Delocalized Chern character for stringy orbifold K-theory

In this paper, we define a stringy product on K^*_{orb}(\XX) \otimes \C , the orbifold K-theory of any almost complex presentable orbifold \XX. We establish that under this stringy product, the de-locaized Chern character ch_{deloc} : K^*_{orb}(\XX) \otimes \C \longrightarrow H^*_{CR}(\XX), after a canonical modification, is a ring isomorphism. Here H^*_{CR}(\XX) is the Chen-Ruan cohomology of \XX. The proof relies on an intrinsic description of the obstruction bundles in the construction of Chen-Ruan product. As an application, we investigate this stringy product on the equivariant K-theory $K^*_G(G)$ of a finite group $G$ with the conjugation action. It turns out that the stringy product is different from the Pontryajin product (the latter is also called the fusion product in string theory).Comment: 34 pages. Final version to appear in Trans. of AMS. Improve the expositions and Change of the title thanks the referee

Political Economy of Village Governance in Contemporary China

Thesis (PhD) - Indiana University, Political Science, 2006Rural development and transformation in post-Mao China is one of the most remarkable scenarios in transition countries. With the dismantlement of collectivized farming and the rural reforms since the late 1970s, villages have become diverse in terms of institutional structure. In some villages, one or a few cadres still dominate decision making over public affairs, while, in others, villagers actively participate in the decision making in one way or another. How do the different institutional structures of villages influence governance performance in terms of providing public goods and services? Do the villages with more peasant participation in decision making over public affairs have better performance than those with less peasant participation? This analysis is aimed at an initial answer to the questions by engaging in empirical, in-depth case studies in contemporary rural China. With the help of four Chinese scholars, I identified four villages with different institutional structures as cases for this project. I have examined and compared the four communities' governance performance in providing roads, primary schools, land allocation, and fiscal management. The findings suggest that the villages with more villager participation in decision making have better performance in providing public goods and services. The implication of the study for rural development in transition societies is to encourage peasants' participation and to draw upon their capabilities and local knowledge. The empirical data for the study rely on my field research of six months in the four communities in 2004. The methods of collecting the data include interviews with villagers and cadres as well as extensive field observations and archival research

Cardiac abnormalities after transaortic constriction are worsened by changing glucose metabolism and benefited by repair of mitochondrial DNA.

Heart failure is a leading cause of morbidity and mortality in the USA. During the development of heart failure, many cardiac parameters change at the same time including fuel metabolism, oxidative stress and mitochondrial function. Each of these changes occurs in the context of multiple other abnormalities in the failing heart. This complexity makes it difficult to discern the importance of each of these parameters. In this dissertation changes in glucose metabolism and mitochondrial DNA repair have been targeted separately and specifically in the heart to test their roles in heart failure independently. Abnormal glucose metabolism is always found in heart failure patients. During heart failure there is a significant increase in cardiac glycolysis. On the other hand, diabetic patients, who are at increased risk of heart failure show the opposite change in glucose metabolism, their level of glycolysis goes down. In these studies separate lines of transgenic mice with increased or decreased glycolysis were used to test if these changes in glucose metabolism altered the development of heart failure induced by pressure overload after transaortic constriction (TAC) surgery. Cardiac glycolysis was targeted by 2 transgenes that alter the level of fructose-2 ,6-P2 (F-2,6-P2), which activates phosphofrucokinase. The Mb trans gene reduces F-2,6-P2 and slows glycolysis. The Mk transgene increases F-2,6-P2 and speeds glycolysis. Mb and Mk transgenic hearts had normal structure and function after sham surgery but they were both much more susceptible to damage from T AC surgery than non-transgenic mice. In both lines of mice TAC produced more fibrosis, more collagen expression, greater hypertrophy, lower fractional shortening, higher lung weight and reduced energy reserves. Mb mice also showed more oxidative stress. These results indicate loss of cardiac flexibility to control glucose metabolism is detrimental to the heart. Cardiac failure is associated with increased levels of oxidized mitochondrial DNA (mtDNA). It is not known if oxidized mtDNA contributes to cardiac dysfunction. To test if protection of mtDNA can reduce cardiac injury, we produced transgenic mice with cardiomyocyte-specific overexpression of the mitochondrial form of the DNA repair enzyme 8-oxoguanine DNA glycosylase 1 (OGG 1). OGG 1 transgenic mice demonstrated significantly lower cardiac mitochondrial levels of the DNA guanine oxidation product 7,8-dihydro-8-oxoguanine (8-oxo-dG). This was true under basal conditions, after Doxorubicin administration or after TAC. OGG 1 mice were tested for protection from TAC surgery. Compared to FVB-TAC mice, hearts from OGG 1-TAC mice had lower levels of ß-MHC mRNA but they did not display significant differences in hypertrophy or function. The principle benefit of OGG 1 overexpression was a significant decrease in T AC induced cardiac fibrosis, indicated by reduced Sirius Red staining and by significantly decreased induction of collagen 1 and 3 mRNA expression. These results provide a new model to assess the cardiac effects of mtDNA damage and demonstrate that oxidation of mtDNA contributes to cardiac pathology

The changes of fructos-2,6-bisphosphate level in transgenic mice causing cardiomyopathy.

Heart failure is recognized as a major cause of death among diabetics. In type I and II diabetes, glucose uptake, glycolysis and pyruvate oxidation are impaired, and fatty acid utilization increases. These alterations in metabolism contribute toward cardiac contractile function. There is a gap in our understanding on how alterations in glycolytic metabolite fructose-2,6-bisphosphate (F-2,6-P 2 ) affects cardiac dysfunction. Two cardiac-specific overexpression of PFK-2 (phosphofructose kinase-2) transgenic models were used to investigate the role of altered metabolism by F-2,6-P 2 in provoking cardiomyopathy. One model is with the PFK-2 kinase active and phosphatase inactive enzyme called MK and another model is the PFK-2 kinase inactive and phosphatase active enzyme called Mb. The effect of PFK2 transgenes was evaluated by Langendorff-perfused heart in vitro. Cardiomyopathy was assessed by measurement of heart to body weight ratio and cardiac histology. The study shows that changes in F-2,6-P 2 level could induce cardiac hypertrophy and fibrosis and cause cardiac dysfunction, and may be important to development of diabetic cardiomyopathy

Field Tuning of Linear Resonant Actuators Using Motion Sensor Feedback

Linear resonant actuators (LRAs) create tactile feedback in consumer devices by generating vibrations. LRA characteristics can change with time due to environmental conditions, thereby degrading the performance of the LRA. Variations in LRA performance can be compensated during operation by using techniques of parameter detection, measurement, and correction, which themselves rely on accurate back EMF measurement. A back EMF test is accurate so long as the LRA is stationary, the device is lying on a flat, vibration-free surface, and is free of external movement. This disclosure describes techniques that ensure accurate measurement of LRA parameters by performing back EMF measurements when onboard motion sensors indicate zero or low device motion

Screening Retinopathy of Prematurity in Extremely Low Birth Weight Infants in China and the Need for Earlier Screening Times

Purpose. To convey the need for a revised screening strategy for retinopathy of prematurity (ROP) for extremely low birth weight (ELBW) infants in China. Design. A retrospective longitudinal study. Methods. The medical charts of infants with a birth weight (BW) of less than 1 kg were reviewed. The infants were divided into three groups: group A, without ROP; group B, with ROP but not up to type 1 prethreshold or threshold ROP; group C, with type 1 prethreshold or threshold ROP. Data collected included gender, gestational age (GA), BW, postmenstrual age (PMA), age of onset of ROP, and age at which treatment was carried out, if required. Results. A total of 77 infants were involved. Fifty-six infants developed ROP at any stage and 38 infants developed type 1 prethreshold or threshold ROP. The mean BW and GA of infants in group A were significantly different compared with groups B and C. The mean PMA of onset of ROP in infants who developed mild ROP was 37 weeks compared with 34 weeks for infants who developed severe ROP. Conclusion. ELBW infants have a higher incidence of ROP in China which highlights the need for optimizing neonatal care for these infants. In ELBW infants, ROP tends to develop more severely when it occurs earlier. It is necessary for ELBW infants, especially for those with a BW less than 800 g or a GA less than 25 weeks, to be initially screened at an earlier time