The common characteristics and mutual effects of heart failure and atrial fibrillation: initiation, progression, and outcome of the two aging-related heart diseases.

Atrial fibrillation (AF) and heart failure (HF) are common chronic diseases noted in humans. AF and HF share several risk factors, such as age, hypertension, obesity, diabetes, and dyslipidemia. They can interact with each other, while both their morbidity and mortality have been considerably increased. And AF and HF often occur together, suggesting a strong association between the two. However, the underlying mechanism behind this association is not well understood. Among them, aging is the most significant common risk factor, which represents an aging heart and is characterized by fibrosis and decreased number of cardiomyocytes, known as senescence-related cardiac remodeling for both atria and ventricles. Finally, it is proposed that cardiac remodeling is the key link between AF and HF.

Circulating plasma galectin-3 predicts new-onset atrial fibrillation in patients after acute myocardial infarction during hospitalization.

BACKGROUND: New-onset atrial fibrillation (NOAF) is a common complication in patients with acute myocardial infarction (AMI) during hospitalization. Galectin-3 (Gal-3) is a novel inflammation marker that is significantly associated with AF. The association between post-AMI NOAF and Gal-3 during hospitalization is yet unclear. OBJECTIVE: The present study aimed to investigate the predictive value of plasma Gal-3 for post-AMI NOAF. METHODS: A total of 217 consecutive patients admitted with AMI were included in this retrospective study. Peripheral venous blood samples were obtained within 24 h after admission and plasma Gal-3 concentrations were measured. RESULTS: Post-AMI NOAF occurred in 18 patients in this study. Patients with NOAF were older (p < 0.001) than those without. A higher level of the peak brain natriuretic peptide (BNP) (p < 0.001) and Gal-3 (p < 0.001) and a lower low-density lipoprotein cholesterol level (LDL-C) (p = 0.030), and an estimated glomerular filtration rate (e-GFR) (p = 0.030) were recorded in patients with post-AMI NOAF. Echocardiographic information revealed that patients with NOAF had a significantly decreased left ventricular eject fraction (LVEF) (p < 0.001) and an increased left atrial diameter (LAD) (p = 0.004) than those without NOAF. The receiver operating characteristic (ROC) curve analysis revealed a significantly higher value of plasma Gal-3 in the diagnosis of NOAF for patients with AMI during hospitalization (area under the curve (p < 0.001), with a sensitivity of 72.22% and a specificity of 72.22%, respectively. Multivariate logistic regression model analysis indicated that age (p = 0.045), plasma Gal-3 (p = 0.018), and LAD (p = 0.014) were independent predictors of post-MI NOAF. CONCLUSIONS: Plasma Gal-3 concentration is an independent predictor of post-MI NOAF.

Predictive value of CHA2DS2-VASc score combined with hs-CRP for new-onset atrial fibrillation in elderly patients with acute myocardial infarction.

BACKGROUND: New-onset atrial fibrillation (NOAF) is common during acute myocardial infarction (AMI) and independently associated with worse prognosis. We aimed to validate the discrimination performance of CHA2DS2-VASc score combined with hs-CRP in the prediction of NOAF after AMI in elderly Chinese population. METHODS: 311 consecutive elderly patients (age ≥ 65 years old) with AMI from 1 January 2018 to 1 January 2019 without atrial fibrillation history were enrolled in our study. Univariable and multivariable logistic regression analyses were used to identify risk factors of NOAF. The discrimination performance of different score models were evaluated using ROC curve analysis and AUCs were compared using the Z test. RESULTS: 30 (9.65%) patients developed NOAF during hospitalization. The NOAF group were older and had higher hs-CRP, initial Killip class, BNP, LAD, CHADS2 score, CHA2DS2-VASc score, in-hospital mortality and lower LVEF and ACEI/ARB use (P < 0.05 vs group without NOAF for all measures). In multivariate regression analyses, age (OR = 1.127, 95% CI 1.063-1.196, P < 0.001) and hs-CRP (OR = 1.034, 95% CI 1.018-1.05, P < 0.001) were independent predictors of NOAF. In ROC curve analyses, both CHADS2 score (AUC = 0.624, 95% CI 0.516-0.733, P = 0.026) and CHA2DS2-VASc score (AUC = 0.687, 95% CI 0.584-0.79, P = 0.001) had acceptable but unsatisfactory discrimination performance in predicting NOAF after AMI. The combined model with CHA2DS2-VASc score and hs-CRP showed a significant better predictive value (AUC = 0.791, 95% CI 0.692-0.891, P < 0.001) compared to that of the CHA2DS2-VASc score alone (Z test, P = 0.008). CONCLUSION: The combined model with CHA2DS2-VASc score and hs-CRP had high accuracy in predicting post-AMI NOAF.

Association of atrial arrhythmias with thrombospondin-1 in patients with acute myocardial infarction.

OBJECTIVES: Atrial remodeling is the main developmental cause of atrial arrhythmias (AA), which may induce atrial fibrillation, atrial flutter, atrial tachycardia, and frequent premature atrial beats in acute myocardial infarction (AMI) patients. Thrombospondin-1 (TSP-1) has been shown to play an important role in inflammatory and fibrotic processes, but its role in atrial arrhythmias is not well described. The purpose of this study was to investigate the role of TSP-1 in AMI patients with atrial arrhythmias. METHODS: A total of 219 patients with AMI who underwent percutaneous coronary intervention and with no previous arrhythmias were included. TSP-1 were analyzed in plasma samples. Patients were classified into 2 groups, namely, with and without AA during the acute phase of MI. Continuous electrocardiographic monitoring was used for AA diagnosis in hospital. RESULTS: Twenty-four patients developed AA. Patients with AA had higher TSP-1 levels (29.01 ± 25.87 µg/mL vs 18.36 ± 10.89 µg/mL, p < 0.001) than those without AA. AA patients also tended to be elderly (65.25 ± 9.98 years vs 57.47 ± 10.78 years, p < 0.001), had higher Hs-CRP (39.74 ± 43.50 mg/L vs 12.22 ± 19.25 mg/L, p < 0.001) and worse heart function. TSP-1 (OR 1.033; 95% CI 1.003-1.065, p = 0.034), Hs-CRP (OR 1.023; 95% CI 1.006-1.041, p = 0.008), age (OR 1.067; 95% CI 1.004-1.135, p = 0.038) and LVDd (OR 1.142; 95% CI 1.018-1.282, p = 0.024) emerged as independent risk factors for AA in AMI patients. CONCLUSION: TSP-1 is a potential novel indicator of atrial arrhythmias during AMI.

Plasma Galectin-3 is associated with progression from paroxysmal to persistent atrial fibrillation.

BACKGROUND: Galectin-3 (Gal-3) is currently recognized as a promising biomarker for myocardial fibrosis. This study aimed to explore the potential association between plasma Gal-3 concentrations and atrial fibrillation (AF) progression in paroxysmal AF (PAF) patients METHODS: A total of 213 PAF patients were included for analysis in this study. All peripheral blood samples were prospectively collected and stored at -80℃ for subsequent Gal-3 quantification. The AF progression was defined as transformation from PAF to persistent AF (PsAF). RESULTS: A total of 51 PAF patients progressed to PsAF during a mean follow-up period of 674.44 ± 19.48 days. Patients with AF progression had significantly higher baseline plasma Gal-3 concentrations than those stayed in PAF status (13.52 ± 0.94 vs. 7.93 ± 0.37, p < 0.001). All PAF patients were divided into two subgroups based on the median value of plasma Gal-3 concentrations. Kaplan-Meier curve analysis showed a significantly higher AF progression rate in the higher plasma Gal-3 concentration group (log-rank test p < 0.001). In the Cox regression analysis, plasma Gal-3 concentration and left atrial diameter (LAD) were showed significantly associated with AF progression, even after adjustment of other potential confounding risk factors. Discrimination for AF progression with a simple model which consists of plasma Gal-3 concentration and LAD was modest with a C-statistic 0.72 (95%CI 0.64-0.80). Plasma Gal-3 concentration significantly improved the predictability by appropriately reclassifying several patients with progression (NRI = 28.3%, p = 0.003). CONCLUSION: Elevated plasma Gal-3 concentration is significantly associated with AF progression from PAF to PsAF. Plasma Gal-3 concentration could be used for PAF progression risk stratification and guiding management for PAF patients.

Research on the epigenetic regulation mechanism of the PTPN6 gene in advanced chronic myeloid leukaemia.

PTPN6, a tyrosine phosphatase protein, plays a negative role in cell signal transduction and is negatively correlated with tumour formation and growth. However, epigenetic regulation mechanism of the PTPN6 gene in advanced chronic myeloid leukaemia (CML) remains unclear. This study investigated bone marrow or blood samples from 44 CML patients and 10 healthy volunteers. KCL22 and K562 cells were cultured and treated with demethylation drugs and histone deacetylase inhibitors. Real time quantitative polymerase chain reaction (qPCR), methylation-specific PCR, bisulfite sequencing PCR, Western blotting, co-immunoprecipitation and chromatin immunoprecipitation (ChIP) was performed. PTPN6 was down-regulated in cell lines and patients with advanced phase CML, whereas DNMT1, DNMT3A, MECP2, MBD2 and HDAC1 were up-regulated. Treatment with 5-azacytidine, decitabine, sodium valproate and LBH589 increased PTPN6 expression, but decreased that of DNMT1, DNMT3A, MECP2, MBD2 and HDAC1. Immunoprecipitation and mass spectrometry showed that HDAC1 combined directly with PTPN6. ChIP-seq showed that HDAC1 did not combine with the promoter region of PTPN6, while MAPK, AKT, STAT5, JAK2 and MYC promoter regions all combined with HDAC1. PTPN6 is associated with progression of CML. Low expression level of PTPN6 was associated with DNA methylation and regulated by histone acetylation. HDAC1 participates in the regulation of PTPN6.

Reproducible fabrication of stable small nano Pt with high activity for sensor applications.

Pt nanoparticles with an average size of 2-3 nm in diameter were reproducibly synthesized by reduction of H2PtCl6 solution containing inositol hexaphosphate (IP6) as the stabilizing agent. Single crystals with Pt(111) faces of the resulting cubic nanoparticles were revealed by the electron diffraction pattern. The PtNPs-IP6 nanoparticles were used to modify an electrode as a nonenzymatic sensor for H2O2 detection, exhibiting a fast response and high sensitivity. A low detection limit of 2.0 × 10⁻7 M (S/N = 3) with two linear ranges between 2.4 × 10⁻7 and 1.3 × 10⁻³ M (R² = 0.9987) and between 1.3 × 10⁻³ and 1.3 × 10⁻² M (R² = 0.9980) was achieved. The attractive electrochemical performance of PtNPs-IP6 enables it to be employed as a promising material for the development of Pt-based analytical systems and other applications.

Solving Biobjective Distributed Flow-Shop Scheduling Problems With Lot-Streaming Using an Improved Jaya Algorithm.

A distributed flow-shop scheduling problem with lot-streaming that considers completion time and total energy consumption is addressed. It requires to optimally assign jobs to multiple distributed factories and, at the same time, sequence them. A biobjective mathematic model is first developed to describe the considered problem. Then, an improved Jaya algorithm is proposed to solve it. The Nawaz-Enscore-Ham (NEH) initializing rule, a job-factory assignment strategy, the improved strategies for makespan and energy efficiency are designed based on the problem's characteristic to improve the Jaya's performance. Finally, experiments are carried out on 120 instances of 12 scales. The performance of the improved strategies is verified. Comparisons and discussions show that the Jaya algorithm improved by the designed strategies is highly competitive for solving the considered problem with makespan and total energy consumption criteria.

The different variant allele frequencies of type I/type II mutations and the distinct molecular landscapes in CALR-mutant essential thrombocythaemia and primary myelofibrosis.

OBJECTIVE: Calreticulin (CALR) mutations have been identified as driver mutations in a quarter of patients with essential thrombocythaemia (ET) and primary myelofibrosis (PMF), which are subgroups of myeloproliferative neoplasms (MPNs). A 52-bp deletion (type I mutation) and a 5-bp insertion (type II mutation) are the most frequent variants. To better understand the impact of different CALR mutant variants, with or without nondriver mutations, on the clinical subtypes of MPN needs further investigation. METHODS: The clinical characteristics, laboratory parameters and genetic mutation statuses were analysed in a cohort of 77 MPN patients with CALR mutations (ET = 24, prePMF = 33, and overt PMF = 20). Targeted NGS using a 38-gene panel was performed to evaluate the variant allele frequency (VAF) of CALR type I/type II mutations and assess the molecular landscape of nondriver gene mutations. RESULTS: A lower VAF of type I vs. type II was observed in CALR-mutant ET, prePMF and overt PMF, and a higher frequency of type I vs. type II was found in CALR-mutant overt PMF. Additional somatic mutations were indicated to be useful in understanding the pathogenesis of MPN. In this study, the mutation landscape was more complex in overt PMF than in ET or in prePMF. Mutations in epigenetic regulators (ASXL1, EZH2 and TET2) were more common in overt PMF. CONCLUSIONS: The two different subtypes of CALR mutations may have different impacts on MPN. A lower VAF of CALR type I indicates a greater contribution to disease progression in MPN, and increased nondriver mutations may be important in myelofibrosis progression.

HNRNPH1 Is a Novel Regulator Of Cellular Proliferation and Disease Progression in Chronic Myeloid Leukemia.

RNA binding proteins act as essential modulators in cancers by regulating biological cellular processes. Heterogeneous nuclear ribonucleoprotein H1 (HNRNPH1), as a key member of the heterogeneous nuclear ribonucleoproteins family, is frequently upregulated in multiple cancer cells and involved in tumorigenesis. However, the function of HNRNPH1 in chronic myeloid leukemia (CML) remains unclear. In the present study, we revealed that HNRNPH1 expression level was upregulated in CML patients and cell lines. Moreover, the higher level of HNRNPH1 was correlated with disease progression of CML. In vivo and in vitro experiments showed that knockdown of HNRNPH1 inhibited cell proliferation and promoted cell apoptosis in CML cells. Importantly, knockdown of HNRNPH1 in CML cells enhanced sensitivity to imatinib. Mechanically, HNRNPH1 could bind to the mRNA of PTPN6 and negatively regulated its expression. PTPN6 mediated the regulation between HNRNPH1 and PI3K/AKT activation. Furthermore, the HNRNPH1-PTPN6-PI3K/AKT axis played a critical role in CML tumorigenesis and development. The present study first investigated the deregulated HNRNPH1-PTPN6-PI3K/AKT axis moderated cell growth and apoptosis in CML cells, whereby targeting this pathway may be a therapeutic CML treatment.

JNK Signaling Pathway Suppresses LPS-Mediated Apoptosis of HK-2 Cells by Upregulating NGAL.

OBJECTIVE: To explore the role of the c-Jun N-terminal kinase (JNK) signaling pathway in upregulated NGAL expression and its antiapoptotic mechanism in lipopolysaccharide (LPS)-mediated renal tubular epithelial cell injury. METHODS: In vitro, HK-2 cells were divided into five groups (Con, LPS 1 h, LPS 3 h, LPS 6 h, and LPS 12 h groups) based on the time of LPS (10 µM) treatment. NGAL and caspase-3 gene expression levels were detected by RT-PCR to assess dynamic changes. HK-2 cells were pretreated with SP600125 (20 µM) for 2 hours, followed by LPS (10 µM) stimulation for 3 hours. NGAL and caspase-3 gene expression levels were then determined. RESULTS: NGAL mRNA was increased significantly within 6 hours, and caspase-3 mRNA was increased within 3 hours after treatment (P < 0.05). Correlation analysis showed a high correlation between their expression (r = 0.448, P < 0.05). After pretreatment with SP600125, mRNA expression of NGAL in the LPS group was inhibited, while that of caspase-3 was increased significantly. The NGAL mRNA expression level in the SB + LPS group was decreased significantly compared with that in the LPS group, but it was slightly higher than that in the SP group (∼1.5 times of that in the Con group). However, caspase-3 mRNA expression was increased significantly in the SB + LPS group (P < 0.001) (3.5 times of that in the Con group). It also showed a significant increase compared with SP and LPS groups (P < 0.001 vs. SB group; P < 0.05 vs. LPS group). We also found that NGAL and caspase 3 proteins were increased significantly in LPS and SP + LPS groups, but SP600125 decreased the NGAL level by almost 35% and increased the caspase 3 level by 50% in the SP + LPS group compared with the LPS group (P < 0.05). CONCLUSIONS: The JNK signaling pathway inhibits LPS-mediated apoptosis of renal tubular epithelial cells by upregulating NGAL.

Applicability of newly derived second and third molar maturity indices for indicating the legal age of 16 years in the Southern Chinese population.

In China, forensic age estimation in the living has become increasingly important in these few years. Due to increasing juvenile crimes, the age of 16 years has become the legal age threshold for determining whether the juvenile criminal law or adult criminal law applies to the citizen. This study aimed to assess new cut-off values of the third molar maturity index (I3M) and second molar maturity index (I2M) at the legal age threshold of 16 years in Southern Chinese population and then to compare the applicability of the cut-off values of I3M and I2M we set for discriminating whether a subject is ≥ 16 years. Orthopantomograms (OPGs) of 671 healthy Southern Chinese subjects (332 males and 339 females), aged between 10 and 20 years, were studied. Logistic regression analysis was performed with chronological age (below 16 years and over 16 years) as a dichotomous dependent variable and, I3M, I2M, and sex as predictive variables. The high p-value for sex (p = 0.861) reveals that this factor was not statistically significant in assessing the legal age of 16. The cut-off values of I3M < 0.38 and I2M < 0.03 were identified and used to distinguish between individuals who were or were not aged ≥ 16 years. Compared with a single predictor (I3M) alone, combining I3M and I2M can be more reliable for determining whether an individual is aged more than 16 years. We found that accuracy was 88.52% (95% confidence interval CI, 86.11-90.94%) and sensitivity and specificity were 77.96% (95% CI, 74.82-81.10%) and 97.28% (95% CI, 96.04-98.51%), respectively. The estimated Bayes post-test probability was 99.12% (95% CI, 98.41-99.83%). In conclusion, combining I3M and I2M may be useful in legal and forensic practices to determine the legal age of 16 years in Southern Chinese individuals.

The Reparative Effects of Human Adipose-Derived Mesenchymal Stem Cells in the Chemotherapy-Damaged Thymus.

Hematological patients who accept chemotherapy always develop secondary tumor or even die of severe infections. As an important central lymphoid organ, the thymus is frequently damaged during chemotherapy. Previous studies showed that the mesenchymal stem cells (MSCs) can promote the proliferation and repair of epithelial cells in thymus. The purpose of our study is to investigate the reparative effects of human adipose-derived mesenchymal stem cells (hADMSCs) in chemotherapy-treated damaged thymus. Eighty mice were randomly divided into four groups: normal group, model control group, hADMSCs untreated group, and hADMSCs treated group. The mice were injected intraperitoneally with dexamethasone sodium phosphate (Dex 20 mg/kg), except the normal group. Then, the chemotherapy models were obtained after 1 week; the treated group was infused intraperitoneally with hADMSCs, whereas the model control group was injected with equal volumes of normal saline. The hADMSC's infusion day was regarded as day 0. The mice were sacrificed at different time points (days 3, 7, 10, and 14). The pathological structure and the function of the thymus, the recovery of T-lymphocyte subpopulation, and the proportion of regulatory T (Treg) cells in spleen and peripheral blood were detected. Additionally, we transfected hADMSCs by lentivirus with green fluorescent protein (GFP) to confirm whether they home to thymus and detected the expressions of cytokines that are associated with the development of thymus in hADMSCs and thymus. The results of the study showed that the hADMSCs treated group had a more rapid recovery in terms of thymic pathological structure and function. The hADMSCs could home to the damaged thymus and secrete cytokines that played important roles in repairing damaged thymus. The results indicated that hADMSCs could repair the damaged thymus caused by chemotherapy and improve the immune microenvironment, which may be a potential treatment for hematological patients.

The Long Noncoding RNA MEG3 and its Target miR-147 Regulate JAK/STAT Pathway in Advanced Chronic Myeloid Leukemia.

BACKGROUND: Long non-coding (lnc) RNAs plays an important role in chronic myeloid leukemia (CML). In this study, we aimed to uncover the mechanism of the lncRNA maternally expressed 3 (MEG3) and its target microRNA-147 (miR-147) in CML. METHODS: Sixty CML patients and 10 healthy donors were included in the study. The methylation of MEG3 and miR-147 promoter was determined by methylation-specific PCR. The relationship of MEG3 and miR-147 was explored by luciferase assay. The interactions of proteins were studied by RNA pull-down assay, RNA immunoprecipitation and co-immunoprecipitation. FINDINGS: Patients in accelerated phase CML (CML-AP) and blast phase CML (CML-BP) showed lower expressions of MEG3 and miR-147 and higher expressions of DNMT1, DNMT3B, MBD2, MECP2 and HDAC1 compared to the controls. These patients also showed a higher degree of methylation of MEG3 and miR-147 while there was a reduction after chidamide treatment. Furthermore, the overexpression of MEG3 and miR-147 inhibited cell proliferation both in vivo and in vitro, promoted apoptosis and decreased the expressions of DNMT1, DNMT3A, DNMT3B, MBD2, HDAC1 and MECP2. We also found MEG3 interacted with DNMT1, JAK2, STAT3, HDAC1, and TYK2, and JAK2 was bound to STAT3, STAT5 and MYC. More interestingly, JAK2 was bound to TYK2 by the bridge of MEG3. INTERPRETATION: LncRNA MEG3 and its target miR-147 may serve as a novel therapeutic target for CML blast crisis, and chidamide might have a potential clinical application in treating CML blast crisis.

Association between methylation of tumor suppressor gene SOCS1 and acute myeloid leukemia.

Suppressor of cytokine signaling­1 (SOCS1) is a widely recognized tumor suppressor gene. Silencing of SOCS1 expression as a result of promoter methylation is associated with occurrence and development of solid tumors such as liver, cervical and pancreatic cancer. However, the association between SOCS1 gene methylation and acute myeloid leukemia (AML) has not been well explored. In the present study, we examined whether gene expression and methylation status of SOCS1 was altered in AML, and whether this was related to disease occurrence and development. To assess this hypothesis, we analyzed SOCS1 in four groups of AML patients: i) Initial treatment group (IT); ii) relapsed/refractory group (RR); iii) remission group (RE); and iv) normal control group (NC). We also used leukemia cell lines U937 and THP­1 to study the underlying molecular mechanism of SOCS1 in AML, mainly the JAK2/STAT pathway. We used several techniques such as quantitative PCR (qPCR), methylation­specific PCR (MS­PCR), western blotting, flow cytometry and cell transfection techniques to analyze the expression and methylation status of SOCS1. We found that the SOCS1 gene methylation rate in the IT and RR groups was significantly higher than that in the RR and NC groups (48, 80 vs. 0 and 0%, respectively). Furthermore, mRNA and protein expression was significantly lower in the IT and RR groups when compared to the RE and NC groups. We also found that the JAK2/STAT signaling pathway was negatively affected by SOCS1. SOCS1 gene methylation caused gene silencing of SOCS1 which overcame the suppression of the downstream JAK2/STAT signaling pathway by SOCS1, and promoted the growth and proliferation of AML cells.

[Cyclin E overexpression and centrosome amplification in squamous cell carcinoma of oral cavity].

OBJECTIVE: To study the correlation between cyclin E protein overexpression and centrosome amplification in oral squamous cell carcinoma (OSCC). METHODS: Formalin-fixed, paraffin-embedded tissues from 12 normal oral epithelium cases and 46 cases of OSCC were studied. Their centrosome status was analyzed by indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The expression of cyclin E protein was studied by immunohistochemical methods. The correlation between cyclin E protein expression and centrosome amplification in OSCC was statistically analyzed by SPSS 12.0. RESULTS: Thirty-seven of the 46 OSCC cases (80.4%) studied showed evidence of centrosome amplification, as signified by enlargement and/or increase in number of centrosomes, while normal oral epithelium possessed centromeres of normal size and number. Positive staining for cyclin E protein was observed in 30 of the 46 OSCC cases (65.2%), while all the normal oral epithelium cases were cyclin E protein-negative. The percentage of centrosome amplification in OSCC with positive cyclin E protein staining (90.0%, 27/30) was higher than that in OSCC with negative cyclin E protein staining (62.5%, 10/16) (chi(2) = 5.014, P < 0.05). Centrosome amplification showed positive correlation with cyclin E protein overexpression (r = 0.330, P < 0.05). CONCLUSION: Up-regulation of cyclin E protein may represent one of the possible mechanisms for centrosome amplification in OSCC.

Dentritic CuPtPd Catalyst for Enhanced Electrochemical Oxidation of Methanol.

The CuPtPd catalyst is designed and synthesized successfully via directly reducing metal ions. The composition, morphology, and structure of the as-prepared CuPtPd nanohybrids are characterized by scanning electron microscopy and transmission electron microscopy, energy-dispersive spectrometry, selected-area electron diffraction, X-ray diffraction, and inductively coupled plasma atomic emission spectrometry. By comparison of the electrocatalytic properties of the ternary CuPtPd catalyst with bimetallic catalysts, we find that ternary nanocomposites perform better electrocatalytic and antipoisoning activity toward oxidation of methanol. The catalytic mass activity of the CuPtPd nanoparticles is 5.51-fold of commercial Pd black and 12.1-fold of Pt black.

[Clinical Analysis of 12 cases of Systemic Lupus Erythematosus Associated with Thrombotic Thrombocytopenic Purpura].

OBJECTIVE: To investigate the clinical manifestations, treatment strategies and outcomes of 12 patients with systemic lupus erythematosus (SLE) associated with thrombotic thrombocytopenic purpura(TTP). METHODS: The clinical data from 12 cases of SLE associated with TTP admitted in the Second Hospital of Hebei Medical University from January 2002 to August 2015 were retrospectively analyzed. RESULTS: 12 cases of SLE associated with TTP included 11 females and 1 male, their median age was 34.5 years old, among them 5 cases of TTP were diagnosed during the treatment of SLE, 7 cases of TTP were comfirmed together with SLE on admission. The hemolytic anemia, thrombocytopenia and neurological deficits appeared in all the patients, the renal impairment was observed in 10 cases, the schistocytes of peripheral blood smears (>1%) were present in 9 cases, a severely reduction of ADAMTS 13 activity (<5%) with inhibitor-positive had been demonstrated in 5 cases, all of the 12 patients were treated with glucocorticoid, and 11 cases were treated in combination with other drug(10 cases combined with cytotoxics, 1 case with intravenous gamma globulin, 1 case with rituximab), plasma exchange were used in 10 cases, and 2 cases died, 2 cases without receiving plasma exchange all died, renal damage was observed in all the dead patients. CONCLUSION: Clinical manifestation and repeated examinations of peripheral blood smears are helpful for early diagnosis of SLE associated with TTP, the plasma exchange combined with glucocortcoids is an effective treatment method, the renal impairment may be a risk factor related with poor prognosis.

[Effect of Rapamycin on Expression of Survivin and Caspase-3 and Its Influence on K562 Cell Ultrastructure].

OBJECTIVE: To investigate the effect of rapamycin on the expression of survivin and caspase-3 at mRNA level in K562 cells and the influence of rapamycin on K562 cell ultrastructure. METHODS: The effects of rapamycin at various concentration on K562 cell proliferation were analyzed by CCK8; the morphological characteristics of K562 cells was observed by transmission electron microscopy; the expression of survivin and caspase-3 at mRNA level in K562 cells treated with rapamycin was detected by RT-PCR. RESULTS: The proliferation of K562 cells was significantly inhibited by rapamycin. The apoptosis level of K562 cells increased with increase of rapamycin concentration, the expression of survivin at mRNA level decreased with increase of rapamycin concentration (P < 0.05). The expression of caspase-3 at mRNA level increased with increase of rapamycin concentration. CONCLUSION: Rapamycin can prornote K562 cell apoptosis through up-regulating caspase-3 level and reduceing survivin level.