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Inorganic n-type metal oxide materials, i.e., ZnO have been developed and employed as interface layers for energy level matching and electron transport in order to achieve high performance perovskites based optoelectronic devices. In this work, we successfully apply atomic layer deposition (ALD) technique to deposit ZnO directly on top of CsPbBr3 to serve as the electron transport layer. A regular perovskite light emitting diode (PeLED) in a configuration of glass/ITO/PEDOT:PSS/CsPbBr3/ZnO/Ag was fabricated. In the CsPbBr3 emitting layer, polyethyleneimine ethoxylated (PEIE) dissolved in an anti-solvent chlorobenzene (CB) was introduced to assist the nucleation and crystal growth of perovskite films, as well as providing surface reactive sites for ALD deposition of ZnO layer particularly. The ALD deposition temperature on the growth, crystallinity and morphology of ZnO and subsequent device performance was investigated. We obtained PeLEDs of the best performance with the best current and external quantum efficiency (EQE) of 0.49 cd/A and 0.14%, respectively, which is as 14 folds high as an inorganic CsPbBr3 device using F8 as the electron transport layer reported previously.

To investigate the prognostic value of the serum calcium level corrected by serum albumin (cCA) and corrected serum lactate dehydrogenase (LDH) level for the risk stratification for newly diagnosed multiple myeloma (MM) patients.The clinical data and survival of 186 newly diagnosed MM patients admitted to our hospital from June 1, 2015 to November 1, 2017 were collected. The patients's survival time was obtained by telephone and follow-up visits to patients and their families. The value of the prognostic system consisting of cCA levels and LDH levels in the survival time of MM patients was retrospectively analyzed. Moreover, the post-corrected hypercalcemia and high LDH as 2 factors were used for risk stratification, then according to these 2 factors, the MM patients were divided into 3 groups: group 1 (no risk factor), group 2 (1 risk factor) and group 3 (2 risk factors), and the effect of risk factors on the prognosis of MM patients was analyzed.The median follow-up time was 16 months. The cumulative OS rate of the post-corrected hypercalcemia group was lower than that of the non-hypercalcemia group. The 1-year cumulative OS rate in the 2 groups was 79.0%±6.7% and 88.6%±3.0%, the 3-year cumulative OS rate was 53.0%±10.5% and 74.6%±6.6% (P=0.016), respectively. The cumulative OS rate of the high LDH group [LDH ＞upper limit of normal (ULN), ULN=250 U/L] was lower than that in the normal LDH group. The 1-year cumulative OS rate in the 2 groups was 71.6%±8.6% and 90.0%±2.8%, the 2-year cumulative OS rate was 44.9%±12.1% and 83.1%±4.0%, respectively, and the median OS time was 19 months (95%CI: 15.32-23.34) and not reached (P=0.001). The risk stratification analysis showed that the median OS time of the 3 group was not reached (n=103, 57%), not reached (n=70, 39%) and 17 months (n=7, 4%, 95%CI: 5.19-28.41, P＜0.001). Patients with two risk factors had a prognosis worse than patients with 0-1 risk factor.The prognostic combination of corrected serum calcium and LDH levels may provide a basis for risk stratification and prognosis in MM patients in clinical practice.校正血钙与血清乳酸脱氢酶对初诊多发性骨髓瘤患者的预后价值.探讨以经血清白蛋白校正后血清钙(校正血钙，cCA)水平和血清乳酸脱氢酶（LDH）水平，作为危险因素建立的风险分层对初诊多发性骨髓瘤（MM）患者的预后价值.收集本院2015年6月1日至2017年11月1日收治的186例初诊MM患者的临床资料。对患者及家属进行电话随访及门诊就诊情况获得患者生存时间。回顾性分析由cCA水平及LDH水平组成的预后系统对MM患者生存时间的价值。以校正后高血钙和高LDH作为2个危险因素设计风险分层，将患者分为3组：第1组（无危险因素），第2组（1个危险因素）和第3组（2个危险因素），比较风险因素对MM患者预后的作用.中位随访时间16个月。校正后高钙组累积生存率低于非高钙组，2组的1年累积OS率分别为79.0%±6.7%和88.6%±3.0%，3年累积OS率分别为53.0%±10.5%和74.6%±6.6%（P=0.016）。高LDH组[LDH＞正常上限（ULN），ULN=250 U/L]累积生存率低于LDH正常组，2组的1年累积OS率分别为71.6%±8.6%和90.0%±2.8%，2年累积OS率分别为44.9%±12.1%和83.1%±4.0%，中位OS时间分别为19个月（95%CI：15.32-23.34）和未达到（P=0.001）。危险分组比较显示，第1组、第2组和第3组中位OS时间分别为未达到（n=103, 57%）、未达到（n=70, 39%）和17个月（n=7，4%，95%CI：5.19-28.41）（P＜0.001）。有2种危险因素的患者预后比0-1个危险因素的患者差.校正血钙和LDH水平的预后组合可以为临床实践中MM患者的风险分层和预后提供依据.

Toxaphene is an organochlorine insecticide, widely used in cereals, vegetables, fruits, tea and other pests. However, in killing pests, increasing agricultural production, while toxaphene aquatic creatures threat. In order to enrich aquatic organisms toxicological data, evaluate the risk to aquatic organisms toxaphene healthy growth, we use the traditional toxicological approach to study the toxic effects of toxaphene goldfish (Carassius auratus)'s. Study 5 toxaphene concentration 7d goldfish exposed catalase (CAT), superoxide dismutase (SOD), acetylcholinesterase (TChE), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) effects, the results showed that: toxaphene in 0.1,0.2,0.3,0.4, 0.5 μg / L in five concentrations, these five enzymes promoting effect, with more toxaphene concentration high, goldfish liver CAT activity is stronger, the stronger the brain and liver SOD activity, the activity of the brain TChE weaker, the stronger the brain activity of GSH-PX, and the contrast with the blank, P

Characterization of an acquired factor VIII inhibitor and plasmapheresis therapy in a patient with bullous pemphigoid

Purpose To explore the effects of Icaritin on chronic myeloid leukemia (CML) cells and underlying mechanisms. Method CML cells were incubated with various concentration of Icaritin for 48 hours, the cell proliferation was analyzed by MTT and the apoptosis was assessed with Annexin V and Hoechst 33258 staining. Cell hemoglobinization was determined. Western blotting was used to evaluate the expressions of MAPK/ERK/JNK signal pathway and Jak-2/Phorpho-Stat3/Phorsph-Akt network-related protein. NOD-SCID nude mice were applied to demonstrate the anti-leukemia effect of Icaritin in vivo. Results Icaritin potently inhibited proliferation of K562 cells (IC50 was 8 µM) and primary CML cells (IC50 was 13.4 µM for CML-CP and 18 µM for CML-BC), induced CML cells apoptosis and promoted the erythroid differentiation of K562 cells with time-dependent manner. Furthermore, Icaritin was able to suppress the growth of primary CD34+ leukemia cells (CML) and Imatinib-resistant cells, and to induce apoptosis. In mouse leukemia model, Icaritin could prolong lifespan of NOD-SCID nude mice inoculated with K562 cells as effective as Imatinib without suppression of bone marrow. Icaritin could up-regulate phospho-JNK or phospho-C-Jun and down-regulate phospho-ERK, phospho-P-38, Jak-2, phospho-Stat3 and phospho-Akt expression with dose- or time-dependent manner. Icaritin had no influence both on c-Abl and phospho-c-Abl protein expression and mRNA levels of Bcr/Abl. Conclusion Icaritin from Chinese herb medicine may be a potential anti-CML agent with low adverse effect. The mechanism of anti-leukemia for Icaritin is involved in the regulation of Bcr/Abl downstream signaling. Icaritin may be useful for an alternative therapeutic choice of Imatinib-resistant forms of CML.

In the present study, 90 patients with newly diagnosed acute promyelocytic leukemia (APL) were studied for all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) combination treatment in remission induction and postremission therapy. In addition, 20 APL patients who had achieved complete remission (CR) with an ATRA-based regimen received ATRA/As2O3 combination for consolidation and maintenance were also enrolled. The results showed that ATRA/As2O3 combination therapy yielded a high CR rate of 93.3% and a significantly shorter time to enter CR (median: 31 days; range: 18–59 days) compared to the ATRA-based regimen (n = 72; median: 39 days; range: 25–62 days). With the ATRA/As2O3 combination for CR maintaining, regardless of the way by which CR was attained, the relapse-free survival was significantly better than with an ATRA plus cytotoxic chemotherapy regimen (92.9 ± 3.2% vs. 72.4 ± 7.6%, for the 3-year Kaplan-Meier estimate of relapse-free survival). The drug toxicity profile showed that with the use of As2O3, the incidence of hepatotoxicity was obviously high during remission induction but decreased significantly during postremission treatment. We conclude that APL patients may benefit from the early use of the combination of ATRA and As2O3, in either remission induction or consolidation/maintenance.

To determine the molecular mechanism of reversing multi-drug resistance of K562/AO2 by puerarin.Effects of ADR and puerarin on NF-kappaB activity of K562,K562/AO2 were tested by immunofluorescence. The expression of survivin of K562,K562/AO2 was examined by immunocytochemistry. The p-gp expression was detected by flow cytometry.The NF-kappaB activity of K562 was significantly higher than that of K562/AO2. The NF-kappaB activity of K562 treated by ADR was significantly higher than untreated. The NF-kappaB activity of K562 which was pretreated by puerarin and then treated by ADR was much lower than that treated by ADR alone. The NF-kappaB activity of K562/AO2 intervened by puerarin was lower than that unintervened by puerarin.The p-gp and survivin expression of K562/AO2 was significantly higher than K562. The p-gp and survivin expression of K562 treated by ADR was higher than that untreated by ADR. But the p-gp and survivin expression of K562 which was pretreated by puerarin and then treated by ADR was much lower than that not pretreated by puerarin.The p-gp and survivin expression of K562/AO2 intervened by puerarin was lower than that unintervened by puerarin. The expression was negatively correlated to the duration of intervention. The inhibition effect demonstrated time dependence.The activation of NF-kappaB can increase the expression of p-gp and survivin, which may be part of the molecular mechanism of multi-drug resistance of K562. Puerarin can prevent and stop the multi-drug resistance in K562 and reverse the multi-drug resistance of K562/AO2 to ADR by inhibiting the activity of NF-kappaB and the expression of p-gp and survivin.

To identify the clinical and laboratory diagnosis of a bullous pemphigoid patient with acquired hemophilia A (AH-A). To identify FVIII binding epitope and IgG subclass of the FVIII inhibitor, and explore the molecular mechanism for AH-A pathogenesis.Plasma FVIII activity( FVIII: C) was determined by one-stage assay, the titre of FYIII inhibitor by Bethesda Unit (BU). IgG purification of patient plasma or normal pooled plasma was finished by protein A-agarose column chromatography. Activated partial thromboplastin time (APTT) was assayed for uncovering FVIII inhibitor effect on FVIII in vivo. Combined Western blot analysis by anti-IgG1, IgG2, IgG3 and IgG4 antibodies was used to determine the relative concentration of patient' s IgG subclass. IgG subclass concentrations were quantified by nephelometric method. Solid-phase binding assay of FVIII and FVIII inhibitor, combined with Western blot was used to recognize the binding epitope at which the FVIII inhibitor bound to FVIII.(1) Plasma APTT value of patient was prolonged evidently and could not be corrected by normal pooled plasma. Patient's FVIII: C was1.5%. The titre of FVIII inhibitor in patient plasma was 147.8 BU. (2) The purified patient IgG was able to inhibit FVIII: C of normal pooled plasma significantly with a dose dependent manner, and the patient plasma could prolong rabbit plasma APTT markedly with a time dependent manner. (3) The FVIII inhibitor was predominantly then of IgG4 subtype with a minority IgG1, and the concentration of IgG4 and IgG1 in the patient was higher than that in normal. The FVIII inhibitor reacted with FVIII 44 x 10(3) fragment epitope.The inhibiting effect of FVIII inhibitors on FVIII: C in the bullous pemphigoid patient with AH-A is determined and the IgG subclass of the FVIII inhibitor is identified. A binding epitope for the FVIII inhibitor is a FVIII 44 x 10(3) fragment. The results provides evidence for understanding the pathogenesis of AH-A.

To study the clinical features and molecular genetics of acute monocytic leukemia (AML) after orthotopic liver transplantation and significance thereof.The clinical manifestations, laboratory findings, development, diagnosis, treatment, and prognosis of the first case of AML after orthotopic liver transplantation in the world, a Chinese, male, aged 46, were observed. RT-PCR was used to analyze the mRNA expression of FLT3, Pim-1, and Hsp-70 in the bone marrow mononuclear cells (BMMCs) of the patient. Nucleotide sequence analysis was used to detect the mutation of FLT3-ITD. Flow cytometry was used to examine the protein expression of C-kit, a stem cell factor receptor, and platelet derived growth factor receptor-alpha (PDGFRalpha).(1) Three months after the orthotopic liver transplantation the patient manifested symptoms and signs of anemia and thrombocytopenia. Laboratory tests found increase of white blood cells and myeloblasts with Auer's rods. Cytogenetic analysis showed a genotype of 46XY/47XY with an extra chromosome 8. Bone marrow examination revealed increased promonocytes. The diagnosis of chronic myelomonocytic leukemia was made. Five months after the liver transplantation the disease developed to AML. The patient underwent combined chemotherapy (HA or DA regimens) for 5 courses and showed a partial remission both hematologically and in bone marrow examination at first, however, became resistant to all chemotherapeutic agents. RT-PCR showed absence of wild type FLT3 allele. At last the patient died of infection. (2) A FLT3-ITD mutation of "insertion" type was identified in the BMMCs. The Pim-1 mRNA was weakly expressed and the expression of Hsp-70 mRNA was upregulated in the BMMCs. (3) The protein expression of C-kit and that of PDGFRalpha were both upregulated in the BMMCs as showed by flow cytometry.Orthotopic liver transplantation may be complicated with acute leukemia heterogeneous in clinical features and hematology. Certain defects in cytogenetics/molecular genetics may attribute to unfavorable prognosis.

To understand the clinical features and histopathology of histocytic necrotizing lymphadenitis (HNL) so as to better recognize the disease.The clinical features, histopathology, and diagnosis of 10 patients admitted to our hospital were retrospectively analyzed.The clinical features of these 10 cases included: young females were the majority; lymphadenopathy and fever were the most common clinical manifestations; some cases were accompanied by connective tissue diseases. Histopathologic examination showed distinctive necrosis and around the necrotic foci, variable proliferations of histocytes but generally without infiltration of neutrophils.HNL has some typical histopathological alterations and relatively fine prognosis,but it tends to be misdiagnosed as lymphoma or lymphoid tuberculosis and may be accompanied by other diseases.