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11.
S A Holland L C Hutton F N McKenzie 《Journal l'Association canadienne des radiologistes》1989,40(2):94-97
The chest radiographic findings and pulmonary radionuclide studies of four patients who underwent heart-lung transplantation between May 1983 and June 1986 were reviewed retrospectively. The two long-term survivors both developed bronchiolitis obliterans (presenting at 32 months postoperatively in the first patient and 14.5 months postoperatively in the second). The etiology of this is likely to be multifactorial and includes pulmonary rejection which may develop without concomitant cardiac rejection. The radiologist must be alert to this complication in heart-lung transplantation. The chest radiographs in our two patients showed diminution of peripheral bronchovascular markings and overinflation. The importance of careful screening of the radiographs of potential donors to detect pneumonia is emphasized. In one patient, a unilateral pneumothorax spread contralaterally due to the absence of normal anatomic barriers. The "reimplantation response" was not a prominent feature and was seen in one patient only. This response has been observed in heart-lung transplant recipients during the second postoperative week. The radiologic appearance is that of interstitial edema not explained by any clinical or hemodynamic findings. 相似文献
12.
Detection of Serum Antibodies to Ovine Progressive Pneumonia Virus in Sheep by Using a Caprine Arthritis-Encephalitis Virus Competitive-Inhibition Enzyme-Linked Immunosorbent Assay 下载免费PDF全文
Lynn M. Herrmann William P. Cheevers Katherine L. Marshall Travis C. McGuire Melinda M. Hutton Gregory S. Lewis Donald P. Knowles 《Clinical and Vaccine Immunology : CVI》2003,10(5):862-865
A competitive-inhibition enzyme-linked immunosorbent assay (cELISA) for detection of antibodies to the surface envelope (SU) of caprine arthritis-encephalitis virus (CAEV) was recently reported (L. M. Herrmann, W. P. Cheevers, T. C. McGuire, D. Scott Adams, M. M. Hutton, W. G. Gavin, and D. P. Knowles, Clin. Diagn. Lab. Immunol. 10:267-271, 2003). The cELISA utilizes CAEV-63 SU captured on microtiter plates using the monoclonal antibody (MAb) F7-299 and measures competitive displacement of binding of the anti-CAEV MAb GPB 74A by goat serum. The present study evaluated the CAEV cELISA for detection of antibodies to ovine progressive pneumonia virus (OPPV) in sheep. Three hundred thirty-two sera were randomly selected from 21,373 sheep sera collected throughout the United States to determine the sensitivity and specificity of cELISA and agar gel immunodiffusion (AGID) based on immunoprecipitation (IP) of [35S]methionine-labeled OPPV antigens as a standard of comparison. A positive cELISA test was defined as >20.9 percent inhibition (% I) of MAb 74A binding based on two standard deviations above the mean % I of 191 IP-negative sheep sera. At this cutoff, there were 2 of 141 false-negative sera (98.6% sensitivity) and 6 of 191 false-positive sera (96.9% specificity). Sensitivity and specificity values for IP-monitored AGID were comparable to those for cELISA for 314 of 332 sera with unambiguous AGID results. Concordant results by cELISA and IP resolved 16 of the 18 sera that were indeterminate by AGID. Additional studies evaluated cELISA by using 539 sera from a single OPPV-positive flock. Based on IP of 36 of these sera, there was one false-negative by cELISA among 21 IP-positive sera (95.5% sensitivity) and 0 of 15 false-positives (100% specificity). We conclude that the CAEV cELISA can be applied to detection of OPPV antibodies in sheep with high sensitivity and specificity. 相似文献
13.
Klein RL Lin WL Dickson DW Lewis J Hutton M Duff K Meyer EM King MA 《The American journal of pathology》2004,164(1):347-353
Neurofibrillary pathology was produced in the brains of adult rats after localized gene transfer of human tau carrying the P301L mutation, which is associated with frontotemporal dementia with parkinsonism. Within 1 month of in situ transfection of the basal forebrain region of normal rats, tau-immunoreactive and argyrophilic neuronal lesions formed. The fibrillar lesions had features of neurofibrillary tangles and tau immunoreactivity at light and electron microscopic levels. In addition to neurofibrillary tangles, other tau pathology, including pretangles and neuropil threads, was abundant and widespread. Tau gene transfer to the hippocampal region of amyloid-depositing transgenic mice produced pretangles and threads, as well as intensely tau-immunoreactive neurites in amyloid plaques. The ability to produce neurofibrillary pathology in adult rodents makes this a useful method to study tau-related neurodegeneration. 相似文献
14.
Willis F Graff-Radford N Pinto M Lawson L Adamson J Epstein D Parfitt F Hutton M O'Brien PC 《Journal of the National Medical Association》2003,95(1):71-76
Through its role in lipid metabolism, Apolipoprotein epsilon4 (ApoE4) may affect "brain repair" in stroke, brain hemorrhage, Alzheimer's disease, and other brain injury syndromes for which African Americans may have greater morbidity and mortality. Cross-cultural evaluations of these and other genetic factors may provide insight on possible ethnic differences in risk of morbidity to acute central nervous system (CNS) injury and chronic neurodegenerative processes. As an initial step toward expanding knowledge of ApoE allele frequencies for persons of African descent, we compared ApoE genotype of a group of 70 young Ugandans to 59 (subset of a larger group of 342 African Americans of all ages) age-matched African Americans and to published frequencies for Caucasians and Asians. We found that the ApoE4 and epsilon2 alleles are more frequent in Ugandans (U) than Caucasians (C) or Asians (A) with corresponding alleles showing significant elevations of epsilon2 (U 15.71%, C 8.40%, A 4.20%) and 14 (U 25%, C 13.70%, A 8.90%) (p < .001). Comparing the differences between Ugandans and age-appropriate African Americans (AA) was not statically significant, but this outcome may be due to small sample size. These results provide the only published ApoE frequencies for Ugandans and the complete set of data provides the largest published community group of ApoE frequencies for African Americans. 相似文献
15.
16.
APOE is a potential modifier gene in an autosomal dominant form of frontotemporal dementia (IBMPFD).
Sarju G Mehta Giles D J Watts Jennifer L Adamson Mike Hutton Geanie Umberger Shuling Xiong Sheena Ramdeen Mark A Lovell Virginia E Kimonis Charles D Smith 《Genetics in medicine》2007,9(1):9-13
PURPOSE: Inclusion-body myopathy, Paget's disease of bone and frontotemporal dementia is an adult-onset autosomal dominant illness (IBMPFD) caused by mutations in the valosin-containing protein (VCP) on chromosome 9p21.1-p12. The penetrance of the gene is 82% for myopathy, 49% for Paget's disease, but may be as low as 30% for frontotemporal dementia. Modifier genes could account for decreased frontotemporal dementia penetrance. In this study apolipoprotein-E (APOE) was evaluated for this role in IBMPFD families based on its known modifier effect in Alzheimer's disease. METHODS: From a database of 231 members of 15 families, 174 had APOE genotype available for analysis. Logistic regressions on APOE genotype and frontotemporal dementia were performed, using appropriate covariates. RESULTS AND CONCLUSION: FTD was associated with APOE 4 genotype (P=0.0002), myopathy (P=0.0006), and age (P=0.01), but not microtubule associated protein tau (MAPT) H2 haplotype (P=0.5) or gender (0.09) after adjustment for membership in pedigrees with at least one APOE 4 genotype. These data suggest a potential link between APOE 4 genotype and the specific form of frontotemporal dementia found in IBMPFD. The molecular basis of this link bears further investigation. We did not observe an association of frontotemporal dementia and H2 MAPT haplotype. 相似文献
17.
Rademakers R Melquist S Cruts M Theuns J Del-Favero J Poorkaj P Baker M Sleegers K Crook R De Pooter T Bel Kacem S Adamson J Van den Bossche D Van den Broeck M Gass J Corsmit E De Rijk P Thomas N Engelborghs S Heckman M Litvan I Crook J De Deyn PP Dickson D Schellenberg GD Van Broeckhoven C Hutton ML 《Human molecular genetics》2005,14(21):3281-3292
18.
Patient motion occurring during data acquisition in single photon emission computed tomography (SPET) can cause serious reconstruction artefacts. We have developed a new approach to correct for head motion in brain SPECT. Prior to motion, projections are assigned to conventional projections. When head motion occurs, it is measured by a motion monitoring system, and subsequent projection data are mapped to 'virtual' projections. The appropriate position of each virtual projection is determined by applying the converse of the patient's accumulated motion to the actual camera projection. Conventional and virtual projections, taken together, form a consistent set that can be reconstructed using a three-dimensional (3D) algorithm. The technique has been tested on a range of simulated rotational movements, both within and out of the transaxial plane. For all simulated movements, the motion corrected images exhibited better agreement with a motion free reconstruction than did the uncorrected images. This technique may help to overcome one of the major remaining limitations on image quality and quantitative accuracy in SPECT. 相似文献
19.
20.
Estimation of the genetic contribution of presenilin-1 and -2 mutations in a population-based study of presenile Alzheimer disease 总被引:11,自引:4,他引:11
Cruts M; van Duijn CM; Backhovens H; Van den Broeck M; Wehnert A; Serneels S; Sherrington R; Hutton M; Hardy J; St George-Hyslop PH; Hofman A; Van Broeckhoven C 《Human molecular genetics》1998,7(1):43-51
Two closely related genes, the presenilins ( PS ), located at chromosomes
14q24.3 and 1q42.1, have been identified for autosomal dominant Alzheimer
disease (AD) with onset age below 65 years (presenile AD). We performed a
systematic mutation analysis of all coding and 5'-non-coding exons of PS -1
and PS -2 in a population-based epidemiological series of 101 unrelated
familial and sporadic presenile AD cases. The familial cases included 10
patients of autosomal dominant AD families sampled for linkage analysis
studies. In all patients mutations in the amyloid precursor protein gene (
APP ) had previously been excluded. Four different PS -1 missense mutations
were identified in six familial cases, two of which where autosomal
dominant cases. Three mutations resulted in onset ages above 55 years, with
one segregating in an autosomal dominant family with mean onset age 64
years (range 50-78 years). One PS -2 mutation was identified in a sporadic
case with onset age 62 years. Our mutation data provided estimates for PS
-1 and PS -2 mutation frequencies in presenile AD of 6 and 1% respectively.
When family history was accounted for mutation frequencies for PS -1 were
9% in familial cases and 18% in autosomal dominant cases. Further,
polymorphisms were detected in the promoter and the 5'-non-coding region of
PS -1 and in intronic and exonic sequences of PS -2 that will be useful in
genetic association studies.
相似文献