The modulated structure of the AlCrFeCoNiCu high‐entropy alloy consists of NiAl intermetallics (β′) and a (α‐Fe, Cr) solid solution (β). The formation of the NiAl intermetallics greatly affects the strengths and magnetic properties of the AlxCrFeCoNiCu alloys. Evidently, the AlCrFeCoNiCu alloy cannot be treated as a solid‐solution alloy.

BackgroundAbnormal activation of PI3K/AKT/mTOR (PAM) pathway, caused by PIK3CA mutation, KRAS mutation, PTEN loss, or AKT1 mutation, is one of the most frequent signaling abnormalities in breast carcinoma. However, distribution and frequencies of mutations in PAM pathway are unclear in breast cancer patients from the mainland of China and the correlation between these mutations and breast cancer outcome remains to be identified.MethodsA total of 288 patients with invasive ductal breast cancer were recruited in this study. Mutations in PIK3CA (exons 4, 9 and 20), KRAS (exon 2) and AKT1 (exon 3) were detected using Sanger sequencing. PTEN loss was measured by immunohistochemistry assay. Correlations between these genetic aberrations and clinicopathological features were analyzed.ResultsThe frequencies of PIK3CA mutation, KRAS mutation, AKT1 mutation and PTEN loss were 15.6%, 1.8%, 4.4% and 35.3%, respectively. However, except for PTEN loss, which was tied to estrogen receptor (ER) status, these alterations were not associated with other clinicopathological features. Survival analysis demonstrated that PIK3CA mutation, PTEN loss and PAM pathway activation were not associated with disease-free survival (DFS). Subgroup analysis of patients with ER positive tumors revealed that PIK3CA mutation more strongly reduced DFS compared to wild-type PIK3CA (76.2% vs. 54.2%; P = 0.011). PIK3CA mutation was also an independent factor for bad prognosis in ER positive patients.Conclusions AKT1, KRAS and PIK3CA mutations and PTEN loss all exist in women with breast cancer in the mainland China. PIK3CA mutation may contribute to the poor outcome of ER positive breast carcinomas, providing evidence for the combination of PI3K/AKT/mTOR inhibitors and endocrine therapy.

Recent studies suggested that green tea has the potential to protect against diet-induced obesity. The presence of caffeine within green tea has caused limitations. Cocoa tea (Camellia ptilophylla) is a naturally decaffeinated tea plant. To determine whether cocoa tea supplementation results in an improvement in high-fat diet-induced obesity, hyperlipidemia and hepatic steatosis, and whether such effects would be comparable to those of green tea extract, we studied six groups (n = 10) of C57BL/6 mice that were fed with (1) normal chow (N); (2) high-fat diet (21% butterfat + 0.15% cholesterol, wt/wt) (HF); (3) a high-fat diet supplemented with 2% green tea extract (HFLG); (4) a high-fat diet supplemented with 4% green tea extract (HFHG); (5) a high-fat diet supplemented with 2% cocoa tea extract (HFLC); and (6) a high-fat diet supplemented with 4% cocoa tea extract (HFHC). From the results, 2% and 4% dietary cocoa tea supplementation caused a dose-dependent decrease in (a) body weight, (b) fat pad mass, (c) liver weight, (d) total liver lipid, (e) liver triglyceride and cholesterol, and (f) plasma lipids (triglyceride and cholesterol). These data indicate that dietary cocoa tea, being naturally decaffeinated, has a beneficial effect on high-fat diet-induced obesity, hepatomegaly, hepatic steatosis, and elevated plasma lipid levels in mice, which are comparable to green tea. The present findings have provided the proof of concept that dietary cocoa tea might be of therapeutic value and could therefore provide a safer and cost effective option for patients with diet-induced metabolic syndrome.

Background This study aimed to describe the design and present the baseline characteristics of a web-based lifestyle intervention program, which comprises of sequentially and simultaneously delivered intervention modules targeting physical activity (PA) and fruit and vegetable consumption (FVC) in Chinese college students. Methods The study adopted a randomized placebo-controlled trial, using the Health Action Process Approach (HAPA) and the Compensatory Carry-Over Action Model (CCAM) as the theoretical backdrops. 556 Chinese college students participated in the 8-week web-based lifestyle intervention program. All eligible participants were randomly assigned to one of four groups: 1) the PA-first arm which received a 4-week intervention addressing PA followed by a 4-week intervention addressing FVC; 2) the FVC-first arm which received a 4-week intervention addressing FVC followed by a 4-week intervention addressing PA; 3) the PA + FVC simultaneous arm that received an 8-week intervention addressing both PA and FVC at the same time; and 4) the placebo-control arm that received 8 weeks of general health information, which is not relevant for changing actual PA and FVC behaviors. Data collection includes four time-points: at the beginning and end of the intervention, and a 3-month and 12-month follow-up after the intervention. Results At baseline, 41.7% of participants were male and 58.3% were female. 41.0% of the participants did not meet the standard PA-recommendations, while 69.6% did not adhere to the standard FVC-recommendations. In total, only 19.6% of participants met both PA and FVC recommendations. Baseline characteristics across the four groups had no significant differences (all P = .17–.99), indicating successful randomization. Conclusions The preliminary results indicate a high prevalence of unhealthy lifestyles in college students in China, which further supports the need for web-based health intervention programs. This is also the first study that examines the comparative effectiveness of simultaneously and sequentially delivered lifestyle interventions in the Chinese population. These findings may contribute to the creation of future web-based health behavior change interventions. Trial registration ClinicalTrails.gov: NCT03627949 , 14 August, 2018. Electronic supplementary material The online version of this article (10.1186/s12889-019-7438-1) contains supplementary material, which is available to authorized users.

Background Increasing evidence showed that carbamylated lipoprotein accelerated atherosclerosis. However, whether such modification of high-density lipoprotein (HDL) particles alters in type 2 diabetes mellitus (T2DM) patients and facilitates vascular complications remains unclear. We aimed to investigate the alteration of the carbamylation in HDL among T2DM patients and clarify its potential role in atherogenesis. Methods A total of 148 consecutive T2DM patients undergoning angiography and 40 age- and gender-matched control subjects were included. HDL was isolated from plasma samples, and the concentration of HDL carbamyl-lysine (HDL-CBL) was measured. Furthermore, the HDL from subjects and in-vitro carbamylated HDL (C-HDL) was incubated with endothelial cells and monocyte to endothelial cell adhesion. Adhesion molecule expression and signaling pathway were detected. Results Compared with the control group, the HDL-CBL level was remarkably increased in T2DM patients (6.13 ± 1.94 vs 12.00 ± 4.06 (ng/mg), P < 0.001). Of note, HDL-CBL demonstrated a more significant increase in T2DM patients with coronary artery disease (CAD) (n = 102) than those without CAD (n = 46) (12.75 ± 3.82 vs. 10.35 ± 4.11(ng/mg), P = 0.001). Multivariate logistic regression analysis demonstrated that higher HDL-CBL level was independently associated with a higher prevalence of CAD in diabetic patients after adjusting for established cofounders (adjusted odds ratio 1.174, 95% confidence Interval 1.045–1.319, p = 0.017). HDL from diabetic patients with CAD enhanced greater monocyte adhesion than that from the non-CAD or the control group (P < 0.001). Such pro-atherogenic capacity of diabetic HDL positively correlated with HDL-CBL level. Furthermore, in-vitro incubation of carbamylated HDL (C-HDL) with endothelial promoted monocyte to endothelial cell adhesion, induced upregulation of cell adhesion molecules expression, and activated NF-κB/p65 signaling in endothelial cells. Inhibiting carbamylation of HDL or NF-κB activation attenuated the monocyte to endothelial cell adhesion and cell surface adhesion molecules expression. Conclusions Our study identified elevated carbamylation modification of HDL from T2DM patients, especially in those with concomitant CAD. We also evidenced that C-HDL enhanced monocyte to endothelial cell adhesion, indicating a potential pro-atherogenic role of C-HDL in atherosclerosis among T2DM patients. Trial registrationhttps://register.clinicaltrials.gov, NCT04390711 Registered on 14 May 2020; Retrospectively registered