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Drilling with prestressed concrete (DPC) pipe pile is a nonsqueezing pile sinking technology, employing drilling, simultaneous pile sinking, a pipe pile protection wall, and pile side grouting. The unloading induced by drilling, the pipe pile supporting effect, and the dissipation of the negative excess pore-water pressure after pile sinking, all of which have significant effects on the recovery of soil pressure on the pile side, are the main concerns of this study, which aim to establish a method to reasonably evaluate the timing selection of pile side grouting. The theoretical solutions for characterizing the unloading and dissipation of the negative excess pore-water pressure are presented based on the cylindrical cavity contraction model and the separated variable method. By inverse-analyzing the measured initial pore pressure change data from borehole unloading, initial soil pressures on the pile side of each soil layer are determined using the presented theoretical solutions. Then, the presented theoretical solutions were verified through a comparative analysis with the corresponding measured results. Moreover, by introducing time-dependent coefficients αt1 and αt2 to characterize the pore pressure dissipation and rheology effects, the effects of the negative excess pore-water pressure dissipation on the pile-side soil pressure recovery are discussed in detail. [ABSTRACT FROM AUTHOR]

A simplified method is presented to investigate the dynamic response of rock-socketed piles embedded in a layered foundation. The finite element method is utilized to derive the dynamic stiffness matrix equations of the pile modelled as a 1D bar, and the exact stiffness matrix method is employed to establish the flexibility matrix equations of the foundation modelled as a 3D body. According to the pilesoil interaction condition, these matrices are incorporated together to obtain the solution for the dynamic response of rock-socketed piles. Finally, some numerical results are given to illustrate the influence of rocksocketed depth on the pile vertical impedance.

Circulating levels of microRNA-221 and 222 (miR-221/222) in patients with coronary artery disease (CAD) are elevated, yet the relationship between circulating miR-221/222 and the severity of coronary lesions in patients with acute coronary syndrome (ACS) remains unknown. In this study, the relative expression levels of circulating miR-221/222 in patients with ACS (n = 267) and controls (n = 71) were compared by real-time fluorescence quantitative-polymerase chain reaction (RT-qPCR). The ACS group was further divided into unstable angina pectoris (UA) group (n = 191) and acute myocardial infarction (AMI) group (n = 76). Significant upregulation of circulating miR-221/222 was observed in ACS. A positive linear correlation between circulating miR-221/222 and Gensini scores was demonstrated. The area under the curve (AUC) of circulating miR-221/222 in the diagnosis of coronary artery stenosis ≥50% was 0.605 and 0.643, respectively. The circulating miRNA-221/222 expression levels in ACS patients were elevated and positively associated with the severity of the coronary artery lesions. Circulating miR-221/222 may be novel biomarkers for the diagnosis of coronary artery stenosis ≥50% and the occurrence of ACS. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues. Histological and morphological analysis demonstrated that STAMP2 gene overexpression reduced adipocyte size, angiogenesis in epididymal and brown adipose tissues. On aortic ring assay, microvessels sprouting from aortas were significantly inhibited after STAMP2 gene overexpression. The cellular effect of STAMP2 on angiogenesis was explored in human umbilical vein endothelial cells ( HUVECs) model. Correlation of STAMP2 and angiogenesis was validated by Ad- STAMP2 transfection and STAMP2 si RNA inhibition. In vitro, overexpression of STAMP2 significantly inhibited endothelial cell migration, tube formation. The effects of Ad- STAMP2 transfection on HUVECs were abolished by treatment with PPARγ antagonist GW9662 (2.5 μM), and the roles of STAMP2 si RNA on HUVECs were also reversed by treatment with PPARγ agonist rosiglitazone ( RSG) (0.1 mM). RT- PCR indicated that STAMP2 could regulate levels of adhesion molecules, vascular endothelial growth factor A and CD36. The expression of PPARγ and CD36 was decreased when STAMP2 was inhibited by si RNA, while PPARγ and CD36 were highly expressed after overexpression of STAMP2. Our results suggested that STAMP2 gene overexpression may improve insulin resistance via attenuating angiogenesis in epididymal and brown adipose tissues through the PPARγ/ CD36 signalling pathway. [ABSTRACT FROM AUTHOR]

Background: Trimetazidine, as an anti-ischemic and antioxidant agent, has been demonstrated to have many cardioprotective effects. However, whether early administration of trimetazidine has an effect on diabetic cardiomyopathy and the mechanisms underlying the effect have not yet been elucidated.Methods: We established a type 2 DCM rat model by high-fat diet and low-dose streptozotocin. Rats were separated into different groups: control, diabetes, and diabetes + trimetazidine (n = 6, each). Cardiac autophagy, cardiac functions, and cardiomyocyte apoptosis were monitored.Results: Rats with type 2 DCM showed severe insulin resistance, left ventricular dysfunction, increased cardiomyocyte apoptosis, and reduced cardiac autophagy. Collagen volume fraction (CVF) and perivascular collagen area/luminal area (PVCA/LA) ratio were significantly higher in the diabetic group than the control group. We found that trimetazidine treatment ameliorated metabolic disturbance and insulin resistance, reduced cardiomyocyte apoptosis, and restored cardiac autophagy. CVF and PVCA/LA ratio were also lower in the diabetes + trimetazidine group than the diabetic group (CVF, 4.75 ± 0.52 % vs. 11.04 ± 1.67 %, p < 0.05; PVCA/LA, 8.37 ± 0.51 vs. 17.97 ± 2.66, p < 0.05). Furthermore, trimetazidine inhibited phosphorylation of ERK and P38 MAPK to reduce myocardial fibrosis. Inhibited phosphorylation of AMPK was restored and the interaction between Bcl-2 and Beclin1 was enhanced in diabetes + trimetazidine group, resulting in the initiation of autophagy and alleviation of apoptosis.Conclusions: Early administration of trimetazidine could ameliorate diabetic cardiomyopathy by inhibiting myocardial fibrosis and cardiomyocyte apoptosis and enhancing autophagy. Therefore, trimetazidine may be a good choice in the prevention of diabetic cardiomyopathy if applied at the early stage of diabetes. [ABSTRACT FROM AUTHOR]