Graphene-wrapped pine needle-like cobalt nanocrystals constructed by cobalt nanorods for efficient microwave absorption performance.

Magnetic metal nanocrystals tend to be advanced microwave absorption substances as they possess simultaneous dielectric and magnetic losses. In this study, the metallic cobalt (Co) nanocrystals with a pine needle-like nanostructure constructed by one-dimensional Co nanorods have been successfully prepared through the polyol approach. By regulating the amount of reduced graphene oxide (rGO), rGO/Co nanocomposites with different mass ratios were acquired. Experimental results demonstrate that the rGO/Co nanocomposites display excellent microwave attenuation capacity. The minimum reflection loss value can reach -57.8 dB at 12.43 GHz with a filler loading of 20 wt% at 1.8 mm. Moreover, the effective absorption bandwidth covers the frequency range of 4.2-15.5 GHz with an integrated thickness of 1.5-4.0 mm. The main absorption mechanisms include dielectric loss caused by dipole and interfacial polarization and magnetic loss arising from ferromagnetic resonance and eddy current loss. In addition, the special nanostructure effect is also beneficial to improve the EM wave absorption performance.

Microwave absorption enhancement by adjusting reactant ratios and filler contents based on 1D K-MnO2@PDA and poly(vinylidene fluoride) matrix.

One-dimensional K-MnO2 nanorods were prepared by a wet chemical process. Dopamine hydrochloride (PDA) layers with various thicknesses were coated and finally, the composites were filled in a poly(vinylidene fluoride) (PVDF) matrix using the hot-molding procedure. The complex permittivity and permeability of the K-MnO2@PDA/PVDF composites could be adjusted by reactant amount ratios and filler contents. The minimum reflection loss could reach -49.4 dB and an effective absorption bandwidth (<-10 dB) covering 11.12 GHz was achieved with 20% filler content when the reactant amount ratio between K-MnO2 and PDA was 4 : 0.375, which was derived from effective internal polarization processes. It is expected that these novel composites can be used as high-performance microwave absorbers.

Potential role of HGF-PARP-1 signaling in invasion of ovarian cancer cells.

We investigated the effects and signaling pathways involved in both HGF-mediated regulation of PARP-1 expression and the invasion ability of ovarian cancer cells. Using a transwell assay, the invasiveness of SKOV-3 cells was tested by incubating them with increasing concentrations of HGF. The relative expression levels of PARP-1 after HGF treatment were analyzed by Real-Time PCR and western blotting. SKOV3 cells were transfected with either negative control siRNA or PARP-1 siRNA, and were divided into different groups as follows: control group; HGF group; PARP-siRNA group; HGF+PARP-siRNA group; NC-siRNA group; and HGF+NC-siRNA group. Western blotting was employed to measure the expression of PARP-1 in the different groups. Transwell tests were used to examine invasiveness. ELISA was applied to measure MMP-2 expression. HGF promotes cell invasion in a concentration- and time-dependent manner in SKOV-3 cells. The expression levels of PARP-1 increased after administration of 40 ng/ml HGF for 24 h. The expression of PARP-1 in the PARP1-siRNA group was lower compared with that in the NC-siRNA group (P < 0.05); PARP1-siRNA transfection significantly reduced the impact of HGF on invasiveness and MMP-2 expression in SKOV-3 cells. HGF promotes the invasiveness and metastasis of ovarian cancer cells. This effect could be related to the induction of increased expression levels of MMP-2 mediated by PARP-1.

Fludarabine and cytarabine versus high-dose cytarabine in consolidation treatment of t(8; 21) acute myeloid leukemia: A prospective, randomized study.

Acute myeloid leukemia (AML) patients with t(8;21) aberration often have favorable outcomes, however, relapse still occurs in 30-40% patients, with only 50-60% of patients with t(8;21) AML cured with regimens containing high-dose cytarabine (HD-Ara-C). To evaluate the effects of fludarabine and cytarabine (FA) consolidation therapy for t(8;21) AML patients, a prospective randomized study was performed. A total of 45 patients with t(8;21) AML after achieving complete remission (CR) were randomly assigned to receive four course consolidation with FA (n = 23) or HD-Ara-C (n = 22). Our study showed that at 36-months, relapse-free survival (RFS) was 81.73% in the FA arm and 50.73% in the HD-Ara-C arm (P = 0.04), overall survival (OS) was 91.1% and 48.4% (P = 0.01) in the FA arm and in the HD-Ara-C arm respectively; whereas cumulative incidence of relapse (CIR) was 18.27% and 47.39%, in the FA arm and in the HD-Ara-C arm respectively (P = 0.05). In our study, treatment with FA, MRD2 status (reduction ≥ 3-log) and absence of c-kit mutations were identified as independent prognostic factors for lower risk of relapse, improved RFS and OS. We also found RFS for patients without c-kit mutations was 100% in FA arm, and 57.8% in HD-Ara-C arm at 36 months (P = 0.005); OS of both groups at 36 months was 100% and 51.4%, respectively (P = 0.004), suggesting a benefit of consolidation therapy with FA for t(8;21) AML patients, especially, those without c-kit mutations (Clinicaltrials.org ID NCT# 02024308). Am. J. Hematol. 92:12-17, 2017. © 2016 Wiley Periodicals, Inc.

CD19(+) CD20(-) CD27(hi) IL-s10-producing B cells are overrepresented in R-CHOP-treated DLBCL patients in complete remission.

Treatment of diffuse large B cell lymphoma (DLBCL) with rituximab, an anti-CD20 monoclonal antibody, has resulted in significantly improved patient responses with longer event-free intervals and higher overall survival rates. However, since rituximab depletes all CD20-expressing cells, including noncancerous B cells, the effects of rituximab on the normal immunity of DLBCL patients under remission need to be examined. Here, we observed that DLBCL patients under remission contained significantly lower frequencies of total B cells, with a significantly overrepresented interleukin (IL)-10-producing B cell (B10) population in the peripheral blood. Further examination confirmed that a large fraction of B10 cells was CD20(-) CD27(hi) plasmablasts, possibly explaining the persistence of B10 cells after R-CHOP treatment. We also observed that the percentage of B10 cells in DLBCL patients in remission gradually reduced during the first year of achieving complete remission, primarily due to the replenishment of non-B10 B cells. Despite this, the percentage of B10 cells in DLBCL patients after 1 year of achieving complete remission was still higher than that in controls. CD4(+) and CD8(+) T cells cocultured with B10-enriched B cells secreted significantly lower levels of proinflammatory cytokines IFN-g and TNF-a, compared to those incubated with B10-depleted B cells. Together, our data observed a long-lasting overrepresentation of B10 cells in DLBCL patients under remission. Whether this change could impact on the overall anti-tumor immunity during remission requires further studies.

PARP-1 may be involved in angiogenesis in epithelial ovarian cancer.

Poly (ADP-ribose) polymerase 1 (PARP-1) is involved in DNA repair and has been implicated in chemoresistance. The present study investigated whether PARP-1 promotes angiogenesis in ovarian cancer. PARP-1 and vascular endothelial growth factor A (VEGF-A) expression and CD34+ microvascular density (MVD) were assessed using immunohistochemistry in 60 human epithelial ovarian cancer specimens. PARP-1 was stably knocked-down in SKOV3 cells using a specific small interfering RNA (siRNA); angiogenic capacity was assessed using the human umbilical vein endothelial cell (HUVEC) tubule formation assay; and PARP-1 and VEGF-A expression were examined by reverse transcription-quantitative polymerase chain reaction, western blotting and ELISA. PARP-1 was found to be expressed in 73.3% (44/60) of the human epithelial ovarian cancer specimens and was significantly associated with VEGF-A, MVD, tumor size, histological grade and lymphatic metastasis (P<0.05). Compared with cells transfected with a negative control siRNA, knockdown of PARP-1 significantly suppressed the ability of SKOV3 cell-conditioned media to promote HUVEC tubule formation on Matrigel in vitro. Knockdown of PARP-1 in SKOV3 cells also significantly reduced VEGF-A mRNA and protein expression and secretion. In summary, PARP-1 is overexpressed and may enhance angiogenesis in epithelial ovarian cancer by upregulating VEGF-A.

MiR-302a inhibits the tumorigenicity of ovarian cancer cells by suppression of SDC1.

MicroRNA plays an important role in tumor proliferation and cell cycle. In this study, we suggested the level of miR-302a was increasing in the human ovarian cancer cells compared to the normal cells. We aimed to explore the role of miR-302a downregulation in human ovarian cancer cells. Functional studies demonstrate over expression of miR-302a could significant suppress ovarian cancer cells proliferation and promote the cell cycle progress. In vitro reporter assay suggested SDC1 is a direct target gene of miR-302a. Furthermore, the expressions of miR-302a in ovarian cancer cells were inversely corrected with that of SDC1. Upregulation of SDC1 could rescue the effect of over expressed miR-302a in the ovarian cancer cells. These findings provide evidence that miR-302a plays a key role in inhibition of the ovarian cancer cells proliferation, and enhancing the cells' apoptosis through targeting SDC1, and strongly suggest that exogenous miR-302a may have therapeutic value in treating ovarian cancer.

Mouse bone marrow-derived mesenchymal stem cells inhibit leukemia/lymphoma cell proliferation in vitro and in a mouse model of allogeneic bone marrow transplant.

The allogeneic hematopoietic stem cell (HSC) transplantation of mesenchymal stem cells (MSCs) contributes to the reconstitution of hematopoiesis by ameliorating acute graft­versus­host disease (aGVHD). However, the role of MSCs in graft­versus­leukemia remains to be determined. In the present study, we co­cultured C57BL/6 mouse bone marrow (BM)­derived MSCs with A20 murine B lymphoma, FBL3 murine erythroleukemia and P388 murine acute lymphocytic leukemia cells. Cell proliferation, apoptosis, cell cycle progression and the amount of cytokine secretion were then measured using a Cell Counting kit­8, Annexin V/propidium iodide staining, flow cytometry and ELISA, respectively. We also established a model of allogeneic bone marrow transplantation (BMT) using BALB/c mice. Following the administration of A20 cells and MSCs, we recorded the symptoms and the survival of the mice for 4 weeks, assessed the T cell subsets present in peripheral blood, and, after the mice were sacrifice, we determined the infiltration of MSCs into the organs by histological staining. Our results revealed that the MSCs inhibited the proliferation of the mouse lymphoma and leukemia cells in vitro, leading to cell cycle arrest and reducing the secretion of interleukin (IL)­10. In our model of allogeneic BMT, the intravenous injection of MSCs into the mice injected wth A20 cells decreased the incidence of lymphoma, improved survival, increased the fraction of CD3+CD8+ T cells, decreased the fraction of CD3+CD4+ T cells and CD4+CD25+ T cells in peripheral blood, and ameliorated the manifestation of aGVHD. The results from the present study indicate that MSCs may be safe and effective when used in allogeneic BMT for the treatment of hemotological malignancies.

Inhibition of proliferation and invasiveness of ovarian cancer C13* cells by a poly(ADP-ribose) polymerase inhibitor and the role of nuclear factor-κB.

OBJECTIVE: To investigate the effect of the poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor PJ34 on the proliferation and invasiveness of ovarian cancer C13* cells and the role of nuclear factor-κB (NF-κB). METHODS: Proliferation of C13* cells was measured using a 3 -(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium bromide assay after incubation with PJ34 at different concentrations and for different treatment durations. In addition, expression of PARP-1 and the NF-κB p65 subunit after treatment with PJ34 was measured using Western blot and immunocytochemistry. The effect of PJ34 on cell invasiveness was examined using a transwell invasion assay. RESULTS: PJ34 inhibited proliferation of C13* cells in a time- and dose-dependent manner. PJ34 treatment was also associated with a dose-dependent decrease in PARP-1 and NF-κB p65 expression and attenuated invasiveness of C13* cells. PARP-1 expression was positively correlated with NF-κB p65 expression. CONCLUSION: The PARP-1 inhibitor PJ34 can markedly inhibit the proliferation and invasiveness of C13* cells, possibly due to PARP-1-mediated attenuation of NF-κB activity.

Skeletal morbidity is strongly associated with poor prognosis in adult acute lymphoblastic leukemia.

The prognostic significance of skeletal morbidity in acute lymphoblastic leukemia (ALL) has been mostly studied in children and yielded disappointing results, while in adult ALL it is seldom reported, and its prognostic value is not clear. To evaluate the prognostic value of skeletal morbidity in de novo adult ALL, we identified 20 patients with ALL with skeletal morbidity and compared them with matched patients with ALL but without skeletal morbidity (n = 60). Compared with controls, patients with skeletal morbidity responded poorly to treatment, with a lower incidence of complete remission (p = 0.02) and shorter continued remission duration (p = 0.031). The overall survival (OS) (38.67% vs. 69.44%, p = 0.03) and event-free survival (EFS) (25.67% vs. 58.77%, p = 0.008) were inferior to those of controls. Allogeneic hematopoietic stem cell transplant (allo-HSCT) may be beneficial to patients with skeletal morbidity. For patients with skeletal morbidity, OS at 12 months was 72.92% in patients who underwent allo-HSCT, while it was 38.5% for patients treated with chemotherapy (p = 0.03). By multivariate analysis, skeletal morbidity was an independent prognostic factor in adult patients with ALL. These results confirm the poor prognosis of patients with ALL with skeletal morbidity and reinforce interest in evaluating the incorporation of allo-HSCT in adult patients with ALL with skeletal morbidity onset.

F-18 FDG PET/CT imaging of solitary liver Langerhans cell histiocytosis: preliminary findings.

Langerhans cell histiocytosis (LCH) is a disorder of clonal proliferation of Langerhans-type cells. The imaging findings of LCH are not specific. A 27-year-old woman was admitted to our hospital because of liver enzyme elevation without other hepatic signs. Radiological studies were originally interpreted as possible metastatic disease to the liver. Fluorine-18 fluorodeoxyglucose positron emission tomography/computed tomography (F-18 FDG PET/CT) images demonstrated a diffuse pattern of nodules in the liver with hypermetabolic activity. LCH was diagnosed histopathologically with an ultrasound-guided liver biopsy. This case illustrates the importance of considering proliferative/benign conditions of the liver when interpreting PET/CT. Failure to do so could result in patient mismanagement.

Risk factors for invasive mold infections following allogeneic hematopoietic stem cell transplantation: a single center study of 190 recipients.

BACKGROUND: Invasive mold infection (IMI) is a major cause of infection-related mortality following allogeneic hematopoietic stem cell transplantation (allo-HSCT). METHODS: We retrospectively analyzed 190 allo-HSCT recipients at Changhai Hospital between the y 2000 and 2007. The survival rate was evaluated with Kaplan-Meier curves. Logistic and Cox regression models were used for multivariate analyses. RESULTS: The 1(st) y cumulative incidence rate of IMI was 12.8%, and invasive aspergillosis was the most commonly observed IMI (85%). Multivariate logistic regression analyses showed that significant predictors of IMI were corticosteroid therapy (odds ratio (OR) 1.656, 95% confidence interval (CI) 1.047-2.621, p = 0.031), positive cytomegalovirus antigenemia (OR 5.301, 95% CI 1.902-14.772, p = 0.001), and secondary neutropenia (OR 5.250, 95% CI 1.741-15.834, p = 0.003). The mortality rate of IMI at 12 weeks after diagnosis was 60%. In Cox regression models, IMI-related mortality was related to the dose of corticosteroid (2 mg/kg/day or more) administered at the time of IMI diagnosis (hazards ratio (HR) 20.841, 95% CI 2.151-201.944, p = 0.009) and neutropenia (HR 7.043, 95% CI 1.186-41.827, p = 0.032). CONCLUSIONS: These data confirm previous findings that the incidence and mortality of IMI are mostly associated with immunodeficiency caused by immunosuppressive therapy or virus infection.

Erythroid 5-aminolevulinate synthase mediates the upregulation of membrane band 3 protein expression by iron.

Iron deficiency leads to abnormal expression and function of band 3 protein in erythrocytes, but the underlying mechanisms remain elusive. The mRNA of erythroid-specific 5-aminolevulinate synthase (eALAS) contains an iron response element and the eALAS protein is an important mediator of iron utilization by erythrocytes. In this study, we investigated the effect of short hairpin RNA (shRNA) mediated silencing of eALAS on the expression of band 3 protein induced by iron. By real-time RT-PCR and Western blot we showed that at mRNA and protein level iron-induced expression of band 3 protein was lower in eALAS-shRNA transfected K562 cells than in control cells. Of note, the lowest expression was detected in K562 cells cultured in iron deficiency condition (p < 0.01). Thus either iron deficiency or depletion of eALAS could suppress the expression of erythroid band 3 protein. These results demonstrated for the first time that iron and the iron-regulatory system regulate the expression of the erythrocyte membrane proteins.