Smoothed Quantile Regression with Large-Scale Inference.

Quantile regression is a powerful tool for learning the relationship between a response variable and a multivariate predictor while exploring heterogeneous effects. This paper focuses on statistical inference for quantile regression in the "increasing dimension" regime. We provide a comprehensive analysis of a convolution smoothed approach that achieves adequate approximation to computation and inference for quantile regression.

The expanding significance of keratin intermediate filaments in normal and diseased epithelia.

Intermediate filaments are assembled from a diverse group of evolutionary conserved proteins and are specified in a tissue-dependent, cell type-dependent, and context-dependent fashion in the body. Genetic mutations in intermediate filament proteins account for a large number of diseases, ranging from skin fragility conditions to cardiomyopathies and premature aging. Keratins, the epithelial-specific intermediate filaments, are now recognized as multi-faceted effectors in their native context.

Type I keratin 17 protein is phosphorylated on serine 44 by p90 ribosomal protein S6 kinase 1 (RSK1) in a growth- and stress-dependent fashion.

Keratin 17 (K17) is a type I intermediate filament protein that is constitutively expressed in ectoderm-derived epithelial appendages and robustly induced in epidermis following injury, during inflammation, and in chronic diseases such as psoriasis and cancer. Mutations within K17 are responsible for two rare diseases related to ectodermal dysplasias. Studies in K17-null mice uncovered several roles for K17, including structural support, resistance to TNFα-induced apoptosis, regulation of protein synthesis, and modulation of cytokine expression.

IFN-gamma-dependent regulatory circuits in immune inflammation highlighted in diabetes.

We demonstrate diverse roles of IFN-gamma in the induction and regulation of immune-mediated inflammation using a transfer model of autoimmune diabetes. The diabetogenic CD4(+)BDC2.5 (BDC) T cell clone upon transfer into NOD.

Matrix metalloproteinases expressed by astrocytes mediate extracellular amyloid-beta peptide catabolism.

It has been postulated that the development of amyloid plaques in Alzheimer's disease (AD) may result from an imbalance between the generation and clearance of the amyloid-beta peptide (Abeta). Although familial AD appears to be caused by Abeta overproduction, sporadic AD (the most prevalent form) may result from impairment in clearance. Recent evidence suggests that several proteases may contribute to the degradation of Abeta.

Location, allocation, relocation: isolating adult tissue stem cells in three dimensions.

The literature on isolation of adult tissue stem cells is vast and disparate. To better organize the field, we redefine 'isolation', re-expressing it as the sum of three component vectors: location, allocation and relocation. Location is the isolation of stem cells in situ by anatomical features.