4,348 research outputs found
Mitochondrial DNA Backgrounds Might Modulate Diabetes Complications Rather than T2DM as a Whole
No full textMitochondrial dysfunction has been implicated in rare and common forms of type 2 diabetes (T2DM). Additionally, rare mitochondrial DNA (mtDNA) mutations have been shown to be causal for T2DM pathogenesis. So far, many studies have investigated the possibility that mtDNA variation might affect the risk of T2DM, however, when found, haplogroup association has been rarely replicated, even in related populations, possibly due to an inadequate level of haplogroup resolution. Effects of mtDNA variation on diabetes complications have also been proposed. However, additional studies evaluating the mitochondrial role on both T2DM and related complications are badly needed. To test the hypothesis of a mitochondrial genome effect on diabetes and its complications, we genotyped the mtDNAs of 466 T2DM patients and 438 controls from a regional population of central Italy (Marche). Based on the most updated mtDNA phylogeny, all 904 samples were classified into 57 different mitochondrial sub-haplogroups, thus reaching an unprecedented level of resolution. We then evaluated whether the susceptibility of developing T2DM or its complications differed among the identified haplogroups, considering also the potential effects of phenotypical and clinical variables. MtDNA backgrounds, even when based on a refined haplogroup classification, do not appear to play a role in developing T2DM despite a possible protective effect for the common European haplogroup H1, which harbors the G3010A transition in the MTRNR2 gene. In contrast, our data indicate that different mitochondrial haplogroups are significantly associated with an increased risk of specific diabetes complications: H (the most frequent European haplogroup) with retinopathy, H3 with neuropathy, U3 with nephropathy, and V with renal failure
Anti-Allergic Cromones Inhibit Histamine and Eicosanoid Release from Activated Human and Murine Mast Cells by Releasing Annexin A1
No full textPMCID: PMC3601088This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
The bed of honour. [electronic resource] : To which is annex'd, The seasons: a poem. Inscribed to the Right Honourable the Earl of Albemarle, &c. By the author of The temple of war and Review.
No full textWith a list of subscribers (*a1).Foxon,Electronic reproduction.English Short Title Catalog,Reproduction of original from British Library
Adenosine A1 receptor activation preferentially protects cultured cerebellar neurons versus astrocytes against hypoxia-induced death
No full textAdministration of adenosine A1 receptor agonists in vivo is neuroprotective in various stroke models. Experiments using either mixed cultures of neurons and astrocytes or brain slices, in which several cell types are present, have demonstrated that activation of A1 receptors also id protective against hypoxia and/or hypoglycemia in vitro. In this study, we have examined the effect of the A1 agonist cyclopentyladenosine (CPA) on cellular damage, measured by efflux of lactate dehydrogenase (LDH), in highly enriched primary cultures of either neurons of astrocytes exposed to different metabolic insults. CPA reduced neuronal LDH release induced by a combination of hypoxia and substrate deprivation ("simulated ischemia"; IC50 = 28 nM) of by hypoxia alone (IC50 = 170 nM). In contrast, CPA had no effect on neuronal damage induced by substrate deprivation alone, not did it affect ischemic death to astrocytes. The neuroprotective effect of CPA during simulated ischemia and hypoxia were reversed by the A1 antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). These data demonstrate that activation of an adenosine A1 receptor on neurons, but not astrocytes, is protective against cellular damage of death induced specifically by hypoxia as opposed to other metabolic insults such as hypoglycemia.LR: 20061115; PUBM: Print; JID: 8910358; 0 (Neuroprotective Agents); 0 (Receptors, Purinergic P1); 41552-82-3 (N(6)-cyclopentyladenosine); 58-61-7 (Adenosine); EC 1.1.1.27 (L-Lactate Dehydrogenase); ppublishSource type: Prin
The restorative role of annexin A1 at the blood-brain barrier.
No full textThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium,
provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/
publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.Annexin A1 is a potent anti-inflammatory molecule that has been extensively studied in the peripheral immune system, but has not as yet been exploited as a therapeutic target/agent. In the last decade, we have undertaken the study of this molecule in the central nervous system (CNS), focusing particularly on the primary interface between the peripheral body and CNS: the blood-brain barrier. In this review, we provide an overview of the role of this molecule in the brain, with a particular emphasis on its functions in the endothelium of the blood-brain barrier, and the protective actions the molecule may exert in neuroinflammatory, neurovascular and metabolic disease. We focus on the possible new therapeutic avenues opened up by an increased understanding of the role of annexin A1 in the CNS vasculature, and its potential for repairing blood-brain barrier damage in disease and aging.SM is supported by Alzheimer’s Research UK (Grant# ARUK-PPG2016B-6) and
the Society for Endocrinology (Early Career Grant); RAL is funded by the CAPES
Foundation, Ministry of Education, Brazil (Grant#7326/2014-09). DV is supported
by Regional Technology Clusters, Regione Puglia, 2015 (cod. MTJU9H8)
and by FCRP-Fondazione Cassa di Risparmio di Puglia, 2015. ES is supported
by Alzheimer’s Research UK (Grant# ARUK-PPG2013B-2) and FISM-Fondazione
Italiana Sclerosi Multipla-cod.2014/R/21
Limiting Conditions of Muckenhoupt and Reverse Hölder Classes on Metric Measure Spaces
No full textFunding Information: Open Access funding provided by Aalto University. The author was supported by the Vilho, Yrjö and Kalle Väisälä Foundation of the Finnish Academy of Science and Letters. Publisher Copyright: © 2023, The Author(s).The natural maximal and minimal functions commute pointwise with the logarithm on A∞. We use this observation to characterize the spaces A1 and RH∞ on metric measure spaces with a doubling measure. As the limiting cases of Muckenhoupt Ap and reverse Hölder classes, respectively, their behavior is remarkably symmetric. On general metric measure spaces, an additional geometric assumption is needed in order to pass between Ap and reverse Hölder descriptions. Finally, we apply the characterization to give simple proofs of several known properties of A1 and RH∞, including a refined Jones factorization theorem. In addition, we show a boundedness result for the natural maximal function.Peer reviewe
Membrane proteome of the thermoalkaliphile Caldalkalibacillus thermarum TA2.A1
No full textProteomics has greatly advanced the understanding of the cellular biochemistry of microorganisms. The thermoalkaliphile Caldalkalibacillus thermarum TA2.A1 is an organism of interest for studies into how alkaliphiles adapt to their extreme lifestyles, as it can grow from pH 7.5 to pH 11. Within most classes of microbes, the membrane-bound electron transport chain (ETC) enables a great degree of adaptability and is a key part of metabolic adaptation. Knowing what membrane proteins are generally expressed is crucial as a benchmark for further studies. Unfortunately, membrane proteins are the category of proteins hardest to detect using conventional cellular proteomics protocols. In part, this is due to the hydrophobicity of membrane proteins as well as their general lower absolute abundance, which hinders detection. Here, we performed a combination of whole cell lysate proteomics and proteomics of membrane extracts solubilised with either SDS or FOS-choline-12 at various temperatures. The combined methods led to the detection of 158 membrane proteins containing at least a single transmembrane helix (TMH). Within this data set we revealed a full oxidative phosphorylation pathway as well as an alternative NADH dehydrogenase type II (Ndh-2) and a microaerophilic cytochrome oxidase ba3. We also observed C. thermarum TA2.A1 expressing transporters for ectoine and glycine betaine, compounds that are known osmolytes that may assist in maintaining a near neutral internal pH when the external pH is highly alkaline.BT/Environmental BiotechnologyBT/Biocatalysi
Free speech: Author reading a popular, and cheap, night on the town
No full textAnne Rice author reading and book signing at Books Inc
Up-Regulation of Annexin-A1 and Lipoxin A(4) in Individuals with Ulcerative Colitis May Promote Mucosal Homeostasis
No full textPubMed ID: 22723974This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
METHOD AND APPARATUS FOR COMBUSTING A CARBONACEOUS MATERIAL
No full textAbstract of WO 9318341 (A1) A method and an apparatus are described for combusting carbonaceous materials in a two-stage process. In a first reaction chamber (2), operating under fuel-rich conditions in a bubbling fluidisation regime, fuel undergoes primary combustion or gasification. Oxidising gas (5) is fed into the first reaction chamber at a velocity sufficient to maintain fluidisation
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