Efficient Multicore Collaborative Filtering

This paper describes the solution method taken by LeBuSiShu team for track1 in ACM KDD CUP 2011 contest (resulting in the 5th place). We identified two main challenges: the unique item taxonomy characteristics as well as the large data set size.To handle the item taxonomy, we present a novel method called Matrix Factorization Item Taxonomy Regularization (MFITR). MFITR obtained the 2nd best prediction result out of more then ten implemented algorithms. For rapidly computing multiple solutions of various algorithms, we have implemented an open source parallel collaborative filtering library on top of the GraphLab machine learning framework. We report some preliminary performance results obtained using the BlackLight supercomputer.Comment: In ACM KDD CUP Workshop 201

iAssist versus conventional total knee arthroplasty in patients with varus and valgus deformities

Background: Accelerometer and gyroscope based iAssist system's accuracy in restoring the hip knee angle (HKA) in valgus and varus deformity patients is compared to that of conventional system.Methods: In this retrospective study we compared the HKA of 26 patients in iAssist group with that of 26 patients in conventional group. The knee joints were evaluated with full leg length radiographs.Results: The iAssist group patients’ post-operative hip knee angle was much near to our target angle when compared to that of patients in conventional technique group.Conclusions: iAssist brings the high accuracy associated with large console CAS systems with lower costs and helps surgeons in low volume hospitals achieve specific intra operative goals with the familiarity of conventional guides

Number of parous events affects the association between physical exercise and glycemic control among women with gestational diabetes mellitus:A prospective cohort study

BACKGROUND: Multiparous women are at a higher risk of gestational diabetes mellitus (GDM) than primiparas. Physical activity during pregnancy has been shown to be beneficial for GDM, but there is little evidence on the association between physical activity and glycemic control among women with GDM, whether primiparas or multiparas. Thus, the objective of the present study was to examine the association between physical activity and glycemic control in women with GDM and to determine what, if any, effects result from number of parous events. METHODS: A prospective cohort of 1162 women with GDM was recruited, with 604 multiparas (51.98%). The general linear model was used to calculate the risk difference and its 95% confidence interval (95%CI) to quantify the impact of parous events on glycemic control in pregnancy as well as the association between physical activity time and glycemic control. RESULTS: Among 1162 women with GDM, the median daily activity time was 65 min (interquartile range (IQR): 45–90 min), and the abnormal plasma glucose (PG) percentage, calculated as number of abnormal PG tests divided by the total number of PG tests, was 40.00% (IQR: 22.22%–66.67%). The percentage of abnormal PG was stabilized and statistically lower with daily physical activity time exceeding 60 min among primiparas (IQR: 30.89%–44.43%) and exceeding 90 min among multiparas (ranged from 27.76% to 38.82%). After adjusting for potential confounders, primiparas tended to have a lower percentage of abnormal PG than do multiparas (rate difference = –0.39, 95%CI: –3.61 to 2.84). The same amount of physical activity time was significantly less effective for multiparas than for primiparas (trend p-value < 0.01). CONCLUSION: In women with GDM, being multiparous is associated with less effective glycemic control through physical activity, such that multiparas need more physical activity to achieve glycemic control at a similar level to primiparas

Molecular Mechanisms of Hepatocellular Carcinoma Related to Aflatoxins: An Update

Hepatocellular carcinoma (hepatocarcinoma) is a major type of primary liver cancer and one of the most frequent human malignant neoplasms. Aflatoxins are I-type chemical carcinogen for hepatocarcinoma. Increasing evidence has shown that hepatocarcinoma induced by aflatoxins is the result of interaction between aflatoxins and hereditary factor. Aflatoxins can induce DNA damage including DNA strand break, adducts formation, oxidative DNA damage, and gene mutation and determine which susceptible individuals feature cancer. Inheritance such as alterations may result in the activation of proto-oncogenes and the inactivation of tumor suppressor genes and determine individual susceptibility to cancer. Interaction between aflatoxins and genetic susceptible factors commonly involve in almost all pathologic sequence of hepatocarcinoma: chronic liver injury, cirrhosis, atypical hyperplastic nodules, and hepatocarcinoma of early stages. In this review, we discuss the biogenesis, toxification, and epidemiology of aflatoxins and signal pathways of aflatoxin-induced hepatocarcinoma. We also discuss the roles of some important genes related to cell apoptosis, DNA repair, drug metabolism, and tumor metastasis in hepatocarcinogenesis related to aflatoxins

Simultaneous measurement of electrostatic charge and its effect on particle motions by electrostatic sensors array in gas-solid fluidized beds

Repeated particle-particle and particle-wall collisions and frictions lead to the generation and accumulation of electrostatic charges in the gas-solid fluidized beds. Variations of electrostatic signals are a rich source of information on particle motions and charging, which have rarely been explored and interpreted. To gain a more comprehensive understanding of the induced electrostatic signals in the fluidized beds, an array of arc-shaped induced electrostatic sensors were attached to the outer wall of a fluidized bed. Combined with cross-correlation method, induced electrostatic voltage signals and correlation velocity of particles were measured simultaneously. It was found that electrostatic charges accumulation restrained the particle motions while the average correlation velocity of particles increased with the amount of injecting liquid antistatic agent. Based on the analyses of induced electrostatic signals, the particle correlation velocity, and the particles charge-to-mass ratio under different charging levels, a predictive model of the average particles charge-to-mass ratio was established. Compared with the results obtained from Faraday cup, the estimated results showed a relative error no more than 40%. Simultaneous measurement of particle correlation velocity and particles charge-to-mass ratio were complemented by arc-shaped induced electrostatic sensors array combined with cross-correlation method

Cocaine Preferentially Potentiates Fast Releasable Vesicle Pool in Mouse Dopaminergic Striatum In Vivo

BiophysicsSCI(E)CPCI-S(ISTP)0MEETING ABSTRACT2498A-499A10

Activation of NLRP3 Inflammasome by Advanced Glycation End Products Promotes Pancreatic Islet Damage

Accumulation of advanced glycation end products (AGEs) contributes to ageing and age-related diseases, especially type 2 diabetes. The NLRP3 inflammasome, as a vital component of the innate immune system, is implicated in the pathogenesis of type 2 diabetes. However, the role of the NLRP3 inflammasome in AGE-induced pancreatic islet damage remains largely unclear. Results showed that administration of AGEs (120 mg/kg for 6 weeks) in C57BL/6J mice induced an abnormal response to glucose (as measured by glucose tolerance and insulin release), pancreatic β-cell ultrastructural lesion, and cell death. These effects were associated with an excessive superoxide anion level, significant increased protein expression levels for NADPH oxidase 2 (NOX2), thioredoxin-interacting protein (TXNIP), NLRP3, and cleaved IL-1β, enhanced caspase-1 activity, and a significant increase in the levels of TXNIP–NLRP3 protein interaction. Ablation of the NLRP3 inflammasome or treatment with antioxidant N-acetyl-cysteine (NAC) clearly ameliorated these effects. In conclusion, our results reveal a possible mechanism for AGE-induced pancreatic islet damage upon NLRP3 inflammasome activation