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Union Catalogue of Agricultural Libraries in the Netherlands The WUR Library Catalogue contains bibliographic data on books and periodicals held by the libraries of Wageningen University and Research Centre and some 15 associated libraries. Holding data are added to each record. Subjects covered include Agrotechnology, Food and Food Production, Plant and Animal Sciences, Soil Science, Geo-information, Landscape and Spatial Planning, Water and Climate, Ecosystem Studies, Economics and Society. The joint collections of the participating libraries cover a substantial part of the internationally available scientific literature in these disciplines. As far as Dutch scientific literature in these fields is concerned, coverage can be considered near 100%, including much of the so-called &grey literature&. All titles are entered in their original language. Keywords are added to facilitate subject searching. The database is updated every day and now contains over 830.000 records.
Record nr. 460985
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Report. Session of the Near East commission on agricultural planning, 1st : Cairo, 16 - 21 December 1963
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STACKS ; VS06557
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To support researchers to publish their research Open Access, deals have been negotiated with various publishers. Depending on the deal, a discount is provided for the author on the Article Processing Charges that need to be paid by the author to publish an article Open Access. A discount of 100% means that (after approval) the author does not have to pay Article Processing Charges.
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Autor:Zhang Y; Xie L; Gunasekar SK; Tong D; Mishra A; Gibson WJ; Wang C; Fidler T; Marthaler B; Klingelhutz A; Abel ED; Samuel I; Smith JK; Cao L; Sah REndere?o:Department of Internal Medicine, Division of Cardiovascular Medicine, University of Iowa, Carver College of Medicine, Iowa City, Iowa 52242, USA.
Título:SWELL1 is a regulator of adipocyte size, insulin signalling and glucose homeostasis.
Fonte:Nat Cell B 19(5):504-517, 2017 05.
ISSN:País de publica??o:England
Idioma:engResumo:Adipocytes undergo considerable volumetric expansion in the setting of obesity. It has been proposed that such marked increases in adipocyte size may be sensed via adipocyte-autonomous mechanisms to mediate size-dependent intracellular signalling. Here, we show that SWELL1 (LRRC8a), a member of the Leucine-Rich Repeat Containing protein family, is an essential component of a volume-sensitive ion channel (VRAC) in adipocytes. We find that SWELL1-mediated VRAC is augmented in hypertrophic murine and human adipocytes in the setting of obesity. SWELL1 regulates adipocyte insulin-PI3K-AKT2-GLUT4 signalling, glucose uptake and lipid content via SWELL1 C-terminal leucine-rich repeat domain interactions with GRB2/Cav1. Silencing GRB2 in SWELL1 KO adipocytes rescues insulin-pAKT2 signalling. In vivo, shRNA-mediated SWELL1 knockdown and adipose-targeted SWELL1 knockout reduce adiposity and adipocyte size in obese mice while impairing systemic glycaemia and insulin sensitivity. These studies identify SWELL1 as a cell-autonomous sensor of adipocyte size that regulates adipocyte growth, insulin sensitivity and glucose tolerance.
Tipo de publica??o: JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
Nome de subst?ncia:0 (Chloride Channels); 0 (FOXO1 protein, human); 0 (Forkhead Box Protein O1); 0 (Foxo1 protein, mouse); 0 (GRB2 Adaptor Protein); 0 (GRB2 protein, human); 0 (Glucose Transporter Type 4); 0 (Grb2 protein, mouse); 0 (Insulin); 0 (LRRC8A protein, human); 0 (LRRC8A protein, mouse); 0 (Membrane Proteins); 0 (SLC2A4 protein, human); 0 (Slc2a4 protein, mouse); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (AKT2 protein, human); EC 2.7.11.1 (Akt2 protein, mouse); EC 2.7.11.1 (GSK3B protein, human); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Gsk3b protein, mouse); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); IY9XDZ35W2 (Glucose)
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Autor:Blanchard A; Bockenhauer D; Bolignano D; Calò LA; Cosyns E; Devuyst O; Ellison DH; Karet Frankl FE; Knoers NV; Konrad M; Lin SH; Vargas-Poussou REndere?o:Faculté de Médecine, Université Paris Descartes, Sorbonne Paris Cité, Paris, F H?pital Européen Georges Pompidou, Assistance Publique H?pitaux de Paris, Centre d'Investigation Clinique, Paris, F Centre d'Investigation Clinique 1418, Institut National de la Santé et de la Recherche Médica
Título:Gitelman syndrome: consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.
Fonte:Kidney I 91(1):24-33, 2017 Jan.
ISSN:País de publica??o:United States
Idioma:engResumo:Gitelman syndrome (GS) is a rare, salt-losing tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. The disease is recessively inherited, caused by inactivating mutations in the SLC12A3 gene that encodes the thiazide-sensitive sodium-chloride cotransporter (NCC). GS is usually detected during adolescence or adulthood, either fortuitously or in association with mild or nonspecific symptoms or both. The disease is characterized by high phenotypic variability and a significant reduction in the quality of life, and it may be associated with severe manifestations. GS is usually managed by a liberal salt intake together with oral magnesium and potassium supplements. A general problem in rare diseases is the lack of high quality evidence to inform diagnosis, prognosis, and management. We report here on the current state of knowledge related to the diagnostic evaluation, follow-up, management, and treatment of GS; ide and propose a research agenda to substantiate a number of issues related to GS. This expert consensus statement aims to establish an initial framework to enable clinical auditing and thus improve quality control of care.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (CLCNKB protein, human); 0 (Chloride Channels); 0 (SLC12A3 protein, human); 0 (Sodium Chloride, Dietary); 0 (Solute Carrier Family 12, Member 3); I38ZP9992A (Magnesium); RWP5GA015D (Potassium); SY7Q814VUP (Calcium)
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Autor:Song S; Ayon RJ; Yamamura A; Yamamura H; Dash S; Babicheva A; Tang H; Sun X; Cordery AG; Khalpey Z; Black SM; Desai AA; Rischard F; McDermott KM; Garcia JG; Makino A; Yuan JXEndere?o:Division of Translational and Regenerative Medicine, The University of Arizona College of Medicine, Tucson, Arizona.
Título:Capsaicin-induced Ca signaling is enhanced via upregulated TRPV1 channels in pulmonary artery smooth muscle cells from patients with idiopathic PAH.
Fonte:Am J Physiol Lung Cell Mol P 312(3):L309-L325, 2017 Mar 01.
ISSN:País de publica??o:United States
Idioma:engResumo:Capsaicin is an active component of chili pepper and a pain relief drug. Capsaicin can activate transient receptor potential vanilloid 1 (TRPV1) channels to increase cytosolic Ca concentration ([Ca ] ). A rise in [Ca ] in pulmonary artery smooth muscle cells (PASMCs) is an important stimulus for pulmonary vasoconstriction and vascular remodeling. In this study, we observed that a capsaicin-induced increase in [Ca ] was significantly enhanced in PASMCs from patients with idiopathic pulmonary arterial hypertension (IPAH) compared with normal PASMCs from healthy donors. In addition, the protein expression level of TRPV1 in IPAH PASMCs was greater than in normal PASMCs. Increasing the temperature from 23 to 43°C, or decreasing the extracellular pH value from 7.4 to 5.9 enhanced capsaicin-induced increases in [Ca ] ; the acidity (pH 5.9)- and heat (43°C)-mediated enhancement of capsaicin-induced [Ca ] increases were greater in IPAH PASMCs than in normal PASMCs. Decreasing the extracellular osmotic pressure from 310 to 200 mOsmol/l also increased [Ca ] , and the hypo-osmolarity-induced rise in [Ca ] was greater in IPAH PASMCs than in healthy PASMCs. Inhibition of TRPV1 (with 5'-IRTX or capsazepine) or knockdown of TRPV1 (with short hairpin RNA) attenuated capsaicin-, acidity-, and osmotic stretch-mediated [Ca ] increases in IPAH PASMCs. Capsaicin induced phosphorylation of CREB by raising [Ca ] , and capsaicin-induced CREB phosphorylation were significantly enhanced in IPAH PASMCs compared with normal PASMCs. Pharmacological inhibition and knockdown of TRPV1 attenuated IPAH PASMC proliferation. Taken together, the capsaicin-mediated [Ca ] increase due to upregulated TRPV1 may be a critical pathogenic mechanism that contributes to augmented Ca influx and excessive PASMC proliferation in patients with IPAH.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Chloride Channels); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Diterpenes); 0 (Potassium Channels); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (iodoresiniferatoxin); LFW48MY844 (capsazepine); S07O44R1ZM (Capsaicin)
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Autor:Atif M; Estrada-Mondragon A; Nguyen B; Lynch JW; Keramidas AEndere?o:Queensland Brain Institute, The University of Queensland, Brisbane, Australia.
Título:Effects of glutamate and ivermectin on single glutamate-gated chloride channels of the parasitic nematode H. contortus.
Fonte:PLoS P 13(10):e17 Oct.
ISSN:País de publica??o:United States
Idioma:engResumo:Ivermectin (IVM) is a widely-used anthelmintic that works by binding to and activating glutamate-gated chloride channel receptors (GluClRs) in nematodes. The resulting chloride flux inhibits the pharyngeal muscle cells and motor neurons of nematodes, causing death by paralysis or starvation. IVM resistance is an emerging problem in many pest species, necessitating the development of novel drugs. However, drug optimisation requires a quantitative understanding of GluClR activation and modulation mechanisms. Here we investigated the biophysical properties of homomeric α (avr-14b) GluClRs from the parasitic nematode, H. contortus, in the presence of glutamate and IVM. The receptor proved to be highly responsive to low nanomolar concentrations of both compounds. Analysis of single receptor activations demonstrated that the GluClR oscillates between multiple functional states upon the binding of either ligand. The G36'A mutation in the third transmembrane domain, which was previously thought to hinder access of IVM to its binding site, was found to decrease the duration of active periods and increase receptor desensitisation. On an ensemble macropatch level the mutation gave rise to enhanced current decay and desensitisation rates. Because these responses were common to both glutamate and IVM, and were observed under conditions where agonist binding sites were likely saturated, we infer that G36'A affects the intrinsic properties of the receptor with no specific effect on IVM binding mechanisms. These unexpected results provide new insights into the activation and modulatory mechanisms of the H. contortus GluClRs and provide a mechanistic framework upon which the actions of drugs can be reliably interpreted.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Anthelmintics); 0 (Chloride Channels); 0 (glutamate-gated chloride channels); 3KX376GY7L (Glutamic Acid);
(Ivermectin)
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Autor:Gabriel SS; Belge H; Gassama A; Debaix H; Luciani A; Fehr T; Devuyst OEndere?o:Institute of Physiology, University of Zürich, Zürich, S Division of Nephrology, University Hospital Zürich, Zürich, Switzerland.
Título:Bone marrow transplantation improves proximal tubule dysfunction in a mouse model of Dent disease.
Fonte:Kidney I 91(4):842-855, 2017 Apr.
ISSN:País de publica??o:United States
Idioma:engResumo:Dent disease is a rare X-linked tubulopathy caused by mutations in the endosomal chloride-proton exchanger (ClC-5) resulting in defective receptor-mediated endocytosis and severe proximal tubule dysfunction. Bone marrow transplantation has recently been shown to preserve kidney function in cystinosis, a lysosomal storage disease causing proximal tubule dysfunction. Here we test the effects of bone marrow transplantation in Clcn5 mice, a faithful model for Dent disease. Transplantation of wild-type bone marrow in Clcn5 mice significantly improved proximal tubule dysfunction, with decreased low-molecular-weight proteinuria, glycosuria, calciuria, and polyuria four months after transplantation, compared to Clcn5 mice transplanted with ClC-5 knockout bone marrow. Bone marrow-derived cells engrafted in the interstitium, surrounding proximal tubule cells, which showed a rescue of the apical expression of ClC-5 and megalin receptors. The improvement of proximal tubule dysfunction correlated with Clcn5 gene expression in kidneys of mice transplanted with wild-type bone marrow cells. Coculture of Clcn5 proximal tubule cells with bone marrow-derived cells confirmed rescue of ClC-5 and megalin, resulting in improved endocytosis. Nanotubular extensions between the engrafted bone marrow-derived cells and proximal tubule cells were observed in vivo and in vitro. No rescue was found when the formation of the tunneling nanotubes was prevented by actin depolymerization or when cells were physically separated by transwell inserts. Thus, bone marrow transplantation may rescue the epithelial phenotype due to an inherited endosomal defect. Direct contacts between bone marrow-derived cells and diseased tubular cells play a key role in the rescue mechanism.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (CLC-5 chloride channel); 0 (Chloride Channels); 0 (Low Density Lipoprotein Receptor-Related Protein-2); 0 (Lrp2 protein, mouse)
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Autor:Zhang Y; Zhang Z; Xiao S; Tien J; Le S; Le T; Jan LY; Yang HEndere?o:Department of Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.
Título:Inferior Olivary TMEM16B Mediates Cerebellar Motor Learning.
Fonte:N 95(5):.e4, 2017 Aug 30.
ISSN:País de publica??o:United States
Idioma:engResumo:Ca -activated ion channels shape membrane excitability and Ca dynamics in response to cytoplasmic Ca elevation. Compared to the Ca -activated K channels, known as BK and SK channels, the physiological importance of Ca -activated Cl channels (CaCCs) in neurons has been largely overlooked. Here we report that CaCCs coexist with BK and SK channels in inferior olivary (IO) neurons that send climbing fibers to innervate cerebellar Purkinje cells for the control of motor learning and timing. Ca influx through the dendritic high-threshold voltage-gated Ca channels activates CaCCs, which contribute to membrane repolarization of IO neurons. Loss of TMEM16B expression resulted in the absence of CaCCs in IO neurons, leading to markedly diminished action potential firing of IO neurons in TMEM16B knockout mice. Moreover, these mutant mice exhibited severe cerebellar motor learning deficits. Our findings thus advance the understanding of the neurophysiology of CaCCs and the ionic basis of IO neuron excitability.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Chloride Channels); 0 (TMEM16B protein, mouse); SY7Q814VUP (Calcium)
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Autor:Valinsky WC; Touyz RM; Shrier AEndere?o:Department of Physiology, McGill University, 3649 Promenade sir William Osler, Montreal, Quebec H3G 0B1, Canada.
Título:Characterization of constitutive and acid-induced outwardly rectifying chloride currents in immortalized mouse distal tubular cells.
Fonte:Biochim Biophys A 07- 08.
ISSN:País de publica??o:Netherlands
Idioma:engResumo:Thiazides block Na reabsorption while enhancing Ca reabsorption in the kidney. As previously demonstrated in immortalized mouse distal convoluted tubule (MDCT) cells, chlorothiazide application induced a robust plasma membrane hyperpolarization, which increased Ca uptake. This essential thiazide-induced hyperpolarization was prevented by the Cl channel inhibitor 5-Nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), implicating NPPB-sensitive Cl channels, however the nature of these Cl channels has been rarely described in the literature. Here we show that MDCT cells express a dominant, outwardly rectifying Cl current at extracellular pH7.4. This constitutive Cl current was more permeable to larger anions (Eisenman sequence I; I >Br &#8805;Cl ) and was substantially inhibited by >100mM [Ca ] , which distinguished it from ClC-K2/barttin. Moreover, the constitutive Cl current was blocked by NPPB, along with other Cl channel inhibitors (4,4'-diisothiocyanatostilbene-2,2'-disulfonate, DIDS; flufenamic acid, FFA). Subjecting the MDCT cells to an acidic extracellular solution (pHBr >Cl ), but was distinguished from the constitutive Cl current by its rectification characteristics, ion sensitivities, and response to FFA. In addition, we have identified similar outwardly rectifying and acid-sensitive currents in immortalized cells from the inner medullary collecting duct (mIMCD-3 cells). Expression of an acid-induced Cl current would be particularly relevant in the acidic IMCD (pH<5.5). To our knowledge, the properties of these Cl currents are unique and provide the mechanisms to account for the Cl efflux previously speculated to be present in MDCT cells.
Tipo de publica??o: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nome de subst?ncia:0 (Chloride Channels); 0 (Chlorides)
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Autor:Yelhekar TD; Druzin M; Johansson SEndere?o:Department of Integrative Medical Biology, Ume? University , Ume?, SE-901 87, Sweden.
Título:Contribution of Resting Conductance, GABA -Receptor Mediated Miniature Synaptic Currents and Neurosteroid to Chloride Homeostasis in Central Neurons.
Fonte:eN 4(2), 2017 Mar-Apr.
ISSN:País de publica??o:United States
Idioma:engResumo:Maintenance of a low intraneuronal Cl concentration, [Cl ] , is critical for inhibition in the CNS. Here, the contribution of passive, conductive Cl flux to recovery of [Cl ] after a high load was analyzed in mature central neurons from rat. A novel method for quantifying the resting Cl conductance, important for [Cl ] recovery, was developed and the possible contribution of GABA and glycine receptors and of ClC-2 channels to this conductance was analyzed. The hypothesis that spontaneous, action potential-independent release of GABA is important for [Cl ] recovery was tested. [Cl ] was examined by gramicidin-perforated patch recordings in medial preoptic neurons. Cells were loaded with Cl by combining GABA or glycine application with a depolarized voltage, and the time course of [Cl ] was followed by measurements of the Cl equilibrium potential as obtained from the current recorded during voltage ramps combined with GABA or glycine application. The results show that passive Cl flux contributes significantly, in the same order of magnitude as does K -Cl cotransporter 2 (KCC2), to [Cl ] recovery and that Cl conductance accounts for ?? 1/4
6% of the total resting conductance. A major fraction of this resting Cl conductance is picrotoxin (PTX)-sensitive and likely due to open GABA receptors, but ClC-2 channels do not contribute. The results also show that when the decay of GABA receptor-mediated miniature postsynaptic currents (minis) is slowed by the neurosteroid allopregnanolone, such minis may significantly quicken [Cl ] recovery, suggesting a possible steroid-regulated role for minis in the control of Cl homeostasis.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Anions); 0 (Chloride Channels); 0 (Chlorides); 0 (ClC-2 chloride channels); 0 (Neurotransmitter Agents); 0 (Receptors, GABA-A); 0 (Symporters); 0 (potassium-chloride symporters)
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Autor:Malyshev AY; Roshchin MV; Smirnova GR; Dolgikh DA; Balaban PM; Ostrovsky MAEndere?o:Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences, Russian Federation. Electronic address: malyshev@ihna.ru.
Título:Chloride conducting light activated channel GtACR2 can produce both cessation of firing and generation of action potentials in cortical neurons in response to light.
Fonte:Neurosci L 640:76-80, 2017 Feb 15.
ISSN:País de publica??o:Ireland
Idioma:engResumo:Optogenetics is a powerful technique in neuroscience that provided a great success in studying the brain functions during the last decade. Progress of optogenetics crucially depends on development of new molecular tools. Light-activated cation-conducting channelrhodopsin2 was widely used for excitation of cells since the emergence of optogenetics. In 2015 a family of natural light activated chloride channels GtACR was identified which appeared to be a very promising tool for using in optogenetics experiments as a cell silencer. Here we examined properties of GtACR2 channel expressed in the rat layer 2/3 pyramidal neurons by means of in utero electroporation. We have found that despite strong inhibition the light stimulation of GtACR2-positive neurons can surprisingly lead to generation of action potentials, presumably initiated in the axonal terminals. Thus, when using the GtACR2 in optogenetics experiments, its ability to induce action potentials should be taken into account. Our results also open an interesting possibility of using the GtACR2 both as cell silencer and cell activator in the same experiment varying the pattern of light stimulation.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Chloride Channels); 0 (Luminescent Proteins); 0 (Recombinant Fusion Proteins)
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Autor:Fuchs O; Gorlanova O; Latzin P; Schmidt A; Schieck M; Toncheva AA; Michel S; Gaertner VD; Kabesch M; Frey UEndere?o:University Children's Hospital (UKBB), University of Basel, Basel, S Dr von Hauner Children's Hospital, Ludwig-Maximilians-Universit?t, Munch, and the Comprehensive Pneumology Center Munich (CPC-M; Member of the German Center for Lung Research [DZL]), Munich, G Division of Respirat
Título:6q12 and 11p14 variants are associated with postnatal exhaled nitric oxide levels and respiratory symptoms.
Fonte:J Allergy Clin I 140(4):, 2017 Oct.
ISSN:País de publica??o:United States
Idioma:engResumo:BACKGROUND: Exhaled nitric oxide (eNO) is a biomarker of airway inflammation and seems to precede respiratory symptoms, such as asthma, in childhood. Identifying genetic determinants of postnatal eNO levels might aid in unraveling the role of eNO in epithelial function or airway inflammation and disease. OBJECTIVE: We sought to identify genetic determinants of early postnatal eNO levels and subsequent respiratory symptoms during the first year of life. METHODS: Within a population-based birth cohort, eNO levels were measured in healthy term infants aged 5 weeks during quiet tidal breathing in unsedated sleep. We assessed associations of single nucleotide polymorphisms with eNO levels in a genome-wide association study and subsequent symptoms of lower respiratory tract infections during the first year of life and asked whether this was modified by prenatal and early-life environmental factors. RESULTS: We identified thus far unknown determinants of infant eNO levels: rs208515 (P = 3.3 × 10 ), which is located at 6q12, probably acting in "trans" and explaining 10.3% of eNO level variance, and rs1441519 (P = 1.6 × 10 ), which is located at 11p14, potentially affecting nitric oxide synthase 3 (NOS3) expression, as shown by means of in vitro functional analyses. Moreover, the 6q12 locus was inversely associated with subsequent respiratory symptoms (P < .05) and time to recovery after first respiratory symptoms during the first year of life (P < .05). CONCLUSION: The identification of novel genetic determinants of infant eNO levels might implicate that postnatal eNO metabolism in healthy infants before first viral infections and sensitization is related to mechanisms other than those associated with asthma, atopy, or increased risk thereof later in life.
Tipo de publica??o: JOURNAL ARTICLE
Nome de subst?ncia:0 (Chloride Channels); 0 (EYS protein, human); 0 (Eye Proteins); 0 (anoctamin 3, human); 31C4KY9ESH (Nitric Oxide)
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