bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neuordnung der Notfallversorgung im ambulanten/präklinischen Bereich
Authors: Sefrin Peter 
Published: July 2018

ZusammenfassungDer Begriff des Notfalls ist in der Bevölkerung nicht gleichbedeutend mit der Sichtweise im medizinischen Bereich und in den gesetzlichen Vorgaben. Daraus resultiert, dass die dafür vorgesehenen Versorgungspfade nicht richtig genutzt werden, was sich z. B. in der überproportionalen Zunahme der „Notfall“-Transporte im Rettungsdienst und der Anzahl der Patienten in den Notaufnahmen der Krankenhäuser zeigt. Die möglichen Ursachen werden aufgezeigt. Verschiedene Institutionen und Organisationen versuchen, durch ihre Stellungnahmen mit konkreten Vorschlägen dazu beizutragen, eine Lösung des Problems zu finden. Zur Umsetzung der Vorschläge bedarf es politischer Entscheidungen, die auch die Finanzierung betreffen.
Soziale Arbeit in der medizinischen Rehabilitation – Eine Literaturübersicht über den aktuellen Stand der Forschung
Authors: Knoop Tobias , Dettmers Stephan , Meyer Thorsten 
Published: July 2018

Zusammenfassung
Hintergrund Qualitätssicherungsaktivitäten der Deutschen Rentenversicherung zeigten die Notwendigkeit der Evidenzbasierung Sozialer Arbeit in der medizinischen Rehabilitation auf. Ziel der Studie ist die Darstellung rehabilitationswissenschaftlicher Forschung zur sozialarbeiterischen Versorgung und ihrer Effektivität.
Methodik Grundlage sind eine Literaturrecherche in 3 Datenbanken (Pubmed, Web of Sciences, Scopus) und eine händische Durchsicht rehabilitationswissenschaftlicher Zeitschriften und Tagungsbände.
Ergebnisse Von 176 Treffern wurden 52 Volltexte aus den Jahren 2000–2016 berücksichtigt. Soziale Arbeit ist im Versorgungsalltag verankert, unterliegt jedoch einer ausgeprägten Variation zwischen Einrichtungen und Indikationen. Sekundärdatenanalysen sowie Beobachtungsstudien ergaben Hinweise auf positive und negative Effekte.
Schlussfolgerungen Die Ergebnisse betonen den Bedarf der stärkeren Evidenzbasierung sozialarbeiterischer Leistungen in der medizinischen Rehabilitation.
Expenditures Of Metabolic Diseases – An Estimation on National Health Care Expenditures of Diabetes and Obesity, Hungary 2013
Authors: Iski Gabriella , Rurik Sarolta , Rurik Imre 
Published: July 2018

Abstract
Background Obesity could be considered as the main consequence of unhealthy nutrition, responsible for many pathological alterations in human. Obese patients usually need more health care services. The aim of the study was to estimate the financial expenditures of health care provisions in Hungary, related to obesity and diabetes, as its main pathological consequence.
Methods Data of the Hungarian National Health Insurance Fund (NHIF) were collected for 2013, regarding finances of secondary care, hospital services, reimbursement for medications and healing aids of diabetic patients together with selected morbidities linked to obesity, based on the codes of the International Classification of Diseases (ICD) and calculated their population prevalence on the population-attributable fraction (PAF).
Results Financial data regarding diabetes care resulted in a 40,311 Million HUF (129 Million EUR) national fund expenses, beside a 7,173 Million HUF (23 Million EUR) contribution from patients. Estimated total health care expenditures related to obesity were 58,986 Million HUF (188 Million EUR) and the financial contribution of patients was calculated as 25,316 Million HUF (81 Million EUR). These data represent a 5.2% and 9.3% of the whole national health services, 16% and 30% of the whole drug-reimbursement budgets, respectively.
Conclusions Although expenditures for some obesity related pathologies analyzed in this paper represent 0.28% of the national GDP, considering other morbidities and other patient’s expenses, the real ratio could be between 0.5–1%. The increasing number of overweight and obese persons requires more focus in public health, higher awareness in the society and more governmental support.
Ultrasonography for the Diagnosis of Carpal Tunnel Syndrome in Diabetic Patients: Missing the Mark?
Authors: Steinkohl Fabian , Loizides Alexander , Gruber Leonhard , Karpf Michael , Mörsdorf Gabriele , Gruber Ingrid , Glodny Bernhard , Löscher Wolfgang , Gruber Hannes 
Published: July 2018

Purpose Diabetes mellitus (DM) and carpal tunnel syndrome (CTS) are common pathologies. The diagnosis of CTS can be facilitated by the use of an ultrasound-based wrist-to-forearm ratio (WFR) of the nerve diameter. However, the applicability of WFR in DM-patients is not yet clear.
Materials and Methods 233 wrists of 153 patients were examined. Cross-sectional areas (CSA) of the median nerve were obtained using a linear array probe. The WFR was calculated.
Results Diabetics with CTS had significantly lower WFR values than non-diabetics with CTS (p = 0.002). There was no difference between the WFR of diabetics with and without CTS (p = 0.06). The diagnostic accuracy between diabetics with and without CTS was low for measurements of WFR (ROC AUC = 0.630, 95 % CI 0.541 – 0.715, p = 0.011).
Conclusion Our findings suggest that the WFR has a low diagnostic accuracy in diabetic patients with CTS and should be used with caution in those patients.
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Thyroid Peroxidase Antibody is Associated with Plasma Homocysteine Levels in Patients with Graves’ Disease
Authors: Li Fang , Aji Gulibositan , Wang Yun , Lu Zhiqiang , Ling Yan 
Published: July 2018

Abstract
Purpose Homocysteine is associated with cardiovascular, inflammation and autoimmune diseases. Previous studies have shown that thyroid peroxidase antibody is associated with homocysteine levels in hypothyroidism. The relationship between thyroid antibodies and homocysteine in hyperthyroidism remains unclear. In this study, we aimed to investigate the association of thyroid antibodies with homocysteine in patients with Graves’ disease.
Methods This was a cross-sectional study including 478 Graves’ disease patients who were consecutively admitted and underwent radioiodine therapy. Homocysteine, thyroid hormones, thyroid antibodies, glucose and lipids were measured.
Results Patients with homocysteine levels above the median were older and had unfavorable metabolic parameters compared to patients with homocysteine levels below the median. Thyroglobulin antibody or thyroid peroxidase antibody was associated with homocysteine levels (β=0.56, 95%CI 0.03-1.08, p=0.04; β=0.75, 95%CI 0.23-1.27, p=0.005). The relationship between thyroid peroxidase antibody and homocysteine remained significant when additionally adjusting for free triiodothyronine (β=0.76, 95%CI 0.24-1.28, p=0.004). The presence of a homocysteine level above the median increased significantly with increasing thyroid peroxidase antibody quartiles in the logistic regression (OR=1.74, 95%CI 1.27-2.39, P for trend=0.001). Homocysteine levels increased significantly with increasing thyroid peroxidase antibody quartiles (p=0.005). Thyroid peroxidase antibody had no significant effect on other traditional cardiovascular risk factors.
Conclusions Thyroid peroxidase antibody is independently and positively associated with homocysteine levels in patients with Graves’ disease. Thyroid peroxidase antibody may be associated with the cardiovascular risk of patients with Graves’ disease through its effect on homocysteine.
Establishment of Enzyme Immunoassay of Human Thrombomodulin in Plasma and Urine Using Monoclonal Antibodies
Authors: Ishii Hidemi , Nakano Masahiko , Tsubouchi Jiro , Ishikawa Taiichi , Uchiyama Hiroyuki , Hiraishi Sayuri , Tahara Chieko , Miyajima Yukari , Kazama Mutsuyoshi 
Published: July 2018

SummaryThrombomodulin, TM, is an endothelial cell membrane protein acting as a cofactor for the activation of plasma protein C. Soluble TM is present in plasma and urine of normal subjects. Enzyme immunoassay, EIA, for human TM was developed using mouse monoclonal antibodies against human placental TM in this paper. We obtained four types of the monoclonal antibodies against human placental TM. EIA sandwich method using three types of the monoclonal antibodies enabled us to measure almost all of 6 and 7 TM subspecies in plasma and urine, respectively, except 1 subspecies, 31 kDa TM. There was no interference from other components of plasma and urine in the assay conditions. Titration curves of purified TM in buffer or in normal plasma were linear within the range from 0.08 to 10 ng/ml. The coefficient of variation at 0.08 ng/ml TM was 4.7%. TM titer with buffer, assayed by this method, was reduced by the addition of thrombin at the final concentration of 20 U/ml, but the titer with plasma was not reduced even at 100 U/ml. These concentrations of thrombin are far larger than those which would be formed in circulation. TM levels in plasma and urine of normal subjects collected in the morning were 35.2 ± 8.32 ng/ml (n = 346) and 111 ± 31.6 ng/ml (n = 33), respectively. TM level in plasma did not differ from the level in serum. Circadian fluctuation of plasma TM was not significant in 10 normal adults, although a tendency of increase in TM excretion to urine was found rather in the day time than the other times. It was concluded that this EIA is reliable for TM assay in human plasma and urine, which will reflect activation or injury of endothelial cells.
Inhibition by Recombinant Hirudins of Experimental Venous Thrombosis and Disseminated Intravascular Coagulation Induced by Tissue Factor in Rats
Authors: Freund Monique , Cazenave Jean-Pierre , Courtney Michael , Degryse Eric , Roitsch Carolyn , Bernat André , Delebassée Denis , Defreyn Guy , Maffrand Jean-Pierre 
Published: July 2018

SummaryAntithrombotic potency of recombinant hirudins rHV2, rHV2–Lys47 and rHV2–Arg47 was studied in a model of experimental thrombosis induced by tissue factor in the rat. Venous thrombosis was induced by i.v. injection of 25 mg/kg tissue factor followed by stasis of the inferior vena cava. In this model natural recombinant hirudins, rHV2 and rHV2–Lys47 injected 5 min before thromboplastin totally inhibited thrombosis in the same μg range as heparin or natural hirudin extracted from leeches. However, the mutant variant rHV2–Arg47 gave a maximal 60% inhibition of thrombosis. Variants rHV2–Lys47 (30 μg/kg) and rHV2–Arg47 (157 μg/kg) injected 5 min before thromboplastin prevented by 90 to 100% the drop in platelet count observed during the disseminated intravascular coagulation induced by thromboplastin injection. Recombinant hirudins were less anticoagulant than heparin as measured by an APTT on rat plasma. After rat tail transection, rHV2–Lys47 caused a 2–fold smaller prolongation of the bleeding time than an equivalent antithrombotic dose of heparin. Plasmatic elimination of rHV2–Lys47 from rat plasma after i.v. injection had a fast distribution phase with a half-life of 3 min during which 90% of injected rHV2–Lys47 was lost and was followed by a slower elimination phase. Thus recombinant hirudin rHV2–Lys47 appears as a promising potent antithrombotic agent for the prevention of thrombin-dependent venous thrombosis and disseminated intravascular coagulation
Characterization of a Mode of Specific Binding of Fibrin Monomer through its Amino-Terminal Domain by Macrophages and Macrophage Cell-Lines
Authors: Shainoff John R , Stearns Deborah J , DiBello Patricia M , Hishikawa-Itoh Youko 
Published: July 2018

SummaryThe studies reported here probe the existence of a receptor-mediated mode of fibrin-binding by macrophages that is associated with the chemical change underlying the fibrinogen-fibrin conversion (the release of fibrinopeptides from the amino-terminal domain) without depending on fibrin-aggregation. The question is pursued by 1) characterization of binding in relation to fibrinopeptide content of both the intact protein and the CNBr-fragment comprising the amino-terminal domain known as the NDSK of the protein, 2) tests of competition for binding sites, and 3) photo-affinity labeling of macrophage surface proteins. The binding of intact monomers of types lacking either fibrinopeptide A alone (α-fibrin) or both fibrinopeptides A and B (αβ-fibrin) by peritoneal macrophages is characterized as proceeding through both a fibrin-specific low density/high affinity (BMAX ≃ 200–800 molecules/cell, KD ≃ 10−12 M) interaction that is not duplicated with fibrinogen, and a non-specific high density/low affinity (BMAX ≥ 105 molecules/cell, KD ≥ 10−6 M) interaction equivalent to the weak binding of fibrinogen. Similar binding characteristics are displayed by monocyte/macrophage cell lines (J774A.1 and U937) as well as peritoneal macrophages towards the NDSK preparations of these proteins, except for a slightly weaker (KD ≃ 10−10 M) high-affinity binding. The high affinity binding of intact monomer is inhibitable by fibrin-NDSK, but not fibrinogen-NDSK. This binding appears principally dependent on release of fibrinopeptide-A, because a species of fibrin (β-fibrin) lacking fibrinopeptide-B alone undergoes only weak binding similar to that of fibrinogen. Synthetic Gly-Pro-Arg and Gly-His-Arg-Pro corresponding to the N-termini of to the α- and the β-chains of fibrin both inhibit the high affinity binding of the fibrin-NDSKs, and the cell-adhesion peptide Arg-Gly-Asp does not. Photoaffinity-labeling experiments indicate that polypeptides with elec-trophoretically estimated masses of 124 and 187 kDa are the principal membrane components associated with specifically bound fibrin-NDSK. The binding could not be up-regulated with either phorbol myristyl acetate, interferon gamma or ADP, but was abolished by EDTA and by lipopolysaccharide. Because of the low BMAX, it is suggested that the high-affinity mode of binding characterized here would be too limited to function by itself in scavenging much fibrin, but may act cooperatively with other, less limited modes of fibrin binding.
Extraction of Protein-Bound ATP and ADP from Human Platelets in Plasma
Authors: Beurling-Harbury Christina , Harbury Pehr B 
Published: July 2018

SummaryActin is the major ATP and ADP binding protein in platelets, 0.9–1.3 nmol/108 cells, 50–70% in the unpolymerized state. The goal of these experiments was to develop a method for extracting all protein-bound ATP and ADP from undisturbed platelets in plasma. Extraction of actin-bound ADP is routine while extraction of actin-bound ATP from platelets in buffer has been unsuccessful. Prior to extraction the platelets were exposed to 14-C adenine, to label the metabolic and actin pools of ATP and ADP. The specific activity was determined from the actin-bound ADP in the 43% ethanol precipitate. Sequential ethanol and perchlorate extractions of platelet rich plasma, and the derived supernatants and precipitates were performed. ATP concentrations were determined with the luciferase assay, and radioactive nucleotides separated by TLC. A total of 1.18 nmol/108 cells of protein-bound ATP and ADP was recovered, 52% ATP (0.61 nmol). The recovery of protein-bound ADP was increased from 0.3 to 0.57 nmol/108 cells. This approach for the first time successfully recovered protein bound ATP and ADP from platelets in a concentration expected for actin.
Factor IX Chongqing: a New Mutation in the Calcium-Binding Domain of Factor IX Resulting in Severe Hemophilia B
Authors: Wang N S , Zhang M , Thompson A R , Chen S-H 
Published: July 2018

SummaryA Chinese patient with sporadic, severe hemophilia B was found to have a low level of total factor IX antigen (3.5 U/dl), but less apparent antigen in an assay using a calcium-dependent antibody fraction (1.1 U/dl). This suggested a defect in the factor IX Gla domain coded mainly by exon 2 of the factor IX gene. Exon 2 was therefore amplified and sequenced. An A to T substitution was found at nucleotide 6455 of the patient’s factor IX gene. This transversion changes the codon for Glu 27 in normal factor IX to a codon for Val. Since Glu 27 becomes an essential Gla residue, the defect should result in altered calcium-binding or calcium-dependent conformation of the patient’s factor IX. The introduction of a hydrophobic side chain also appears to affect the hemophilic protein’s stability.In leukocyte DNA from the patient’s mother, the nucleotide sequence of exon 2 was entirely normal. Thus, barring somatic mosaicism within her germ cells, the new mutation occurred in oogenesis of her ovary.
Characterization of the Anticoagulant Activities from a Brazilian Arrow Poison
Authors: Jacobs John W , Petroski Christopher , Friedman Paul A , Simpson Ellen 
Published: July 2018

SummaryA recent report indicated that an arrow poison used by the native Indians of Rondonia, Brazil, to kill small animals was associated with profuse bleeding (1). The arrow poison was prepared from the bark of a tree, known locally as Tike-Uba. We have obtained bark and sap specimens from this tree and have characterized a potent anticoagulant activity in both the crude bark and sap samples as well as in more highly purified preparations. An aqueous extract of the bark significantly prolongs both prothrombin times and activated partial thromboplastin times in plasma based assays. Further fractionation of the bark extract and sap by molecular weight indicated that all of the anticoagulant activity could be isolated in a molecular weight fraction of equal to or greater than 30,000 daltons. The anticoagulant activity was also further purified by C-18 reverse phase chromatography. When highly purified preparations of the anticoagulant activity from the Tike-Uba tree were examined in specific blood coagulation enzyme assays utilizing chromogenic substrates, the highest inhibitory potency was found versus thrombin, followed by factor Xa. These studies establish the presence of a compound(s) in a Brazilian arrow poison, which potently disrupts mammalian blood clotting, and which may account for some of the observed toxicities associated with the arrows.
Detection of both Type 1 and Type 2 Plasminogen Activator Inhibitors in Human Monocytes
Authors: Castellote Joan C , Grau Enric , Linde Maria A , Pujol-Moix Nuria , Rutllant Miquel LI 
Published: July 2018

SummaryIncreasing evidence suggests the involvement of leukocytes in the fibrinolytic system. Monocytes secrete pro-urokinase (Grau, Thromb Res 1989; 53: 145) and it has been shown that these cells have specific receptors for urokinase and plasminogen (Miles, Thromb Haemostas 1987; 58: 936). The aim of this study was to analyse the presence of plasminogen activator inhibitor(s) in platelet-free suspensions of human peripheral blood monocytes and polymorphonuclear leukocytes (PMN). SDS-PAGE and reverse fibrin autography showed an inhibitory band of 50 kDa in the monocyte extracts (Triton X-100) but not in the PMN extracts. Urokinase (u-PA) was mixed with increasing amounts of monocyte extract for 10 min and the mixtures were added to 125Ifibrin coated wells containing plasminogen. A dose-dependent decrease in the u-PA fibrinolytic activity was observed. The amount of inhibition increased when the monocyte releasates were preincubated with u-PA (40% inhibition after 5 min preincubation and 80% after 15 min), indicating a direct interaction between this activator and an inhibitor(s). After SDS-PAGE of monocyte extracts, immunoblotting and peroxidase staining identified both PAI1 and PAI2, with an apparent molecular weight of 47-50 kDa. Monocyte-associated PAI1 formed complexes with single chain t-PA with a molecular mass 50 kDa higher than the molecular mass of the free PAI1. However, a significant amount of PAI remained unbound to t-PA. This inactive PAI1 could have come from a rapid inactivation of the primary active PAI1. These PAI1 and PAI2 detected in human monocytes may be transcendent in the regulation of the fibrinolytic system.
A Plasma Clot Lysis Assay Based on the Release of Fibrin Degradation Products: Application to the Diagnosis of Hypofibrinolytic States
Authors: Gaussem Pascale , Gandrille Sophie , Molho-Sabatier Pascale , Capron Loïc , Fiessinger Jean-Noël , Aiach Martine 
Published: July 2018

SummaryUsing a monoclonal antibody-based assay, we measured the fibrin degradation product release in the supernatant of plasma clots obtained before and after venous occlusion (VO) in 30 patients with definite or suspected vascular thrombosis (19 definite and 2 suspected deep vein thrombosis, 6 recurrent superficial thrombophlebitis, 3 arterial occlusions of lower limbs). tPA and PAI-1 concentrations were determined using ELISA assays; the post-occlusion values were corrected for haemoconcentration. The increase in tPA during VO was correlated with haemoconcentration (r = 0.74), but 3 patients had ineffective VO (<2% increase in proteins). The fibrinolytic response to VO was evaluated using the shortening of the time necessary for the release of 200 μg of fibrin degradation products per mg of fibrinogen (Δ T 200). Two among the 27 patients with effective VO were bad responders with a Δ T 200 <3 h (whereas all the others had Δ T 200 >10 h). These patients had respectively a deficient tPA release (Δ tPA = 1 ng/ml) and an elevated PAI-1 level at rest (33 ng/ml). Several other patients were bad responders in terms of tPA release or of shortening of the euglobulin clot lysis time but they had a normal Δ T 200. This plasma clot test reflects the ability of free tPA to bind to fibrin (the amount of which depends on the level of tPA and PAI-1), and may be useful in the diagnosis of a hypofibrinolytic state.
Effect of Angiotensin II on Collagen-Induced Platelet Activation in Normotensive Subjects
Authors: Swartz Stephen L , Moore Thomas J 
Published: July 2018

SummaryWe examined the effect of angiotensin II (AII) on platelet activation in 15 normotensive volunteers. By measuring the initial phase of platelet aggregation on the optical density aggregation tracing and generation of thromboxane production, we demonstrated that AII enhances collagen-induced platelet activation. This enhancement in platelet activation is significantly greater when subjects are on a high salt than on a low salt diet. Furthermore, the increase in platelet activation parallels an increase in platelet AII receptor number. These parallel changes in platelet activation and platelet AII receptors provide a possible mechanism through which AII may affect platelet function.
A Resolution of Reported Discrepancies in the Characteristics of Platelet Glycoproteins IV (GPIV) and III b (GPIII b)
Authors: Yamamoto Naomasa , Romeuf Christophe de , Tandon Narendra N , Jamieson G A 
Published: July 2018

SummaryThe terms glycoprotein IV (GPIV) and glycoprotein IIIb (GPIIIb) have been used interchangeably and reports in the literature have indicated this glycoprotein as having a molecular weight variously described as either 88,000 or 97,000, a fast anodal mobility on crossed electrophoresis and either 13 or <1 methionine residues on amino acid analysis of the purified glycoprotein. To resolve these discrepancies, we have evaluated the characteristics of GPIV both in whole platelets and after isolation. These studies have shown that the term GPIV defines a protease-resistant platelet surface glycoprotein with Mr 88,330 ± 2,240 which is immunologically identical with the CD36 differentiation antigen, which migrates with a relatively slow anodal mobility on crossed immunoelectrophoresis and which contains ∼13 methionine residues per mole.