SMUG1 DNA glycosylase modulates reward behaviour through regulation of olfactory receptor gene expression.

The SMUG1 DNA glycosylase is the primary enzyme responsible for excising 5-hydroxymethyluracil (5hmU) from genomic DNA. SMUG1 activity is high in the brain, suggesting its crucial role in controlling 5hmU levels in this organ. 5hmU has been proposed as an epigenetic mark, but it is still unclear whether, and in which contexts, it may have regulatory functions.

NEIL3 influences adult neurogenesis and behavioral pattern separation via WNT signaling.

Adult neurogenesis in the hippocampus, involving the generation and integration of new neurons, is essential for behavioral pattern separation, which supports accurate memory recall and cognitive plasticity. Here, we explore the role of the DNA repair protein NEIL3 in adult hippocampal neurogenesis and behavioral pattern separation. NEIL3 is required for efficient proliferation and neuronal differentiation of neonatal NSPCs and adult-born NPCs in the hippocampus following a behavioral pattern separation task.

A new blood based epigenetic age predictor for adolescents and young adults.

Children have special rights for protection compared to adults in our society. However, more than 1/4 of children globally have no documentation of their date of birth. Hence, there is a pressing need to develop biological methods for chronological age prediction, robust to differences in genetics, psychosocial events and physical living conditions.

NEIL1 and NEIL2 DNA glycosylases modulate anxiety and learning in a cooperative manner in mice.

Oxidative DNA damage in the brain has been implicated in neurodegeneration and cognitive decline. DNA glycosylases initiate base excision repair (BER), the main pathway for oxidative DNA base lesion repair. NEIL1 and NEIL3 DNA glycosylases affect cognition in mice, while the role of NEIL2 remains unclear.

Age assessment by Demirjian's development stages of the third molar: a systematic review.

Objectives: Radiographic evaluation of the wisdom teeth (third molar) formation is a widely used age assessment method for adolescents and young adults. This systematic review examines evidence on the agreement between Demirjian's development stages of the third molar and chronological age.

Methods: We searched four databases up until May 2016 for studies reporting Demirjian's stages of third molar and confirmed chronological age of healthy individuals aged 10-25 years.

BioAlder: a tool for assessing chronological age based on two radiological methods.

We have created the tool BioAlder as an age prediction model based on the systems Greulich and Pyle (hand) and the Demirjian's grading of the third molar tooth. The model compiles information from studies representing a total of 17,151 individuals from several parts of the world. The model offers a solution where issues as group-wise data format and age mimicry bias are bypassed.

A systematic review of the agreement between chronological age and skeletal age based on the Greulich and Pyle atlas.

Objectives: This systematic review examines the agreement between assessed skeletal age by the Greulich and Pyle atlas (GP skeletal age) and chronological age.

Methods: We searched electronic databases until January 2017 for studies reporting GP skeletal age and confirmed chronological age in healthy individuals aged 10-25 years. Results are presented as forest plots and meta-analyses (random-effects models).

Advancing estimation of chronological age by utilizing available evidence based on two radiographical methods.

This paper describes a strategy for estimating chronological age of individuals based on age indicators of X-ray of the hand and the third molar tooth. The great majority of studies in the field provide group-wise data of different formats, which makes them difficult to compare and utilize in a model. In this paper, we have provided a framework to utilize different types of data formats to build a common model for estimating chronological age.

No cancer predisposition or increased spontaneous mutation frequencies in NEIL DNA glycosylases-deficient mice.

Base excision repair (BER) is a major pathway for removal of DNA base lesions and maintenance of genomic stability, which is essential in cancer prevention. DNA glycosylases recognize and remove specific lesions in the first step of BER. The existence of a number of these enzymes with overlapping substrate specificities has been thought to be the reason why single knock-out models of individual DNA glycosylases are not cancer prone.

Synergistic Actions of Ogg1 and Mutyh DNA Glycosylases Modulate Anxiety-like Behavior in Mice.

Ogg1 and Mutyh DNA glycosylases cooperate to prevent mutations caused by 8-oxoG, a major premutagenic DNA lesion associated with cognitive decline. We have examined behavior and cognitive function in mice deficient of these glycosylases. Ogg1(-/-)Mutyh(-/-) mice were more active and less anxious, with impaired learning ability.

The acceptability of volunteer, repeat blood donations in a hospital setting in the Adamaoua region of Cameroon.

Background And Objectives: The knowledge of factors that may influence blood donation in Cameroon is limited. The objectives of this study are to assess the characteristics of previous and potential blood donors by exploring the religious beliefs, and knowledge and understanding of blood donations among individuals present at a district hospital.

Materials And Methods: Forty-nine in-depth, semi-structured interviews were conducted among consenting, randomly selected 18 years or older community members present at a district hospital in the Adamaoua region during October and November 2011.

Loss of Neil3, the major DNA glycosylase activity for removal of hydantoins in single stranded DNA, reduces cellular proliferation and sensitizes cells to genotoxic stress.

7,8-Dihydro-8-oxoguanine (8-oxoG) is one of the most common oxidative base lesions in normal tissues induced by a variety of endogenous and exogenous agents. Hydantoins are products of 8-oxoG oxidation and as 8-oxoG, they have been shown to be mutagenic lesions. Oxidative DNA damage has been implicated in the etiology of various age-associated pathologies, such as cancer, cardiovascular diseases, arthritis, and several neurodegenerative diseases.

Hippocampal adult neurogenesis is maintained by Neil3-dependent repair of oxidative DNA lesions in neural progenitor cells.

Accumulation of oxidative DNA damage has been proposed as a potential cause of age-related cognitive decline. The major pathway for removal of oxidative DNA base lesions is base excision repair, which is initiated by DNA glycosylases. In mice, Neil3 is the main DNA glycosylase for repair of hydantoin lesions in single-stranded DNA of neural stem/progenitor cells, promoting neurogenesis.

X-ray studies of carbon dioxide intercalation in Na-fluorohectorite clay at near-ambient conditions.

We show experimentally that gaseous CO(2) intercalates into the interlayer space of the synthetic smectite clay Na-fluorohectorite at conditions not too far from ambient. The mean interlayer repetition distance of the clay when CO(2) is intercalated is found to be 12.5 Å for the conditions -20 °C and 15 bar.

Endonuclease VIII-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia.

Neural stem/progenitor cell proliferation and differentiation are required to replace damaged neurons and regain brain function after hypoxic-ischemic events. DNA base lesions accumulating during hypoxic-ischemic stress are removed by DNA glycosylases in the base-excision repair pathway to prevent cytotoxicity and mutagenesis. Expression of the DNA glycosylase endonuclease VIII-like 3 (Neil3) is confined to regenerative subregions in the embryonic and perinatal brains.

Widespread distribution of DNA glycosylases removing oxidative DNA lesions in human and rodent brains.

High metabolic activity and low levels of antioxidant enzymes make neurons particularly prone to damage by reactive oxygen species. Thus, repair of oxidative DNA damage is essential for normal brain function. Base excision repair is the major pathway for repair of oxidative DNA damage, and is initiated by DNA glycosylases recognizing and removing the damaged base.

Base excision repair activities in organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation.

The capacity for DNA repair is likely to be one of the factors that determine the vulnerability of neurons to ischemic stress and may influence the pathological outcome of stroke. In this report, initiation of base excision repair (BER) was assessed by analysis of enzyme activity and gene expression level of DNA glycosylases and AP-endonucleases in rat organotypic hippocampal slice cultures exposed to oxygen and glucose deprivation (OGD) - an in vitro model of stroke. Under basal conditions, AP-endonuclease activity and base removal of ethenoadenine and 8-oxoguanine (8-oxoG) were higher (by approximately 20-35 %) in CA3/fascia dentata (FD) than in CA1.

Human NEIL1 localizes with the centrosomes and condensed chromosomes during mitosis.

The DNA glycosylase hNEIL1 initiates base excision repair (BER) of a number of oxidized purines and pyrimidines in cellular DNA and is one of three mammalian orthologs of the Escherichia coli Nei/Fpg enzymes. Human NEIL1 has been purified and extensively characterized biochemically, however, not much is known about its intracellular distribution. In the present work, we have studied the cellular localization of hNEIL1 using both antibodies raised against the full-length recombinant protein and a stable HeLa cell line expressing hNEIL1 fused N-terminal to EGFP.

Dynamic relocalization of hOGG1 during the cell cycle is disrupted in cells harbouring the hOGG1-Cys326 polymorphic variant.

Numerous lines of evidence support the role of oxidative stress in different types of cancer. A major DNA lesion, 8-oxo-7,8-dihydroguanine (8-oxoG), is formed by reactive oxygen species in the genome under physiological conditions. 8-OxoG is strongly mutagenic, generating G.

Human DNA glycosylases of the bacterial Fpg/MutM superfamily: an alternative pathway for the repair of 8-oxoguanine and other oxidation products in DNA.

The mild phenotype associated with targeted disruption of the mouse OGG1 and NTH1 genes has been attributed to the existence of back-up activities and/or alternative pathways for the removal of oxidised DNA bases. We have characterised two new genes in human cells that encode DNA glycosylases, homologous to the bacterial Fpg (MutM)/Nei class of enzymes, capable of removing lesions that are substrates for both hOGG1 and hNTH1. One gene, designated HFPG1, showed ubiquitous expression in all tissues examined whereas the second gene, HFPG2, was only expressed at detectable levels in the thymus and testis.

Additive toxicity of limonene and 50% oxygen and the role of glutathione in detoxification in human lung cells.

Limonene has many commercial applications and has been introduced as an environmentally acceptable solvent replacing halogenated hydrocarbons. Occupational exposure to limonene presumably occurs simultaneously with other chemicals including oxidative agents and may exert a heavy strain on cellular detoxifying capacity resulting in synergistic effects. The present study used oxygen as an example of an ubiquitous oxidative and radical forming agent and investigated the combination effects with limonene on human lung cells.

5-Formyluracil and its nucleoside derivatives confer toxicity and mutagenicity to mammalian cells by interfering with normal RNA and DNA metabolism.

Oxidation of the methyl group of thymine yields 5-(hydroxymethyl)uracil (5-hmU) and 5-formyluracil (5-foU) as major products. Whereas 5-hmU appears to have normal base pairing properties, the biological effects of 5-foU are rather poorly characterised. Here, we show that the colony forming ability of Chinese hamster fibroblast (CHF) cells is greatly reduced by addition of 5-foU, 5-formyluridine (5-foUrd) and 5-formyl-2'-deoxyuridine (5-fodUrd) to the growth medium.