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991.
992.
SM Mulders DG Bichet JP Rijss EJ Kamsteeg MF Arthus M Lonergan M Fujiwara K Morgan R Leijendekker P van der Sluijs CH van Os PM Deen 《Canadian Metallurgical Quarterly》1998,102(1):57-66
Calcyclin (CaCY) is a member of the S100 subfamily of helix-loop-helix (EF-hand) calcium-binding proteins. Human CaCY was overexpressed in Escherichia coli and purified with an overall yield of 40 mg/l culture. Ca2+ and Zn2+ binding properties of CaCY were examined with respect to the oxidation state of the single Cys residue at position 3. CaCY with the SH group either reduced, blocked or oxidized stays as a dimer as shown by analytical ultracentrifugation. Upon binding of Ca2+, CaCY exhibits 30% enhancement of the Tyr fluorescence, the apparent binding constant (Ka) being 2.8-5.8x10(4) M(-1). Oxidized CaCY binds Ca2+ approximately twice as weakly than its reduced form. The affinity for Ca2+ is increased in the presence of caldesmon, which could be a potential target molecule. Fully reduced CaCY binds Zn2+ with an affinity of at least 1.0x10(7) M(-1). As compared to Ca2+, Zn2+ binding results in a three times greater enhancement of the Tyr fluorescence. Saturation occurs at a Zn2+/CaCY ratio of 2:1. The reactivity of Cys3 is reduced by Zn2+ binding, although oxidized CaCY still binds Zn2+. On the basis of the effects of thiol-directed labels on the affinities for Ca2+ and Zn2+, the fluorescence changes accompanying the binding, and the CaCY reactivity with a hydrophobic probe, it was concluded that the two cations bind to CaCY at different sites: Ca2+ binds probably at the EF-hand type sites, whereas binding of at least one Zn2+ ion involves the Cys residue, and results in a different structural change. 相似文献
993.
Six healthy men completed three 1-hr bouts of treadmill walk-jogging at low (L; 42 +/- 3.9% VO2max), moderate (M; 55 +/- 5.6%), and high (H; 67 +/- 4.5%) exercise intensity in order to determine whether moderate physical activity affects dietary protein needs. Both sweat rate and sweat urea N loss were greater (p < .10) with increasing exercise intensity. Seventy-two hour postexercise urine urea N excretion was elevated (p < .05) over nonexercise control (26.6 +/- 2.96 g) with both M (31.0 +/- 3.65) and H (33.6 +/- 4.39), but not L (26.3 +/- 1.86), intensities. Total 72-hr postexercise urea N excretion (urine + sweat) for the M and H exercise was greater than control by 4.6 and 7.2 g, respectively. This suggests that 1 hr of moderate exercise increases protein oxidation by about 29-45 g, representing approximately 16-25% of the current North American recommendations for daily protein intake. These data indicate that the type of exercise typically recommended for health/wellness can increase daily protein needs relative either to sedentary individuals or to those who exercise at lower intensities. 相似文献
994.
We evaluated the gait of thirty-five neurologically normal children who had a limb-length discrepancy of the lower extremities that ranged from 0.8 to 15.8 per cent of the length of the long extremity (0.6 to 11.1 centimeters). The twenty-two boys and thirteen girls had an average age of thirteen years (range, eight to seventeen years). No patient had a substantial angular or rotational deformity of the lower extremities. We found no correlation between the actual discrepancy or the per cent discrepancy and any of the dependent kinematic or kinetic variables, including pelvic obliquity. Discrepancies of less than 3 per cent of the length of the long extremity were not associated with compensatory strategies. When a discrepancy was 5.5 per cent or more, more mechanical work was performed by the long extremity and there was a greater vertical displacement of the center of body mass. Clinically, this degree of discrepancy was manifested by the use of toe-walking as a compensatory strategy. Children who had less of a discrepancy were able to use a combination of compensatory strategies to normalize the mechanical work performed by the lower extremities. 相似文献
995.
JV Bowler M Eliasziw R Steenhuis DG Munoz R Fry H Merskey VC Hachinski 《Canadian Metallurgical Quarterly》1997,54(6):697-703
OBJECTIVE: To compare the evolution of Alzheimer disease (AD), vascular dementia (VaD), and mixed dementia by cognitive domain. SETTING: The University of Western Ontario Dementia Study, which is a registry of cases of dementia seen for secondary and tertiary assessment in a university memory disorders clinica with extensive follow-up data and histopathological confirmation of clinical diagnoses. PATIENTS: One hundred twenty-nine patients with definite or probable AD, 12 patients with definite or probable VaD, and 36 patients with definite or probable mixed dementia. METHODS: Patients were grouped as having an early, moderate, or advanced stage of disease according to the extended scale for dementia (ESD). The ESD was subdivided into cognitive domains, and the domain scores were compared for each stage of disease by diagnostic category with the use of a 2-way analysis of variance with repeated measures. RESULTS: As expected, the scores in all domains decreased significantly with increasing severity. There was a significant difference in the decline in memory among the diagnostic groups (P = .02) that was mostly attributable to the difference between AD and mixed dementia (P = .03), with the difference between AD and VaD only approaching significance (P = .06). There was a similar finding for praxis. The interaction between diagnosis (AD and VaD) and severity was significant only for memory (P = .02), showing a less severe memory deficit at onset but a proportionately more rapid progression in VaD and arithmetic ability (AD and mixed dementia [P = .03]). CONCLUSIONS: Alzheimer disease, VaD, and mixed dementia evolve similarly as assessed using cognitive domains obtained by subdivision of the ESD in a patient population derived from a memory clinic and by analyzing VaD as a single entity. Only memory impairment evolves differently between AD and VaD, with this depending on the severity. Memory is more severely impaired in the early stage of AD; however, with increasing severity of dementia, memory impairment in VaD accelerates and catches up with AD at the level of moderate impairment. The differences between AD and mixed dementia are greater than those between mixed dementia and VaD, suggesting an important role for the ischemic component of mixed dementia. Simple neuropsychological tools (eg, the ESD) may be incapable of distinguishing between AD and VaD, and more focused instruments may be required. Inherent bias in case selection may prevent extrapolation of these results to VaD in general, but the neuropsychological criteria for VaD may need to vary, depending on the severity. 相似文献
996.
DR Alessi M Deak A Casamayor FB Caudwell N Morrice DG Norman P Gaffney CB Reese CN MacDougall D Harbison A Ashworth M Bownes 《Canadian Metallurgical Quarterly》1997,7(10):776-789
BACKGROUND: The activation of protein kinase B (PKB, also known as c-Akt) is stimulated by insulin or growth factors and results from its phosphorylation at Thr308 and Ser473. We recently identified a protein kinase, termed PDK1, that phosphorylates PKB at Thr308 only in the presence of lipid vesicles containing phosphatidylinositol 3,4,5-trisphosphate (Ptdlns(3,4,5)P3) or phosphatidylinositol 3,4-bisphosphate (Ptdlns(3,4)P2). RESULTS: We have cloned and sequenced human PDK1. The 556-residue monomeric enzyme comprises a catalytic domain that is most similar to the PKA, PKB and PKC subfamily of protein kinases and a carboxy-terminal pleckstrin homology (PH) domain. The PDK1 gene is located on human chromosome 16p13.3 and is expressed ubiquitously in human tissues. Human PDK1 is homologous to the Drosophila protein kinase DSTPK61, which has been implicated in the regulation of sex differentiation, oogenesis and spermatogenesis. Expressed PDK1 and DSTPK61 phosphorylated Thr308 of PKB alpha only in the presence of Ptdlns(3,4,5)P3 or Ptdlns(3,4)P2. Overexpression of PDK1 in 293 cells activated PKB alpha and potentiated the IGF1-induced phosphorylation of PKB alpha at Thr308. Experiments in which the PH domains of either PDK1 or PKB alpha were deleted indicated that the binding of Ptdlns(3,4,5)P3 or Ptdlns(3,4)P2 to PKB alpha is required for phosphorylation and activation by PDK1. IGF1 stimulation of 293 cells did not affect the activity or phosphorylation of PDK1. CONCLUSIONS: PDK1 is likely to mediate the activation of PKB by insulin or growth factors. DSTPK61 is a Drosophila homologue of PDK1. The effect of Ptdlns(3,4,5)P3/Ptdlns(3,4)P2 in the activation of PKB alpha is at least partly substrate directed. 相似文献
997.
998.
DG Blanchard JL Sobel J Hope A Raisinghani S Keramati AN DeMaria 《Canadian Metallurgical Quarterly》1998,11(11):1078-1083
Infrahepatic interruption of the inferior vena cava (IVC) with azygos or hemiazygos continuation is a rare finding. In this anatomic entity, the intrahepatic segment of the IVC is absent, and the hepatic veins empty directly into the right atrium. Venous blood flow from the lower body is directed from the IVC into the azygos system at the level of the renal veins, with resultant dilation of the azygos and/or hemiazygos veins. Because these enlarged vessels lie parallel to the descending thoracic aorta, they may be mistaken for aortic pathology (dissection, aneurysm, or rupture) during transesophageal echocardiography (TEE). We describe a case of azygos continuation of the IVC initially misdiagnosed by TEE as partial aortic rupture. Repeat TEE with intravenous agitated saline injection correctly identified the condition, and the echocardiographic features are described. 相似文献
999.
The Monte Carlo computer code MCNP (version 4A) has been used to develop a personal computer-based model of the Swansea in vivo neutron activation analysis (IVNAA) system. The model included specification of the neutron source (252Cf), collimators, reflectors and shielding. The MCNP model was 'benchmarked' against fast neutron and thermal neutron fluence data obtained experimentally from the IVNAA system. The Swansea system allows two irradiation geometries using 'short' and 'long' collimators, which provide alternative dose rates for IVNAA. The data presented here relate to the short collimator, although results of similar accuracy were obtained using the long collimator. The fast neutron fluence was measured in air at a series of depths inside the collimator. The measurements agreed with the MCNP simulation within the statistical uncertainty (5-10%) of the calculations. The thermal neutron fluence was measured and calculated inside the cuboidal water phantom. The depth of maximum thermal fluence was 3.2 cm (measured) and 3.0 cm (calculated). The width of the 50% thermal fluence level across the phantom at its mid-depth was found to be the same by both MCNP and experiment. This benchmarking exercise has given us a high degree of confidence in MCNP as a tool for the design of IVNAA systems. 相似文献
1000.
DG Baskin RJ Seeley JL Kuijper S Lok DS Weigle JC Erickson RD Palmiter MW Schwartz 《Canadian Metallurgical Quarterly》1998,47(4):538-543
BACKGROUND: Graft coronary artery disease (CAD) is an increasingly important problem during long-term survival after heart transplantation, but the importance of cellular rejection, in particular late after transplantation, remains undetermined. METHODS and RESULTS: We analyzed 492 coronary angiographies (967+/-705 days after transplantation; range, 49 days to 9.4 years) and 5201 endomyocardial biopsies (518+/-648 days after transplantation) from 156 patients (age, 47+/-11 years). Patients with angiographically detectable graft CAD had significantly more episodes of rejection requiring augmentation of immunosuppressive therapy (i.e., International Society of Heart and Lung Transplantation score > or = 3A) than those without graft CAD during the first (3.7+/-2.6 vs. 2.2+/-2.0, P<0.001) as well as subsequent years after transplantation (1.2+/-1.9 vs. 0.4+/-0.9, P<0.01). Multivariate logistic regression analysis including established risk factors for CAD, ischemic time, gender and age of donors and recipients, number of mismatches, cytomegalovirus infection, and drug therapy showed that the number of rejections during the first [odds ratio (OR)=1.39, P<0.005] as well as subsequent years (OR=1.49, P<0.05), previous cytomegalovirus infection (OR=3.21, P<0.05), donor age >40 years (OR=2.97, P<0.05), and current or former smoker status (OR=2.76, P<0.05) were independent predictors of graft CAD. In patients without angiographically detectable graft CAD 1 year after transplantation, the number of rejections after the first year was even more strongly related to graft coronary artery disease than in the total patient population, underlining the importance of late cellular rejection (OR=1.74, P<0.005). CONCLUSION: Rejection requiring augmentation of immunosuppression early and late after transplantation is an independent risk factor for the development of angiographically detectable graft CAD. Hence, the search for and treatment of moderate or severe rejection seems to be prudent even late after transplantation. 相似文献