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排序方式: 共有348条查询结果,搜索用时 31 毫秒
91.
Transformed T lymphocytes infected by a novel isolate of human T cell leukemia virus type II 总被引:1,自引:0,他引:1
Chorba TL; Brynes R; Kalyanaraman VS; Telfer M; Ramsey R; Mawle A; Palmer EL; Chen AT; Feorino P; Evatt BL 《Blood》1985,66(6):1336-1342
Human T cell leukemia virus type II (HTLV-II) has been isolated from a patient (Mo) with features of leukemic reticuloendotheliosis (LRE) and from a patient with acquired immunodeficiency syndrome (AIDS). We have obtained another isolate of HTLV-II from a patient (CM) with severe hemophilia A, pancytopenia, and a 14-year history of staphylococcal and candidal infections but no evidence of T cell leukemia/lymphoma, AIDS, or LRE. Fresh mononuclear cells and cultured lymphocytes from CM express retroviral antigens indistinguishable by molecular criteria from HTLV-IIMo. Leukocyte cultures from CM yield hyperdiploid (48,XY, +2, +19) continuous lymphoid lines; human fetal cord blood lymphocytes (CBL) are transformed by cocultivation with these CM cell cultures but retain normal cytogenetic constitution. Electron microscopic examination of the CM cultures and transformed CBL reveals budding of extracellular viral particles, intracellular tubuloreticular structures, and viral particles contained within intracellular vesicles. CM cell cultures and the transformed CBL do not require exogenous interleukin 2, have T cell cytochemical features and mature T helper phenotypes, and exhibit minimal T helper and profound T suppressor activity on pokeweed mitogen-stimulated differentiation of normal B cells. These characteristics, which are similar to those observed with the first HTLV-II isolate, may represent properties of all HTLV-II-infected T cells. 相似文献
92.
Paul TL Chiam MBBS MRCP Howard A Cohen MD Carlos E. Ruiz MD PhD 《Catheterization and cardiovascular interventions》2008,71(4):564-567
Percutaneous closure of sedundum atrial septal defects (ASD) has been shown to be safe and effective. Usually crossing the defect is relatively straightforward. Occasionally, with fenestrated ASDs, trying to cross the defect(s) may be challenging. We report the use of a “paralle wire” (0.018 or 0.014 inch wire) technique to maintain access and be able to recross the same defect easily in case of misplacement until just before the device was secured and released. This technique could be used also as a “body wire” for large ASDs with deficient rims to reduce the incidence of device prolapse, and for patent foramen ovale and ventricular septal defect closures. This is a simple and easily reproducible method with the equipment readily available in virtually all catheterization laboratories. © 2008 Wiley‐Liss, Inc. 相似文献
93.
ML Von Linstow V Rosenfeldt AM Lebech M Storgaard T Hornstrup TL Katzenstein G Pedersen T Herlin NH Valerius N Weis 《HIV medicine》2010,11(7):448-456
Objectives
The aim of this study was to describe trends in the management of pregnancies in HIV‐infected women and their outcomes over a 14‐year period in Denmark on a national basis.Methods
The study was a retrospective cohort study of all HIV‐infected women in Denmark giving birth to one or more children between 1 June 1994 and 30 June 2008.Results
We identified 210 HIV‐infected women with 255 pregnancies, ranging from 7 per year in 1995 to 39 per year in 2006. Thirty per cent of the women were Caucasian and 51% were Black African. Knowledge of HIV status before pregnancy increased from 8% (four of 49) in 1994–1999 to 80% (164 of 206) in 2000–2008. Only 29% (53 of 183) of the women chose to consult an infectious disease specialist when planning pregnancy, while 14% (27 of 199) received assistance with fertility. The proportion of women on antiretroviral therapy (ART) increased from 76% (37 of 49) in 1994–1999 to 98% (201 of 206) in 2000–2008. Vaginal deliveries ranged from 0 in 2003 to 35% of pregnancies in 2007. Mother‐to‐child transmission (MTCT) of HIV decreased from 10.4% in 1994–1999 to 0.5% in 2000–2008. All women giving birth to an HIV‐positive child were diagnosed with HIV during or after delivery and did not receive prophylactic ART.Conclusions
The annual number of HIV pregnancies increased fivefold during this 14‐year period and substantial changes in pregnancy management were seen. No woman treated according to the national guidelines, i.e. ART before week 22, intravenous zidovudine (ZDV) during labour, neonatal ZDV for 4 to 6 weeks and no breastfeeding, transmitted HIV to her child. 相似文献94.
Kirkman NJ Libbey JE Sweeten TL Coon HH Miller JN Stevenson EK Lainhart JE McMahon WM Fujinami RS 《Journal of autism and developmental disorders》2008,38(2):333-341
Controversy exists over the role of autoantibodies to central nervous system antigens in autism and Tourette Syndrome. We investigated plasma autoantibody titers to glial fibrillary acidic protein (GFAP) in children with classic onset (33) and regressive onset (26) autism, controls (25, healthy age- and gender-matched) and individuals with Tourette Syndrome (24) by enzyme-linked immunosorbent assays. We found a significant difference in autoantibody titers to GFAP, not accounted for by age, between the Tourette (significantly lower) and regressive autism groups. However, no differences were found between: classic/regressive; classic/controls; classic/Tourette; regressive/controls; or controls/Tourette. Autoantibody responses against GFAP are unlikely to play a pathogenic role in autism or Tourette Syndrome. 相似文献
95.
Libbey JE Coon HH Kirkman NJ Sweeten TL Miller JN Lainhart JE McMahon WM Fujinami RS 《Journal of neurovirology》2007,13(3):252-259
The role that virus infections play in autism is not known. Others have reported that antibodies against measles virus are higher in the sera/plasma of children with autism versus controls. The authors investigated antibody titers to measles, mumps, and rubella viruses and diphtheria toxoid in children with autism, both classic onset (33) and regressive onset (26) forms, controls (25, healthy age- and gender-matched) and individuals with Tourette's syndrome (24) via enzyme-linked immunosorbent assays. No significant differences in antibody titers to measles, mumps, and rubella viruses and diphtheria toxoid were found among the four groups. Additionally, there were no significant differences between the four groups for total immunoglobulin (Ig)G or IgM. Interestingly, the authors did find a significant number (15/59) of autism subjects (classic and regressive onset combined) who had a very low or no antibody titer against rubella virus, compared to a combine control/Tourette's group (2/49). 相似文献
96.
97.
TL Carter CH Cole CF Mews PJ Price DL Baker 《Journal of paediatrics and child health》1997,33(3):238-241
Objective: To assess the prevalence of hepatitis C in 200 patients with paediatric malignancies, surviving in remission more than 5 years from diagnosis, who had received blood product transfusions before 1990 when routine screening of blood products for hepatitis C began.
Method: The second and third generation Abbott Diagnostics ELISA was used to assess hepatitis C seropositivity. Seropositive patients and those with abnormal liver transaminases were assessed by hepatitis C virus RNA polymerase chain reaction (PCR).
Results: A low incidence (4%) of seropositivity for hepatitis C was found in survivors of paediatric malignancy who were transfused prior to routine screening of blood products in this cohort.
Conclusions: All patients identified have evidence of hepatitis and may be at high risk of developing cirrhosis. 相似文献
Method: The second and third generation Abbott Diagnostics ELISA was used to assess hepatitis C seropositivity. Seropositive patients and those with abnormal liver transaminases were assessed by hepatitis C virus RNA polymerase chain reaction (PCR).
Results: A low incidence (4%) of seropositivity for hepatitis C was found in survivors of paediatric malignancy who were transfused prior to routine screening of blood products in this cohort.
Conclusions: All patients identified have evidence of hepatitis and may be at high risk of developing cirrhosis. 相似文献
98.
Mooney LA; Bell DA; Santella RM; Van Bennekum AM; Ottman R; Paik M; Blaner WS; Lucier GW; Covey L; Young TL; Cooper TB; Glassman AH; Perera FP 《Carcinogenesis》1997,18(3):503-509
Prior epidemiological evidence suggests that genes controlling the
metabolism of carcinogens and antioxidant/nutritional status are associated
with lung cancer risk, possibly through their ability to modulate DNA
damage by carcinogens. We performed a cross-sectional analysis of 159 heavy
smokers from a cohort of subjects enrolled in a smoking cessation program.
A total of 159 blood samples were analyzed to determine the relative
contributions of genetic polymorphisms [CYP1A1 MspI and exon 7 and
glutathione S-transferase M1 (GSTM1)] and plasma micronutrients to
polycyclic aromatic hydrocarbon-DNA (PAH-DNA) adduct levels. DNA damage in
smokers was affected by genetic polymorphisms and nutritional status.
Smokers with the CYP1A1 exon 7 valine polymorphism had significantly higher
(2-fold, P < or = 0.03) levels of DNA damage than those without. In
parallel models, PAH-DNA adducts were inversely associated with plasma
levels of retinol (beta = -0.93, P = 0.01), beta-carotene (beta = -0.18, P
= 0.09), and alpha- tocopherol (beta = -0.28, P = 0.21) in 159 subjects.
The association between smoking-adjusted plasma beta-carotene levels and
DNA damage was only significant in those subjects lacking the GSTM1
detoxification gene (beta = -0.30, P = 0.05, n = 75). There was a
statistical interaction between beta-carotene and alpha-tocopherol; when
beta- carotene was low, alpha-tocopherol had a significant protective
effect (beta = -0.78, P = 0.04) on adducts, but not when beta-carotene was
high (beta = -0.16, P = 0.57). Plasma alpha-tocopherol was significantly
correlated with beta-carotene (r = 0.36, P = 0.0005) and less strongly with
retinol (r = 0.20, P = 0.0005). These results suggest that several
micronutrients may act in concert to protect against DNA damage and
highlight the importance of assessing overall antioxidant status. In
conclusion, a subset of smokers may be at increased risk of DNA damage and
possibly lung cancer due to the combined effect of low plasma
micronutrients and genetic susceptibility factors. The use of biological
markers to assess efficacy of interventions and to study mechanisms of
micronutrients is timely given the current debate regarding the use of
chemopreventive agents in high risk populations.
相似文献
99.
Wolf DC; Goldsworthy TL; Donner EM; Harden R; Fitzpatrick B; Everitt JI 《Carcinogenesis》1998,19(11):2043-2047
Hormonal influences are known to affect the development of renal cell
carcinoma in man and laboratory animal models. We tested the hypothesis
that estrogen treatment or ovariectomy of rats modulates renal tumor
development using tuberous sclerosis 2 (Tsc2) heterozygous mutant (Eker)
rats in which a germline mutation predisposes the animals to renal cell
tumor development. Two-month-old female wild-type and Eker rats were
ovariectomized or sham-operated and treated with placebo or 5 mg
17beta-estradiol in s.c. pellets for 6 or 10 months. Rats were examined at
8 or 12 months of age, at which time the numbers of renal tumors and
preneoplastic foci were quantitated and the severity of nephropathy was
assessed. In contrast to what may have been expected, prolonged estrogen
treatment enhanced the development of hereditary renal cell tumors, with a
2-fold greater number of preneoplastic and neoplastic renal lesions
compared with untreated Eker rats. Ovariectomized Eker rats had 33% fewer
renal lesions than the unmanipulated control group. No tumors or
preneoplastic lesions were present in wild-type rats at either time point.
Estrogen treatment increased the severity of nephropathy in both wild-type
and Eker rats, whereas ovariectomy was protective against nephropathic
changes. Although estrogen is not a rat renal carcinogen, it enhanced the
development of hereditary renal cell tumors when administered to Eker rats.
Eker rats heterozygous for a mutation in the Tsc2 locus provide a good
model in which to study how genetic and hormonal factors contribute to the
development of renal cell tumors and to understand the influence genetic
susceptibility has on the development of renal cell carcinoma.
相似文献
100.
WL Greer DC Riddell S Murty TL Gillan GS Girouard SM Sparrow C Tatlidil MJ Dobson PE Neumann 《Clinical genetics》1999,55(4):248-255
Niemann-Pick type D (NPD) disease is a severe degenerative disorder of the nervous system characterized by the accumulation of tissue cholesterol and sphingomyelin. Because of a founder effect, it is unusually common in southwestern Nova Scotia, Canada. We have confirmed that almost all patients from 20 affected sibships descended on both sides from a small group of Acadians who settled in this region in about the year 1767. Previously using classic linkage analysis of this large kindred, we defined the critical gene region to a 13-cM chromosome segment between D18S869 and D18S66. Seven ESTs have been positioned within this interval. Carstea et al. (Niemann Pick C disease gene: homology to mediators of cholesterol homeostasis. Science 1997: 277: 232-235) recently demonstrated that one of these ESTs is the Niemann-Pick type C (NPCI) gene, the gene disrupted in most patients with NPC disease, and we have shown that a G3097-->T mutation in the NPC1 gene is also responsible for NPD. Here we report the development of five new polymorphic microsatellite markers and the testing for complete linkage disequilibrium in our single large NPD kindred that allowed us to reduce the NPD critical region to a 1-cM (1.3-1.6 Mb) interval between D18S1398 and D18S1108. In contrast, Carstea et al., using classic linkage analysis, required more than 18 unrelated NPC families to reduce the NPC1 critical region to a 5-cM interval. Our work supports the finding that NPD is an allelic variant of NPC1, and illustrates the power of large kindreds, which are common in Atlantic Canada and other relatively isolated areas, for gene mapping and identification. 相似文献