Aim To investigate the efficacy of a virtual reality rehabilitation system of wearable multi‐inertial sensors to improve upper‐limb function in children with brain injury. Method Eighty children (39 males, 41 females) with brain injury including cerebral palsy aged 3 to 16 years (mean age 5y 8mo, SD 2y 10mo) were assessed as part of a multicentre, single‐blind, randomized controlled trial. The intervention group received a 30‐minute virtual reality intervention and a 30‐minute session of conventional occupational therapy while the control group received 60 minutes of conventional occupational therapy per session, with 20 sessions over 4 weeks. The virtual reality rehabilitation system consisted of games promoting wrist and forearm articular movements using wearable inertial sensors. The Melbourne Assessment of Unilateral Upper Limb Function‐2 (MA‐2), Upper Limb Physician’s Rating Scale, Pediatric Evaluation of Disability Inventory Computer Adaptive Test, and computerized three‐dimensional motion analysis were performed. Results Both groups (virtual reality, n=40; control, n=38) significantly improved after treatment compared to baseline; however, the virtual reality group showed more significant improvements in upper‐limb dexterity functions (MA‐2, virtual reality group: Δ=10.09±10.50; control: Δ=3.65±6.92), performance of activities of daily living, and forearm supination by kinematic analysis (p<0.05). In the virtual reality group, children with more severe motor impairment showed significant improvements compared to those with less severe impairment. Interpretation The virtual reality rehabilitation system used in this study, which consists of wearable inertial sensors and offers intensive, interactive, and repetitive motor training, is effective in children with brain injury. What this paper adds Both virtual reality rehabilitation and conventional occupational therapy were effective for upper‐limb training. Virtual reality training was superior in improving dexterity, performance of activities of daily living, and active forearm supination motion. The effect of virtual reality training was significant in children with more severe motor impairments.

This study aims to evaluate the effect of the regulatory relationship between microRNA-383 (miR-383) and PARP2 in the cell migration and invasion in human with cervical cancer (CC) via the PI3K-AKT-MTOR signaling pathway. Cancerous tissues and corresponding paracancerous tissues were collected from 115 patients with CC. The positive expression rate of PARP2 was detected by immunohistochemistry. HeLa cells with highest miR-383 expression were selected and assigned into the blank, negative control (NC), miR-383 mimic, miR-383 inhibitor, si-PARP2, and miR-383 inhibitor + si-PARP2 groups. qRT-PCR and Western blot were performed to evaluate the expression of miR-383, PI3K, AKT, mTOR, PARP2, and p70S6K. MTT assay were utilized to measure cell viability. Transwell assay were applied to evaluate cell invasion and metastasis. Dual luciferase reporter assay identified that PARP2 is a target gene of miR-383. Cancerous tissues manifested higher expression of PI3K, AKT, mTOR, PARP2, and p70S6K but lower miR-383 expression than paracancerous tissues. Compared with the blank and NC groups, the miR-383 mimic and si-PARP2 groups had decreased expression of PI3K, AKT, mTOR, PARP2, and p70S6K mRNA and protein. In the miR-383 mimic and si-PARP2 groups, the cell viability, migration, and invasion were descended, in comparison to the blank and NC groups. All above parameters showed an opposite trend in the miR-383 inhibitor group when compared with the blank and NC groups. This study demonstrates that miR-383 could down-regulate PARP2 to protect against CC by inhibiting PI3K-AKT-MTOR signaling pathway.

This study assessed the hypothesis that the protein levels of high mobility group box 1 (HMGB1) and hepsin can be used as markers for diagnosis and prognosis in cervical carcinoma. Seventy patients with cervical cancer who were hospitalized in Xuzhou Central Hospital from May 2008 to June 2010 and underwent surgical treatment were selected for the observation group. At the same time, 20 patients with cervical benign lesions who underwent tumor stripping or accessory resection were selected for the control group. Immunohistochemical (SP) detection methods were used to detect hepsin and HMGB1 protein levels in tissues. The positive rates of HMGB1 cells in normal, paracancerous and cancerous cervical tissues were 5.0% (1/20), 22.9% (16/70) and 95.7% (67/70) (F=24.581, P=0.001) respectively. The positive rates of hepsin in normal, paracancerous and cancerous cervical tissues were respectively 10% (2/20), 61% (43/70) and 90% (63/70) (F=11.538, P=0.001). The HMGB1 expression level was related to the degree of tumor differentiation, lymph node metastasis and TNM stage (P<0.05). While the level of hepsin expression was related to the degree of tumor differentiation, invasion depth, lymph node metastasis and TNM stage (P<0.05). Furthermore, a positive correlation between the levels of hepsin and HMGB1 was found (r=15.27, P<0.05). The overall 5-year survival rates of patients with high expression of HMGB1 (+++) and low expression of HMGB1 (+ to ++) were respectively 51.2 and 29.2% (HR=11.637, 95% CI=4.351–38.213; P=0.002). The overall 5-year survival rates of patients with high hepsin expression (+++) and low hepsin expression (+ to ++) were respectively 41.3 and 35.3% (HR=10.143, 95% CI=4.285–33.275; P=0.006). Based on our results, the higher the levels of expression of hepsin and HMGB1 in tissues the higher the degree of invasiveness of the cervical cancers, and the worse the prognoses for the patient.

PurposeCervical cancer (CC) is one of the most common malignant tumors among women. The present study aimed at integrating two expression profile datasets to identify critical genes and potential drugs in CC.Materials and methodsExpression profiles, GSE7803 and GSE9750, were integrated using bioinformatics methods, including differentially expressed genes analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and protein–protein interaction (PPI) network construction. Subsequently, survival analysis was performed among the key genes using Gene Expression Profiling Interactive Analysis websites. Connectivity Map (CMap) was used to query potential drugs for CC.ResultsA total of 145 upregulated genes and 135 downregulated genes in CC were identified. The functional changes of these differentially expressed genes related to CC were mainly associated with cell cycle, DNA replication, p53 signaling pathway, and oocyte meiosis. A PPI network was identified by STRING with 220 nodes and 2,111 edges. Thirteen key genes were identified as the intersecting genes of the enrichment pathways and the top 20 nodes in PPI network. Survival analysis revealed that high mRNA expression of MCM2, PCNA, and RFC4 was significantly associated with longer overall survival, and the survival was significantly better in the low-expression RRM2 group. Moreover, CMap predicted nine small molecules as possible adjuvant drugs to treat CC.ConclusionOur study found key dysregulated genes involved in CC and potential drugs to combat it, which might provide insights into CC pathogenesis and might shed light on potential CC treatments.

Breast cancer stem cells (bCSCs) are considered an obstacle in breast cancer therapy because they exhibit long-term proliferative potential, phenotypic plasticity and high resistance to the current therapeutics. CXC chemokine receptor type 7 (CXCR7), which provides a growth advantage to breast cancer cells, has recently been demonstrated to play an important role in the maintenance of stem cell-like properties in the CSCs of glioblastoma and lung cancer, yet its role in bCSCs remains elusive. In this study, CD44/CD24 bCSC-enriched cells (bCSCs for short) were isolated from MCF-7 cells, and CXCR7 was stably knocked down in bCSCs via lentivirus-mediated transduction with CXCR7 short hairpin RNA (shRNA). Knockdown of CXCR7 in bCSCs decreased the proportion of CD44/CD24 cells, and markedly reduced the clonogenicity of the cells. Moreover, silencing of CXCR7 downregulated the expression of stem cell markers, such as aldehyde dehydrogenase 1 (ALDH1), Oct4, and Nanog. In addition, CXCR7 silencing in bCSCs suppressed cell proliferation and G1/S transition in vitro, and delayed tumor growth in vivo in a xenograft mouse model. In situ immunohistochemical analysis revealed a reduction in Ki-67 expression and enhanced apoptosis in the xenograft tumors as a result of CXCR7 silencing. Furthermore, combined treatment with CXCR7 silencing and epirubicin displayed an outstanding anti-tumor effect compared with either single treatment. Our study demonstrates that CXCR7 plays a critical role in the maintenance of stem cell-like properties and promotion of growth in bCSCs, and suggests that CXCR7 may be a candidate target for bCSCs in breast cancer therapy.