bluuebunny/crossref_metadata_2025_split huggingface dataset:
Flexible distribution network: definition, configuration, operation, and pilot project
Authors: Xiao Jun , Wang Ying , Luo Fengzhang , Bai Linquan , Gang Fayun , Huang Renle , Jiang Xun , Zhang Xinsong 
Published: August 2018

In this article, a new concept of flexible distribution network (FDN) is proposed for the power grid with increasing distributed energy resources (DERs) and power electronic devices. First, the authors define FDN as a flexible closed‐loop operation smart distribution network with the capability of wide‐area energy exchange. In FDNs, flexible networking devices are the key facilities, which upgrade traditional networking devices by soft open point (SOP). Second, several typical network configurations of FDN are presented, which facilitate smooth upgrades from traditional networks to FDNs. Third, the normal operation mode, N  − 1 mode, and the related analysis methods of FDN are presented. Finally, the world's first three‐terminal SOP‐based FDN pilot project is introduced and analysed to demonstrate the advantages of FDN in controlling power flow and integrating DERs.
Checkpoint Patientensicherheit
Authors: Ehrengruber Maximilian , Wurm Claudius 
Published: August 2018

ZusammenfassungEin Verwechslungsfall ist für den Patienten und das Behandlungsteam ein katastrophales Ereignis, mit oft schwerwiegenden Folgen. Als gängiger Standard hat sich
hierzu die Patientensicherheitscheckliste etabliert. Dem Trend der Digitalisierung folgend, haben unsere Autoren die Checkliste einem kompletten Redesign
unterzogen, indem sie diese digitalisiert und in die OP-Dokumentationssoftware integriert haben. Kombiniert mit dem innovativen Checkpoint-System, welches der
Patient vor Operationsbeginn passieren muss, kann dabei garantiert werden, dass alle sicherheitsrelevanten Information zum richtigen Zeitpunkt, am richtigen
Ort, durch die richtige Berufsgruppe abgefragt und kommuniziert werden.
Leben mit Rheuma: Rehabilitation und adjuvante Therapien
Authors: Clasen Marina , Schwarting Andreas 
Published: August 2018

ZusammenfassungDie Entwicklung neuer zielgerichteter medikamentöser Therapien hat zu einer deutlichen Verbesserung der Behandlung der akuten Entzündungsaktivität geführt. Die größere Herausforderung stellt im Alltag oftmals jedoch der Umgang mit bereits eingetretenen Behinderungen und Schmerzen dar. Hierfür gibt es zahlreiche adjuvante Möglichkeiten, deren Stellenwert im Beitrag erörtert wird.
Palladium(II)-Catalyzed Redox-Neutral Cyclizations of Alkynes Containing Alkenyl or Electrophilic Functional Groups:
A Convenient Synthesis of Carbocycles and Heterocycles
Authors: Han Xiuling , Lu Xiyan 
Published: August 2018

The palladium(II)-catalyzed redox-neutral cyclizations of alkynes bearing alkenyl or electrophilic functional groups, such as carbonyl, imino, or cyano groups, were developed to provide convenient approaches to various carbocycles and heterocycles. These tandem reactions are initiated by nucleopalladation of alkynes, transmetalation of arylboron reagents with palladium, or hydropalladation of alkynes, and they are quenched by β-heteroatom elimination, addition to electron-deficient alkenes, or addition to carbon–heteroatom multiple bonds. This account reviews these types of reaction, with a focus on our contributions to the field.1	Introduction2	Tandem Reactions of Functionalized Alkynes Initiated by Nucleo­palladation3	Tandem Reactions Of Functionalized Alkynes Initiated by Transmetalation of Palladium(Ii) with Arylboron Reagents4	Tandem Reactions of Functionalized Alkynes Initiated by Hydro­palladation5	Conclusion
Modifications in Coagulation Parameters Induced by Treatment Associating Urokinase (2000 u CTA/kg/h) with Heparin
Authors: Juhan I , Calas M F , Buonocore M , Mathieu P , Isnard G , Cazenave B , Serradimigni A 
Published: August 2018

SummaryTwenty-nine patients with deep venous thrombosis of the lower limbs were treated for 48 hours by intravenous infusion of urokinase (2000 u CTA/kg/h) and heparin (5 mg/kg/24 h).Plasma coagulation parameters were measured every 12 hours. After 36 hours of therapy the following results were obtained – decrease in: fibrinogen levels (9% fall), plasminogen (40% decrease), α2-macroglobulin (9% decrease, but no change during the first 12 hours) and fast acting α2-antiplasmin (60% decrease); bidimensional electrophoresis consistently revealed 2 spikes during treatment: the first corresponded to complexed plasmin-fast acting α2-antiplasmin, the second corresponded to free, unconsumed fast acting α2-antiplasmin. Levels of α1-antitrypsin increased by 20% whereas the antithrombin III level remained stable. FDP levels increased slightly. Recalcified plasma coagulation times progressively increased.Therapeutic results were evaluated on phlebography and showed, after 48 hours urokinase administration, improvement in 6 patients and no improvement in 17 cases. Consumption of plasminogen and production of FDP were both greater in the improved patient group.The authors discuss these results and suggest that the dosage level of urokinase used in this study should be modified; it is concluded that a therapeutic regimen associating a loading dose with higher hourly administration levels is needed to achieve neutralization of fast acting α2-antiplasmin, a prerequisite to development of thrombolytic activity.
Fibrinolysis in the Pigeon (Columba livia)
Authors: Ahmad Nasreen , Dube B , Agarwal G P , Dube Ramakanta 
Published: August 2018

SummaryThe presence of plasminogen activator in the euglobulin fraction of pigeon plasma, was demonstrated by conspicuous lysis on unheated fibrin plates; human as well as bovine fibrin were susceptible to lysis. The presence of free plasmin in euglobulin fraction was indicated by lysis on heated fibrin plates.
Changes of Platelet Function and Blood Clotting in Diabetes Mellitus
Authors: Gensini G F , Abbate R , Favilla S , Neri Serneri G G 
Published: August 2018

SummaryWe investigated some aspects of blood clotting and of platelet functions in 48 diabetics (12 affected by preclinical diabetes, 15 by clinical diabetes, 21 with complications of diabetes, peripheral vascular disease, ischaemic heart disease or diabetic nephropathy with or without hypertension) in 35 age matched controls and in 7 prediabetics.Blood clotting has been investigated by gel-chromatography of fibrin soluble complexes, by factor VIIICOAG two stage assay, by factor VIIIAGN electroimmunodiffusion assay and by factor VIIIvWF assay. Platelet functions have been investigated by the determination of circulating platelet aggregates associated with megathrombocytes count, by the malondial- dehyde formation after thrombin and after arachidonic acid. In order to clarify some mechanisms responsible for platelet aggregating plasmatic activity (PAPA) has been investigated by plasmaplatelet cross-matches.Our results indicate early changes of platelet functions in diabetics, already demonstrable in preclinical diabetes. Platelets are hyperaggregable and produce increased amounts of malondialdehyde after stimulation by thrombin and arachidonic acid, thus suggesting an increased activity of the intraplatelet endoperoxide-thromboxane forming metabolic pathway. An increased concentration of fibrin soluble complexes can be shown in clinical and complicated diabetes whereas in preclinical diabetes the fibrogen complexes concentration is within the normal range.Factor VIIIvWF results significantly increased in all groups of diabetics, and even in the subjects with prediabetes. Factor VHICoag and Factor VIIIAGN, besides factor VIIIvWF, were significantly increased in clinical and in complicated diabetes. The increased concentration of factor VIIICOAG and of soluble fibrinogen complexes suggest the existence of a hypercoagulable condition in patients with clinical and above all with complicated diabetes.In these patients a platelet aggregating plasmatic activity can be frequently found. The indication is that platelet hyperaggregation in diabetes is due to various mechanisms. In preclinical diabetes and in some patients with clinical diabetes platelet hyperaggregability is mainly due to a primary platelet hypersensitivity whereas in complicated diabetes, specially when hypercoagulability occurs, platelet hyperaggregation is due to a plasmatic factor related to blood clotting activation.
Thrombus Weight as a Measure of Hypercoagulability Induced by Drugs
Authors: MacIomhair Maura , Lavelle S M 
Published: August 2018

SummaryThrombus weight was used as a measure of the thrombus enhancing effect of drugs in 135 rats. The weight of thrombus formed in one hour, on a 20 × 0.5 mm platinum wire, inserted in the vena cava was taken as a measure of thrombosis. The change in thrombus weight which followed the injection of ellagic acid to activate the coagulation system, adenosine diphosphate to activate the platelets, and epsilon-aminocaproic acid to inhibit the fibrinolytic system, was measured. Pilot studies showed that the drug doses used brought about the appropriate changes in the factors named. The mean thrombus weight in 45 control animals was 1.93 mg. Ellagic acid increased it about five-fold, and epsilon- aminocaproic acid almost two-fold, while adenosine diphosphate reduced it by almost a half. Concurrent controls were used in each case. Clotting tests (whole blood clotting time, kaolin-activated whole blood clotting time, thrombin time, and partial thromboplastin time), performed at the end of the hour, showed no significant correlation with thrombus weight.
VIIIR: Ag in Platelets from Patients with Various Forms of von Willebrand’s Disease
Authors: Holmbeg L , Nilsson Inga Marie 
Published: August 2018

SummaryThirty patients with various forms of von Willebrand’s disease were investigated for VIIIR: Ag in their platelets. VIIIR: Ag was extracted from washed platelets and measured both with electroimmunoassay and a sensitive immunoradiometric assay. Six patients had severe von Willebrand’s disease, type I, with very low or no VIIIR: Ag in their plasma. None of these patients had any VIIIR: Ag detectable in their platelets. All 19 patients with mild von Willebrand’s disease had VIIIR: Ag in their platelets but the values often fell below those of normal controls. Five patients with genetic variants of von Willebrand’s disease also had values in their platelets corresponding to those in plasma.Von Willebrand’s disease is a bleeding disorder caused by an inherited defect in so-called factor VIII related antigen (VIIIR: Ag), which is a protein normally occurring in plasma (Zimmerman et al. 1971), endothelial cells (Bloom et al. 1973), platelets (Howard et al. 1974) and megakaryocytes (Piovella et al. 1974). The defect leads to a prolonged bleeding time and as a rule a secondary decrease in factor VIII clotting activity (VIII: C) in plasma. Von Willebrand’s disease is a heterogeneous condition (Holmberg and Nilsson 1972). It varies widely in severity, and a genetic variation causing a qualitative abnormality of VIIIR :Ag is also known (Peake et al. 1974). The disease is, as a rule, transmitted as an autosomal and dominant trait, but some severely affected individuals have been suspected to be homozygous for an autosomal and more or less recessive gene (Italian Working Group 1977, Shoa’i et al. 1977).The clinical severity of the disease varies with the amount of functional VIIIR :Ag (VIIIR: RCF) in plasma (Holmberg and Nilsson 1972, Meyer et al. 1974). Patients with severe von Willebrand’s disease have very little or no VIIIR: Ag in their plasma. They also lack the protein in their endothelial cells (Holmberg et al. 1974 b). There is evidence that also their platelets are devoid of VIIIR :Ag. In the present investigation we studied the platelet content of VIIIR: Ag in a series of patients with various types of von Willebrand’s disease. Both electroimmunoassay (EIA) and a more sensitive immunoradiometric assay (IRMA) for VIIIR: Ag were used.
The Optimal Therapeutic Range in Oral Anticoagulation
History and Proposal
Authors: Loeliger E A 
Published: August 2018

SummaryFor patients on oral anticoagulation controlled with Quick’s prothrombin time test using rabbit brain thromboplastin American clinicians proposed in the early 1940s that the lower limit of prolongation be taken at 1.5 and the upper limit at 3, corresponding to 10-30 per cent prothrombin activity on a saline dilution curve. Thromboplastins derived from other tissues and species were later introduced, methods were modified, and adsorbed plasma was used instead of saline in the construction of the dilution curve to obtain percentage prothrombin activity; ratios and percentages lost their initial significance, but too often without the clinicians� awareness. With the detection of PIVKAs, finally, it became clear that transformation of prothrombin times into percentage activity, as obtained from dilution curves, could never be a valid means of standardization. It also became evident that only direct comparison of thromboplastins with (fresh) plasma from patients on stabilized oral anticoagulants could be used to determine equivalent therapeutic ranges for different types of thromboplastins. Reference thromboplastins were established and calibration procedures developed. A series of well-controlled clinical trials has provided sufficient information to define, in terms of these reference thromboplastins, therapeutic ranges for the prophylaxis and treatment of venous as well as arterial thrombosis. Definition of the ranges in terms of the biochemical defect induced by coumarin congeners remains, however, to be established.
Anticoagulant Kinetics Following Bolus Injection of Heparin
Authors: Mockros Lyle F , Hirsch Samuel D , Zuckerman Leon , Caprini Joseph A , Robinson William P , Vagher J Paul 
Published: August 2018

SummaryBolus injections of beef-lung heparin at doses of 50, 100 and 200 u/kg body weight were administered to mongrel dogs. Neutralization of the anticoagulant effect was evaluated using sequential samples withdrawn from the animals (in vivo samples) and aliquots from a 100 ml sample withdrawn from the dog at 30 minutes post-injection (in vitro samples). Tests of the activated partial thromboplastin time (APTT) and prothrombin time (PT) did not indicate the degree of anticoagulation. Tests of the whole blood clotting time (WBCT), celite- activated whole blood clotting time (ACT), and celite-activated thromboelastography (ATEG) indicated pronounced hypocoagulability immediately after the injection, followed by a fairly rapid decay in anticoagulability, and a slight Ziype/coagulability at three to four hours post injection. The results from the in vitro ATEG samples were essentially identical to those on the in vivo samples, whereas the in vitro WBCT and ACT generally indicated higher degrees of anticoagulation. Calculated half-lives of the anticoagulant effect are significantly shorter than previously reported, being 18 to 36 minutes, and slightly dose dependent. The decay of the effects, however, does not appear to follow a single exponential curve, dropping very rapidly immediately post-injection and at a somewhat slower rate 60 or more minutes post-injection.
Relationship Between Kallikrein Release and Factor XII in Normal Persons and Carriers of the Hageman Trait
Authors: Torres M , Ercoreca L , Lucia J F , Giralt M , Raichs A 
Published: August 2018

SummaryIn four healthy subjects with Factor XII levels equal to or below 50% (selected at random from 100 persons) the release of Kallikrein was studied in order to establish the relationship between the above data and those found in four Hageman trait carriers showing levels of Factor XII above the lowest normal limits. It was found that for similar amounts of Hageman activity three of the carriers showed significantly less release of Kallikrein than the control subjects in whom it was normal.The conclusion was reached that the additional determination of the amount of Kallikrein released may be of value in the detection of carriers of the Hageman trait.
In Vitro Stability of Human Fibrinopeptide B
Authors: Qureshi G D , Vennart William C 
Published: August 2018

SummaryIn anticipation of a future clinical application of plasma fibrinopeptide B (FPB) measurement, we studied the stability of FPB in an ultrafiltrate of normal plasma, normal urine and alkaline buffer by measuring the immunoreactivity of the peptide by FPB radioimmunoassay using anti FPB serum (R-29). FPB was unstable in an ultrafiltrate of plasma and urine and demonstrated a temperature dependent loss of activity. In plasma ultrafiltrate the loss of immunoreactivity was not significant during the first 24 hours, however, 92% of the peptide activity was lost at the end of seven days at 25° C and 37° C. The rate of FPB degradation in urine was comparable. The peptide was stable in an alkaline buffer (pH 8.5) at temperatures ranging from �10° C to 37° C or in plasma ultrafiltrate or urine when incubated at �10° C. Treatment with carboxypeptidase B or leucine aminopep- tidase for two hours at 37° C (enzyme/substrate molar ratio of up to 1:100) did not cause a loss of FPB immunoreactivity. EDTA (1.0 mM) and Trasylol (500 units/ml) completely stabilized the peptide in a plasma ultrafiltrate.
In Vitro Thrombogenicity Tests of Factor IX Concentrates. II: Effects of Phospholipids and Heparin
Authors: Prowse C V , Boffa M C , Guthrie C , Pepper D S 
Published: August 2018

SummaryMeasurement of the total phospholipid (and that portion active in coagulation) in factor IX concentrates revealed no correlation with in vitro tests of potential thrombogenicity, except in the case of the recalcification time and the thrombin generation test which may detect coagulant phospholipid as well as the presence of thrombogenic enzymes. This is probably due to separation of the prothrombin complex proteins from most phospholipid during ion-exchange chromatography. Although low levels of phospholipid remain in the final product these are apparently insufficient to effect appreciable activation of factor IX concentrates despite low levels of antithrombin III.Two tests which measure the formation of thrombin and factor Xa after recalcification of concentrates were affected by the addition of exogenous phospholipid. However this is a relative effect such that differences are quantitative rather than qualitative.Heparin addition during production of factor IX concentrate was found to have only minor effects on the results of in vitro thrombogenicity tests of the final product. This was confirmed in the laboratory by incubation of unheparinised products with heparin for periods of up to 6 hr.
Fibrinogen-Induced Polymerization Via the Process of Methylation
Authors: Osbahr A J 
Published: August 2018

SummaryFibrinogen is polymerized by a number of group specific reagents including diazomethane, thionyl chloride and di-methyl sulfate at pH 7.4. The relationship between the number of methyl groups incorporated into fibrinogen and the extent of polymerization was evaluated. With diazomethane and thionyl chloride as modifying agents, polymerization ensued in approximately IV2 hr with extensive modification of fibrinogen. On the other hand, m�thylation via di-methyl sulfate-induced polymer formation occurs in approximately 35 min with primarily carboxylic acid group esterification. The polymerized fibrinogen formed under these conditions exhibited properties that were closely similar with the physiological fibrin clot.Amino group determinations revealed the m�thylation of amino acid residues other than the expected esterification of carboxylic acid groups. Diazomethane induced both N- methylation of lysine, as well as O-methylation of tyrosine, as estimated from spectrophotometric analysis. On the other hand, thionyl chloride modified only a small number of amino groups, and di-methyl sulfate modification resulted in no significant amounts of amino group methylation during the process of modification induced polymerization of fibrinogen.The profile of the number of methoxyl groups incorporated into fibrinogen with time for diazomethane modification may reflect a conformational change in the protein due to a more nonspecific m�thylation. Both the reagent and the conditions of modification were found to be important in achieving a selective modification of fibrinogen.A possible interpretation of these results is the esterification of carboxylic acid groups in the fibrinogen with reduction in the prevailing carboxylate ion negative repulsion, thereby achieving an increased protein-protein interaction with a resulting polymerization.
Isolation of Peptides with Anti-Urokinase Activity from the Human Placenta
Authors: Uszynski Mieczyslaw 
Published: August 2018

SummaryIt is known that the fibrinolysis inhibitors in the human placenta are proteins which, in vitro, block urokinase plasminogen activation and are for this reason called urokinase inhibitors. In the present study it was found, for the first time, that a low-molecular urokinase inhibitor also occurs in the human placenta. It is a peptide which can be isolated through a three-step procedure: dialysis of human placenta homogenate, extraction of peptides from a filtrable fraction, and ion exchange chromatography of peptides on a Dowex-50 column.
Differential Effects of Cytochalasin B on Platelet Release, Aggregation and Contractility: Evidence against a Contractile Mechanism for the Release of Platelet Granular Contents
Authors: Kirkpatrick John P , McIntire Larry V , Moake Joel L , Cimo Philip L 
Published: August 2018

SummaryCytochalasin B alters the structure and functional properties of filamentous actin. Platelet-mediated clot retraction in dilute platelet-rich plasma (PRP) is inhibited progressively at cytochalasin B concentrations of 0.01 mg/ml, 0.05 mg/ml and 0.1 mg/ml. Dynamic rheological measurements of recalcified PRP in a Weissenberg Rheogoniometer indicate that platelet contractility (as reflected in measurements of elastic moduli) is reduced by 33%, 57% and 63% at cytochalasin B concentrations of 0.01, 0.05 and 0.1 mg/ml, respectively.In contrast, pre-incubation of human platelet-rich plasma (PRP) with 0.01 mg/ml or 0.05 mg/ml cytochalasin B does not inhibit collagen-induced [14C-]serotonin release or collagen-induced-platelet aggregation, which is dependent on the release of ADP from platelet dense granules. Even at a cytochalasin B concentration of 0.1 mg/ml, collagen-induced [14C-]serotonin release and aggregation are impaired only moderately. Cytochalasin B does not interfere with the uptake by platelets of [14C-]-serotonin, or with the kinetics and extent of clot formation in platelet-free plasma.Thus, concentrations of cytochalasin B which impair platelet contractility do not inhibit the release of platelet dense granule contents. It is concluded that neither the platelet release reaction nor platelet aggregation is dependent on platelet contractile mechanisms.
Increased Plasma Fibrinogen and Platelet-Aggregates in Type II Hyperlipoproteinaemia
Authors: Lowe G D O , Drummond Maureen M , Third Jane L H C , Bremner W F , Forbes C D , Prentice C R M , Lawrie T D V 
Published: August 2018

SummaryPlasma fibrinogen and platelet-aggregates (method of Wu and Hoak) were measured in 21 patients with familial Type II hyperlipoproteinaemia and 21 matched control subjects. Patients with hyperlipoproteinaemia had increased levels of fibrinogen and platelet- aggregates (p<0.01). Young patients with hyperlipoproteinaemia had prematurely high fibrinogen levels, and the normal rise in fibrinogen during adult life was abolished. There were no statistically significant correlations within the patient group between fibrinogen, platelet-aggregates, and plasma lipids. High fibrinogen and platelet-aggregate levels may play a part in the development of the premature arterial disease associated with Type II hyperlipoproteinaemia, or may be markers of arterial injury.