The effect of quenching and Mn substitution for Ni on the magnetic properties of Mn25+xNi50-xGa25.

Ni-Mn based Heusler alloys have attracted widespread attention due to their novel physical properties. However, the structure of Mn2NiGa is metastable at room temperature, making it difficult to obtain its intrinsic physical properties and limiting its application. In this study, we obtained Mn2NiGa by replacing Ni in the precursor alloy Ni2MnGa with Mn and studied its magnetic properties, structures, and phase transitions with floating composition. In addition, we focused on the compositional segregation characteristics of Mn2NiGa caused by different heat treatment and quenching conditions. It was found that the samples quenched after annealing at 773 K for 48 hours exhibited abnormalities in magnetism, phase transformation, and structure. The further electron probe scanning characterization results reveal that the changes in these physical properties were related to component segregation caused by heat treatment.

The effect of Cr doping on the magnetic and magnetocaloric properties of Ni45Co5Mn36.5In13.5 Heusler alloys.

Herein, Ni45-xCrxCo5Mn36.5In13.5 (x = 0, 0.2, 0.4, and 0.6 at%) and Ni45Co5Mn36.5-yCryIn13.5 (y = 0.2, 0.4, and 0.6 at%) polycrystalline Heusler alloys are prepared by arc melting and then characterized using X-ray diffraction and a vibrating sample magnetometer. A single L21 austenitic phase is confirmed at room temperature. Meanwhile, we studied the effect of Cr doping on the magnetic properties of Ni45Co5Mn36.5In13.5 alloys. It is observed that, with the incorporation of Cr atoms, both the lattice constant and valence electron concentration of the alloys have changed, resulting in the phase transition temperature, saturation magnetization and magnetic entropy changing significantly. In addition, when Cr is replaced by Mn, the change of phase transition temperature (ΔT) induced by the magnetic field decreases; therefore, in the Ni45Co5Mn36.1Cr0.4In13.5 samples, the magnetic entropy change reaches a maximum value of up to 37.1 J kg-1 K-1 under an external magnetic field of 3T, which is more than 50% higher than that of other Ni-Mn based Heusler alloys reported in the literature.

Long ncRNA MALAT1 promotes cell proliferation, migration, and invasion in prostate cancer via sponging miR-145.

BACKGROUND: The long non-coding (lncRNA) RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1) is known to promote tumorigenesis, whereas microRNA-145 (miR-145) plays an antitumor role in several cancers. In this study, we aimed to elucidate the role of MALAT1 and miR-145 in prostate cancer cells and investigate the effect of MALAT1 downregulation on prostate cancer (PCa) cells in vitro in vivo. METHODS: The Cancer Genome Atlas (TCGA) datasets were used to carry out the initial bioinformatics analysis; the findings were then tested in LNCaP and CWR22Rv1 cell lines. Western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to evaluate the levels of MALAT1 and miR-145 along with related biomarkers. Furthermore, wound-healing and Transwell assays were performed to test the migratory and invasive abilities of PCa cells. Luciferase reporter assays were used to validate the relationship between MALAT1 and miR-145; their down-stream target genes were also studied. To further substantiate these findings in an animal model, tumor studies including immunofluorescence staining of tissues were carried in nude mice. RESULTS: The expression of MALAT1 was upregulated in both LNCaP cell lines and CWR22Rv1 cell lines (F=2.882, t=13.370, P<0.001; F=2.268, t=15.859, P<0.001). Knockdown of MALAT1 reduced the migratory and invasive capabilities of PCa cells (F=0.017, t=12.212, P<0.001; F=10.723, t=6.016, P=0.002). Using direct binding, MALAT1 suppressed the antitumor function of miR-145, which in turn upregulated transforming growth factor-ß1 (TGF-ß1)-induced epithelial-mesenchymal transition (EMT) via SMAD3 and TGFBR2 (F=2.097, t=5.389, P=0.006; F=1.306, t=4.155, P=0.014). CONCLUSIONS: We confirmed that MALAT1 acts as a competing endogenous RNA (ceRNA) of miR-145. The MALAT1 based regulation of MiR-145-5p-SMAD3/TGFBR2 interactions could be an intriguing molecular pathway for the progression of PCa.

MicroRNA-423-5p as a biomarker for early diagnosis and outcome prediction of acute kidney injury in patients with acute decompensated heart failure.

OBJECTIVE: To evaluate the clinical significance of serum and urinary microRNA-423-5p in the prediction of acute kidney injury onset and survival in patients with acute decompensated heart failure. METHODS: A total of 180 acute decompensated heart failure patients, including 57 acute kidney injury cases and 123 non-acute kidney injury cases, were included in this study. Serum and urinary neutrophil gelatinase-associated lipocalin, a biomarker of renal injury of acute kidney injury, was detected using an enzyme-linked immunosorbent assay. Expression of microRNA-423-5p in serum and urine samples was examined using quantitative real-time polymerase chain reaction. The clinical significance of microRNA-423-5p was evaluated using receiver operating characteristic curve and Kaplan-Meier survival analysis. RESULTS: The levels of neutrophil gelatinase-associated lipocalin and microRNA-423-5p in serum and urine samples were elevated in patients with acute kidney injury compared with the non-acute kidney injury cases (all P < 0.05). Serum and urinary microRNA-423-5p had relatively high predictive performance for acute kidney injury onset in acute decompensated heart failure patients, and this predictive value was more significant when combined with urinary neutrophil gelatinase-associated lipocalin. In addition, serum and urinary elevated levels of microRNA-423-5p predicted a poor 180-day survival in the acute kidney injury group. CONCLUSION: Increased serum and urinary microRNA-423-5p can predict the occurrence of acute kidney injury in acute decompensated heart failure patients, and is associated with poor survival of acute kidney injury patients. In addition, the diagnostic value of urine neutrophil gelatinase-associated lipocalin for the early screening of acute kidney injury from acute decompensated heart failure patients might be improved by considering the changes in urinary microRNA-423-5p.

Diagnostic and prognostic significance of aberrant miR-652-3p levels in patients with acute decompensated heart failure and acute kidney injury.

OBJECTIVE: This study aimed to examine a novel microRNA (miR-652-3p) biomarker to improve early diagnosis of acute kidney injury (AKI) in patients with acute decompensated heart failure (ADHF) and to evaluate the survival predictive value of miR-652-3p. METHODS: We retrospectively analyzed the data of 196 patients with ADHF, including 65 who developed AKI during hospitalization. Neutrophil gelatinase-associated lipocalin (NGAL) levels were measured in serum and urine samples. Real-time quantitative PCR was applied to evaluate miR-652-3p mRNA expression. The diagnostic performance of miR-652-3p was examined using receiver operating characteristic curve analysis. The prognostic value of miR-652-3p was also analyzed. RESULTS: Serum and urinary NGAL and miR-652-3p levels were elevated in patients with ADHF and AKI. Serum and urinary miR-652-3p expression had diagnostic value in predicting AKI onset in patients with ADHF, and it had improved diagnostic performance when used with NGAL. Patients with AKI and high miR-652-3p levels had a high failure rate of renal recovery and poor 180-day survival. CONCLUSION: Serum and urinary miR-652-3p may be a candidate biomarker for early diagnosis of AKI in patients with ADHF and for predicting the prognosis of AKI. The combination of NGAL and miR-652-3p may accurately predict AKI onset in ADHF.

[A study of the influence of the guideline on the treatment of chronic congestive heart failure in the elderly].

OBJECTIVE: To investigate the changes in drug treatment in elderly inpatients with chronic congestive heart failure (CHF) after the publication of the guideline. METHODS: Three thousands one hundred and seventy-four hospitalized patients over 60 years old with CHF admitted from January 1990 to July 2007 to Second Hospital of Tianjin Medical University were enrolled, and the patients were divided into three groups according to every 6 years by the time when guideline of the American College of Cardiology/American Heart Association (ACC/AHA) was published. The changes in drug treatment were analyzed retrospectively. RESULTS: The proportion of enrolled patients was 79.2% (3 174/4 010) of total number of CHF patients. The number of male patients was 1 639, and that of the female 1 535. The age ranged 60-98 years old with the mean age (71.94±7.07) years old. Three groups were from 1990 to 1995 (group A), from 1996 to 2001 (group B) and from 2002 to 2007 (group C) respectively. The patients' age (years old) of three groups increased year by year (mean age of each group was 68.99±6.71, 71.56±6.86, 73.79±7.01 respectively, F=91.142, P<0.01). The three major causes of heart failure were coronary heart disease (55.3%, 64.5%, 81.8%), pulmonary heart disease (21.9%, 19.3%,5.5%) and rheumatic heart disease (16.5%, 10.3%, 7.5%). The difference among the three causes was statistically significant (χ(2)=217.979, P<0.01 ). Cardiac function on admission was mostly New York Heart Association (NYHA) grade III or IV (1 561 cases of NYHA III, 1 433 cases of NYHA IV, χ(2)=75.828, P<0.01 ). The outcome was mostly improved (the proportion of three groups was 88.9%, 88.3%, 92.7%, respectively, χ(2)=35.002, P<0.01). The frequency of using nitrate esters, ß-blocker, angiotensin receptor blocker (ARB), aldosterone antagonist was increased year by year (all P<0.05). The use of digitalis was decreased gradually (both P<0.05). The angiotensin converting enzyme inhibitor (ACEI) and ß-blocker were mostly used in coronary heart disease, and their frequency was 81.3% (1 698/2 088) and 87.8% (768/875) respectively. CONCLUSION: The guidelines made positive effects on the treatment of elderly inpatients with CHF. The treatment drugs that can improve the prognosis of CHF should be used in this group in time.

[Renal dysfunction and survival in hospitalized patients with chronic heart failure: a retrospective analysis].

OBJECTIVE: To analyze the impact of renal dysfunction on survival in hospitalized chronic heart failure (CHF) patients. METHODS: In this retrospective analysis, we collected all clinical data from eligible patients hospitalized in the second hospital of Tianjin Medical University between Jan 1980 and Aug 2007. CHF patients were divided into three groups according to glomerular filtration rate (GFR): A, normal renal function; B, mild renal dysfunction; C, renal dysfunction. Patients in group C were further divided into three subgroups according to hospitalization year: D, 1980.01 - 1989.12; E, 1990.01 - 1999.12; F, 2000.01 - 2007.08. RESULTS: Renal dysfunction was found in 714 patients. Compared with group A (n = 817) and group B (n = 928), patients in group C were older, had worse heart function and major medications included nitrates, diuretics and digitalis. From 1980 to 2007, use of Angiotensin II receptor antagonist, beta-blocker, statins significantly increased and the in-hospital mortality significantly decreased in group C patients. Percent of angiotensin converting enzyme inhibitor (ACEI) use was the highest in 1990s. The hospital stay was significantly longer and all cause in-hospital mortality was significantly higher in group C compared to group A and group B (all P < 0.01). After adjustment for other risk factors by multivariate analysis, renal dysfunction was an independent risk factor of in-hospital all cause mortality. Patients faced 16.7% higher risk of all cause in-hospital mortality for every 10 mlxmin(-1) x1.73 m(-2) decrease in GFR. CONCLUSIONS: The incidence of renal dysfunction was high in CHF patients. The hospital stay was longer, in-hospital all-cause mortality was higher in CHF patients with renal dysfunction compared to CHF patients without or with mild renal dysfunction. Renal dysfunction was an independent risk factor for all-cause in-hospital mortality. Increased use of ACEI, ARB, beta-blocker and statins might be responsible for reduced in-hospital mortality in CHF with renal dysfunction patients in recent years.