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1دورية أكاديمية
المؤلفون: Thors, Brynhildur, Jónsson, Helgi Már
المساهمون: Landspítali
مصطلحات موضوعية: Myndgreining (læknisfræði), Consciousness, Humans, Unconsciousness/diagnosis, stroke, loss of conciousness, basilar artery, thrombolysis, thrombectomy, Almenn læknisfræði
الوصف: Peer reviewed
وصف الملف: 455-456
العلاقة: Læknablaðið; 108(10); http://www.scopus.com/inward/record.url?scp=85138477564&partnerID=8YFLogxKTest; Thors , B & Jónsson , H M 2022 , ' Tilfelli mánaðarins. Skyndilegt meðvitundarleysi hjá hraustri konu ' , Læknablaðið , bind. 108 , nr. 10 , bls. 455-456 . https://doi.org/10.17992/lbl.2022.10.711Test; 94d2e7b2-4d70-48cd-9ebe-a3b8d33e210e; 85138477564; unpaywall: 10.17992/lbl.2022.10.711; https://hdl.handle.net/20.500.11815/3603Test
الإتاحة: https://doi.org/20.500.11815/3603Test
https://doi.org/10.17992/lbl.2022.10.711Test
https://hdl.handle.net/20.500.11815/3603Test -
2دورية أكاديمية
المؤلفون: Thors, Brynhildur, Sveinsson, Ólafur Árni
المساهمون: Læknadeild, Landspítali
مصطلحات موضوعية: Taugasjúkdómafræði, Arteries, Female, Humans, Infarction, Stroke, Thalamus, Unconsciousness/etiology
الوصف: Brátt heilaslag á grunni lokunar á Percheron slagæðar til miðheila og stúku er sjaldgæf og snúin greining vegna ósértækra klínískra einkenna. Skjót greining og meðferð er afar mikilvæg þar sem um er að ræða brátt og alvarlegt ástand. Hér er kynnt tilfelli ungrar konu sem fékk skyndilegan höfuðverk og skerta meðvitund. Sjáöldur voru misvíð og brugðust illa við ljósáreiti og iljaviðbrögð voru jákvæð beggja megin. Fram komu flogalíkar hreyfingar í öllum útlimum. Tölvusneiðmynd af heila og heilaæðum var eðlileg en bráð segulómun sýndi byrjandi drep í stúku beggja megin. Á grunni einkenna og segulómunar fékk sjúklingur segaleysandi meðferð í æð 70 mínútum eftir komu á bráðamóttöku og náði sér að fullu. Acute cerebral infarction due to occlusion of the artery of Percheron (AOP) is rare and poses a diagnostic challenge due to unspecific clinical symptoms. A prompt diagnosis and treatment is vital due to a potentially very serious outcome. Here we represent a healthy young woman who developed sudden headache and loss of consciousness. At admission she was unconscious with GCS of 4, pupils were unevenly dilated and poorly reactive and the plantar reflex was upward bilaterally. She had seizure like movements in all limbs. CT of brain and CT angiography were normal but acute MRI showed bilateral paramedian thalamic diffusion restriction. The patient was treated with i.v. thrombolysis (tPA) 70 minutes after hospital arrival and recovered fully. ; Peer reviewed
وصف الملف: 186-188
العلاقة: Læknablaðið; 107(4); Thors , B & Sveinsson , Ó Á 2021 , ' Skyndileg meðvitundarskerðing vegna lokunar á æð Percherons - sjúkratilfelli ' , Læknablaðið , bind. 107 , nr. 4 , bls. 186-188 . https://doi.org/10.17992/lbl.2021.04.631Test; feb7f36b-5d55-443d-94f1-5aa177a3f2dc; 85103608111; https://hdl.handle.net/20.500.11815/3566Test
الإتاحة: https://doi.org/20.500.11815/3566Test
https://doi.org/10.17992/lbl.2021.04.631Test
https://hdl.handle.net/20.500.11815/3566Test -
3مراجعة
المصدر: Laeknabladid ; ISSN:1670-4959 ; Volume:110 ; Issue:7
مصطلحات موضوعية: CADASIL, NOTCH 3, cerebral infarction, migraine with aura, small vessel disease
الوصف: Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is a hereditary small vessel disease of the brain characterized by progressive white matter lesions, subcortical infarcts, and cognitive decline. This autosomal dominant disorder is caused by mutations in the NOTCH3 gene located on chromosome 19, resulting in the accumulation of granular osmiophilic material within the walls of small arteries and arterioles. Clinically, CADASIL typically manifests in mid-adulthood with recurrent ischemic events, migraine with aura, mood disturbances, and cognitive impairment. Neuroimaging plays a crucial role in the diagnosis of CADASIL, with characteristic findings including white matter hyperintensities particularly in the anterior temporal lobe and external capsule.
العلاقة: https://doi.org/10.17992/lbl.2024.0708.801Test; https://pubmed.ncbi.nlm.nih.gov/38934718Test
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4دورية أكاديمية
المساهمون: University of Iceland, Landspitali University Hospital, Council for Science and Technology, Helga Jonsdottir and Sigurlidi Kristjansson Memorial Fund, Eimskipafelag University Fund
المصدر: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ; volume 1813, issue 2, page 322-331 ; ISSN 0167-4889
مصطلحات موضوعية: Cell Biology, Molecular Biology
الإتاحة: https://doi.org/10.1016/j.bbamcr.2010.12.001Test
https://api.elsevier.com/content/article/PII:S0167488910003083?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0167488910003083?httpAccept=text/plainTest -
5دورية أكاديمية
المصدر: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research ; volume 1783, issue 10, page 1893-1902 ; ISSN 0167-4889
مصطلحات موضوعية: Cell Biology, Molecular Biology
الإتاحة: https://doi.org/10.1016/j.bbamcr.2008.07.003Test
https://api.elsevier.com/content/article/PII:S0167488908002528?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0167488908002528?httpAccept=text/plainTest -
6دورية أكاديمية
المصدر: FEBS Letters ; volume 573, issue 1-3, page 175-180 ; ISSN 0014-5793 1873-3468
الوصف: Histamine and thrombin cause phosphorylation and activation of endothelial NO‐synthase (eNOS) on Ser1177. We tested the role of various protein kinases in mediating this effect in human umbilical vein endothelial cells. Inhibition of the Ca 2+ /calmodulin‐dependent protein kinase II or phosphoinositide 3‐kinase (PI3K) had no effect. H89, an inhibitor of both protein kinase A (PKA) and 5 ′ ‐AMP‐activated protein kinase (AMPK), strongly inhibited phosphorylation and activity of eNOS. Conversely, the PKA inhibitor Rp‐adenosine 3 ′ 5 ′ ‐cyclic monophosphate (cAMPS) had no effect and eNOS was not phosphorylated by treatments that affect cAMP levels. Thrombin and histamine caused phosphorylation of AMPK on Thr172 as well as on its downstream target acetyl‐CoA carboxylase. Activation of AMPK using AICAR or CCCP also resulted in eNOS phosphorylation. We conclude that histamine and thrombin cause eNOS phosphorylation in an AMPK mediated manner, independent of P13K‐Akt.
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7دورية أكاديمية
المصدر: Journal of the American College of Cardiology ; volume 43, issue 5, page A499-A500 ; ISSN 0735-1097
مصطلحات موضوعية: Cardiology and Cardiovascular Medicine
الإتاحة: https://doi.org/10.1016/s0735-1097Test(04)92113-4
https://api.elsevier.com/content/article/PII:S0735109704921134?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S0735109704921134?httpAccept=text/plainTest -
8دورية أكاديمية
المساهمون: 1 Univ Iceland, Pharmacol, Fac Med, IS-101 Reykjavik, Iceland 2 Univ Iceland, Dept Med, Fac Med, Landspitali Univ Hosp, IS-101 Reykjavik, Iceland
مصطلحات موضوعية: Poly(ADP-ribose) Polymerases/metabolism, Endothelium, Thrombin
الوصف: To access publisher's full text version of this article click on the hyperlink at the bottom of the page ; To test the hypothesis that a fall in cellular ATP following stimulation of endothelial cells with thrombin is secondary to a decrease in NAD levels caused by poly(ADP-Ribose)polymerase (PARP), we measured the levels of NAD and ATP in endothelial cells after treatment with thrombin, the Ca(++)-ionophore A23187, or hydrogen peroxide (H2O2), and compared the effects of inhibitors of PARP, NAD synthesis, and ADP-ribose breakdown on these responses. Neither thrombin nor A23187 caused a reduction in endothelial NAD levels and A23187 affected ATP levels independently of NAD levels or PARP activity. H2O2 induced lowering of NAD caused modest lowering of ATP but marked additional ATP-lowering, independent of PARP and NAD, was also demonstrated. We conclude that in endothelial cells ATP levels are largely independent of NAD and PARP, which do not play a role in thrombin or Ca(++)-ionophore-mediated lowering of ATP. H2O2 caused ATP lowering through a similar mechanism as thrombin and A23187 but, additionally, caused a further ATP lowering through its intense stimulation of PARP and marked lowering of NAD. ; University of Iceland Research Fund Research Fund of Landspitali, University Hospital Helga Jonsdottir and Sigurlidi Kristjansson Memorial fund
العلاقة: http://dx.doi.org/10.1080/15257770.2014.984072Test; Nucleosides Nucleotides Nucleic Acids 2015, 34 (4):246-57; http://hdl.handle.net/2336/566205Test; Nucleosides, nucleotides & nucleic acids
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9دورية أكاديمية
مصطلحات موضوعية: 1-Phosphatidylinositol 3-Kinase, Ca(2+)-Calmodulin Dependent Protein Kinase, Thrombin, Signal Transduction, Proto-Oncogene Protein, Phosphoserine, Nitric Oxide Synthase Type III, Multienzyme Complexes
الوصف: To access publisher full text version of this article. Please click on the hyperlink in Additional Links field ; Histamine and thrombin cause phosphorylation and activation of endothelial NO-synthase (eNOS) on Ser1177. We tested the role of various protein kinases in mediating this effect in human umbilical vein endothelial cells. Inhibition of the Ca2+/calmodulin-dependent protein kinase II or phosphoinositide 3-kinase (PI3K) had no effect. H89, an inhibitor of both protein kinase A (PKA) and 5'-AMP-activated protein kinase (AMPK), strongly inhibited phosphorylation and activity of eNOS. Conversely, the PKA inhibitor Rp-adenosine 3 '5'-cyclic monophosphate (cAMPS) had no effect and eNOS was not phosphorylated by treatments that affect cAMP levels. Thrombin and histamine caused phosphorylation of AMPK on Thr172 as well as on its downstream target acetyl-CoA carboxylase. Activation of AMPK using AICAR or CCCP also resulted in eNOS phosphorylation. We conclude that histamine and thrombin cause eNOS phosphorylation in an AMPK mediated manner, independent of P13K-Akt.
وصف الملف: YES
العلاقة: http://www.sciencedirect.com/science/article/B6T36-4D2C7CS-D/2/0602dcd9f2daacfc90a7c0dbf93de7b2Test; FEBS Lett. 2004, 573(1-3):175-80; http://hdl.handle.net/2336/13600Test; FEBS letters
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10دورية أكاديمية
مصطلحات موضوعية: Cells, Cultured, Endothelium, Vascular, Enzyme Activation, Epidermal Growth Factor, Histamine, Humans, Isoenzymes, Lysophosphatidylcholines, Lysophospholipids, Mitogen-Activated Protein Kinases, Nitric Oxide Synthase, Nitric Oxide Synthase Type III, Phospholipase C delta, Phosphorylation, Protein Kinase C, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-akt, Sphingosine, Thrombin, Type C Phospholipases
الوصف: To access publisher full text version of this article. Please click on the hyperlink in Additional Links field ; The protein kinase Akt is involved in embryonic vascular development and neoangiogenesis as well as in several endothelial cell functions, including activation of endothelial NO-synthase (eNOS) and promotion of endothelial cell survival. We have examined the effects of G-protein activators thrombin and histamine as well as lysophosphatidylcholine (LPC) on Akt phosphorylation in cultured human umbilical vein endothelial cells (HUVEC). Akt phosphorylation was analyzed with the phosphospecific Akt (Ser473) antibody by Western blotting. While epidermal growth factor (EGF) was a potent stimulator of Akt phosphorylation histamine, thrombin and LPC blocked its activation when used in cotreatment with EGF. Following inhibition or downregulation of protein kinase C (PKC), the inhibitory effect of both histamine and thrombin on the endothelial response to EGF was prevented. Furthermore, stimulation of PKC, using short-term 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment, markedly inhibited the stimulatory effects of EGF on Akt phosphorylation. Rottlerin, an inhibitor of the PKCdelta, but not Gö6976, which is an inhibitor of alpha, beta, gamma and isoforms, reversed the inhibitory effects of histamine. Conversely, inhibition or downregulation of PKC did not prevent the inhibitory effect of LPC. Akt phosphorylation was also increased by sphingosine 1-phosphate (S1P) treatment and this activity was influenced by the various cotreatments in the same way as the activation by EGF. Overall, this study demonstrated that the G-protein activators thrombin and histamine inhibited both EGF- and S1P-mediated Akt phosphorylation in HUVEC by activation of PKCdelta, while the inhibitory effects of LPC were independent of PKCdelta.
العلاقة: http://www.sciencedirect.com/science/article/B6T12-48JK65S-2/2/6a3cfbb8c99d7ed73cd4a1ce150835cbTest; Atherosclerosis. 2003, 168(2):245-53; http://hdl.handle.net/2336/15742Test; Atherosclerosis
الإتاحة: https://doi.org/10.1016/S0021-9150Test(03)00127-8
http://hdl.handle.net/2336/15742Test