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[PMID]: 29471143
[Au] Autor:Hutton ARJ; Quinn HL; McCague PJ; Jarrahian C; Rein-Weston A; Coffey PS; Gerth-Guyette E; Zehrung D; Larrañeta E; Donnelly RF
[Ad] Address:School of Pharmacy, Queen's University, Belfast, Medical Biology Centre, 97 Lisburn Road, Belfast BT9 7BL, United Kingdom.
[Ti] Title:Transdermal delivery of vitamin K using dissolving microneedles for the prevention of vitamin K deficiency bleeding.
[So] Source:Int J Pharm;541(1-2):56-63, 2018 Feb 19.
[Is] ISSN:1873-3476
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Vitamin K deficiency within neonates can result in vitamin K deficiency bleeding. Ensuring that newborns receive vitamin K is particularly critical in places where access to health care and blood products and transfusions is limited. The World Health Organization recommends that newborns receive a 1 mg intramuscular injection of vitamin K at birth. Evidence from multiple surveillance studies shows that the introduction of vitamin K prophylaxis reduces the incidence of vitamin K deficiency bleeding. Despite these recommendations, coverage of vitamin K prophylactic treatment in low-resource settings is limited. An intramuscular injection is the most common method of vitamin K administration in neonates. In low- and middle-income countries, needle sharing may occur, which may result in the spread of bloodborne diseases. The objective of our study was to investigate the manufacture of microneedles for the delivery of vitamin K. Following microneedle fabrication, we performed insertion studies to assess the microneedle's mechanical properties. Results indicate that vitamin K in a microneedle array was successfully delivered in vitro across neonatal porcine skin with 1.80 ±â€¯0.08 mg delivered over 24 h. Therefore, this initial study shows that microneedles do have the potential to prevent vitamin K deficiency bleeding. Future work will assess delivery of vitamin K in microneedle array in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

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[PMID]: 29401369
[Au] Autor:Ardell S; Offringa M; Ovelman C; Soll R
[Ad] Address:Pediatrics Division of Newborn Medicine, University of Pittsburgh Medical Center, 300 Halket Street, Pittsburgh, Pennsylvania, USA, 15219.
[Ti] Title:Prophylactic vitamin K for the prevention of vitamin K deficiency bleeding in preterm neonates.
[So] Source:Cochrane Database Syst Rev;2:CD008342, 2018 02 05.
[Is] ISSN:1469-493X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Vitamin K is necessary for the synthesis of coagulation factors. Term infants, especially those who are exclusively breast fed, are deficient in vitamin K and consequently may have vitamin K deficiency bleeding (VKDB). Preterm infants are potentially at greater risk for VKDB because of delayed feeding and subsequent delay in the colonization of their gastrointestinal system with vitamin K producing microflora, as well as immature hepatic and hemostatic function.  OBJECTIVES: To determine the effect of vitamin K prophylaxis in the prevention of vitamin K deficiency bleeding (VKDB) in preterm infants. SEARCH METHODS: We used the standard search strategy of Cochrane Neonatal to search the Cochrane Central Register of Controlled Trials (CENTRAL 2016, Issue 11), MEDLINE via PubMed (1966 to 5 December 2016), Embase (1980 to 5 December 2016), and CINAHL (1982 to 5 December 2016). We also searched clinical trials databases, conference proceedings, and the reference lists of retrieved articles. SELECTION CRITERIA: Randomized controlled trials (RCTs) or quasi-RCTs of any preparation of vitamin K given to preterm infants. DATA COLLECTION AND ANALYSIS: We evaluated potential studies and extracted data in accordance with the recommendations of Cochrane Neonatal. MAIN RESULTS: We did not identify any eligible studies that compared vitamin K to no treatment.One study compared intravenous (IV) to intramuscular (IM) administration of vitamin K and compared various dosages of vitamin K. Three different prophylactic regimes of vitamin K (0.5 mg IM, 0.2 mg vitamin K , or 0.2 mg IV) were given to infants less than 32 weeks' gestation. Given that only one small study met the inclusion criteria, we assessed the quality of the evidence for the outcomes evaluated as low.Intramuscular versus intravenousThere was no statistically significant difference in vitamin K levels in the 0.2 mg IV group when compared to the infants that received either 0.2 or 0.5 mg vitamin K IM (control) on day 5. By day 25, vitamin K levels had declined in all of the groups, but infants who received 0.5 mg vitamin K IM had higher levels of vitamin K than either the 0.2 mg IV group or the 0.2 mg IM group.Vitamin K 2,3-epoxide (vitamin K O) levels in the infants that received 0.2 mg IV were not statistically different from those in the control group on day 5 or 25 of the study. All of the infants had normal or supraphysiologic levels of vitamin K concentrations and either no detectable or insignificant amounts of prothrombin induced by vitamin K absence-II (PIVKA II).Dosage comparisonsDay 5 vitamin K levels and vitamin K O levels were significantly lower in the 0.2 mg IM group when compared to the 0.5 mg IM group. On day 25, vitamin K O levels and vitamin K levels in the 0.2 mg IM group and the 0.5 mg IM group were not significantly different. Presence of PIVKA II proteins in the 0.2 mg IM group versus the 0.5 mg IM group was not significantly different at day 5 or 25 of the study. AUTHORS' CONCLUSIONS: Preterm infants have low levels of vitamin K and develop detectable PIVKA proteins during the first week of life. Despite being at risk for VKDB, there are no studies comparing vitamin K versus non-treatment and few studies that address potential dosing strategies for effective treatment. Dosage studies suggest that we are currently giving doses of vitamin K to preterm infants that lead to supraphysiologic levels. Because of current uncertainty, clinicians will have to extrapolate data from term infants to preterm infants. Since there is no available evidence that vitamin K is harmful or ineffective and since vitamin K is an inexpensive drug, it seems prudent to follow the recommendations of expert bodies and give vitamin K to preterm infants. However, further research on appropriate dose and route of administration is warranted.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Process
[do] DOI:10.1002/14651858.CD008342.pub2

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[PMID]: 29246447
[Au] Autor:Chollet ME; Andersen E; Skarpen E; Myklebust CF; Koehler C; Morth JP; Chuansumrit A; Pinotti M; Bernardi F; Thiede B; Sandset PM; Skretting G
[Ad] Address:Department of Hematology, Oslo University Hospital, NO-0424 Oslo, Norway; Research Institute of Internal Medicine, Oslo University Hospital, NO-0424 Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address: Maria.Eugenia.Chollet.Dugarte@rr-research.no.
[Ti] Title:Factor VII deficiency: Unveiling the cellular and molecular mechanisms underlying three model alterations of the enzyme catalytic domain.
[So] Source:Biochim Biophys Acta;1864(3):660-667, 2018 Mar.
[Is] ISSN:0006-3002
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Activated factor (F) VII is a vitamin K-dependent glycoprotein that initiates blood coagulation upon interaction with tissue factor. FVII deficiency is the most common of the rare congenital bleeding disorders. While the mutational pattern has been extensively characterized, the pathogenic molecular mechanisms of mutations, particularly at the intracellular level, have been poorly defined. Here, we aimed at elucidating the mechanisms underlying altered FVII biosynthesis in the presence of three mutation types in the catalytic domain: a missense change, a microdeletion and a frameshift/elongation, associated with severe or moderate to severe phenotypes. Using CHO-K1 cells transiently transfected with expression vectors containing the wild-type FVII cDNA (FVIIwt) or harboring the p.I289del, p.G420V or p.A354V-p.P464Hfs mutations, we found that the secretion of the FVII mutants was severely decreased compared to FVIIwt. The synthesis rate of the mutants was slower than the FVIIwt and delayed, and no degradation of the FVII mutants by proteasomes, lysosomes or cysteine proteases was observed. Confocal immunofluorescence microscopy studies showed that FVII variants were localized into the endoplasmic reticulum (ER) but were not detectable within the Golgi apparatus. These findings suggested that a common pathogenic mechanism, possibly a defective folding of the mutant proteins, was triggered by the FVII mutations. The misfolded state led to impaired trafficking of these proteins causing ER retention, which would explain the low to very low FVII plasma levels observed in patients carrying these mutations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180207
[Lr] Last revision date:180207
[St] Status:In-Data-Review

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[PMID]: 29269514
[Au] Autor:Weitz JI; Fredenburgh JC
[Ad] Address:From the Department of Medicine (J.I.W., J.C.F.) and Department of Biochemistry and Biomedical Sciences (J.I.W.), McMaster University, Hamilton, Ontario, Canada; and Thrombosis and Atherosclerosis Research Institute (J.I.W., J.C.F.), Hamilton, Ontario, Canada. weitzj@taari.ca.
[Ti] Title:2017 Scientific Sessions Sol Sherry Distinguished Lecture in Thrombosis: Factor XI as a Target for New Anticoagulants.
[So] Source:Arterioscler Thromb Vasc Biol;, 2017 Dec 21.
[Is] ISSN:1524-4636
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The goal of anticoagulant therapy is to attenuate thrombosis without compromising hemostasis. Although the direct oral anticoagulants are associated with less intracranial hemorrhage than vitamin K antagonists, bleeding remains their major side effect. Factor XI has emerged as a promising target for anticoagulants that may be safer than those currently available. The focus on factor XI stems from epidemiological evidence of its role in thrombosis, the observation of attenuated thrombosis in factor XI-deficient mice, identification of novel activators, and the fact that factor XI deficiency is associated with only a mild bleeding diathesis. Proof-of-concept comes from the demonstration that compared with enoxaparin, factor XI knockdown reduces venous thromboembolism without increasing bleeding after elective knee arthroplasty. This article rationalizes the selection of factor XI as a target for new anticoagulants, reviews the agents under development, and outlines a potential path forward for their development.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 171222
[Lr] Last revision date:171222
[St] Status:Publisher

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[PMID]: 29139025
[Au] Autor:Zeynelabidin S; Klouwer FCC; Meijers JCM; Suijker MH; Engelen M; Poll-The BT; van Ommen CH
[Ad] Address:Department of Pediatric Neurology, Emma Children's Hospital, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
[Ti] Title:Coagulopathy in Zellweger spectrum disorders: a role for vitamin K.
[So] Source:J Inherit Metab Dis;, 2017 Nov 14.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Zellweger spectrum disorders (ZSDs) are caused by an impairment of peroxisome biogenesis, resulting in multiple metabolic abnormalities. This leads to a range of symptoms, including hepatic dysfunction and coagulopathy. This study evaluated the incidence and severity of coagulopathy and the effect of vitamin K supplementation orally and IV in ZSD. METHODS: Data were retrospectively retrieved from the medical records of 30 ZSD patients to study coagulopathy and the effect of vitamin K orally on proteins induced by vitamin K absence (PIVKA-II) levels. Five patients from the cohort with a prolonged prothrombin time, low factor VII, and elevated PIVKA-II levels received 10 mg of vitamin K IV. Laboratory results, including thrombin generation, at baseline and 72 h after vitamin K administration were examined. RESULTS: In the retrospective cohort, four patients (13.3%) experienced intracranial bleedings and 14 (46.7%) reported minor bleeding. No thrombotic events occurred. PIVKA-II levels decreased 38% after start of vitamin K therapy orally. In the five patients with a coagulopathy, despite treatment with oral administration of vitamin K, vitamin K IV caused an additional decrease (23%) of PIVKA-II levels and increased thrombin generation. CONCLUSION: Bleeding complications frequently occur in ZSD patients due to liver disease and vitamin K deficiency. Vitamin K deficiency is partly corrected by vitamin K supplementation orally, and vitamin K administered IV additionally improves vitamin K status, as shown by further decrease of PIVKA-II and improved thrombin generation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171115
[Lr] Last revision date:171115
[St] Status:Publisher
[do] DOI:10.1007/s10545-017-0113-8

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[PMID]: 29126301
[Au] Autor:Winter WE; Flax SD; Harris NS
[Ad] Address:Department of Pathology, Immunology & Laboratory Medicine, University of Florida, Gainesville, FL.
[Ti] Title:Coagulation Testing in the Core Laboratory.
[So] Source:Lab Med;48(4):295-313, 2017 Nov 08.
[Is] ISSN:1943-7730
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Primary hemostasis begins with endothelial injury. VWF, produced by endothelial cells, binds to platelets and links them to subendothelial collagen. Platelet-derived ADP and thromboxane activate non-adhered platelets via their GPIIb/IIIa receptors, allowing these platelets to participate in platelet aggregation. Secondary hemostasis is initiated with the binding of factor VII to extravascular tissue factor (TF). Factors II, VII, IX and X are vitamin K-dependent factors. The role of vitamin K is to assist in the addition of gamma carboxylate groups to glutamic acids in the "GLA" domains of these factors.In vitro the intrinsic pathway is initiated when fresh whole blood is placed in a glass tube. The negative charge of the glass initiates the "contact pathway" where FXII is activated and then FXIa cleaves FIX to FIXa. The extrinsic pathway is triggered when tissue factor, phospholipid and calcium are added to plasma anticoagulated with citrate. In vitro, FVII is activated to FVIIa, and TF-FVIIa preferentially converts FX to FXa activating the common pathway.The prothrombin time is commonly used to monitor warfarin anticoagulant therapy. To correct for differences in reagent and instrument, the international normalized ratio was developed to improve standardization of PT reporting globally. The activated partial thromboplastin time (aPTT) is used to evaluate the intrinsic and common pathways of coagulation. The aPTT is useful clinically as a screening test for inherited and acquired factor deficiencies as well as to monitor unfractionated heparin therapy although the anti-Xa assay is now the preferred measure of the effects of unfractionated heparin. The Clauss assay is the most commonly performed fibrinogen assay and uses diluted plasma where clotting is initiated with a high concentration of reagent thrombin.The mixing study assists in the assessment of an abnormally prolonged PT or aPTT. An equal volume of citrated patient plasma is mixed with normal pooled plasma and the PT or aPTT are repeated on the 1:1 mix. Factor activity assays are most commonly performed as a one-stage assay. The patient's citrated plasma is diluted and mixed 1-to-1 with a single factor-deficient substrate plasma. A PT or aPTT is performed on the above mix, depending on the factor being tested.Factor inhibitors are antibodies that are most commonly diagnosed in male patients with severe hemophilia A (FVIII deficiency) where they are induced by factor replacement therapy.Factor inhibitors can also appear in the form of spontaneous autoantibodies in both male and female individuals who were previously well. This is an autoimmune condition called "acquired hemophilia."Most coagulation laboratories can measure the plasma concentration of VWF protein (VWF antigen) by an immunoturbidimetric technique. Testing the functional activity of VWF, utilizes the drug ristocetin.The state of multimerization of VWF is important and is assessed by electrophoresis on agarose gels. Type 2a and 2b VWD are associated with the lack of intermediate- and high molecular weight multimers.The antiphospholipid syndrome (APLS) is an acquired autoimmune phenomenon associated with an increased incidence of both venous and arterial thromboses, as well as fetal loss. Typically, there is a paradoxical prolongation of the aPTT in the absence of any clinical features of bleeding. This is the so-called "lupus anticoagulant (LA) effect." The laboratory definition of the APLS requires the presence of either a "lupus anticoagulant" or a persistent titer of antiphospholipid antibodies.There are now 2 broad classes of direct-acting oral anticoagulants (DOACs): [1] The oral direct thrombin inhibitors (DTIs) such as dabigatran; and [2] The oral direct factor Xa inhibitors such as rivaroxaban and apixaban. The PT and aPTT are variably affected by the DOACs and are generally unhelpful in monitoring their concentrations. Most importantly, a normal PT or aPTT does NOT exclude the presence of any of the DOACs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171110
[Lr] Last revision date:171110
[St] Status:In-Process
[do] DOI:10.1093/labmed/lmx050

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[PMID]: 28928999
[Au] Autor:Zekavat OR; Fathpour G; Haghpanah S; Dehghani SJ; Zekavat M; Shakibazad N
[Ad] Address:Hematology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
[Ti] Title:Acquired Vitamin K Deficiency as Unusual Cause of Bleeding Tendency in Adults: A Case Report of a Nonhospitalized Student Presenting with Severe Menorrhagia.
[So] Source:Case Rep Obstet Gynecol;2017:4239148, 2017.
[Is] ISSN:2090-6684
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We report a rare case of acquired vitamin K deficiency presenting with severe menorrhagia and without any gynecological problem. Partial thromboplastin time (59.2 seconds) and prothrombin time (33.1 seconds, INR: 5.97) were considerably prolonged in laboratory evaluations. A complete coagulation factor assay test was performed for the patient: factor IX, 24%; factor II, 41%; factor VII, 3%; and factor X, 52%. She had been taking many high-energy drinks and she had inadequate dietary intake for the past 6 months. Given that she had vitamin K deficiency (VKD), a course of vitamin K therapy was started for her in the hospital. This case showed the potential for menorrhagia due to VKD with use of high-energy drinks and the value of a complete and detailed history in early diagnosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 170922
[Lr] Last revision date:170922
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2017/4239148

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[PMID]: 28870850
[Au] Autor:Angles E; Mouton C; Perino J; Remy A; Ouattara A
[Ad] Address:Department of Anaesthesia and Critical Care II, CHU Bordeaux, 33600 Pessac, France; UMR 1034, Inserm, Biology of Cardiovascular Diseases, University Bordeaux, 33600 Pessac, France.
[Ti] Title:Hypoprothrombinemia and severe perioperative haemorrhagic complications in cardiac surgery patients treated with high-dose cefazolin for infective endocarditis.
[So] Source:Anaesth Crit Care Pain Med;, 2017 Sep 01.
[Is] ISSN:2352-5568
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Endocarditis is a serious and common disease that requires prolonged antimicrobial therapy. The recent shortage of oxacillin has led to the use of other antimicrobial agents such as cefazolin to treat endocarditis due to methicillin-sensitive Staphylococcus aureus. We describe four cases of life-threatening haemorrhagic complications (fatal in two cases) in patients treated with high-dose cefazolin. All of these patients with major bleeding presented with hypoprothrombinemia secondary to hypovitaminosis K. This adverse event may be due to inhibition of vitamin K epoxide reductase and/or gamma-glutamyl-carboxylase by the 2-methyl-1,2,3-thiadiazol-5-thiol group of cefazolin. This inhibition may result in hypoprothrombinemia by altering the synthesis of vitamin K-dependent coagulation factors. The increasing use of cefazolin, especially at a high dose and for a prolonged period of time, should be accompanied by regular monitoring of coagulation, including prothrombin index, and vitamin K supplementation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1709
[Cu] Class update date: 171001
[Lr] Last revision date:171001
[St] Status:Publisher

  9 / 1246 MEDLINE  
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[PMID]: 28652649
[Au] Autor:Gurvits GE; Fradkov E
[Ad] Address:Grigoriy E Gurvits, Division of Gastroenterology, New York University School of Medicine/Langone Medical Center, New York, NY 10016, United States.
[Ti] Title:Bleeding with the artificial heart: Gastrointestinal hemorrhage in CF-LVAD patients.
[So] Source:World J Gastroenterol;23(22):3945-3953, 2017 Jun 14.
[Is] ISSN:2219-2840
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Continuous-flow left ventricular assist devices (CF-LVADs) have significantly improved outcomes for patients with end-stage heart failure when used as a bridge to cardiac transplantation or, more recently, as destination therapy. However, its implantations carries a risk of complications including infection, device malfunction, arrhythmias, right ventricular failure, thromboembolic disease, postoperative and nonsurgical bleeding. A significant number of left ventricular assist devices (LVAD) recipients may experience recurrent gastrointestinal hemorrhage, mainly due to combination of antiplatelet and vitamin K antagonist therapy, activation of fibrinolytic pathway, acquired von Willebrand factor deficiency, and tendency to develop small intestinal angiodysplasias due to increased rotary speed of the pump. Gastrointestinal bleeding in LVAD patients remains a source of increased morbidity including the need for blood transfusions, extended hospital stays, multiple readmissions, and overall mortality. Management of gastrointestinal bleeding in LVAD patients involves multidisciplinary approach in stabilizing the patients, addressing risk factors and performing structured endoluminal evaluation with focus on upper gastrointestinal tract including jejunum to find and eradicate culprit lesion. Medical and procedural intervention is largely successful and universal bleeding cessation occurs in transplanted patients.
[Pt] Publication type:EDITORIAL
[Em] Entry month:1706
[Cu] Class update date: 170714
[Lr] Last revision date:170714
[St] Status:In-Process
[do] DOI:10.3748/wjg.v23.i22.3945

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[PMID]: 28577108
[Au] Autor:Ackermann S; Schimpf J; Richter M
[Ad] Address:Klinik für Anästhesiologie und Operative Intensivmedizin, Klinikum Augsburg, Stenglinstraße 2, 86156, Augsburg, Deutschland. Sven.Ackermann@klinikum-augsburg.de.
[Ti] Title:Intrakranielle Vitamin-K-Mangel-Blutung trotz oraler Vitamin-K-Gabe bei einem Säugling : Auch eine anästhesiologische Herausforderung. [Intracranial hemorrhage secondary to vitamin K deficiency in an infant despite oral vitamin K prophylaxis : Also a challenge for the anesthesiologist].
[So] Source:Anaesthesist;, 2017 Jun 02.
[Is] ISSN:1432-055X
[Cp] Country of publication:Germany
[La] Language:ger
[Ab] Abstract:This article presents the case of a 6-week-old infant who, despite oral vitamin K prophylaxis and otherwise normal developmental progress, suffered a severe intracerebral and subdural hemorrhage, which required surgical evacuation. The interdisciplinary approach is described with emphasis on the management of hemostasis. Furthermore, the clinical picture of intracranial bleeding due to vitamin K deficiency, which is nowadays rare in the Western World, is described in the anesthesiology literature for the first time. The usual recommendations regarding prophylaxis as well as certain risk factors are presented.
[Pt] Publication type:ENGLISH ABSTRACT; JOURNAL ARTICLE
[Em] Entry month:1706
[Cu] Class update date: 170810
[Lr] Last revision date:170810
[St] Status:Publisher
[do] DOI:10.1007/s00101-017-0307-3


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