selenoprotein/fever

A number of distinct viruses are known as hemorrhagic fever viruses based on a shared ability to induce hemorrhage by poorly understood mechanisms, typically involving the formation of blood clots ("disseminated intravascular coagulation"). It is well documented that selenium plays a significant

BACKGROUND Pathogen colonization inside tick tissues is a significant aspect of the overall competence of a vector. Amblyomma maculatum is a competent vector of the spotted fever group rickettsiae, Rickettsia parkeri. When R. parkeri colonizes its tick host, it has the opportunity to dynamically

The genomes of both bacteria and eukaryotic organisms are known to encode selenoproteins, using the UGA codon for seleno-cysteine (SeC), and a complex cotranslational mechanism for SeC incorporation into polypeptide chains, involving RNA stem-loop structures. These common features and similar codon

Selenium, a vital trace element, is incorporated into selenoproteins to produce selenocysteine. Our previous studies have revealed an adaptive co-evolutionary process that has enabled the spotted fever-causing tick-borne pathogen Rickettsia parkeri to survive by manipulating an antioxidant defense

The aim of this study was to explore the impacts of heat stress (HS) on expressions of selenoprotein genes in IPEC-J2 cells. Cells were cultured with 5 % CO2-humidified chamber at 37 °C until the cells grew to complete confluence and then exposed to a mild hyperthermia at 41.5 °C (HS) or 37 °C

This study was conducted to profile the selenoprotein encoding genes or proteins in mouse C2C12 cells and integrate their roles in the skeletal cell damage induced by heat stress (HS). Cells were cultured at 37.0 °C or 41.5 °C for 4, 6 or 8 days. The mRNA expression of 24 selenoprotein encoding

BACKGROUND Congenital myopathies include many genetically distinct diseases which have in common the early appearance of symptoms and characteristic morphological findings. OBJECTIVE To resume clinical, pathological and genetic findings of the most frequent myopathies in this group. METHODS The most

BACKGROUND Congenital myopathies are a heterogeneous group of diseases that share clinical early onset and specific hystopathological alterations in muscle. Genetic studies allow to determine the causative mutation in most cases. Genotypic and phenotypic heterogeneity exists, which is illustrated by

BACKGROUND Minicore myopathy (multi-minicore disease [MmD]) is a congenital myopathy characterized by multifocal areas with loss of oxidative activity on muscle biopsy. MmD is clinically heterogeneous and distinct phenotypes have been associated with recessive mutations in either the selenoprotein N

Multi-minicore Disease (MmD) is a recessively inherited neuromuscular disorder characterized by multiple cores on muscle biopsy and clinical features of a congenital myopathy. Prevalence is unknown. Marked clinical variability corresponds to genetic heterogeneity: the most instantly recognizable