Caffeic acid prevents non-alcoholic fatty liver disease induced by a high-fat diet through gut microbiota modulation in mice.

Caffeic acid (CA) is derived from many plants and may have the ability to reduce hepatic lipid accumulation. The gut microbiota produces lipopolysaccharides and further influences hepatic lipid metabolism, and thus plays an important role in the development of nonalcoholic fatty liver disease (NAFLD). However, whether the beneficial effects of CA are associated with the gut microbiota remains unclear. The present study aimed to investigate the benefits of experimental treatment with CA on the gut microbiota and metabolic functions in a mouse model of NAFLD. In this study, C57BL/6J mice received a high-fat diet (HFD) for 8 weeks and were then fed a HFD supplemented with or without CA for another 8 weeks. HFD induced obesity and increased accumulation of intrahepatic lipids, serum biochemical parameters and gene expression related to lipid metabolism. Microbiota composition was determined via 16S rRNA sequencing, and analysis revealed that HFD led to dysbiosis, accompanied by endotoxemia and low-grade inflammation. CA reverted the imbalance in the gut microbiota and related lipopolysaccharide-mediated inflammation, thus inhibiting deregulation of lipid metabolism-related gene expression. Our results support the possibility that CA can be used as a therapeutic approach for obesity-associated NAFLD via its anti-inflammatory and prebiotic integrative response.

Nifedipine inhibits ox-LDL-induced lipid accumulation in human blood-derived macrophages.

Studies have shown that nifedipine, an anti-hypertensive drug, protects against atherosclerotic progression, but the underlying mechanisms remain elusive. Oxidized low-density lipoprotein (ox-LDL) is critically implicated in macrophage lipid deposition seen in atherosclerosis. In this study, we examined the effects of nifedipine on some ox-LDL-associated changes in human blood-derived macrophages. We isolated monocytes from normal human blood and differentiated them into macrophages. We then treated these human macrophages with ox-LDL and/or nifedipine, and examined lipid accumulation and expression levels of two scavenge receptors CD36 and SR-A as well as a protein kinase PKC-θ. Nifedipine treatment substantially reduced lipid accumulation and the expression of CD36, SR-A, and protein kinase C (PKC)-θ in human macrophages treated with ox-LDL. Silencing of PKC-θ using siRNA also reduced the expression of CD36 and SR-A in these cells. Our results thus suggest that nifedipine may inhibit atherosclerosis by reducing ox-LDL-induced lipid deposition through suppression of the CD36/SR-A-mediated uptake of ox-LDL by macrophages via a PKC-θ-dependent mechanism.

Cylinder detection in large-scale point cloud of pipeline plant.

The huge number of points scanned from pipeline plants make the plant reconstruction very difficult. Traditional cylinder detection methods cannot be applied directly due to the high computational complexity. In this paper, we explore the structural characteristics of point cloud in pipeline plants and define a structure feature. Based on the structure feature, we propose a hierarchical structure detection and decomposition method that reduces the difficult pipeline-plant reconstruction problem in IR³ into a set of simple circle detection problems in IR². Experiments with industrial applications are presented, which demonstrate the efficiency of the proposed structure detection method.

[Evaluation of soft tissue lesions affecting the masticator space with dynamic contrast enhanced MRI].

OBJECTIVE: To determine the characteristics and diagnostic value of dynamic contrast enhanced MRI (DCE-MRI) in differentiating benign soft tissue lesions from malignant tumors affecting the masticator space (MS). METHODS: Prior to managements, conventional MRI and DCE-MRI were performed in 53 patients who suffered from primary or secondary soft tissue lesions affecting the MS. The time to peak (TTP), relative maximum enhancement (RME) and relative washout ratio (RWO) were separately calculated. RESULTS: Mean TTP of benign and malignant lesions were (130.3 ± 13.2) and (69.6 ± 6.9) s, respectively. Mean RWO of benign and malignant lesions were (29.7 ± 5.5)% and (8.7 ± 2.1)%, respectively. Malignant lesions had a significantly shorter TTP(P = 0.001) and lower RWO (P = 0.003) than benign lesions. When TTP was less than 92.2 s and RWO less than or equal to 16.0%, malignant tumors were considered. DCE-MRI had a sensitivity of 72.3%, specificity of 93.5%, accuracy of 84.9%, positive predictive value of 88.9%, and negative predictive value of 82.9%. CONCLUSIONS: As a non-invasive imaging technique, DCE-MRI is valuable to differentiate benign soft tissue lesions from malignant tumors affecting the MS.

[Expression of estrogen sulfotransferase (EST) gene and bridging integrator protein-1 (BIN1) gene and their significance in breast tissues].

BACKGROUND & OBJECTIVE: Estrogen sulfotransferase (EST) is an enzyme which metabolizes estrogen into inactive estrogen sulphate. Bridging integrator protein-1 (BIN1) is a novel c-myc-interacting protein with the features of tumor suppressor. EST and BIN1 may be protective in tumorigenesis. This study was to detect the gene expression of EST and BIN1 in breast cancer tissues,and further investigate the carcinogenesis mechanism of breast cancer. METHODS: The mRNA levels of EST and BIN1 in 12 specimens of normal human breast tissue, and 24 specimens of breast cancer were measured by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: EST mRNA and BIN1 mRNA were expressed in all normal human breast tissues, while EST mRNA was decreased in 75.0% (18/24), and lost in 25.0% (6/24) breast cancer specimens; BIN1 mRNA was decreased in 25.0%(16/24), and lost in 66.7.0% (16/24) breast cancer specimens. CONCLUSION: Down-regulation of EST mRNA and BIN1 mRNA may play an important role in the molecular mechanisms of breast carcinogenesis.

[Expression of estrogen sulfotransferase in breast tissues and the regulation of ESTmRNA by estrogen].

OBJECTIVE: To detect the expression of estrogen sulfotransferase (EST) in breast tissues, and to investigate its significance in breast carcinogenesis and the relationship between EST mRNA and estrogen. METHODS: Seven specimens of normal human breast tissues from patients with benign breast diseases were implanted subcutaneously into athymic nude mice, one specimen divided into many pieces to be implanted into 2 groups of mice, totalling 14 mice. Then the 14 mice were divided into 2 groups: as control and the other injected intramuscularly with estradiol benzoate (B-E(2)) every other day for 6 weeks. Six weeks after, the implanted tissues were taken out. Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of EST mRNA in 24 specimens of breast cancer, 6 specimens of normal breast tissues around the breast fibroadenoma, all resected during operation, and the specimens of implanted normal breast tissues from the mice (control group and B-E(2) group). The protein expression of estrogen receptor (ER) was detected by immunohistochemistry in the 24 specimens of breast cancer. RESULTS: EST mRNA was expressed in all normal human breast tissues and the expression was increased in the grafts from mice of B-E(2) group. However, the specimens of breast cancer showed decrease or absence of EST mRNA expression. CONCLUSION: EST mRNA expression is decreased or lost in breast cancer tissues. EST mRNA can be regulated by estrogen in normal breast tissues.

Effect of Exogenous Rb Gene on Expression of p21 Gene in Vascular Smooth Muscle Cells.

The level of p21 mRNA and protein in cultured human umbilical arterial vascular smooth muscle cells were assayed by immunochemical staining and RT-PCR. The expression and phosphorylation status of Rb protein were examined by Western blot. It was observed that the senescent vascular smooth muscle cells exerted morphological changes with transmission electron microscope and characterized with beta-galactosidase staining. The flow cytometry was used for cell cycle analysis. Introduction of exogenous Rb gene could induce the expression of p21 gene leading to inhibition of phosphorylation of Rb protein. The senescent vascular smooth muscle cells at G0/G1 phase of the cell cycle were found following transfection of Rb gene recombinant adenovirus. These results show that exogenous Rb gene regulate cell cycle progression and promote cell senescence by induction of p21 gene expression.