Chinese Academy | Date: 2012-09-19
The present invention provides a device system structure based on hybrid orientation SOI and channel stress and a preparation method thereof. According to the preparation method provided in the present invention, first, a (100)/(110) global hybrid orientation SOI structure is prepared; then, after epitaxially growing a relaxed silicon-germanium layer and strained silicon layer sequentially on the global hybrid orientation SOI structure, an (110) epitaxial pattern window is formed; then, after epitaxially growing a (110) silicon layer and a non-relaxed silicon-germanium layer at the (110) epitaxial pattern window, a surface of the patterned hybrid orientation SOI structure is planarized; then, an isolation structure for isolating devices is formed; and finally, a P-type high-voltage device structure is prepared in a (110) substrate portion, an N-type high-voltage device structure and/or low voltage device structures are prepared in the (100) substrate portion. In this manner, a carrier mobility is improved, Rdson of a high-voltage device is reduced, and performance of devices are improved, thereby facilitating further improvement of integration and reduction of power consumption.
Chinese Academy | Date: 2011-09-25
The present invention provides an equivalent electrical model of a Silicon On Insulator (SOI) Field Effect Transistor (FET) of a body leading-out structure, and a modeling method thereof. The equivalent electrical model is formed by an internal FET and an external FET connected in parallel, where the SOI FET of a body leading-out structure is divided into a body leading-out part and a main body part, the internal FET represents a parasitic transistor of the body leading-out part, and the external FET represents a normal transistor of the main body part. The equivalent electrical model provided in the present invention completely includes the influence of parts of a physical structure of the SOIMOSFET device of a body leading-out structure, that is, the body leading-out part and the main body part, on the electrical properties, thereby improving a fitting effect of the model on the electrical properties of the device.
News Article | August 30, 2016
In an effort to determine if stem cell therapy can prevent or improve a condition called "diabetic foot" caused by poor blood flow in patients with diabetes, a team of researchers in China has found that transplanting human placenta-derived mesenchymal stem cells (MSCs) into rats modeled with diabetes can affect blood vessel growth, potentially improving blood flow and preventing critical limb ischemia (CLI), a condition that results in diabetic foot and frequently leads to amputation. The study will be published in a future issue of Cell Transplantation and is currently freely available on-line as an unedited, early epub at: http://www.ingentaconnect.com/content/cog/ct/pre-prints/content-ct-1594_liang_et_al "CLI describes an advanced stage of peripheral artery disease characterized by obstruction of the arteries and a markedly reduced blood flow to the extremities. CLI is associated with high rates of mortality and morbidity, putting the patients at high-risk for major amputation," said study co-author Dr. Zhong Chao Han of the Beijing Institute of Stem Cells, Health and Biotech. "Mesenchymal stem cells are ideal candidates for transplantation because they have both angiogenic (potential to form new blood vessels) and immunomodulatory properties and are capable of differentiating into three different lineages. The utility of placenta-derived MSCs is poorly understood, so we sought to investigate the efficacy of combined regular therapy and cell therapy in treating diabetes-related CLI." According to the researchers, human placenta was obtained from full-term cesarean section deliveries with written informed consent of the mother. The use of human-derived cells was approved by the Institutional Biomedical Research Ethics Committee of the Chinese Academy of Medical Science and Peking Union Medical College. After injection into rats surgically modeled with CLI, the stem cells were traced and counted at various points in time. The researchers found that the stem cell counts decreased dramatically over time, but a few cells differentiated into vascular cells. The infused cells also secreted cytokines, which are small proteins secreted by cells that have a specific effect on the interactions and communications between cells. "We believe that cytokines secreted by MSCs attract endothelial cells, a type of cells that make up the tissues lining the interior surface of blood vessels," said the researchers. "These cells participate in building new vascular tissues and also inhibit inflammation." The researchers concluded that their experimental data implied that MSCs improved ischemia recovery in diabetic rats via direct cell differentiation and paracrine (protein-mediated) mechanisms, although the two mechanisms exist simultaneously. The paracrine mechanisms, said the researchers, were likely more important than direct cell differentiation. "So far, MSC therapy represents a simple, safe and effective therapeutic approach for diabetes and its complications," the researchers concluded. "Our studies lay the groundwork for the transition from the experimental bench to the clinical bedside." "Diabetes is becoming more prevalent across the globe and stem cell therapy may be a vital approach to serious vascular complications," said Dr. Maria Carolina Oliveira Rodrigues of the Ribeirão Preto Medical School - University of São Paulo, Brazil and section editor of Cell Transplantation. "Future studies should aim to expound upon previous findings in MSC transplantation studies and confirm the efficacy of placenta-derived MSCs for CLI."
On one hand, a UK-based animal genetics firm was able to breed pigs totally immune to PRRSv, a previously incurable porcine syndrome that costs farmers hundreds of millions of euros per year. At the same time another team of researchers, also based in the UK, engineered a genetic change in malaria-transmitting mosquitoes which would see their population fall dramatically – eventually stopping malaria from spreading. Both findings were made possible by using CRISPR-Cas9, a novel technology that enables scientists not only to easily cut and paste genes as they like, but also to ensure that the newly-created traits are inherited and spread rapidly through populations. The new technique is about 1 000 cheaper than other gene modification techniques. But while scientists generally hail the performance – and as businesses get ready to take over this emerging market – ideas of using CRISP-Cas9 to get rid of human diseases or even bolster genetic traits like intelligence, beauty or strength are causing concerns. Many say that it is too soon and potentially too dangerous to modify the human genome in a way that is passed down to the next generation, and that the complexity of biological systems would most likely result in unforeseen consequences. This week in Washington, a panel of experts met to decide on whether or not the technology should be banned altogether. 'We could be on the cusp of a new era in human history,' Nobel laureate David Baltimore of the California Institute of Technology said in the introduction of international summit. 'The overriding question is when, if ever, would we want to use gene editing to change human inheritance?' After three days of debate, panelists released a consensus document that leaves the door open and makes three recommendations. First, that basic and preclinical research is clearly needed and should continue. Then, that gene editing of somatic cells – whose genome is not transmitted to the next generation – should be carefully evaluated and regulated. And finally, that it would be irresponsible at this point to proceed with germ-line editing. China's recent experiment in the field, which saw 86 embryos being modified to alter the gene that causes thalassemia, eventually resulted in only a handful surviving with not all of them having the correct edits – certainly is a case in point. Although fruitful, these discussions barely scratched the surface of the gene editing ethical challenge. The organizers – the U.S. National Academies of Sciences, Engineering and Medicine; the United Kingdom's Royal Society; and the Chinese Academy of Science – acknowledged that it is only the first step and that more countries and stakeholders should be involved in the future. However a question remains open: will the regulatory measures be able to keep up with the science? Judging by the comments of Dana Carroll of the University of Utah, who said that 'germline applications will be done, probably before anyone in this room is ready for it', or by the enthusiasm of families who have been afflicted by a genetic disease generations, there certainly is room for doubt. Explore further: UNESCO experts call for ban on genetic 'editing'
Certain antibiotic resistance genes are easily transferred from one bacterial species to another, and can move between farm animals and the human gut. A team led by Chinese researchers has characterized this "mobile resistome," which they say is largely to blame for the spread of antibiotic resistance. They found that many antibiotic resistance genes that are shared between the human and animal gut microbiome are also present in multiple human pathogens. These findings are published September 9 in Applied and Environmental Microbiology, a journal of the American Society for Microbiology. "This is an incredibly robust study," said Harold Drake, PhD, editor of the journal. "The so-called "transfer network" of antibiotic resistance genes described in the paper is very forward reaching and will have great impact not only on our understanding of this modern microbial dilemma but also on how human healthcare agencies and research institutes attempt to cope with it." In China, the human and chicken gut microbiomes share 36 mobile resistance genes, said corresponding author Baoli Zhu, PhD, professor of pathogenomics, University of Chinese Academy of Sciences Medical School. The human gut microbiomes in China, Europe, and the US share more mobile resistance genes with the chicken gut microbiome than with any other livestock gut microbiomes. Among 84 mobile antibiotic resistance genes shared between at least two gut databases, 41 had recently moved between human and animal guts, said Zhu. Collectively, genes from among these 41 are capable of disabling all of six major classes of antibiotics, including tetracyclines, aminoglycosides, and beta-lactams. Transfer of resistance genes between bacterial species occurs chiefly among four of the 11 major bacterial phyla—Proteobacteria, Firmicutes, Bacteroidetes, and Actinobacteria, said Zhu. The investigators found a total of 515 mobile resistance genes, which were distributed among 790 individual bacterial species. The resistance gene sharing can be quite promiscuous. "We found a total of 11 species that each shared at least one mobile [resistance gene] with more than 200 other species," the investigators wrote. The species displaying the most sharing of resistance genes were E. coli, Bacteroides fragilis, and Staphylococcus aureus, all of which can be pathogenic. These species shared resistance genes with 302, 266, and 260 other species, respectively. The network of horizontal gene transfer is shaped largely by phylogeny and ecological constraints, said Zhu. That is, resistance gene transfers from one species of bacteria to another are more common within the same phylum than between different phyla, and more common within a single microbiome than between microbiomes. On the latter point, the investigators wrote that successful gene transfer requires contact between donor and recipient. The recent mobile resistance gene transfer that has taken place between livestock and human gut microbiomes is especially important for policy-makers. Much of the resistance in farm animals is generated by feeding them large quantities of antibiotics, which is done because it encourages the animals to grow faster. "One consideration, from the worldwide ecological view, is that bacteria of animal origin may face more antibiotic selection pressure because more antibiotics (nearly 80 percent in the United states) are consumed by animals as growth-promotors, infection prevention, and clinical treatments," the investigators wrote. "The high exchange frequency of mobile [antibiotic resistance genes] between animals and humans or environmental bacteria is also noteworthy."