Role of strain in the blistering of hydrogen-implanted silicon

The authors investigated the physical mechanisms underlying blistering in hydrogen-implanted silicon by examining the correlation between implantation induced damage, strain distribution, and vacancy diffusion. Using Rutherford backscattering, scanning electron microscopy, and atomic force microscopy, they found that the depth of blisters coincided with that of maximum implantation damage. A model based on experimental results is presented showing the effect of tensile strain on the local diffusion of vacancies toward the depth of maximum damage, which promotes the nucleation and growth of platelets and ultimately blisters. © 2006 American Institute of Physics

Plasma hydrogenation of strained Si/SiGe/Si heterostructure for layer transfer without ion implantation

We have developed an innovative approach without the use of ion implantation to transfer a high-quality thin Si layer for the fabrication of silicon-on-insulator wafers. The technique uses a buried strained SiGe layer, a few nanometers in thickness, to provide H trapping centers. In conjunction with H plasma hydrogenation, lift-off of the top Si layer can be realized with cleavage occurring at the depth of the strained SiGe layer. This technique avoids irradiation damage within the top Si layer that typically results from ion implantation used to create H trapping regions in the conventional ion-cut method. We explain the strain-facilitated layer transfer as being due to preferential vacancy aggregation within the strained layer and subsequent trapping of hydrogen, which lead to cracking in a well controlled manner. © 2005 American Institute of Physics

H-induced platelet and crack formation in hydrogenated epitaxial Si/Si <inf>0.98</inf>B <inf>0.02</inf>/Si structures

An approach to transfer a high-quality Si layer for the fabrication of silicon-on-insulator wafers has been proposed based on the investigation of platelet and crack formation in hydrogenated epitaxial Si Si0.98 B0.02 Si structures grown by molecular-beam epitaxy. H-related defect formation during hydrogenation was found to be very sensitive to the thickness of the buried Si0.98 B0.02 layer. For hydrogenated Si containing a 130 nm thick Si0.98 B0.02 layer, no platelets or cracking were observed in the B-doped region. Upon reducing the thickness of the buried Si0.98 B0.02 layer to 3 nm, localized continuous cracking was observed along the interface between the Si and the B-doped layers. In the latter case, the strains at the interface are believed to facilitate the (100)-oriented platelet formation and (100)-oriented crack propagation. © 2006 American Institute of Physics

β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death

Tumor necrosis factor (TNF)-alpha induces caspase-independent cell death in the fibrosarcoma cell line L929. This cell death has a necrotic phenotype and is dependent on production of reactive oxygen species (ROS) in the mitochondria. To identify genes involved in this TNF-induced, ROS-dependent cell death pathway, we utilized retrovirus insertion-mediated random mutagenesis to generate TNF-resistant L929 cell lines and we subsequently identified genes whose mutations are responsible for the TNF-resistant phenotype. In one such resistant line, beta-actin was disrupted by viral insertion, and subsequent reconstitution of P-actin expression levels in the mutant line Actin(mut) restored its sensitivity to TNF Resistance to TNF in Actin(mut) cells is signal specific since the sensitivity to other death stimuli is either unchanged or even increased. Comparable NF-kappaB activation and p38 phosphorylation in TNF-treated wild-type and Actin(mut) cells also indicates that reduced expression of actin only selectively blocked some of the TNF-induced cellular changes. Actin cleavage involved in apoptosis does not occur in TNF-treated L929 cell death, as in HeLa cells. Consistent over-expression of a caspase-cleaved product, a 15 kDa actin fragment, had no effect on TNF-induced necrosis of L929 cell. By contrast, TNF-induced mitochondria clustering and ROS production were dramatically reduced in Actinmut cells, indicating that actin-deficiency-mediated TNF resistance is most likely due to impaired mitochondrial responses to TNF stimulation. Our findings suggest that a full complement of actin is required for transduction of a cell death signal to mitochondria in TNF-treated L929 cells

The detector system of the Daya Bay reactor neutrino experiment

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DNMT3a methylation in neuropathic pain

Cuijie Shao,&nbsp;Yong Gao,&nbsp;Dan Jin,&nbsp;Xin Xu,&nbsp;Shuying Tan,&nbsp;Hui Yu,&nbsp;Qingxiang Zhao,&nbsp;Li Zhao,&nbsp;Wansheng Wang,&nbsp;Deqiang Wang Department of Pain, Binzhou Medical University Hospital, Binzhou, China Background: Mu opioid receptor (MOR) plays a crucial role in mediating analgesic effects of opioids and is closely associated with the pathologies of neuropathic pain. Previous studies have reported that peripheral nerve injury downregulates MOR expression, but the epigenetic mechanisms remain unknown.Objective:&nbsp;Therefore, we investigated DNA methyltransferase3a (DNMT3a) expression or methylation changes within MOR promoter in the spinal cord in a neuropathic pain induced by a chronic constriction injury (CCI) mouse model and further determined whether these injury-associated changes are reversible by pharmacological interventions.Methods: A CCI mouse model was established and tissue specimens of lumbar spinal cords were collected. The nociception threshold was evaluated by a Model Heated 400 Base. DNMT3a and MOR mRNA and protein level were detected by real-time-polymerase chain reaction and Western blot, respectively. Methylation of DNMT3a gene was measured by methylation-specific PCR.Results: Our data showed that chronic nerve injury led to a significant upregulation of DNMT3a expression that was associated with increased methylation of MOR gene promoter and decreased MOR protein expression in the spinal cord. Inhibition of DNMT3a catalytic activity with DNMT inhibitor RG108 significantly blocked the increase in methylation of the MOR promoter, and then upregulated MOR expression and attenuated thermal hyperalgesia in neuropathic pain mice.Conclusion: This study demonstrates that an increase of DNMT3a expression and MOR methylation epigenetically play an important role in neuropathic pain. Targeting DNMT3a to the promoter of MOR gene by DNMT inhibitor may be a promising approach to the development of new neuropathic pain therapy. Keywords: DNMT3A, pain, MOR, RG108, neuropathic pai

Selenium supplementation increases renal glomerular filtration rate.

Selenium (Se) is a trace element variously distributed in the human body and especially concentrated in certain organs, such as the renal cortex. We report results obtained during a ten weeks' oral Se supplementation. Experiments were devised to evaluate previous preliminary observations which suggested a possible effect of Se addition on the renal glomerular filtration rate. Eleven healthy volunteers have given increasing oral Se (as a sodium selenite solution) as follows: on the first week they have given 100 micrograms Se per day; this was progressively increased 100 micrograms per day for each of the following 6 weeks; the last dose (700 micrograms per day) was maintained for three further weeks. Serum and 24-hour urine were collected weekly for creatinine determination by kinetic Jaff\ue9 reaction and Se measurement by proton-induced X ray emission (PIXE). The final mean serum creatinine concentration was 13% lower than the initial mean value (p less than 0.01). Mean creatinine clearance increased significantly (p less than 0.05) and showed a direct correlation with mean Se clearance (r = 0.79; p less than 0.001). As the increase of creatinine clearance was concomitant with a reduction of serum creatinine levels, we excluded the possibility of toxic effects. Our results seem to suggest a positive influence of Se supplementation on the rate of glomerular filtration and we hypothesize that Se might be involved in the vascular regulatory mechanism of the kidney

beta-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death

Tumor necrosis factor (TNF)-alpha induces caspase-independent cell death in the fibrosarcoma cell line L929. This cell death has a necrotic phenotype and is dependent on production of reactive oxygen species (ROS) in the mitochondria. To identify genes involved in this TNF-induced, ROS-dependent cell death pathway, we utilized retrovirus insertion-mediated random mutagenesis to generate TNF-resistant L929 cell lines and we subsequently identified genes whose mutations are responsible for the TNF-resistant phenotype. In one such resistant line, beta-actin was disrupted by viral insertion, and subsequent reconstitution of P-actin expression levels in the mutant line Actin(mut) restored its sensitivity to TNF Resistance to TNF in Actin(mut) cells is signal specific since the sensitivity to other death stimuli is either unchanged or even increased. Comparable NF-kappaB activation and p38 phosphorylation in TNF-treated wild-type and Actin(mut) cells also indicates that reduced expression of actin only selectively blocked some of the TNF-induced cellular changes. Actin cleavage involved in apoptosis does not occur in TNF-treated L929 cell death, as in HeLa cells. Consistent over-expression of a caspase-cleaved product, a 15 kDa actin fragment, had no effect on TNF-induced necrosis of L929 cell. By contrast, TNF-induced mitochondria clustering and ROS production were dramatically reduced in Actinmut cells, indicating that actin-deficiency-mediated TNF resistance is most likely due to impaired mitochondrial responses to TNF stimulation. Our findings suggest that a full complement of actin is required for transduction of a cell death signal to mitochondria in TNF-treated L929 cells