The antitumor effect of natural killer T cells has been reported in several studies analyzing the expression of CD1d on antigen-presenting cells (APCs). Therefore, the present study questioned whether APCs may be abnormal in the peripheral blood (PB) of acute leukemia (AL) patients, particularly the levels of CD1d. To improve the understanding of the role of CD1d on APCs, the levels of CD1d on monocytes were analyzed in healthy controls, AL patients and AL patients with complete remission (CR). In addition, the correlation between the number of CD3+CD56+ T lymphocytes and levels of CD1d on monocytes was analyzed. Flow cytometry was used to determine the levels of CD1d on monocytes and lymphocytes. A significant decrease was observed in the levels of CD1d on monocytes in the PB of acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) patients compared with the healthy controls. Simultaneously, significantly different levels of CD1d on monocytes were identified between the CR-AML and the CR-ALL patients; the levels of CD1d on monocytes remained low in the CR-AML patients, while the levels of CD1d on monocytes recovered in the CR-ALL patients. A significantly negative correlation was observed between the number of CD3+CD56+ T lymphocytes and the levels of CD1d on monocytes in AL patients. However, a significantly positive correlation was identified between the cytotoxicity of the CD3+CD56+ T lymphocytes and the levels of CD1d on monocytes. These results suggested that the significantly low levels of CD1d on monocytes may contribute to AML and ALL progression. In addition, a significant correlation was observed between the levels of CD1d on monocytes and the number/cytotoxicity of CD3+CD56+ T lymphocytes in AML and ALL patients.
Abstract The study aims to examine the treatment effect and adverse reactions of patients with newly diagnosed MM receiving different bortezomib-based regimens. This was a retrospective study of patients with newly diagnosed MM and who were treated with bortezomib-based combined chemotherapy at the Department of Hematology of the 2 affiliated hospitals of Wenzhou Medical University between July 2009 and May 2016. Cox proportion hazard multivariate analyses were carried out to assess the differences in treatment effect and adverse events between standard (1.3 mg/m 2 on days 1, 4, 8, 11) and weekly (1.6 mg/m 2 on days 1, 8, 15) cohorts, as well as the differences between intravenous injection and subcutaneous injection therapy. Progression-free survival (PFS) and overall survival (OS) were assessed using Kaplan–Meier method and the log-rank test. Among the 117 patients, 78 patients were treated with bortezomib standard therapy and 39 patients were treated with bortezomib weekly therapy (all with intravenous injection). In all patients, the treatment strategy was not independently associated with PFS or OS. The patients in the weekly therapy group had less thrombocytopenia events than those in the standard therapy group. The subcutaneous route had similar treatment effect as the intravenous route, but the incidence of peripheral neuropathy was lower. The once-weekly bortezomib regimen was similar in effectiveness to standard therapy in treating patients with newly diagnosed MM, but the incidence of thrombocytopenia was lower with the weekly regimen compared with the standard regimen.
Objective
To evaluate the applicability of the Chinese version of SF-36(v.2) scale for evaluating the quality of life of hospitalized patients with chronic heart failure.
Methods
From September 2013 to December 2014, 159 patients with chronic heart failure(NYHA I-IV), who were older than 18 years, clear mind and well self-expressed, were selected as participants. Questionnaire surveys included general survey and SF-36(v.2) scale. Internal consistency reliability, binary reliability and construct validity were all analyzed as indicators to evaluate SF-36(v.2) scale.
Results
A total of 159 questionnaires were issued and 159 valid questionnaires were recovered. The eight dimensions of SF-36(v.2) scale including physical function (PF), role-physical (RP), bodily pain (BP), general health (GH), social function (SF), vitality (VT), role-emotion(RE), and mental health (MH) score conversion were (41.57±24.86), (48.35±21.64), (69.18±25.68), (31.28±16.01), (48.90±19.53), (45.05±22.76), (59.43±24.31), (57.55±19.03); the floor effects were 2.5%, 4.4%, 3.1%, 4.4%, 3.1%, 6.3%, 0.6%, 1.3%; the ceiling effects were 0.0%, 3.8%, 21.4%, 0.0%, 0.0%, 1.9%, 3.1%, 0.0%. The item-convergent validity all achieved the standard (r≥0.4), and the total scaling success rate of item-convergent was 100.00%; the dimensions′ success rates of item-discriminant validity of RP, BP, RE and SF were all 100%, the rest of four dimensions were PF 95.71%, GH 85.71%, VT 89.29%, MH 94.29%, and the total success rate was 94.69%. Internal consistency reliability ranged from 0.738 to 0.919; the binary reliability ranged from 0.808 to 0.963. Within factors analysis, two common factors were confirmed, separately representing physical health and mental health, altogether making contribution of 61.66% cumulative variance.
Conclusions
As the revision of SF-36(v.1), SF-36(v.2) scale seemed more friendly in layout for questions and answers, the floor and ceiling effects significantly reduced. Additionally, it also shows good reliability and validity in the evaluation of quality of life of hospitalized patients with chronic heart failure, and the SF-36(v.2) scale can be used to evaluate the quality of life (QOL) of patients with chronic heart failure.
Key words:
Quality of life; Chronic heart failure; SF-36; Reliability and validity; Scale evaluation
Previous studies showed that Chidamide enhances the cytotoxicity of drugs in acute myeloid leukemia (AML) cells. Therefore, we examined whether Chidamide enhanced the cytotoxicity of drugs in AML cells by affecting H3K9me3 and autophagy levels. AML cells (THP-1 and MV4-11 cells) were treated with Chidamide, Cytarabine (Ara-c), or Sorafenib alone or in combination. Cell proliferation and survival rates were analyzed by MTT, flow cytometry, and western blotting assays. The results showed that a low dose of Chidamide enhanced the cytotoxicity of Ara-c or Sorafenib in AML cells, decreasing proliferation and increasing apoptosis. H3K9me3 levels as assessed by western blotting were upregulated by Chidamide treatment. ChIP-seq, which was used to investigate potential signaling pathways, indicated that the autophagy pathway might play a role in the effects of Chidamide. The level of autophagy induced in AML cells upon treatment with Ara-c or Sorafenib was inhibited by Chidamide, and autophagy markers (LC3, P62) were tested by western blotting. SIRT1 mRNA and protein levels were lower in AML cells treated with Ara-c or Sorafenib in combination with Chidamide than in cells treated with these drugs alone. Additionally, the Integrative Genomics Viewer results indicate that the H3K9me3 changes were related to SIRT1-binding sites. Together, these results show that Chidamide enhances the cytotoxicity of two chemotherapy drugs in AML cells by increasing the H3K9me3 level and inhibiting autophagy via decreasing the expression of SIRT1. Chidamide may be a potential treatment strategy for AML in the future, especially for refractory AML patients.
Recent reports have highlighted the role of cellular immunity in anti-tumor defenses. T lymphocytes are known to play important part in anti-cancer immunity. The number and function of T lymphocytes are altered in chronic leukemia patients. CD3(+)CD56(+) T lymphocytes have also been found to be abnormal in cancer patients. We therefore investigated changes in the number and cytotoxicity of CD3(+)CD56(+) T lymphocytes in the peripheral blood of acute leukemia (AL) patients (excluding acute promyelocytic leukemia), to improve our understanding of the role of this T lymphocyte subset. We analyzed CD3(+)CD56(+) T lymphocyte numbers and cytotoxicities in healthy controls, AL patients, and AL patients with complete remission. Lymphocyte counts were performed in peripheral blood and flow cytometry was used to determine cell numbers and cytotoxicities. The absolute number of CD3(+)CD56(+) T lymphocytes was increased in AL patients (including acute myeloid [AML] and acute lymphocytic leukemia [ALL]) compared with healthy controls (P<0.05), but their functioning was significantly reduced (P<0.05). The number of CD3(+)CD56(+) T lymphocytes in AML and ALL patients who achieved remission following chemotherapy was close to healthy controls (P>0.05), but their functioning was still significantly reduced (P<0.05). In addition, the number of CD3(+)CD56(+) T lymphocytes increased significantly in AML patients with increased peripheral blood white blood cell (WBC) counts, and in ALL patients without increased WBCs. These results suggest that cellular immunity may respond to AML and ALL, but that lymphocyte cytotoxicity remains impaired. Dysfunction of CD3(+)CD56(+) T lymphocytes in AML and ALL patients may contribute to the failure of the host immune response against leukemic blasts.
Abstract Background: Cytogenetic abnormalities are considered initiating events in the pathogenesis of multiple myeloma (MM) and are assumed to be of clinical significance. Methods: Fluorescence in situ hybridization (FISH) was used to analyze chromosomal architecture in 101 patients with MM. We evaluated overall patient survival and assessed cytotoxicity of imatinib against MM cells using a CCK8 assay. Results: ABL gene amplification was detected in 67 patients (66.3%). However, ABL gene amplification was not associated with clinical features, cytogenetic abnormalities (c-Myc amplification, IGH rearrangement, RB1 deletion, p53 deletion, or 1q21 amplification), or overall survival. ABL amplification in MM cell lines (LP-1 and U266) was revealed by FISH. Furthermore, the ABL protein was easily detectable in MM cell lines and some tumor cells by western blotting. A CCK8 assay indicated limited cytotoxicity of imatinib against MM cells. Conclusions: Our study firstly discussed ABL gene amplification was prevalent in MM cells, and we believe ABL gene would potentially be a useful target in the treatment of combination strategy for MM with ABL amplification in future.
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