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91.
AR Rezaie 《Canadian Metallurgical Quarterly》1998,91(12):4572-4580
A recent study indicated that negatively charged substances such as heparin and dextran sulfate accelerate thrombin activation of coagulation factor XI by a template mechanism. Because the serine proteinase of the natural anticoagulant pathway, activated protein C, can bind heparin, it was reasonable to think that these compounds may also bind protein C (PC) and accelerate its activation by thrombin or other heparin binding plasma serine proteinases by a similar mechanism. To test this, PC activation by thrombin and factor Xa (fXa) was studied in the presence of these polysaccharides. With thrombin in the absence of thrombomodulin (TM), these polysaccharides markedly reduced the Km for PC and Gla-domainless PC (GDPC) activation in the presence of Ca2+. With TM containing chondroitin sulfate, heparin did not influence PC activation by thrombin, but with TM lacking chondroitin sulfate, the characteristic high-affinity PC interaction at low Ca2+ (approximately 50 to 100 micromol/L) was largely eliminated by heparin. In EDTA, heparin enhanced thrombin activation of GDPC by reducing the Km, but it inhibited PC activation by increasing the Km. PC activation in EDTA was insensitive to the presence of heparin if the exosite 2 mutant, R93,97,101A thrombin, was used for activation. These results suggest that, when the Gla-domain of PC is not fully stabilized by Ca2+, it interacts with the anion binding exosite 2 of thrombin and that heparin binding to this site prevents this interaction. Additional studies indicated that, in the presence of phospholipid vesicles, heparin and dextran sulfate dramatically accelerate PC activation by fXa by also reducing the Km. Interestingly, on phospholipids containing 40% phosphatidylethanolamine, the activation rate of near physiological PC concentrations ( approximately 80 nmol/L) by fXa in the presence of dextran sulfate was nearly comparable to that observed by the thrombin-TM complex. The biochemical and potential therapeutical ramifications of these findings are discussed. 相似文献
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OBJECTIVES: To confirm the presence of an outbreak of postoperative infections following laminectomy and to determine the infection rate after interventions were instituted. DESIGN: Retrospective cohort study. Medical records were reviewed, personnel interviewed, and premises examined. SETTING: Surgical unit of hospital A in Pakistan. SUBJECTS: Patients who had surgical laminectomy between January 1993 and July 1994. INTERVENTION: Instructive program for nursing and medical staff in December 1993. RESULTS: From January to December 1993, 6 (15%) of 41 laminectomy patients developed postoperative discitis. The risk of discitis varied significantly by surgeon (P = .016); patients who had one particular surgeon, surgeon A, were nine times more likely to develop postoperative infections than patients who did not have surgeon A. Patients were not consistently cleaned or shaved before coming to the operating room, and personnel moved back and forth between the operation theater and other parts of the hospital without changing their gowns or slippers. After the instructional intervention, between January and July 1994, 2 (6%) of 31 laminectomy patients developed postoperative discitis, a rate not significantly lower than in the preceding 12 months (P = .45). Overall, from January 1993 through July 1994, female patients were more likely to develop discitis than males (31% vs 7%; relative risk, 4.4; 95% confidence interval, 1.3-15.6; P < .032). CONCLUSION: Endemic conditions require that laminectomy at hospital A be limited to those situations where the benefits of the surgery exceed the considerable risk of postoperative discitis. 相似文献
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AR Zinn VS Tonk Z Chen WL Flejter HA Gardner R Guerra H Kushner S Schwartz VP Sybert DL Van Dyke JL Ross 《Canadian Metallurgical Quarterly》1998,63(6):1757-1766
Turner syndrome is the complex human phenotype associated with complete or partial monosomy X. Principle features of Turner syndrome include short stature, ovarian failure, and a variety of other anatomic and physiological abnormalities, such as webbed neck, lymphedema, cardiovascular and renal anomalies, hypertension, and autoimmune thyroid disease. We studied 28 apparently nonmosaic subjects with partial deletions of Xp, in order to map loci responsible for various components of the Turner syndrome phenotype. Subjects were carefully evaluated for the presence or absence of Turner syndrome features, and their deletions were mapped by FISH with a panel of Xp markers. Using a statistical method to examine genotype/phenotype correlations, we mapped one or more Turner syndrome traits to a critical region in Xp11.2-p22.1. These traits included short stature, ovarian failure, high-arched palate, and autoimmune thyroid disease. The results are useful for genetic counseling of individuals with partial monosomy X. Study of additional subjects should refine the localization of Turner syndrome loci and provide a rational basis for exploration of candidate genes. 相似文献
95.
RF Bury AR Cowen AG Davies EL Baker P Hawkridge AJ Bruijns H Reitsma 《Canadian Metallurgical Quarterly》1998,53(12):923-928
This paper presents a brief technical evaluation and first review of clinical experiences with an experimental direct digital X-ray image detector designed to support both dynamic and snap-shot imaging. Derivatives of this type of image detector can potentially fulfil the majority of the fluoroscopic and radiographic imaging requirements of clinical radiology departments, and initial results suggest that imaging systems using the new technology will provide a high quality dose-efficient solution to the search for a universal digital X-ray image detector. 相似文献
96.
Experimental data from protein engineering studies and NMR spectroscopy have been used by theoreticians to develop algorithms for helix propensity and to benchmark computer simulations of folding pathways and energy landscapes. Molecular dynamic simulations of the unfolding of chymotrypsin inhibitor 2 (CI2) have provided detailed structural models of the transition state ensemble for unfolding/folding of the protein. We now have used the simulated transition state structures to design faster folding mutants of CI2. The models pinpoint a number of unfavorable local interactions at the carboxyl terminus of the single alpha-helix and in the protease-binding loop region of CI2. By removing these interactions or replacing them with stabilizing ones, we have increased the rate of folding of the protein up to 40-fold (tau = 0.4 ms). This correspondence, and other examples of agreement between experiment and theory in general, Phi-values and molecular dynamics simulations, in particular, suggest that significant progress has been made toward describing complete folding pathways at atomic resolution by combining experiment and simulation. 相似文献
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WP Petros J Rabinowitz JP Gibbs IH Hall AR Stuart WP Peters 《Canadian Metallurgical Quarterly》1998,18(4):816-823
Marshall syndrome is a rare, autosomal dominant skeletal dysplasia that is phenotypically similar to the more common disorder Stickler syndrome. For a large kindred with Marshall syndrome, we demonstrate a splice-donor-site mutation in the COL11A1 gene that cosegregates with the phenotype. The G+1-->A transition causes in-frame skipping of a 54-bp exon and deletes amino acids 726-743 from the major triple-helical domain of the alpha1(XI) collagen polypeptide. The data support the hypothesis that the alpha1(XI) collagen polypeptide has an important role in skeletal morphogenesis that extends beyond its contribution to structural integrity of the cartilage extracellular matrix. Our results also demonstrate allelism of Marshall syndrome with the subset of Stickler syndrome families associated with COL11A1 mutations. 相似文献
100.