A method to experimentally investigate injection-induced activation of fractures

Natural fractures are generally well developed in most hydrocarbon and geothermal reservoirs,which can produce complex fracture networks due to the activation of fractures during hydraulic stimulation.The present paper is devoted to developing a method to investigate the activation characteristics of fracture under injection-shearing coupled condition at laboratory scale.The fluid is injected into the single-fractured granite until the fracture is activated based on the triaxial direct shear tests.The results show that injection process can significantly influence the shear stress distribution field,resulting in release of shear stress and relative slip between the opposite sides of the fractured surface.The injectioninduced activation of fracture is strongly dependent on the stress states.When the normal stress increases,the injection-induced activation pressure increases,and the comparatively high normal stress can restrain the fracture activation.The fracture deformation mechanisms during fluid injection are also discussed preliminarily with the experimental data.The sensitivity of shear stress to fluid injection increases with increase of shear stress level,while it decreases under high normal stress.The results can facilitate our understanding of the natural fracture activation behavior during fluid pressure stimulation.

Degradation effects on dichlorvos by a biocontrol strain,Trichoderma atroviride T23

Excessive use of organophosphate pesticides(OP),such as dichlorvos,in farming system poses a threat to human health through potential contamination of environment.To date,biodegradation has been prospected most promising approach to eliminate environmental OP residues.Trichoderma species as a biological control microorganism is often exposed to the chemical pesticides applied in environments,so it is necessary to understand the mechanism of degradation of dichlorvos by Trichoderma.In this study,dichlorvos significantly inhibited the growth,sporulation and pigmentation of T.atroviride T23,and the dichlorvos degradation activity of T23 required the initial induction effect of dichlorvos and the culture conditions,including the nutrient and pH values of the medium.Various changed primary and secondary metabolites released from T23 in the presence of dichlorvos were speculated as the energy and antioxidants for the strain itself to tolerate dichlorvos stress.The results showed that T23 could produce a series of enzymes,especially the intracellular enzymes,to degrade dichlorvos.The activities of the intracellular enzyme generated by T23 were differentially changed along time course and especially relied on initial dichlorvos concentration,ammonium sulfate and phosphate added in the medium.In conclusion,some dichlorvos-induced chemical degradation related enzymes of T23 were proved to be involved in the degradation of dichlorvos.

Effects of compressing and remelting in SIMA processing on semi-solid structure evolution of an Al-Zn wrought alloy

Structure evolution of an Al-Zn wrought alloy in remelting processing in thestrain induced melt activated (SIMA) serai-solid procedure was observed, and effects of factors, theremelting temperature, the holding time, and the compression strain, on structures and grain sizesof the alloy were investigated. The results show that (1) the proper temperature of remelting is inthe range of 610 to 615℃; (2) the grain size in specimen with greater compression strain is smallerthan that with smaller compression strain in condition of the same remelting temperature andholding time, and the grain size in local area with great local equivalent strain is smaller thanthat with small one; (3) liquid occurs in form of cluster in matrix during remelting and itsquantity increases with remelting time increasing; liquid in specimen with great compression strainoccurs earlier than that with small one, and quantity of liquid in the center of specimen withgreater local equivalent strain is greater than that in the two ends of it; (4) distortion energyafter deforming in matrix of the alloy is the significant factor to activate melting of matrix atlocal area with great local equivalent strain.

Effect of IFNα-2a on Fas expression and apoptosis rate of peripheral blood cytotoxic T cells in patients with hepatitis B

Interferon(IFN) with antiviral and im-munomodulatory activities is one of the most important therapeutic agents for the treatment of chronic hepatitis. The apoptotic effect of IFN is influenced by cell type and the types of IFN, which suppresses proliferation and induces apoptosis in some cell types while inhibiting apoptosis in others. The aim of this study was to explore the effect of IFNα-2a on Fas expression and the apoptosis rate of peripheral blood cytotoxic T cells (CTLs) in patients with hepatitis B. METHODS:Peripheral blood mononuclear cells were isolated from 26 patients with hepatitis B including 16 patients with chronic hepatitis B and 10 patients with chronic severe hepatitis B. Fas expression and apoptosis rate of CTLs were analyzed with flow cytometry before and after IFNα-2a treatment. RESULTS:Before IFNα-2a treatment, Fas expression and apoptosis rate of CTLs from patients with chronic hepatitis B were significantly higher than those from patients with chronic severe hepatitis B and healthy controls respectively. No significant difference was observed between Fas expression and apoptosis rate of CTLs from patients with chronic severe hepatitis B and healthy controls. After IFNα-2a treatment,Fas expression and apoptosis rate of CTLs from different groups were compared with those before IFNα-2a treatment, showing no significant difference despite alternation of different degree. CONCLUSIONS:Activation induced cell death (AICD) exists in peripheral blood CTLs from patients with hepatitis B. No effect of IFNα-2a exerts on Fas expression and apoptosis rate of Fas in patients with hepatitis B.

The Function and Meaning of Receptor Activator of NF-κB Ligand in Arterial Calcification

Osteoclast-like cells are known to inhibit arterial calcification. Receptor activator of NF-κB ligand（RANKL） is likely to act as an inducer of osteoclast-like cell differentiation. However,several studies have shown that RANKL promotes arterial calcification rather than inhibiting arterial calcification. The present study was conducted in order to investigate and elucidate this paradox. Firstly,RANKL was added into the media,and the monocyte precursor cells were cultured. Morphological observation and Tartrate resistant acid phosphatase（TRAP） staining were used to assess whether RANKL could induce the monocyte precursor cells to differentiate into osteoclast-like cells. During arterial calcification,in vivo and in vitro expression of RANKL and its inhibitor,osteoprotegerin（OPG）,was detected by real-time PCR. The extent of osteoclast-like cell differentiation was also assessed. It was found RANKL could induce osteoclast-like cell differentiation. There was no in vivo or in vitro expression of osteoclast-like cells in the early stage of calcification. At that time,the ratio of RANKL to OPG was very low. In the late stage of calcification,a small amount of osteoclast-like cell expression coincided with a relatively high ratio of RANKL to OPG. According to the results,the ratio of RANKL to OPG was very low during most of the arterial calcification period. This made it possible for OPG to completely inhibit RANKL-induced osteoclast-like cell differentiation. This likely explains why RANKL had the ability to induce osteoclast-like cell differentiation but acted as a promoter of calcification instead.

The influence of HDL and purified apoprotein E on platelet activation induced by serotonin

Elevated plasma levels of high density lipoprotein (HDL) are recognized as having a beneficial influence on the progression of atherosclerosis. As platelets are closely involved in atherosclerogenesis, it is difficult to evaluate if the protective effect of HDL is associated with its ability to affect platelet structure and function. Previous studies give conflicting reports concerning the HDL platelet interaction. In our in vitro experiments, washed human blood platelets were preincubated with HDL (100 800 μg/ml) and then stimulated by serotonin (5 Hydroxytryptamine, 1 5 μM), a potent agonist and mediator in the process of atherosclerosis. Aggregatory studies and electron microscopy revealed that HDL could not prevent morphological alterations of blood platelets treated with serotonin. Furthermore, high dosages of HDL led to platelet activation. These findings indicate that HDL may not inhibit agonist induced platelet activation. As HDL is a heterogeneous group of different subclasses with opposite effects on platelet function, it Platelet Research Unit, Institute of Anatomy, University of Münster, Germany (Pfennig O and Dierichs R) Institute of Physiology, Ruhr University Bochum, Bochum, Germany (Liu B) can be concluded that HDL platelet interaction reflects relative concentrations of the particular sample. Our findings suggest that the protective influence of HDL may not be associated with decreased platelet function. Apoprotein E rich subclasses of HDL (HDL 2), particularly HDL enriched apoprotein E (HDL E), inhibit agonist induced platelet activation. In order to enlighten the role of apo E in this process, platelets in suspensions were preincubated with purified apoprotein E (50 400 μg/ml) and then stimulated by serotonin (5 μM). Apoprotein E of 300 μg/ml prevented morphological alterations of blood platelets and suppressed serotonin induced activation. Lower concentrated apoprotein E showed no clear effects. There is evidence that apoprotein E is an important factor in the prevention of atherosclerosis, by enhancing the reversed cholesterol transport to the liver and modifiing the functional status of different cell types such as macrophages and smooth muscle cells. Because results showed effects of apo R on platelet activation, we suggest that apoprotein E may be a principal factor when platelet aggregability is suppressed by HDL subclasses or liposomes and that the antiatherogenic potency of apo E correlates with this process.