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11.
E K Lancaster R A Evans S Kos E Hills C R Dunstan S Y Wong 《Journal of bone and mineral research》1989,4(4):507-514
Bone mineral content (BMC) was measured in the os calcis of 232 normal subjects aged 17-82 years. The mean reproducibility (coefficient of variation) of the measurement was 1.8%. Substantial bone loss occurred between the ages of 20 and 50 years, and in females the menopause was associated with additional bone loss. There was no significant difference in the rate of bone loss in females and males, but the mean BMC was greater at all ages in males than in females. We also compared os calcis BMC with spinal bone mineral density (BMD), measured by quantitative computed tomographic (CT) scanning, in 85 subjects: 33 were normal controls, 19 had osteoporosis defined by the presence of one or more pathological fractures, and in the remainder the CT examination was performed at the patient's request. Os calcis BMC correlated with spinal BMD in both females (r = 0.69, p less than 0.001) and males (r = 0.84, p less than 0.001). However, the os calcis BMC did not reliably predict spine values around the CT "fracture threshold" of 90-100 mg/cm3 and did not correlate with osteoporotic fracture as well as did spinal BMD. It is concluded that measurement of the os calcis BMC is of limited clinical usefulness for the early diagnosis of osteoporosis. 相似文献
12.
Linkage of the MHC to familial multiple sclerosis suggests genetic heterogeneity. The Multiple Sclerosis Genetics Group 总被引:5,自引:0,他引:5
Haines JL; Terwedow HA; Burgess K; Pericak-Vance MA; Rimmler JB; Martin ER; Oksenberg JR; Lincoln R; Zhang DY; Banatao DR; Gatto N; Goodkin DE; Hauser SL 《Human molecular genetics》1998,7(8):1229-1234
Multiple sclerosis (MS) is a demyelinating autoimmune disease of the
central nervous system. While its etiology is not well understood, genetic
factors are clearly involved. Until recently, most genetic studies in MS
have been association studies using the case-control design testing
specific candidate genes and studying only sporadic cases. The only
consistently replicated finding has been an association with the HLA-DR2
allele within the major histocompatibility complex (MHC) on chromosome 6.
Using the genetic linkage design, however, evidence for and against linkage
of the MHC to MS has been found, fostering suggestions that sporadic and
familial MS have different etiologies. Most recently, two of four genomic
screens demonstrated linkage to the MHC, although specific allelic
associations were not tested. Here, a dataset of 98 multiplex families was
studied to test for an association to the HLA-DR2 allele in familial MS and
to determine if genetic linkage to the MHC was due solely to such an
association. Three highly polymorphic markers (HLA-DR, D6S273 and TNFbeta)
in the MHC demonstrated strong genetic linkage (parametric lod scores of
4.60, 2.20 and 1.24, respectively) and a specific association with the
HLA-DR2 allele was confirmed (TDT; P < 0.001). Stratifying the results
by HLA-DR2 status showed that the linkage results were limited to families
segregating HLA-DR2 alleles. These results demonstrate that genetic linkage
to the MHC can be explained by the HLA-DR2 allelic association. They also
indicate that sporadic and familial MS share a common genetic
susceptibility. In addition, preliminary calculations suggest that the MHC
explains between 17 and 62% of the genetic etiology of MS. This
heterogeneity is also supported by the minority of families showing no
linkage or association with loci within the MHC.
相似文献
13.
Missed opportunities for the prevention of cardiovascular disease among British hypertensives in primary care. 下载免费PDF全文
F A Foss E Dickinson M Hills A Thomson V Wilson S Ebrahim 《The British journal of general practice》1996,46(411):571-575
BACKGROUND: High-risk strategies for the prevention of cardiovascular disease (CVD) among hypertensive patients require knowledge of the prevalence and interaction of modifiable risk factors to ensure effective targeting of interventions. Comparatively little is known of risk-factor profiles and their modification among hypertensives in primary care. AIM: The present study was designed to explore relationships between patients' knowledge of CVD risk factors, their perception of personal risk and health behaviours, and their use of lifestyle interventions. METHOD: A cross-sectional survey of 2676 men and women with mild to moderate hypertension (diastolic blood pressure 95-115 mmHg), and their general practitioners, recruited from 1044 general practices throughout the UK, was conducted. RESULTS: Levels of modifiable risk factors were high, although there was considerable variation by age and sex; most (98.5%) patients had at least one additional CVD risk factor. A lower standard of living was associated with a higher prevalence of 'unhealthy' behaviours. Out of those with a current lifestyle problem, 85% of obese patients, 59% of smokers, 47% of excess drinkers, 49% of those with dietary risk factors and 32% of inactive patients claimed to have adopted healthier behaviours within the past 3 months. Older subjects and those with a lower standard of living were less likely to acknowledge risks, and those who did were less likely to report improving their lifestyles. While 71% of patients recalled receiving lifestyle advice, the coverage and targeting of specific interventions was generally poor. Overall, 60% of the sample had received advice on weight control, 47% on diet, 38% on exercise, 38% on smoking and 36% on alcohol. Women and older people were less likely to be given relevant counseling, and there was no evidence of targeting with respect to subjects' social class, level of hypertension or duration of diagnosis. CONCLUSION: Lifestyle interventions are welcomed and are viewed as helpful by patients receiving them. Potential health gains among high-risk hypertensives are being lost because of poor targeting and coverage of those at greatest risk. 相似文献
14.
Y chromosome microdeletions, in azoospermic or near-azoospermic subjects, are located in the AZFc (DAZ) subregion 总被引:9,自引:2,他引:9
Submicroscopic deletions of the Y chromosome and polymorphisms of the
androgen receptor (AR) gene in the X chromosome have been observed in men
with defective spermatogenesis. To further define the subregions/genes in
the Y chromosome causing male infertility and its relationship to
polymorphisms of the AR polyglutamine tract, we screened the genomic DNA of
202 subfertile males and 101 healthy fertile controls of predominantly
Chinese ethnic origin. Y microdeletions were examined with 16
sequence-tagged site (STS) probes, including the RBM and DAZ genes,
spanning the AZFb and AZFc subregions of Yq11, and related to the size of
trinucleotide repeat encoding the AR polyglutamine tract. Y microdeletions
were detected and confirmed in three out of 44 (6.8%) of azoospermic and
three out of 86 (3.5%) severely oligozoospermic patients. No deletions were
detected in any of the patients with sperm counts of >0.5 x 10(6)/ml,
nor in any of the 101 fertile controls. All six affected patients had
almost contiguous Y microdeletions spanning the entire AZFc region
including the DAZ gene. The AZFb region, containing the RBM1 gene, was
intact in five of the six subjects. Y deletions were not found in those
with long AR polyglutamine tracts. Our study, the first in a Chinese
population, suggest a cause and effect relationship between Y
microdeletions in the AZFc region (possibly DAZ), and azoospermia or
near-azoospermia. Y microdeletions and long AR polyglutamine tracts appear
to be independent contributors to male infertility.
相似文献
15.
Catt SL; Sakkas D; Bizzaro D; Bianchi PG; Maxwell WM; Evans G 《Molecular human reproduction》1997,3(9):821-825
Controlling the sex of offspring by the separation of X and Y
chromosome-bearing spermatozoa using flow cytometry has been reported as a
clinical technique aiding prevention of X-linked diseases. Although this
technique has resulted in several hundred normal births in animals and at
least one human birth, there is still concern over its genetic safety due
to the involvement of two potentially mutagenic agents: UV light and the
fluorochrome dye, Hoechst 33342 (H33342). Human spermatozoa, particularly
those considered abnormal, may be more likely to suffer DNA damage
following exposure to mutagenic agents, compared with other mammalian
species. The stability of normal fresh and decondensed human spermatozoa
were examined after exposure to a range of levels of UV and H33342
staining, using an assay that detects endogenous nicks in the DNA of
spermatozoa. The stability of abnormal and normal, fresh and frozen-thawed
human spermatozoa was examined following UV laser, H33342 staining and flow
cytometry treatments utilizing the same assay. There was an increase in the
presence of endogenous nicks when spermatozoa were decondensed compared
with fresh spermatozoa. There was no increase in the incidence of nicks in
any group of spermatozoa after UV and fluorochrome exposure compared with
controls without exposure.
相似文献
16.
Winberg JO; Hammami-Hauasli N; Nilssen O; Anton-Lamprecht I; Naylor SL; Kerbacher K; Zimmermann M; Krajci P; Gedde-Dahl T Jr; Bruckner-Tuderman L 《Human molecular genetics》1997,6(7):1125-1135
Dystrophic epidermolysis bullosa (EBD) is a clinically heterogeneous skin
disorder, characterized by abnormal anchoring fibrils (AF) and loss of
dermal-epidermal adherence. EBD has been linked to the COL7A1 gene at
chromosome 3p21 which encodes collagen VII, the major component of the AF.
Here we investigated two unrelated EBD families with different clinical
phenotypes and novel combinations of recessive and dominant COL7A1
mutations. Both families shared the same recessive heterozygous 14 bp
deletion at the exon-intron 115 boundary of the COL7A1 gene. The deletion
caused in-frame skipping of exon 115 and the elimination of 29 amino acid
residues from the pro-alpha1(VII) polypeptide chain. As a result,
procollagen VII was not converted to collagen VII and the C-terminal NC-2
propeptide which is normally removed from the procollagen VII prior to
formation of the anchoring fibrils was retained in the skin. All affected
individuals also carried missense mutations in exon 73 of COL7A1 which lead
to different glycine- to-arginine substitutions in the triple-helical
domain of collagen VII. Combination of the deletion mutation with a G2009R
substitution resulted in a mild phenotype. In contrast, combination of the
deletion with a G2043R substitution led to a severe phenotype. The G2043R
substitution was a de novo mutation which alone caused a mild phenotype.
Thus, different combinations of dominant and recessive COL7A1 mutations can
modulate disease activity of EBD and alter the clinical presentation of the
patients.
相似文献
17.
Experiments were carried out in which unfractionated spleen cells, and T lymphocyte subpopulations characterized by certain experimental criteria, were isolated at various times from rats infected with Plasmodium berghei. By adoptive transfer it was shown that unfractionated spleen cells, and T cells alone, could transfer protection to syngenic recipients as early as 11 days after infection of the cell donors. The protection conferred by T cells increased with the duration of the infection in the donors, at least up to 100 days. The additional presence of B cells in transferred lymphocyte populations enhanced their protective capacity over that shown by T cells alone. The role of T cells in protective immunity to malaria is discussed. 相似文献
18.
Bone histology was quantitated in 10 osteoporotic patients aged between 17 and 51 years and in six healthy subjects aged between 23 and 43 years. The osteoporosis was of varying aetiology and was clinically stable. All patients were given tetracycline before biopsy and double tetracycline labelling was used in seven patients. Bone forming and resorbing surfaces were defined by the presence of osteoblasts and osteoclasts, respectively, which were identified by histochemical techniques. The associations between bone forming and resorbing surfaces were similar in patients and controls, though the range of values was wider in the patients than in the controls. Mineral apposition rate was normal in the osteoporotic patients, but there was a reduction in mineralising (tetracycline) surface, whether related to osteoid surface or to osteoblast surface. This did not indicate osteomalacia as the directly and indirectly measured mineralisation lag times were normal. The osteoid seams were thinner in osteoporotic patients than in controls. The data suggest that osteoclast and osteoblast numbers were normal in this group of osteoporotic patients but that the metabolic activity of osteoblasts was impaired. 相似文献
19.
B A Hills 《Undersea biomedical research》1992,19(2):107-120
Various endothelial surfaces from sheep and humans have been studied for their hydrophobicity using a standard method based on the angle of contact (theta) of the surface with a droplet of saline placed on it. Most surfaces were relatively hydrophilic (theta less than 25 degrees) but some were distinctly hydrophobic with theta exceeding 65 degrees for sheep pulmonary vein, left ventricle, and aorta, and human umbilical vein. These results are discussed as compatible with the theory that surface-active phospholipid (surfactant) migrates from lung tissue into the pulmonary circulation or reaches intravascular sites from other sources. Transmission electron microscopy of cerebral vessels demonstrated an oligolamellar lining of surfactant on many endothelial surfaces, bridging the "tight" junctions between endothelial cells in many cases. Lamellar bodies were found adjacent to the endothelium. The oligolamellar surfactant lining and lamellar bodies are discussed as potentially very important factors in influencing bubble formation on vessel walls. It is believed to impart hydrophobicity while it could also determine the microgeometry of any crevices vital for bubble formation or retention. 相似文献
20.