Technology Courage: Implications for Faculty Development.

This article was migrated. The article was marked as recommended. From a decade of technology-focused faculty development, the authors recognized that academic physicians adopt educational technology at varying rates and with variable confidence.

Abuse Characteristics and Individual Differences Related to Disclosing Childhood Sexual, Physical, and Emotional Abuse and Witnessed Domestic Violence.

Many adult survivors of childhood abuse hide their victimization, avoiding disclosure that could identify perpetrators, end the abuse, and bring help to the victim. We surveyed 1,679 women undergraduates to understand disclosure of childhood sexual, physical, and emotional abuse, and, for the first time, witnessed domestic violence, which many consider to be emotionally abusive. A substantial minority of victims failed to ever disclose their sexual abuse (23%), physical abuse (34%), emotional abuse (20%), and witnessed domestic violence (29%).

Next-generation sequencing of small RNAs from inner ear sensory epithelium identifies microRNAs and defines regulatory pathways.

Background: The mammalian inner ear contains sensory organs, the organ of Corti in the cochlea and cristae and maculae in the vestibule, with each comprised of patterned sensory epithelia that are responsible for hearing and balance. The development, cell fate, patterning, and innervation of both the sensory and nonsensory regions of the inner ear are governed by tight regulation involving, among others, transcription factors and microRNAs (miRNAs). In humans, mutations in specific miRNA genes are associated with hearing loss.

microRNA-224 regulates Pentraxin 3, a component of the humoral arm of innate immunity, in inner ear inflammation.

microRNAs (miRNAs) are regulators of differentiation and development of inner ear cells. Mutations in miRNAs lead to deafness in humans and mice. Among inner ear pathologies, inflammation may lead to structural and neuronal defects and eventually to hearing loss and vestibular dysfunction.

MicroRNAs in sensorineural diseases of the ear.

Non-coding microRNAs (miRNAs) have a fundamental role in gene regulation and expression in almost every multicellular organism. Only discovered in the last decade, miRNAs are already known to play a leading role in many aspects of disease. In the vertebrate inner ear, miRNAs are essential for controlling development and survival of hair cells.

Egr2::cre mediated conditional ablation of dicer disrupts histogenesis of mammalian central auditory nuclei.

Histogenesis of the auditory system requires extensive molecular orchestration. Recently, Dicer1, an essential gene for generation of microRNAs, and miR-96 were shown to be important for development of the peripheral auditory system. Here, we investigated their role for the formation of the auditory brainstem.

microRNAs: the art of silencing in the ear.

MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression through the RNA interference (RNAi) pathway and by inhibition of mRNA translation. miRNAs first made their appearance in the auditory and vestibular systems in 2005, with the discovery of a triad of hair cell-specific miRNAs later found to be involved in both human and mouse deafness. Since then, miRNAs have been implicated in other medical conditions related to these systems, such as cholesteatomas, vestibular schwannomas and otitis media.

Integration of transcriptomics, proteomics, and microRNA analyses reveals novel microRNA regulation of targets in the mammalian inner ear.

We have employed a novel approach for the identification of functionally important microRNA (miRNA)-target interactions, integrating miRNA, transcriptome and proteome profiles and advanced in silico analysis using the FAME algorithm. Since miRNAs play a crucial role in the inner ear, demonstrated by the discovery of mutations in a miRNA leading to human and mouse deafness, we applied this approach to microdissected auditory and vestibular sensory epithelia. We detected the expression of 157 miRNAs in the inner ear sensory epithelia, with 53 miRNAs differentially expressed between the cochlea and vestibule.

Expression of urokinase-type plasminogen activator receptor (uPAR) in primary central nervous system neoplasms.

The cellular receptor for urokinase-type plasminogen activator receptor (uPAR) is a member of the glycosylphosphatidylinositol (GPI) anchored protein family. It is a specific cell surface receptor for its ligand, urokinase-type plasminogen activator, which catalyzes the formation of plasmin from plasminogen to generate the proteolytic cascade and leads to the breakdown of the extracellular matrix. uPAR has been shown to correlate with a propensity to tumor invasion and metastasis in several types of non-central nervous system tumors.

Calpain mediates calcium-induced activation of the erk1,2 MAPK pathway and cytoskeletal phosphorylation in neurons: relevance to Alzheimer's disease.

Aberrant phosphorylation of the neuronal cytoskeleton is an early pathological event in Alzheimer's disease (AD), but the underlying mechanisms are unclear. Here, we demonstrate in the brains of AD patients that neurofilament hyperphosphorylation in neocortical pyramidal neurons is accompanied by activation of both Erk1,2 and calpain. Using immunochemistry, Western blot analysis, and kinase activity measurements, we show in primary hippocampal and cerebellar granule (CG) neurons that calcium influx activates calpain and Erk1,2 and increases neurofilament phosphorylation on carboxy terminal polypeptide sites known to be modulated by Erk1,2 and to be altered in AD.

Age-related increase of pulse pressure and gene polymorphisms in essential hypertension: a preliminary study.

Genes may modulate the changes of blood pressure (BP) with age; this possibility has never been studied for the age-related increase of pulse pressure (PP), although in older populations, PP is considered the stronger mechanical factor predicting cardiovascular mortality. In humans, the presence of the mutant allele C of the angiotensin II (Ang II) AT(1)-receptor or of the mutant allele T of the eNOS G(298) T gene polymorphisms is associated with enhanced contractile properties of conduit arteries in response to vasoconstrictive agents. In this study, we evaluated, in subjects with untreated essential hypertension, whether the presence of these mutant alleles or their combination might influence the age-related increase of PP.

Comparative effects of aging in men and women on the properties of the arterial tree.

Objectives: We measured the properties of the arterial tree, seeking differences between men and women as they aged.

Background: There are many differences between men and women, besides menopause, which might account for such disparities. These include body height, heart rate, stroke volume and smaller arterial diameters.

Brain expression of presenilins in sporadic and early-onset, familial Alzheimer's disease.

Background: Mutations in the presenilin proteins cause early-onset, familial Alzheimer's disease (FAD).

Materials And Methods: We characterized the cellular localization and endoproteolysis of presenilin 2 (PS2) and presenilin 1 (PS1) in brains from 25 individuals with presenilin-mutations causing FAD, as well as neurologically normal individuals and individuals with sporadic Alzheimer's disease (AD).

Results: Amino-terminal antibodies to both presenilins predominantly decorated large neurons.

Changes in arterial structure and function under trandolapril-verapamil combination in hypertension.

Background And Purpose: Converting enzyme inhibition and calcium blockade alter large arteries in hypertension. However, the heterogeneity of the response according to the site of cardiovascular measurements has never been investigated.

Methods: In a double-blind study, we compared for 180 days 3 hypertensive patient groups treated with verapamil, trandolapril, or their combination.

Enalapril in the treatment of mild-to-moderate heart failure in general medical practice: a prospective and multicentre study concerning 17,546 patients.

The objective of this study was to test the efficacy and tolerability of a precise dosage regimen of enalapril in general medical practice, in combination with conventional therapy, in patients with mild-to-moderate (NYHA classes II and III) congestive heart failure (CHF). 17,546 patients were prospectively included in this multicentre study. After three months of treatment with enalapril, 53.