ABSTRACT
Intensity-based image registration is critical for neuroimaging tasks, such as 3D reconstruction, times-series alignment, and common coordinate mapping. The gradient-based optimization methods commonly used to solve this problem require a careful selection of step-length. This limitation imposes substantial time and computational costs. Here we propose a gradient-independent rigid-motion registration algorithm based on the majorization-minimization (MM) principle. Each iteration of our intensity-based MM algorithm reduces to a simple point-set rigid registration problem with a closed form solution that avoids the step-length issue altogether. The details of the algorithm are presented, and an error bound for its more practical truncated form is derived. The performance of the MM algorithm is shown to be more effective than gradient descent on simulated images and Nissl stained coronal slices of mouse brain. We also compare and contrast the similarities and differences between the MM algorithm and another gradient-free registration algorithm called the block-matching method. Finally, extensions of this algorithm to more complex problems are discussed.
ABSTRACT
Inflammation often induces regeneration to repair the tissue damage. However, chronic inflammation can transform temporary hyperplasia into a fertile ground for tumorigenesis. Here, we demonstrate that the microRNA miR-34a acts as a central safeguard to protect the inflammatory stem cell niche and reparative regeneration. Although playing little role in regular homeostasis, miR-34a deficiency leads to colon tumorigenesis after Citrobacter rodentium infection. miR-34a targets both immune and epithelial cells to restrain inflammation-induced stem cell proliferation. miR-34a targets Interleukin six receptor (IL-6R) and Interleukin 23 receptor (IL-23R) to suppress T helper 17 (Th17) cell differentiation and expansion, targets chemokine CCL22 to hinder Th17 cell recruitment to the colon epithelium, and targets an orphan receptor Interleukin 17 receptor D (IL-17RD) to inhibit IL-17-induced stem cell proliferation. Our study highlights the importance of microRNAs in protecting the stem cell niche during inflammation despite their lack of function in regular tissue homeostasis.
