Browsing by Author "Ma, J"
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Item Open Access Analysis of main risk factors causing stroke in Shanxi Province based on machine learning models(Informatics in Medicine Unlocked, 2021-01-01) Liu, J; Sun, Y; Ma, J; Tu, J; Deng, Y; He, P; Li, R; Hu, F; Huang, H; Zhou, X; Xu, SBackground: In China, stroke has been the first leading cause of death in recent years. It is a major cause of long-term physical and cognitive impairment, which bring great pressure on the National Public Health System. On the other hand, China is a big country, evaluation of the risk of getting stroke is important for the prevention and treatment of stroke in China. Methods: A data set with 2000 hospitalized stroke patients in 2018 and 27583 residents during the year 2017 to 2020 is analyzed in this study. With the cleaned data, three models on stroke risk levels are built by using machine learning methods. The importance of “8+2” factors from China National Stroke Prevention Project (CSPP) is evaluated via decision tree and random forest models. The importance of more detailed features and their SHAP values are evaluated and ranked via random forest model. Furthermore, a logistic regression model is applied to evaluate the probability of getting stroke for different risk levels. Results: Among all “8+2” risk factors of getting stroke, the decision tree model reveals that top three factors are Hypertension (0.4995), Physical Inactivity (0.08486) and Diabetes Mellitus (0.07889), and the random forest model shows that top three factors are Hypertension (0.3966), Hyperlipidemia (0.1229) and Physical Inactivity (0.1146). In addition to “8+2” factors the importance of features for lifestyle information, demographic information and medical measurement are evaluated via random forest model. It shows that top five features are Systolic Blood Pressure (SBP) (0.3670), Diastolic Blood Pressure (DBP) (0.1541), Physical Inactivity (0.0904), Body Mass Index (BMI) (0.0721) and Fasting Blood Glucose (FBG)(0.0531). SHAP values show that DBP, Physical Inactivity, SBP, BMI, Smoking, FBG, and Triglyceride(TG) are positively correlated to the risk of getting stroke. High-density Lipoprotein (HDL) is negatively correlated to the risk of getting stroke. Combining with the data of 2000 hospitalized stroke patients, the logistic regression model shows that the average probabilities of getting stroke are 7.20%±0.55% for the low-risk level patients, 19.02%±0.94% for the medium-risk level patients and 83.89%±0.97% for the high-risk level patients. Conclusion: Based on the census data from Shanxi Province, we investigate stroke risk factors and their ranking. It shows that Hypertension, Physical Inactivity, and Overweight are ranked as the top three high stroke risk factors in Shanxi. The probability of getting a stroke is also estimated through our interpretable machine learning methods.Item Open Access Dysferlin, annexin A1, and mitsugumin 53 are upregulated in muscular dystrophy and localize to longitudinal tubules of the T-system with stretch.(Journal of neuropathology and experimental neurology, 2011-04) Waddell, LB; Lemckert, FA; Zheng, XF; Tran, J; Evesson, FJ; Hawkes, JM; Lek, A; Street, NE; Lin, P; Clarke, NF; Landstrom, AP; Ackerman, MJ; Weisleder, N; Ma, J; North, KN; Cooper, STMutations in dysferlin cause an inherited muscular dystrophy because of defective membrane repair. Three interacting partners of dysferlin are also implicated in membrane resealing: caveolin-3 (in limb girdle muscular dystrophy type 1C), annexin A1, and the newly identified protein mitsugumin 53 (MG53). Mitsugumin 53 accumulates at sites of membrane damage, and MG53-knockout mice display a progressive muscular dystrophy. This study explored the expression and localization of MG53 in human skeletal muscle, how membrane repair proteins are modulated in various forms of muscular dystrophy, and whether MG53 is a primary cause of human muscle disease. Mitsugumin 53 showed variable sarcolemmal and/or cytoplasmic immunolabeling in control human muscle and elevated levels in dystrophic patients. No pathogenic MG53 mutations were identified in 50 muscular dystrophy patients, suggesting that MG53 is unlikely to be a common cause of muscular dystrophy in Australia. Western blot analysis confirmed upregulation of MG53, as well as of dysferlin, annexin A1, and caveolin-3 to different degrees, in different muscular dystrophies. Importantly, MG53, annexin A1, and dysferlin localize to the t-tubule network and show enriched labeling at longitudinal tubules of the t-system in overstretch. Our results suggest that longitudinal tubules of the t-system may represent sites of physiological membrane damage targeted by this membrane repair complex.Item Open Access Junctophilin-2 expression silencing causes cardiocyte hypertrophy and abnormal intracellular calcium-handling.(Circulation. Heart failure, 2011-03) Landstrom, AP; Kellen, CA; Dixit, SS; Van Oort, RJ; Garbino, A; Weisleder, N; Ma, J; Wehrens, XHT; Ackerman, MJJunctophilin-2 (JPH2), a protein expressed in the junctional membrane complex, is necessary for proper intracellular calcium (Ca(2+)) signaling in cardiac myocytes. Downregulation of JPH2 expression in a model of cardiac hypertrophy was recently associated with defective coupling between plasmalemmal L-type Ca(2+) channels and sarcoplasmic reticular ryanodine receptors. However, it remains unclear whether JPH2 expression is altered in patients with hypertrophic cardiomyopathy (HCM). In addition, the effects of downregulation of JPH2 expression on intracellular Ca(2+) handling are presently poorly understood. We sought to determine whether loss of JPH2 expression is noted among patients with HCM and whether expression silencing might perturb Ca(2+) handling in a prohypertrophic manner.JPH2 expression was reduced in flash-frozen human cardiac tissue procured from patients with HCM compared with ostensibly healthy traumatic death victims. Partial silencing of JPH2 expression in HL-1 cells by a small interfering RNA probe targeted to murine JPH2 mRNA (shJPH2) resulted in myocyte hypertrophy and increased expression of known markers of cardiac hypertrophy. Whereas expression levels of major Ca(2+)-handling proteins were unchanged, shJPH2 cells demonstrated depressed maximal Ca(2+) transient amplitudes that were insensitive to L-type Ca(2+) channel activation with JPH2 knockdown. Further, reduced caffeine-triggered sarcoplasmic reticulum store Ca(2+) levels were observed with potentially increased total Ca(2+) stores. Spontaneous Ca(2+) oscillations were elicited at a higher extracellular [Ca(2+)] and with decreased frequency in JPH2 knockdown cells.Our results show that JPH2 levels are reduced in patients with HCM. Reduced JPH2 expression results in reduced excitation-contraction coupling gain as well as altered Ca(2+) homeostasis, which may be associated with prohypertrophic remodeling.Item Open Access Robust Bayesian inference for multivariate longitudinal data using normal/independent distributions(Statistics in Medicine, 2013) Luo, Sheng; Ma, J; Kieburtz, KDItem Open Access Robust Bayesian inference for multivariate longitudinal data using normal/independent distributions(Statistics in Medicine, 2013) Luo, S; Ma, J; Kieburtz, KDItem Open Access Thermoelectric transport properties of CaMg 2Bi 2, EuMg 2Bi 2, and YbMg 2Bi 2(Physical Review B - Condensed Matter and Materials Physics, 2012-01-11) May, AF; McGuire, MA; Singh, DJ; Ma, J; Delaire, O; Huq, A; Cai, W; Wang, HThe thermoelectric transport properties of CaMg 2Bi 2, EuMg 2Bi 2, and YbMg 2Bi 2 were characterized between 2 and 650 K. As synthesized, the polycrystalline samples are found to have lower p-type carrier concentrations than single-crystalline samples of the same empirical formula. These low carrier concentration samples possess the highest mobilities yet reported for materials with the CaAl 2Si 2 structure type, with a mobility of ∼740 cm2/V/s observed in EuMg 2Bi 2 at 50 K. Despite decreases in the Seebeck coefficient (α) and electrical resistivity (ρ) with increasing temperature, the power factor (α2ρ) increases for all temperatures examined. This behavior suggests a strong asymmetry in the conduction of electrons and holes. The highest figure of merit (zT) is observed in YbMg 2Bi 2, with zT approaching 0.4 at 600 K for two samples with carrier densities of approximately 2×1018cm -3 and 8×1018 cm -3 at room temperature. Refinements of neutron powder diffraction data yield similar behavior for the structures of CaMg 2Bi 2 and YbMg 2Bi 2, with smooth lattice expansion and relative expansion in c being ∼35% larger than relative expansion in a at 973 K. First-principles calculations reveal an increasing band gap as Bi is replaced by Sb and then As, and subsequent Boltzmann transport calculations predict an increase in α for a given n associated with an increased effective mass as the gap opens. The magnitude and temperature dependence of α suggests higher zT is likely to be achieved at larger carrier concentrations, roughly an order of magnitude higher than those in the current polycrystalline samples, which is also expected from the detailed calculations. © 2012 American Physical Society.