Genome-wide profiling of tRNA modifications by Induro-tRNAseq reveals coordinated changes.

While all native tRNAs undergo extensive post-transcriptional modifications as a mechanism to regulate gene expression, mapping these modifications remains challenging. The critical barrier is the difficulty of readthrough of modifications by reverse transcriptases (RTs). Here we use Induro-a new group-II intron-encoded RT-to map and quantify genome-wide tRNA modifications in Induro-tRNAseq.

Spinal TNF-α receptor 1 is differentially required for phrenic long-term facilitation (pLTF) over the course of motor neuron death in adult rats.

Introduction: Intrapleural injections of cholera toxin B conjugated to saporin (CTB-SAP) result in selective respiratory (, phrenic) motor neuron death and mimics aspects of motor neuron disease [(, amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA)], such as breathing deficits. This rodent model allows us to study the impact motor neuron death has on the output of surviving phrenic motor neurons as well as the compensatory mechanisms that are recruited. Microglial density in the phrenic motor nucleus as well as cervical gene expression of markers associated with inflammation (.

A gigantic intraosseous and dural-based calvarial metastatic follicular thyroid carcinoma: illustrative case.

Background: Metastatic follicular thyroid carcinoma to the central nervous system (CNS), including the skull and dura, is exceedingly rare.

Observations: The authors present the case of a gigantic, intraosseous, dural-based follicular thyroid carcinoma, highlighting the operative strategy for this mass. They also provide a literature review of CNS metastases of differentiated thyroid carcinoma.

Ighmbp2 mutations and disease pathology: Defining differences that differentiate SMARD1 and CMT2S.

Mutations in the Immunoglobulin mu DNA binding protein 2 (IGHMBP2) gene result in two distinct diseases, SMA with Respiratory Distress Type I (SMARD1) and Charcot Marie Tooth Type 2S (CMT2S). To understand the phenotypic and molecular differences between SMARD1 and CMT2S, and the role of IGHMBP2 in disease development, we generated mouse models based on six IGHMBP2 patient mutations. Previously, we reported the development and characterization of Ighmbp2 mice and in this manuscript, we examine two mutations: D565N (D564N in mice) and H924Y (H922Y in mice) in the Ighmbp2 and Ighmbp2 contexts.