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51.
H. K. DÜRR CHRISTIANE BODE R. KRUPINSKI J. CH. BODE 《European journal of clinical investigation》1978,8(3):189-191
Macroamylasaemia was produced in vitro by incubation of hydroxyethylstarch with serum, and in vivo by intravenous infusion of hydroxyethylstarch. Gel filtration on Sephadex G-100 revealed distinct differences in molecular size distribution between such hydroxyethylstarch-induced macroamylase and the usual form of naturally occurring macroamylase which was observed in a few patients from our hospital. Further studies demonstrated that the gel filtration elution pattern of amylase activity in serum containing hydroxyethylstarch-induced macroamylase is significantly altered with time in vitro and in vivo, probably because of an enzymatic degradation of the hydroxyethylstarch components of the macromolecular complexes. In a healthy volunteer the serum amylase activity was elevated to a maximum of 797 u/l and the renal clearance rate of amylase was diminished to a minimum of 0.3 ml/min after infusion of 500 ml of a 6% solution of hydroxyethylstarch, as compared to 300 u/l, and 0.95 ml/min, respectively, during the pre-infusion period. 相似文献
52.
Migraine genetics: An update 总被引:1,自引:0,他引:1
Haan J Kors EE Vanmolkot KR van den Maagdenberg AM Frants RR Ferrari MD 《Current pain and headache reports》2005,9(3):213-220
A growing interest in genetic research in migraine has resulted in the identification of several chromosomal regions that
are involved in migraine. However, the identification of mutations in the genes for familial hemiplegic migraine (FHM) forms
the only true molecular genetic knowledge of migraine thus far. The increased number of mutations in the FHM1 (CACNA1A) and the FHM2 (ATP1A2) genes allow studying the relationship between genetic findings in both genes and the clinical features in patients. A wide
spectrum of symptoms is seen in patients. Additional cerebellar ataxia and (childhood) epilepsy can occur in FHM1 and FHM2.
Functional studies show a dysfunction in ion transport as the key factor in the pathophysiology of (familial hemiplegic) migraine
that predict an increased susceptibility to cortical spreading depression—the underlying mechanism of migraine aura. 相似文献
53.
Familial hemiplegic migraine: a clinical comparison of families linked and unlinked to chromosome 19 总被引:5,自引:0,他引:5
GM Terwindt RA Ophoff J Haan RR Frants MD Ferrari for the DMGRG 《Cephalalgia : an international journal of headache》1996,16(3):153-155
We compared the clinical characteristics of 50 patients from three unrelated families with familial hemiplegic migraine (FHM) linked to chromosome 19, with those of 20 patients from two families with FHM not linked to chromosome 19. We found no significant differences for age at onset, frequency and duration of attacks, duration of the paresis, and occurrence of basilar migraine symptoms. In the linked families, significantly more patients reported unconsciousness during attacks (39%, vs 15%; p<0.05) and provocation of attacks by mild head trauma (70% vs 40%; p< 0.05). In one linked family patients also displayed chronic progressive cerebellar ataxia, whereas in one unlinked family benign infantile convulsions occurred in addition to FHM. Interestingly, so far an association with cerebellar ataxia was only described in chromosome 19-linked families. FHM linked to chromosome 19 and FHM unlinked to chromosome 19 do not differ with respect to clinical features. 相似文献
54.
J Défize G Pals J C Pronk R R Frants G Rimmelzwaan B D Westerveld A W Eriksson 《Scandinavian journal of clinical and laboratory investigation》1985,45(7):649-655
Total human pepsinogen (PG) was isolated from gastric fundic mucosa and PGA (formerly called PGI) from urine, using standard ion-exchange and gel filtration techniques. Gastric PGA was separated from PGC (formerly called PGII) either by immunoaffinity or high resolution ion-exchange chromatography (fast protein liquid chromatography, Pharmacia, Uppsala, Sweden). The individual PGA isozymogens 2, 3, 4 and 5 could be isolated to homogeneity with the aid of the same ion-exchanger. Evidence was obtained for the existence of secondary modifications of the PGA fractions 3, 4 and 5, electrophoretically overlapping the primary (genetic) isozymogens. 相似文献
55.
G Pals V R?s?nen S G Meuwissen R R Frants P J Kostense A W Eriksson 《Scandinavian journal of clinical and laboratory investigation》1987,47(1):29-33
The determination of serum pepsinogen A (= pepsinogen I) levels is of clinical importance in the study of duodenal ulcer, atrophic gastritis and gastric cancer. In the present study two different quantitative immunological techniques for serum pepsinogen A were compared: a radioimmunoassay (RIA) (Helsinki) and an enzyme-linked immunosorbent assay (ELISA) (Amsterdam). Serum samples of 177 subjects with various gastric diseases were tested in a double blind study. The correlation was excellent (r = 0.954 in the range 0-760 micrograms/l and r = 0.971 in the range 0-100 micrograms/l). The functional relationship between ELISA (x) and RIA (y), determined by weighted model II regression, was y = 1.12x-0.54. Initially the use of goat anti-PGA in the ELISA resulted in falsely high values in about 10% of the individuals. This was caused by circulating antibodies cross-reacting with goat IgG. This artefact was eliminated by pre-incubation of all samples with non-immune goat serum. 相似文献
56.
Red cell loss following orthopedic surgery: the case against postoperative blood salvage 总被引:3,自引:0,他引:3
J Umlas ; RR Foster ; SA Dalal ; SM O'Leary ; L Garcia ; MS Kruskall 《Transfusion》1994,34(5):402-406
BACKGROUND: Expensive devices have been developed for the collection and transfusion of blood salvaged after hip or knee arthroplasty. STUDY DESIGN AND METHODS: The volume of salvaged red cells was measured for the first 6 hours after operation. This volume was compared to total red cell loss during hospitalization and to the volume of allogeneic red cells transfused. RESULTS: Mean postoperative red cell loss in 31 patients following hip replacement was 55 +/− 29 mL and that in 20 patients following knee replacement was 121 +/− 50 mL. The 6-hour wound drainage represented 8.7 and 16.8 percent of overall red cell loss during hospitalization for hip and knee replacement, respectively. The transfusion of postoperatively salvaged red cells would have supplanted transfusion of less than one-third of a unit of allogenic blood after hip replacement and two-thirds of a unit after knee replacement. Only three patients (5.9%) lost red cell volume in the drainage equivalent to or in excess of 1 unit of red cells (180 mL). The volume of red cells salvaged postoperatively bore no relationship to perioperative red cell losses as a whole. CONCLUSION: The relatively small red cell loss in the postoperative period in most arthroplasty patients does not appear to justify the routine use of this technique for the recovery of autologous blood. 相似文献
57.
Jessica C. de Greef Richard J.L.F. Lemmers Baziel G.M. van Engelen Sabrina Sacconi Shannon L. Venance Rune R. Frants Rabi Tawil Silvère M. van der Maarel 《Human mutation》2009,30(10):1449-1459
Facioscapulohumeral muscular dystrophy (FSHD), caused by partial deletion of the D4Z4 macrosatellite repeat on chromosome 4q, has a complex genetic and epigenetic etiology. To develop FSHD, D4Z4 contraction needs to occur on a specific genetic background. Only contractions associated with the 4qA161 haplotype cause FSHD. In addition, contraction of the D4Z4 repeat in FSHD patients is associated with significant D4Z4 hypomethylation. To date, however, the methylation status of contracted repeats on nonpathogenic haplotypes has not been studied. We have performed a detailed methylation study of the D4Z4 repeat on chromosome 4q and on a highly homologous repeat on chromosome 10q. We show that patients with a D4Z4 deletion (FSHD1) have D4Z4‐restricted hypomethylation. Importantly, controls with a D4Z4 contraction on a nonpathogenic chromosome 4q haplotype or on chromosome 10q also demonstrate hypomethylation. In 15 FSHD families without D4Z4 contractions but with at least one 4qA161 haplotype (FSHD2), we observed D4Z4‐restricted hypomethylation on chromosomes 4q and 10q. This finding implies that a genetic defect resulting in D4Z4 hypomethylation underlies FSHD2. In conclusion, we describe two ways to develop FSHD: (1) contraction‐dependent or (2) contraction‐independent D4Z4 hypomethylation on the 4qA161 subtelomere. Hum Mutat 30:1–11, 2009. © 2009 Wiley‐Liss, Inc. 相似文献
58.
Pons D Monraats PS de Maat MP Pires NM Quax PH van Vlijmen BJ Rosendaal FR Zwinderman AH Doevendans PA Waltenberger J de Winter RJ Tio RA Frants RR van der Laarse A van der Wall EE Jukema JW 《Thrombosis and haemostasis》2007,98(6):1323-1328
Since activation of the haemostatic system is an important feature of the wound healing response triggered by arterial injury, variations in genes involved in thrombus formation may play a role in restenosis after percutaneous coronary interventions (PCI). Therefore, our aim was to examine the relationship between polymorphisms that are known to play a role in the haemostatic system and the risk of clinical restenosis in the GENetic DEterminants of Restenosis (GENDER) study, a multicenter prospective study design that enrolled 3,104 consecutive patients after successful PCI. Target vessel revascularization (TVR) was the primary endpoint. All patients were genotyped for six polymorphisms in the Factor II, Factor V, Factor VII and PAI-1 genes. The PAI-1 4G variant was associated with an increased risk of TVR. When compared to 5G/5G homozygotes, heterozygous patients were at higher risk for TVR (HR: 1.46, 95% CI: 1.05-2.03), whereas patients with the 4G/4G genotype had an even further increased risk (HR: 1.69, 95% CI: 1.19-2.41). In contrast, the factor V 506Gln (factor V Leiden) amino acid substitution was associated with a decreased risk of TVR (HR: 0.41, 95% CI: 0.19-0.86). Our findings indicate that polymorphisms in the factorV and PAI-1 genes may play a role in the process of restenosis. 相似文献
59.
Boukje de Vries Anine H. Stam Martin Kirkpatrick Kaate R.J. Vanmolkot Jan B. Koenderink Jeroen J.M.W. van den Heuvel Bas Stunnenberg David Goudie Jay Shetty Vivek Jain Judith van Vark Gisela M. Terwindt Rune R. Frants Joost Haan Arn M.J.M. van den Maagdenberg Michel D. Ferrari 《Epilepsia》2009,50(11):2503-2504
60.