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OBJECTIVE: MiRNAs have been verified to play a role in the development and progression of prostate cancer (PCa). However, the role of miR-492 in PCa has not been mentioned. We aim to detect the expression of miR-492 in PCa and explore its underlying mechanism. PATIENTS AND METHODS: T he r elative e xpression of miR-492 in PCa tissue samples to normal prostate tissues was detected using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The level of miR-492 in PCa-derived cell lines compared with the normal prostate cell line was also measured. Cell counting kit-8 (CCK-8) and colony formation assays were employed to investigate the cell proliferation ability. Transwell assay and wound-healing assays were utilized to explore the cell invasion and migration abilities. Luciferase assay and Western blot were utilized to explore the underlying mechanism of miR-492 in PCa cells. RESULTS: MiR-492 expressed significantly higher in PCa tissues than that in the normal tissues. Its expression level was also over-expressed in PCa cells compared with that in the normal cells. The up-regulation of miR-492 promoted the growth, invasion, and migration of the cells, while down-regulation had the opposite effects. SOCS2 was identified as a potential target for miR-492 in PCa. Silencing of SOCS2 could neutralize the inhibitory function of miR-492 inhibitor in PCa cells. CONCLUSIONS: This study demonstrated that miR-492 was over-expressed in PCa and exerted tumor-promoting function in PCa cells via repressing SOCS2 expression. This might provide a new sight for future accurate therapy for PCa. [ABSTRACT FROM AUTHOR]

OBJECTIVE: JAK-STAT3 signaling pathway widely participates in cell proliferation and apoptosis. Suppressor of cytokine signaling 3 (SOCS3) is a negative regulator of JAK-STAT3. SOCS3 downregulation is associated with drug resistance in breast cancer and leukemia. However, its role in bladder cancer drug resistance is still unclear. This study established ADM resistant bladder cancer cell model to investigate the role of SOCS3-JAK/STAT3 signaling pathway ADM resistance. MATERIALS AND METHODS: ADM drug resistant cell line T24/ADM was established. SOCS3, p-JAK2, p-JAK3, and Bcl-2 expressions in T24/ADM, T24, and HBEC cells were compared. Cell proliferation and apoptosis were evaluated by flow cytometry. T24/ADM cells were divided into five groups, including control, pSicoR-blank, pSicoR-SOCS3, FLLL32, and pSicoR-SOCS3 + FLLL32 groups. Cell proliferation was determined by EdU staining. RESULTS: SOCS3 was reduced, while p-JAK2, p-STAT3, and Bcl-2 expressions upregulated in T24 cells compared with HBEC cells. T24/ADM cells exhibited lower SOCS3, higher p-JAK2, p-STAT3, and Bcl-2 levels than T24 cells. Cell apoptosis was higher, whereas cell proliferation was weaker in T24 cells compared with T24/ADM cells. SOCS3 overexpression and/or FLLL32 treatment significantly downregulated p-JAK2, p-STAT3, and Bcl-2 expressions, attenuated cell proliferation, and elevated sensitivity to ADM induced cell apoptosis. CONCLUSIONS: SOCS3 reduction was associated with bladder cancer sensitivity to ADM. SOCS3 overexpression decreased JAK-STAT3 signaling pathway activity, declined Bcl-2 expression, inhibited cell proliferation, elevated cell apoptosis, and enhanced ADM sensitivity in T24 cells. [ABSTRACT FROM AUTHOR]

The influence of substitutional alloying elements (Al, Nb and W) on the mechanical properties of MoSi2 with both C11b and C40 structures was explored by first principles calculations. Using the shear modulus/bulk modulus ratio (G/B), Poisson's ratio and Peierls stress, the change in the mechanical properties of the C40 and C11b structured MoSi2 due to the addition of the solute atom has been investigated. The results showed that the ductility of C11b MoSi2 was increased by alloying with the elements (Al and Nb) that form a C40 structured disilicide but decreased by alloying with the elements (W) that form a C11b structured disilicide. In contrast, the effect of alloying elements on the ductility of C40 MoSi2 showed a reverse trend to that of C11b MoSi2. [ABSTRACT FROM AUTHOR]

The optimal dose and schedule of G-CSF for mobilization of peripheral blood stem cells (PBSC) is not well defined. G-CSF mobilization was performed in a group of healthy donors and paediatric patients for autologous back-up before receiving allogeneic stem cell transplant. Seventeen consecutive subjects who received G-CSF at 5 μg/kg/dose twice daily (group A) were compared with a historical control group of 25 subjects who received a single daily dose of 10 μg/kg/day G-CSF (group B). Double blood volume apheresis for PBSC collection was started on day 5. G-CSF was continued and apheresis repeated until the targeted CD34+ cell dose was achieved. Both groups were comparable for sex, age, body weight and reason for PBSC collection. Over two-thirds of the subjects in both groups were less than 16 years of age. The G-CSF priming and apheresis were well tolerated. When the first day apheresis products were analyzed, group A resulted in significantly higher yield of total nucleated cells (5.91 vs 3.92 × 108/kg, P = 0.013), mononuclear cells (5.73 vs 3.92 × 108/kg, P = 0.017), CD34+ cells (2.80 vs 1.69 × 106/kg, P = 0.049) and colony-forming units (107 vs 54 × 104/kg, P = 0.010) as compared with group B. We conclude that the two dose schedule is more efficient in mobilizing PBSC in normal donors and children with non-malignant diseases. This approach may reduce the number of aphereses required and thus reduce the transplant cost. Bone Marrow Transplantation (2000) 25, 931–935. [ABSTRACT FROM AUTHOR]

Thirty thalassaemia patients received iron reduction starting at around 3 months post transplant. Sixteen received desferrioxamine and nine had phlebotomy, five patients had desferrioxamine followed by phlebotomy. The desferrioxamine group had higher serum ferritin levels at the start of iron reduction as compared to the phlebotomy group (5292 vs 2453 μg/l, P EQ 0.001). After 444 and 407 days of iron reduction, serum ferritins at cessation of iron reduction in both groups was similar (665 vs 588 μg/l). The rate of decline of serum ferritin in both groups was similar. There was no graft rejection during the programme. Early institution of iron reduction in ex-thalassaemia is safe. Bone Marrow Transplantation (2000) 25, 653–656. [ABSTRACT FROM AUTHOR]

The article "SOCS3 overexpression enhances ADM resistance in bladder cancer T24 cells, by M.-Z. Li, D.-H. Lai, H.-B. Zhao, Z. Chen, Q.-X. Huang, J. Situ, published in Eur Rev Med Pharmacol Sci 2017; 21 (13): 3005-3011–PMID: 28742207".

A 7-year-old boy with Ph+ ALL received an allogeneic BMT in second remission. Conditioning included cyclophosphamide 60 mg/kg for 2 days, TBI 2 Gy twice daily for 3 days (12 Gy) and a single testicular boost of 4 Gy. He remained in hematological remission after BMT but developed isolated testicular relapse at 17 months. He underwent orchiectomy of the affected testis, 24 Gy testicular radiotherapy and systemic chemotherapy. He remains in remission 24 months after the testicular relapse. This is the first report of isolated testicular relapse which received a testicular irradiation boost included in the conditioning. [ABSTRACT FROM AUTHOR]

We determined the species specificity and function of structural domains of the interferon-gamma receptor (IFN-gamma R) by construction of human/murine chimeric IFN-gamma R cDNA clones and their expression in various cells. We demonstrate that we can reconstitute a biologically active IFN-gamma R in eukaryotic cells with chimeric receptors as long as the extracellular domain and an accessory factor are from the same species. These results indicate that the extracellular domain of the receptor interacts directly or indirectly with the species-specific accessory factor.