| 1. |
- Clarke, Robert, et al.
(författare)
-
Lowering blood homocysteine with folic acid based supplements : Meta-analysis of randomised trials
- 1998
-
Ingår i: British Medical Journal. - : BMJ. - 0959-8146. ; 316:7135, s. 894-898
-
Forskningsöversikt (refereegranskat)abstract
- Objective: To determine the size of reduction in homocysteine concentrations produced by dietary supplementation with folic acid and with vitamins B-12 or B-6. Design: Meta-analysis of randomised controlled trials that assessed the effects of folic acid based supplements on blood homocysteine concentration. Multivariate regression analysis was used to determine the effects on homocysteine concentrations of different doses of folic acid and of the addition of vitamin B-12 or B-6. Subjects: Individual data on 1114 people included in 12 trials. Findings: The proportional and absolute reductions in blood homocysteine produced by folic acid supplements were greater at higher pretreatment blood homocysteine concentrations (P < 0.001) and at lower pretreatment blood folate concentrations (P < 0.001). After standardisation to pretreatment blood concentrations of homocysteine of 12 μmol/l and of folate of 12 nmol/l (approximate average concentrations for Western populations), dietary folic acid reduced blood homocysteine concentrations by 25% (95% confidence interval 23% to 28%; P < 0.001), with similar effects in the range of 0.5-5 mg folic acid daily. Vitamin B-12 (mean 0.5 mg daily) produced an additional 7% (3% to 10%) reduction in blood homocysteine. Vitamin B-6 (mean 16.5 mg daily) did not have a significant additional effect. Conclusions: Typically in Western populations, daily supplementation with both 0.5-5 mg folic acid and about 0.5 mg vitamin B-12 would be expected to reduce blood homocysteine concentrations by about a quarter to a third (for example, from about 12 μmol/l to 8-9 μmol/l). Large scale randomised trials of such regimens in high risk populations are now needed to determine whether lowering blood homocysteine concentrations reduces the risk of vascular disease.
|
|
| 2. |
- West, Jay B., et al.
(författare)
-
Comparison and evaluation of retrospective intermodality image registration techniques
- 1997
-
Ingår i: SPIE - The International Society for Optical Engineering. - : SPIE - International Society for Optical Engineering. ; , s. 332-347
-
Konferensbidrag (refereegranskat)abstract
- All retrospective image registration methods have attached to them some intrinsic estimate of registration error. However, this estimate of accuracy may not always be a good indicator of the distance between actual and estimated positions of targets within the cranial cavity. This paper describes a project whose principal goal is to use a prospective method based on fiducial markers as a ’gold standard’ to perform an objective, blinded evaluation of the accuracy of several retrospective image-to-image registration techniques. Image volumes of three modalities – CT, MR, and PET – were taken of patients undergoing neurosurgery at Vanderbilt University Medical Center. These volumes had all traces of the fiducial markers removed, and were provided to project collaborators outside Vanderbilt, who then performed retrospective registrations on the volumes, calculating transformations from CT to MR and/or from PET to MR, and communicated their transformations to Vanderbilt where the accuracy of each registration was evaluated. In this evaluation the accuracy is measured at multiple ’regions of interest,’ i.e. areas in the brain which would commonly be areas of neurological interest. A region is defined in the MR image and its centroid C is determined. Then the prospective registration is used to obtain the corresponding point C’ in CT or PET. To this point the retrospective registration is then applied, producing C’ in MR. Statistics are gathered on the target registration error (TRE), which is the disparity between the original point C and its corresponding point C’. A second goal of the project is to evaluate the importance of correcting geometrical distortion in MR images, by comparing the retrospective TRE in the rectified images, i.e., those which have had the distortion correction applied, with that of the same images before rectification. This paper presents preliminary results of this study along with a brief description of each registration technique and an estimate of both preparation and execution time needed to perform the registration.
|
|
| 3. |
|
|
| 4. |
- Hägerhäll, Cecilia, et al.
(författare)
-
An Escherichia coli Mutant Quinol:Fumarate Reductase Contains an EPR-detectable Semiquinone Stabilized at the Proximal Quinone-binding Site
- 1999
-
Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 274:37, s. 26157-26164
-
Tidskriftsartikel (refereegranskat)abstract
- The EPR and thermodynamic properties of semiquinone (SQ) species stabilized by mammalian succinate:quinone reductase (SQR) in situ in the mitochondrial membrane and in the isolated enzyme have been well documented. The equivalent semiquinones in bacterial membranes have not yet been characterized, either in SQR or quinol:fumarate reductase (QFR) in situ. In this work, we describe an EPR-detectable QFR semiquinone using Escherichia coli mutant QFR (FrdC E29L) and the wild-type enzyme. The SQ exhibits a g = 2.005 signal with a peak-to-peak line width of ~1.1 milliteslas at 150 K, has a midpoint potential (Em(pH 7.2)) of 56.6 mV, and has a stability constant of ~1.2 × 102 at pH 7.2. It shows extremely fast spin relaxation behavior with a P1/2 value of 500 milliwatts at 150 K, which closely resembles the previously described SQ species (SQs) in mitochondrial SQR. This SQ species seems to be present also in wild-type QFR, but its stability constant is much lower, and its signal intensity is near the EPR detection limit around neutral pH. In contrast to mammalian SQR, the membrane anchor of E. coli QFR lacks heme; thus, this prosthetic group can be excluded as a spin relaxation enhancer. The trinuclear iron-sulfur cluster FR3 in the [3Fe-4S]1+ state is suggested as the dominant spin relaxation enhancer of the SQFR spins in this enzyme. E. coli QFR activity and the fast relaxing SQ species observed in the mutant enzyme are sensitive to the inhibitor 2-n-heptyl-4-hydroxyquinoline N-oxide (HQNO). In wild-type E. coli QFR, HQNO causes EPR spectral line shape perturbations of the iron-sulfur cluster FR3. Similar spectral line shape changes of FR3 are caused by the FrdC E29L mutation, without addition of HQNO. This indicates that the SQ and the inhibitor-binding sites are located in close proximity to the trinuclear iron-sulfur cluster FR3. The data further suggest that this site corresponds to the proximal quinone-binding site in E. coli QFR.
|
|
| 5. |
- Kihl, Maria, et al.
(författare)
-
Measuring real-time performance in distributed object oriented systems
- 1999
-
Ingår i: Performance and control of network systems III : 20-21 September 1999, Boston, Massachusetts. - 0819434345 ; , s. 248-258
-
Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- The principles of distributed object oriented programming offer great possibilities for flexible architectures in multiple fields. In telecommunications, an architecture called Telecommunication Information Networking Architecture (TINA) has been developed using these very principles. It allows telecommunication services to be implemented using software objects that in turn can be executed in a location transparent way in a network. The location transparency offers great flexibility for service creation, but as the software must be executed somewhere in the network on nodes of finite capacity, performance problems can arise due to inefficient placement of objects causing either overloaded nodes or excessive and unneccesary inter-node communication. To ensure good performance, various measures of load control and load balancing must be taken. We discuss how to measure the performance of a distributed object oriented system and examine two load balancing algorithms that can be used in such systems. of finite capacity, performance problems can arise due to inefficient placement of objects causing either overloaded nodes or excessive and unneccesary inter-node communication. To ensure good performance, various measures of load control and load balancing must be taken. We discuss how to measure the performance of a distributed object oriented system and examine two load balancing algorithms that can be used in such systems.
|
|
| 6. |
|
|
| 7. |
- Pugliese, Alberto, et al.
(författare)
-
Sequence analysis of the diabetes-protective human leukocyte antigen-DQB1*0602 allele in unaffected, islet cell antibody-positive first degree relatives and in rare patients with type 1 diabetes
- 1999
-
Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 84:5, s. 1722-1728
-
Tidskriftsartikel (refereegranskat)abstract
- The human leukocyte antigen (HLA)-DQA1*0102/DQB1*0602/DRB1*1501 (DR2) haplotype confers strong protection from type 1 diabetes. Growing evidence suggests that such protection may be mostly encoded by the DQB1*0602 allele, and we reported that even first degree relatives with islet cell antibodies (ICA) have an extremely low diabetes risk if they carry DQB1*0602. Recently, novel variants of the DQB1*0602 and *0603 alleles were reported in four patients with type 1 diabetes originally typed as DQB1*0602 with conventional techniques. One inference from this observation is that DQB1*0602 may confer absolute protection and may never occur in type 1 diabetes. By this hypothesis, all patients typed as DQB1*0602 positive with conventional techniques should carry one of the above diabetes-permissive variants instead of the protective DQB1*0602. Such variants could also occur in ICA/DQB1*0602-positive relatives, with the implication that their diabetes risk could be significantly higher than previously estimated. We therefore sequenced the DQB1*0602 and DQA1*0102 alleles in all ICA/DQB1*0602-positive relatives (n = 8) previously described and in six rare patients with type 1 diabetes and DQB1*0602. We found that all relatives and patients carry the known DQB1*0602 and DQA1*0102 sequences, and none of them has the mtDNA A3243G mutation associated with late-onset diabetes in ICA-positive individuals. These findings suggest that diabetes-permissive DQB1*0602/3 variants may be very rare. Thus, although the protective effect associated with DQB1*0602 is extremely powerful, it is not absolute. Nonetheless, the development of diabetes in individuals with DQB1*0602 remains extremely unlikely, even in the presence of ICA, as confirmed by our further evaluation of ICA/DQB1*0602-positive relatives, none of whom has yet developed diabetes.
|
|
| 8. |
- Saalman, Robert, 1952, et al.
(författare)
-
Antibody-dependent cell-mediated cytotoxicity to gliadin-coated cells with sera from children with coeliac disease.
- 1998
-
Ingår i: Scandinavian journal of immunology. - 0300-9475. ; 47:1, s. 37-42
-
Tidskriftsartikel (refereegranskat)abstract
- Antibody-dependent cell-mediated cytotoxicity (ADCC) has been suggested as a contributing immunological mechanism in the disease process of coeliac disease. In the present study, sera from coeliac children were examined for their capacity to mediate ADCC against gliadin-coated target cells. The ADCC-mediating efficacy of sera were tested using monocytes from healthy adults as effector cells and gliadin-coated erythrocytes from the same donor as targets. Using monocytes as effector cells, sera from children with active coeliac disease (untreated or challenged), demonstrated significantly higher ADCC-mediating capacity than sera from healthy and disease references as well as children with treated coeliac disease. A positive correlation was found between the ADCC-mediating capacity and serum IgG as well as IgA anti-gliadin antibody levels. The results suggest that an antibody-dependent monocyte/macrophage-induced cytotoxic reaction might be involved in the disease process of coeliac disease.
|
|
| 9. |
- Wheelersburg, Robert P.
(författare)
-
Introduction
- 1996
-
Ingår i: Northern People Southern States. - Umeå : UmU Tryckeri. - 9171912142 ; , s. 1-11
-
Bokkapitel (övrigt vetenskapligt/konstnärligt)
|
|
| 10. |
|
|
