Effects of dietary fats on the bioaccessibility and bioavailability of carotenoids: a systematic review and meta-analysis of in vitro studies and randomized controlled trials.

CONTEXT: Dietary fats are one of the well-known stimulators of carotenoid absorption, but the effects of the quantity and the type of dietary fats on carotenoid absorption have not yet been studied systematically. OBJECTIVE: This review aimed to analyze data from both in vitro studies and randomized controlled trials (RCTs) to examine the effects of dietary fats on the bioaccessibility and bioavailability of carotenoids. DATA SOURCES: A systematic search of 5 databases (Scopus, PubMed, Embase, CINAHL and the Cochrane Library) was conducted. STUDY SELECTION: In vitro studies and RCTs were selected according to the PICOS criteria and were reviewed independently by 2 investigators. DATE EXTRACTION: Key study characteristics from the eligible in vitro studies and RCTs were extracted independently by 2 investigators using a standardized table. RESULTS: A total of 27 in vitro studies and 12 RCTs were included. The meta-regression of in vitro studies showed that the bioaccessibility of carotenoids, except for lycopene, was positively associated with the concentration of dietary fats. The meta-analysis of RCTs showed that the bioavailability of carotenoids was enhanced when a higher quantity of dietary fats was co-consumed. Moreover, fats rich in unsaturated fatty acids resulted in greater improvement in carotenoid bioavailability (SMD 0.90; 95%CI, 0.69-1.11) as compared with fats rich in saturated fatty acids (SMD 0.27; 95%CI, 0.08-0.47). CONCLUSIONS: Co-consuming dietary fats, particularly those rich in unsaturated fatty acids, with carotenoid-rich foods can improve the absorption of carotenoids. SYSTEMATIC REVIEW REGISTRATION: PROSPERO registration number CRD42020188539.

miR-515-5p inhibits the proliferation, migration and invasion of human breast cancer cells by targeting CBX4.

microRNA (miR)-515-5p has been previously suggested to function as a tumor suppressor in various types of human cancer. Therefore, the role of miR-515-5p in breast cancer (BC) was explored in the present study. A series of assays were performed to study the function of miR-515-p in BC cells, including Cell Counting Kit-8, TUNEL, flow cytometric and colony formation to detect cell viability and apoptosis, wound healing and Transwell assays to measure cell motility. In addition, reverse transcription quantitative PCR and western blot analysis were used to assess miR-515-5p, CBX4, Cox-2, MMP2, MMP9, CDK2, p21 and Cyclin D1 respectively. Bioinformatics and dual-luciferase reporter assays were used to analyze the target genes of miR-515-5p, which confirmed the direct binding between miR-515-5p and polycomb chromobox 4 (CBX4). It was found that the expression of miR-515-5p is lower in BC cells compared with that in normal breast cells (MCF10A). Overexpression of miR-515-5p using the miR-515 mimic was found to reduce cell viability, facilitate cell apoptosis, inhibit cell proliferation and arrest cell cycle progressio at G1 phase. In addition, miR-515-5p overexpression could inhibit cell migration and invasion, whilst decreasing the expression levels of prostaglandin-endoperoxide synthase 2, MMP2 and MMP9 proteins. In addition, miR-515-5p overexpression could reduce the expression levels of CBX4 in MCF7 and ZR-75-30 cells. By contrast, overexpression of CBX4 reversed the effects of the miR-515-5p mimic transfection on cell proliferation, migration and invasion in MCF7 and ZR-75-30 cells. In combination, these results suggest that miR-515-5p inhibits BC cell proliferation, migration and invasion by directly targeting CBX4.

MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3.

MiR-548 has been reported to be involved in a variety of tumor processes, but its function in breast cancer remains unclear. In this study, we found that miR-548 was low expressed in breast cancer tissues and cells compared with normal control. We then examined whether up-regulation of miR-548 could improve the progression of breast cancer. Our results indicate that up-regulation of miR-548 significantly inhibits cell proliferation, migration andinvasion, and induces apoptosis in breast cancer cells. Further studies showed that miR-548 could specifically inhibit E2F3 expression. Moreover, rescue test showed that up-regulation of E2F2 could reverse the effect of miR-548 on proliferation, migration, invasion and apoptosis of breast cancer cells. In general, miR-548 could improve the progression of breast cancer. By targeting E2F2, which may make a potential target for the treatment of breast cancer.

[Evolution of fibrinolysis status with D-dimer level and the rate of plasminogen activator inhibitor type-1/D-dimer in acute coronary syndrome patients complicated with impaired glucose tolerance].

OBJECTIVE: To study the status of fibrinolytic inhibition in patients with acute coronary syndrome (ACS) complicated with impaired glucose tolerance (IGT) and to evaluate the effect of fibrinolytic inhibition on treatment and prognosis. METHODS: The subjects were divided into three groups included 39 patients with ACS without diabetes mellitus, 37 patients with IGT+ACS and 36 patients with ACS+noninsulin-dependent diabetes mellitus (NIDDM). Twenty healthy people were randomized to be control group. The plasma levels of tissue type plasminogen activator (t-PA), plasminogen activator inhibitor type-1 (PAI-1) and plasma D-dimer were detected by enzyme linked immunoadsorbent assay (ELISA) technique. The index of status of fibrinolysis was detected with the plasma levels of PAI-1, D-dimer and the ratio of PAI-1/D-dimer. This index was used to evaluate the status of fibrinolytic inhibition and the clinical out come in patients with AMI. RESULTS: Plasma level of PAI-1 was significantly higher in IGT+ACS patients and NIDDM +ACS patients than that in ACS(P<0.05), but the plasma level of D-dimer raised from basic level was significantly lower in IGT+ ACS patients and NIDDM+ACS patients than that in ACS (P<0.05). The ratio of PAI-1/D-dimer was significantly higher in IGT+ACS patients and NIDDM +ACS patients than that in ACS or in control group (P<0.01). For AMI patients in treatment groups, the rate of reperfusion after the thrombolytic was significantly lower and the rate of incidences in pump failure was significantly higher in IGT+ACS patients and NIDDM+ACS patients than that in ACS, too (P<0.01 and P<0.05). The incidences of serious arrhythmia, re-infarction and death were also higher in IGT+ACS patients and NIDDM +ACS patients. CONCLUSION: The fibrinolytic inhibition is existed in IGT+ACS group patients. The plasma level of D-dimer combined with the ratio of PAI-1/D-dimer could be used to be the evidence and to be the index to evaluate the status of fibrinolytic inhibition and prognosis.

Generalizable mass spectrometry mining used to identify disease state biomarkers from blood serum.

We bring a "spectrum" of classical data mining and statistical analysis methods to bear on discrimination of two groups of spectra from 24 diseased and 17 normal patients. Our primary goal is to accurately estimate the generalizability of this small dataset. After an aggressive preprocessing step that reduces consideration to only 55 peaks, we conduct over 35 out-of-sample cross-validation simulations of logistic regression, binary decision trees, and linear discriminant analysis. Misclassification rates grow worse as the size of the holdout sample increases, with many exceeding 30 percent. The ability to generalize is clearly tempered by the statistical, instrumentation, and biophysical characteristics of the study.