Geary (2018, 2019) suggested that heritable and environmentally caused differences in mitochondrial functioning affect the integrity and efficiency of neurons and supporting glia cells and may thus ...contribute to individual differences in higher-order cognitive functioning and physical health. In our comment, we want to pose three questions aimed at different aspects of Geary’s theory that critically evaluate his theory in the light of evidence from neurocognitive, cognitive enhancement, and behavioral genetics research. We question (1) if Geary’s theory explains why certain cognitive processes show a stronger age-related decline than others; (2) if intervention studies in healthy younger adults support the claim that variation in mitochondrial functioning underlies variation in human intelligence; and (3) if predictions arising from the matrilineal heredity of mitochondrial DNA are supported by behavioral genetics research. We come to the conclusion that there are likely many more biological and social factors contributing to variation in human intelligence than mitochondrial functioning.
A large fraction of globally produced methane is converted to CO2
by anaerobic oxidation in marine sediments. Strong geochemical
evidence for net methane consumption in anoxic sediments is based on ...methane
profiles, radiotracer experiments and stable carbon
isotope data. But the elusive microorganisms mediating this
reaction have not yet been isolated, and the pathway of anaerobic oxidation
of methane is insufficiently understood. Recent data suggest that certain
archaea reverse the process of methanogenesis by interaction with sulphate-reducing
bacteria. Here we provide microscopic evidence for a
structured consortium of archaea and sulphate-reducing bacteria, which we
identified by fluorescence in situ hybridization using specific 16S
rRNA-targeted oligonucleotide probes. In this example of a structured archaeal-bacterial
symbiosis, the archaea grow in dense aggregates of about 100 cells and are
surrounded by sulphate-reducing bacteria. These aggregates were abundant in
gas-hydrate-rich sediments with extremely high rates of methane-based sulphate
reduction, and apparently mediate anaerobic oxidation of methane.
Celotno besedilo
Dostopno za:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Aicardi-Goutières syndrome (AGS), a hereditary autoimmune disease, clinically and biochemically overlaps with systemic lupus erythematosus (SLE) and, like SLE, is characterized by spontaneous type I ...interferon (IFN) production. The finding that defects of intracellular nucleases cause AGS led to the concept that intracellular accumulation of nucleic acids triggers inappropriate production of type I IFN and autoimmunity. AGS can also be caused by defects of SAMHD1, a 3′ exonuclease and deoxynucleotide (dNTP) triphosphohydrolase. Human SAMHD1 is an HIV-1 restriction factor that hydrolyzes dNTPs and decreases their concentration below the levels required for retroviral reverse transcription. We show in gene-targeted mice that also mouse SAMHD1 reduces cellular dNTP concentrations and restricts retroviral replication in lymphocytes, macrophages, and dendritic cells. Importantly, the absence of SAMHD1 triggered IFN-β-dependent transcriptional upregulation of type I IFN-inducible genes in various cell types indicative of spontaneous IFN production. SAMHD1-deficient mice may be instrumental for elucidating the mechanisms that trigger pathogenic type I IFN responses in AGS and SLE.
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•Murine SAMHD1 depletes cellular dNTP pools and restricts retroviral replication•SAMHD1−/− mice reproduce the spontaneous type I IFN response of SLE and AGS patients
Aicardi-Goutières syndrome (AGS), a hereditary autoimmune disease, clinically and biochemically overlaps with systemic lupus erythematosus (SLE) and, like SLE, is characterized by spontaneous type I interferon (IFN) production. AGS can be caused by defects in SAMHD1, a 3′-exonuclease and dinucleotide triphosphate (dNTP) triphosphohydrolase that restricts HIV-1 infection. Roers and colleagues now show that mouse SAMHD1 also restricts retroviral replication. SAMHD1-deficient mice featured IFN-β-dependent upregulation of IFN-inducible genes indicative of spontaneous IFN production. These mice may be instrumental in the investigation of pathogenic type I IFN responses in AGS and SLE.
Lung failure is responsible for significant morbidity and is a frequent cause of death in ataxia-telangiectasia (A-T). Disturbance in the redox balance of alveolar epithelial cells must be considered ...as a causal factor for respiratory disease in A-T. To investigate bronchoalveolar sensitivity to reactive oxygen species (ROS) and ROS-induced DNA damage, we used bleomycin (BLM) to induce experimental inflammation and fibrotic changes in the Atm-deficient mouse model.
BLM or saline was administered by oropharyngeal instillation into the lung of Atm-deficient mice and wild-type mice. Mice underwent pulmonary function testing at days 0, 9, and 28, and bronchoalveolar lavage (BAL) was analysed for cell distribution and cytokines. Lung tissue was analysed by histochemistry.
BLM administration resulted in a tremendous increase in lung inflammation and fibrotic changes in the lung tissue of Atm-deficient mice and was accompanied by irreversible deterioration of lung function. ATM (ataxia telangiectasia mutated) deficiency resulted in reduced cell viability, a delay in the resolution of γH2AX expression and a significant increase in intracellular ROS in pulmonary epithelial cells after BLM treatment. This was confirmed in the human epithelial cell line A549 treated with the ATM-kinase inhibitor KU55933.
Our results demonstrate high bronchoalveolar sensitivity to ROS and ROS-induced DNA damage in the Atm-deficient mouse model and support the hypothesis that ATM plays a pivotal role in the control of oxidative stress-driven lung inflammation and fibrosis.
An open and shut case: The competition between charge separation and recombination in artificial photosynthetic systems can be controlled by using photochromic dynamic bridge. The photoinduced ...opening and closing of the bridge mediates the electronic coupling between donor (D) and acceptor (A).
The in vivo phenotypic profile of T cells reactive to severe acute respiratory syndrome (SARS)-CoV-2 antigens remains poorly understood. Conventional methods to detect antigen-reactive T cells ...require in vitro antigenic re-stimulation or highly individualized peptide-human leukocyte antigen (pHLA) multimers. Here, we use single-cell RNA sequencing to identify and profile SARS-CoV-2-reactive T cells from Coronavirus Disease 2019 (COVID-19) patients. To do so, we induce transcriptional shifts by antigenic stimulation in vitro and take advantage of natural T cell receptor (TCR) sequences of clonally expanded T cells as barcodes for 'reverse phenotyping'. This allows identification of SARS-CoV-2-reactive TCRs and reveals phenotypic effects introduced by antigen-specific stimulation. We characterize transcriptional signatures of currently and previously activated SARS-CoV-2-reactive T cells, and show correspondence with phenotypes of T cells from the respiratory tract of patients with severe disease in the presence or absence of virus in independent cohorts. Reverse phenotyping is a powerful tool to provide an integrated insight into cellular states of SARS-CoV-2-reactive T cells across tissues and activation states.
Fullerene Van der Waals Oligomers as Electron Traps Shubina, Tatyana E.; Sharapa, Dmitry I.; Schubert, Christina ...
Journal of the American Chemical Society,
08/2014, Letnik:
136, Številka:
31
Journal Article
Recenzirano
Odprti dostop
Density functional theory calculations indicate that van der Waals fullerene dimers and larger oligomers can form interstitial electron traps in which the electrons are even more strongly bound than ...in isolated fullerene radical anions. The fullerenes behave like “super atoms”, and the interstitial electron traps represent one-electron intermolecular σ-bonds. Spectroelectrochemical measurements on a bis-fullerene-substituted peptide provide experimental support. The proposed deep electron traps are relevant for all organic electronics applications in which non-covalently linked fullerenes in van der Waals contact with one another serve as n-type semiconductors.
Försters resonance energy transfer (FRET) microscopy is widely used for the analysis of protein interactions in intact cells. However, FRET microscopy is technically challenging and does not allow ...assessing interactions in large cell numbers. To overcome these limitations we developed a flow cytometry-based FRET assay and analysed interactions of human and simian immunodeficiency virus (HIV and SIV) Nef and Vpu proteins with cellular factors, as well as HIV Rev multimer-formation.
Amongst others, we characterize the interaction of Vpu with CD317 (also termed Bst-2 or tetherin), a host restriction factor that inhibits HIV release from infected cells and demonstrate that the direct binding of both is mediated by the Vpu membrane-spanning region. Furthermore, we adapted our assay to allow the identification of novel protein interaction partners in a high-throughput format.
The presented combination of FRET and FACS offers the precious possibility to discover and define protein interactions in living cells and is expected to contribute to the identification of novel therapeutic targets for treatment of human diseases.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
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