A new species of Dicaelotus Wesmael (Hymenoptera, Ichneumonidae, Ichneumoninae) parasitizing Asclerobia sinensis (Lepidoptera) in seed pods of Caragana spp.

A new species of Ichneumoninae, Dicaelotus caraganae Sheng & Li, sp. nov.,is described and illustrated. Specimens were reared from the cocoon of Asclerobia sinensis (Caradja, 1937) (Lepidoptera, Pyralidae), from Hangjinqi, Inner Mongolia Autonomous Region, China. The new species is characterized by face very short, median length shorter than clypeus; clypeus 2.9 × as wide as long, apical margin with weak median convex; area basalis of propodeum very short, lateral carinae indistinct; hind coxa partly irregularly black; fourth and subsequent metasomal tergites black. A key to species of Dicaelotus known in China is provided.

Survival Trends of Patients With Surgically Resected Gastric Cardia Cancer From 1988 to 2015: A Population-based Study in the United States.

BACKGROUND: The incidence of gastric cardia cancer (GCC) patients has been increasing, while the survival trends of GCC patients over time remains unclear. Thus, the aim of our study was to determine the survival trends of GCC patients over time using a population-based data in the United States. METHODS: A total of 9044 surgically resected GCC patients during 1988 to 2015 from the Surveillance, Epidemiology, and End Results (SEER) database were identified. The survival probabilities were calculated by Kaplan-Meier method and the different survival probabilities between groups were examined by log-rank test. RESULTS: The median overall survival time was 27 (interquartile range, 12 to 99) months, and the median disease-specific survival time was 32 (interquartile range, 13 to 320) months for GCC patients. There was a statistically significant increase in median overall survival time (17 to 46 mo; P<0.001) and disease-specific survival time (19 to 67 mo; P<0.001) from 1988 to 1997 to 2008 to 2015. More GCC patients were diagnosed at an early stage in recent years. Meanwhile, adequate lymph nodes examined (eLNs) were obtained in more GCC patients during surgery. Also, the proportion of GCC patients who received chemoradiotherapy increased significantly. Moreover, early diagnosis, adequate eLNs, and chemoradiotherapy were associated with mortality. CONCLUSIONS: The survival rates of surgically resected GCC patients had a significant improvement from 1988 to 1997 to 2008 to 2015 in the United States, which might relate to the early discovery of GCC, greater utilization of adequate eLNs, and chemoradiotherapy.

[Predicting Therapeutic Response by Lymphocyte Level at 28th Day after DAC Treatment in Patients with MDS].

OBJECTIVE: To investigate a reliable clinical indication for predicting the therapeutic response of decitabine therapy in the patients with myelodysplastic syndromes (MDS). METHODS: The clinical efficacy of decitabine for 55 cases of MDS was analyzed retrospectively. According to the lymphocyte level at d28 after the first time treatment with decitabine, the patients were divided into high lymphocyte level group (H-Lym≥1.2×109/L) and low lymphocyte level group (L-Lym<1.2×109/L), and the overall response rate (ORR) and the progression-free survival (PFS) time in 2 groups were compared. RESULTS: As compared with L-Lym group, the ORR and PFS time in H-Lym group were significantly enhanced ï¼»(76.0% vs 50.0%) (P<0.05) and median time (15.7 months vs 8.5 months)(P<0.05), respectivelyï¼½;the ratio of platelet level ≥100×109/L in H-Lym group was very significantly higher than that in L-Lym group (72.0% vs 20.0%)(P<0.01). Multivariat analysis showed that the risk of disease progression in L-Lym group was 4.45-fold of H-Lym group (95% CI:1.58-12.59)(P<0.05). CONCLUSION: The patients with lymphocyte level ≥1.2×109/L at day 28 after the first time treatment with decitabine show the higher ORR and longer PFS time, therefore. the lymphocyte level at day 28 after first time treatment with decitabine can be used as an early clinical indicator for predecting the response to decitabine treatment.

Microvesicles shed from bortezomib-treated or lenalidomide-treated human myeloma cells inhibit angiogenesis in vitro.

Angiogenesis plays a significant role in the pathogenesis of multiple myeloma (MM). Microvesicles (MVs), a type of extracellular vesicles, are known as important players in cell-to-cell communication. MM-derived MVs have exhibited the activity of promoting angiogenesis. Bortezomib and lenalidomide are important drugs for treating myeloma. Therefore, the aim of the present study was to investigate whether and how MVs secreted from human myeloma cells exposed to bortezomib and lenalidomide affect angiogenesis. RPMI-8226 human myeloma cells and human umbilical vein endothelial cells (HUVECs) were used. MVs were isolated from the drug-treated RPMI-8226 cells. The number of the MVs were analyzed with flow cytometry. The expression of pro-angiogenic factors was analyzed with PCR and ELISA. The angiogenic potential of HUVECs was examined. NF-κB activation was analyzed using PCR, immunofluorescent staining and western blotting assays. We showed that bortezomib treatment induced an increase in the number of MVs shed from myeloma cells, but the number of MVs was not significantly altered by lenalidomide. The expression levels of vascular endothelial growth factor (VEGF), interleukin 6 (IL-6) and basic fibroblast growth factor (bFGF) were reduced in the MVs from the RPMI-8226 cells exposed to bortezomib and lenalidomide. Consequently, these MVs exhibited reduced angiogenic potential, as evaluated by wound healing tests, Boyden chamber assays and tube formation assays. Co-culturing HUVECs with drug-treated MVs inhibited NF-κB activation in the HUVECs and reduced the secretion of pro-angiogenic factors. In conclusion, bortezomib and lenalidomide treatment of cultured myeloma cells can block MV-induced angiogenesis and hence provides another mechanism for anti-angiogenic therapy.

[Efects of Inhibiting miR-155 Expression on the Proliferation and Apoptosis of Leukemia THP-1 Cells].

The aim of this study was to investigate the effects of miR-155 inhibitor transfection on the proliferation and apoptosis of THP-1 cells. The miR-155 inhibitor was transfected into THP-1 cells (THP-1I) by using X-treme GENE siRNA transfection reagent. Cells without transfection (THP-1C) and cells with negative transfection (THP-1IC) were used as controls. Quantitative real-time polymerase chain reaction (RT-PCR) was performed to detect the expression of miR-155 and relative expression of SHIP1 mRNA in the cells. Cell proliferation was assayed using CCK-8 method. Cell apoptosis were detected by flow cytometry. The expression of SHIP1, TAKT and pAKT in THP-1 cells were detected by Western blot. The results indicated that compared with THP-1C and THP-1IC, the expression of miR-155 in THP-1I cells was significantly reduced; miR-155 inhibition significantly increased apoptosis rate in THP-1 cells (P < 0.05) ; miR-155 inhibition in THP-1 cells caused no significant alteration in SHIP1 mRNA level but significantly increased its protein content, indicating some post-transcriptional modulations might exist underlying the modulation of miR-155 to SHIP1, the miR-155 caused significantly reduced protein level of pAKT (P < 0.05) without interfering TAKT protein content. It is concluded that the miR-155 inhibition may promote THP-1 cell apoptosis through increasing SHIP1 protein content and impairing its downstream PI3K/AKT signaling pathway. This study suggests that miR-155 inhibition may be a promising therapy strategy for treating acute myeloid leukemia (AML).