and phospho-AKT in clinical bladder recurrent tumors compared with their non-recurrent counterparts. CONCLUSIONS The ITGB8/TRIM59/AKT/mTOR/glycolysis axis plays a crucial role in modulating tumor softness and stemness. Meanwhile, the soft tumor cells become more sensitive to chemotherapy after stiffening, that offers new insights for hampering tumor progression and recurrence.
Animals ; Mice ; Humans ; Proto-Oncogene Proteins c-akt/metabolism* ; Actins/metabolism* ; Neoplasm Recurrence, Local ; TOR Serine-Threonine Kinases/metabolism* ; Urinary Bladder Neoplasms ; Glycolysis ; Cell Line, Tumor ; Cell Proliferation ; Mammals/metabolism* ; Tripartite Motif Proteins/metabolism* ; Intracellular Signaling Peptides and Proteins/metabolism* ; Integrin beta Chains