T- and L-Type Calcium Channels Maintain Calcium Oscillations in the Murine Zona Glomerulosa.

Background: The zona glomerulosa of the adrenal gland is responsible for the synthesis and release of the mineralocorticoid aldosterone. This steroid hormone regulates salt reabsorption in the kidney and blood pressure. The most important stimuli of aldosterone synthesis are the serum concentrations of angiotensin II and potassium.

Isradipine therapy in Cacna1dIle772Met/+ mice ameliorates primary aldosteronism and neurologic abnormalities.

Somatic gain-of-function mutations in the L-type calcium channel CaV1.3 (CACNA1D gene) cause adrenal aldosterone-producing adenomas and micronodules. De novo germline mutations are found in a syndrome of primary aldosteronism, seizures, and neurologic abnormalities (PASNA) as well as in autism spectrum disorder.

Oxidative Stress Resistance 1 Gene Therapy Retards Neurodegeneration in the rd1 Mutant Mouse Model of Retinopathy.

Purpose: Oxidative stress is a major factor underlying many neurodegenerative diseases. However, antioxidant therapy has had mixed results, possibly because of its indiscriminate activity. The purpose of our study was to determine if the human OXR1 (hOXR1) antioxidant regulatory gene could protect neurons from oxidative stress and delay photoreceptor cell death.

Development of a new COVID-19 panel survey: the IAB high-frequency online personal panel (HOPP).

Since January 2020, the COVID-19 crisis has affected everyday life around the world, and rigorous government lockdown restrictions have been implemented to prevent the further spread of the pandemic. The consequences of the corona crisis and the associated lockdown policies for public health, social life, and the economy are vast. In view of the rapidly changing situation during this crisis, policymakers require timely data and research results that allow for informed decisions.

Preventing Neurodegeneration by Controlling Oxidative Stress: The Role of OXR1.

Parkinson's disease, diabetic retinopathy, hyperoxia induced retinopathy, and neuronal damage resulting from ischemia are among the notable neurodegenerative diseases in which oxidative stress occurs shortly before the onset of neurodegeneration. A shared feature of these diseases is the depletion of (oxidation resistance 1) gene products shortly before the onset of neurodegeneration. In animal models of these diseases, restoration of has been shown to reduce or eliminate the deleterious effects of oxidative stress induced cell death, delay the onset of symptoms, and reduce overall severity.

Molecular Assessment of Epiretinal Membrane: Activated Microglia, Oxidative Stress and Inflammation.

Fibrocellular membrane or epiretinal membrane (ERM) forms on the surface of the inner limiting membrane (ILM) in the inner retina and alters the structure and function of the retina. ERM formation is frequently observed in ocular inflammatory conditions, such as proliferative diabetic retinopathy (PDR) and retinal detachment (RD). Although peeling of the ERM is used as a surgical intervention, it can inadvertently distort the retina.

Stabilization of Crystalline Carotenoids in Carrot Concentrate Powders: Effects of Drying Technology, Carrier Material, and Antioxidants.

Coloring concentrates of carotenoid-rich plant materials are currently used in the food industry to meet the consumer's demand for natural substitutes for food colorants. The production of shelf-stable powders of such concentrates comes with particular challenges linked to the sensitivity of the active component towards oxidation and the complexity of the composition and microstructure of such concentrates. In this study, different strategies for the stabilization of crystalline carotenoids as part of a natural carrot concentrate matrix during drying and storage were investigated.

What You See Is What You Remember: Visual Chunking by Temporal Integration Enhances Working Memory.

Human memory benefits from information clustering, which can be accomplished by chunking. Chunking typically relies on expertise and strategy, and it is unknown whether perceptual clustering over time, through temporal integration, can also enhance working memory. The current study examined the attentional and working memory costs of temporal integration of successive target stimulus pairs embedded in rapid serial visual presentation.

RNA polymerase II depletion promotes transcription of alternative mRNA species.

Background: Cells respond to numerous internal and external stresses, such as heat, cold, oxidative stress, DNA damage, and osmotic pressure changes. In most cases, the primary response to stress is transcriptional induction of genes that assist the cells in tolerating the stress and facilitate the repair of the cellular damage. However, when the transcription machinery itself is stressed, responding by such standard mechanisms may not be possible.

Acute Catecholamine Exposure Causes Reversible Myocyte Injury Without Cardiac Regeneration.

Rationale: Catecholamines increase cardiac contractility, but exposure to high concentrations or prolonged exposures can cause cardiac injury. A recent study demonstrated that a single subcutaneous injection of isoproterenol (ISO; 200 mg/kg) in mice causes acute myocyte death (8%-10%) with complete cardiac repair within a month. Cardiac regeneration was via endogenous cKit(+) cardiac stem cell-mediated new myocyte formation.

The Sub1 nuclear protein protects DNA from oxidative damage.

Reactive oxygen species are a by-product of aerobic metabolism that can damage lipid, proteins, and nucleic acids. Oxidative damage to DNA is especially critical, because it can lead to cell death or mutagenesis. Previously we reported that the yeast sub1 deletion mutant is sensitive to hydrogen peroxide treatment and that the human SUB1 can complement the sensitivity of the yeast sub1 mutant.

Induction of a unique isoform of the NCOA7 oxidation resistance gene by interferon β-1b.

We demonstrate that interferon (IFN)-β-1b induces an alternative-start transcript containing the C-terminal TLDc domain of nuclear receptor coactivator protein 7 (NCOA7), a member of the OXR family of oxidation resistance proteins. IFN-β-1b induces NCOA7-AS (alternative start) expression in peripheral blood mononuclear cells (PBMCs) obtained from healthy individuals and multiple sclerosis patients and human fetal brain cells, astrocytoma, neuroblastoma, and fibrosarcoma cells. NCOA7-AS is a previously undocumented IFN-β-inducible gene that contains only the last 5 exons of full-length NCOA7 plus a unique first exon (exon 10a) that is not found in longer forms of NCOA7.

From zero to hero - production of bio-based nylon from renewable resources using engineered Corynebacterium glutamicum.

Polyamides are important industrial polymers. Currently, they are produced exclusively from petrochemical monomers. Herein, we report the production of a novel bio-nylon, PA5.

Differential requirement for SUB1 in chromosomal and plasmid double-strand DNA break repair.

Non homologous end joining (NHEJ) is an important process that repairs double strand DNA breaks (DSBs) in eukaryotic cells. Cells defective in NHEJ are unable to join chromosomal breaks. Two different NHEJ assays are typically used to determine the efficiency of NHEJ.

UV damage regulates alternative polyadenylation of the RPB2 gene in yeast.

Alternative polyadenylation (APA) is conserved in all eukaryotic cells. Selective use of polyadenylation sites appears to be a highly regulated process and contributes to human pathogenesis. In this article we report that the yeast RPB2 gene is alternatively polyadenylated, producing two mRNAs with different lengths of 3'UTR.

Structural/functional analysis of the human OXR1 protein: identification of exon 8 as the anti-oxidant encoding function.

Background: The human OXR1 gene belongs to a class of genes with conserved functions that protect cells from reactive oxygen species (ROS). The gene was found using a screen of a human cDNA library by its ability to suppress the spontaneous mutator phenotype of an E. coli mutH nth strain.

Preferential DNA damage prevention by the E. coli AidB gene: A new mechanism for the protection of specific genes.

aidB is one of the four genes of E. coli that is induced by alkylating agents and regulated by Ada protein. Three genes (ada, alkA, and alkB) encode DNA repair proteins that remove or repair alkylated bases.

Specific DNA binding and regulation of its own expression by the AidB protein in Escherichia coli.

Upon exposure to alkylating agents, Escherichia coli increases expression of aidB along with three genes (ada, alkA, and alkB) that encode DNA repair proteins. While the biological roles of the Ada, AlkA, and AlkB proteins have been defined, despite many efforts, the molecular functions of AidB remain largely unknown. In this study, we focused on the biological role of the AidB protein, and we demonstrated that AidB shows preferential binding to a DNA region that includes the upstream element of its own promoter, PaidB.

A functional genomics approach to identify and characterize oxidation resistance genes.

In order to develop a more complete understanding of the genes required for resistance to oxidative DNA damage, we devised methods to identify genes that can prevent or repair oxidative DNA damage. These methods use the oxidative mutator phenotype of a repair deficient E. coli strain to measure the antimutator effect resulting from the expression of human cDNAs.

The OXR domain defines a conserved family of eukaryotic oxidation resistance proteins.

Background: The NCOA7 gene product is an estrogen receptor associated protein that is highly similar to the human OXR1 gene product, which functions in oxidation resistance. OXR genes are conserved among all sequenced eukaryotes from yeast to humans. In this study we examine if NCOA7 has an oxidation resistance function similar to that demonstrated for OXR1.

Base excision repair sensitizes cells to sulfur mustard and chloroethyl ethyl sulfide.

DNA repair generally functions to improve survival and reduce mutagenesis of cells that have suffered DNA damage. In this study we examine the role of nucleotide excision repair (NER) and base excision repair (BER) in recovery, mutagenesis and DNA repair in response to DNA damage inflicted by the mustard compounds, sulfur mustard (SM) and chloroethyl ethyl sulfide (CEES) in bacteria and mammalian cells. SM and CEES are compared because SM produces cross-links and monoadducts, whereas CEES produces only monoadducts that are similar to those produced by SM, thus allowing the examination of which types of lesions may be responsible for the effects seen.

Deregulation of DNA damage signal transduction by herpesvirus latency-associated M2.

Infected cells recognize viral replication as a DNA damage stress and elicit a DNA damage response that ultimately induces apoptosis as part of host immune surveillance. Here, we demonstrate a novel mechanism where the murine gamma herpesvirus 68 (gammaHV68) latency-associated, anti-interferon M2 protein inhibits DNA damage-induced apoptosis by interacting with the DDB1/COP9/cullin repair complex and the ATM DNA damage signal transducer. M2 expression constitutively induced DDB1 nuclear localization and ATM kinase activation in the absence of DNA damage.

Palliative irradiation of Scottish Fold osteochondrodysplasia.

This report describes palliative irradiation as treatment for Scottish Fold osteochondrodysplasia. A 3-year-old female spayed Scottish Fold cat suffering from osteochondrodysplasia was referred to the Veterinary Teaching Hospital, University of Zurich. Based on the breed, history, clinical signs, radiographic findings, and the histologic diagnosis of a biopsy specimen, Scottish Fold osteochondrodysplasia was confirmed.

The single-strand DNA binding activity of human PC4 prevents mutagenesis and killing by oxidative DNA damage.

Human positive cofactor 4 (PC4) is a transcriptional coactivator with a highly conserved single-strand DNA (ssDNA) binding domain of unknown function. We identified PC4 as a suppressor of the oxidative mutator phenotype of the Escherichia coli fpg mutY mutant and demonstrate that this suppression requires its ssDNA binding activity. Saccharomyces cerevisiae mutants lacking their PC4 ortholog Sub1 are sensitive to hydrogen peroxide and exhibit spontaneous and peroxide-induced hypermutability.