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181.
Dal Maso L La Vecchia C Franceschi S Preston-Martin S Ron E Levi F Mack W Mark SD McTiernan A Kolonel L Mabuchi K Jin F Wingren G Galanti MR Hallquist A Glattre E Lund E Linos D Negri E 《Cancer causes & control : CCC》2000,11(2):137-144
Objective: To assess the relation between anthropometric factors and thyroid cancer risk in a pooled analysis of individual data from 12 case–control studies conducted in the US, Japan, China and Europe.
Methods: 2056 female and 417 male cases, 3358 female and 965 male controls were considered. Odds ratios (OR) were derived from logistic regression, conditioning on age, A-bomb exposure (Japan) and study, and adjusting for radiotherapy.
Results: Compared to the lowest tertile of height, the pooled OR was 1.2 for females for the highest one, and 1.5 for males, and trends in risk were significant. With reference to weight at diagnosis, the OR for females was 1.2 for the highest tertile, and the trend in risk was significant, whereas no association was observed in males. Body mass index (BMI) at diagnosis was directly related to thyroid cancer risk in females (OR = 1.2 for the highest tertile), but not in males. No consistent pattern of risk emerged with BMI during the late teens. Most of the associations were observed both for papillary and follicular cancers, and in all age groups. However, significant heterogeneity was observed across studies.
Conclusions: Height and weight at diagnosis are moderately related to thyroid cancer risk. 相似文献
182.
Anita Langer?d Ida R K Bukholm André Breg?rd Per Eystein L?nning Tone Ikdal Andersen Torleiv O Rognum Gunn Iren Meling Ragnhild A Lothe Anne-Lise B?rresen-Dale 《Cancer epidemiology, biomarkers & prevention》2002,11(12):1684-1688
An Arg/Pro polymorphism in codon 72 of the TP53 gene was analyzed in blood samples from 390 breast and 162 colorectal cancer patients previously investigated for TP53 mutations in their tumors. Among the breast cancer cases, 228 were homozygous for the Arg72 allele, of which, 65 (28.5%) also had a TP53 mutation in their tumors. In contrast, of 26 cases that were homozygous for the Pro72 allele, only 1 case (3.8%) had a TP53 mutation in the tumor (P = 0.004). Cloning the TP53 gene from tumor DNA followed by sequencing was performed in 14 heterozygotes with tumor mutation, and 9 of the mutations resided on the Arg72 allele. Among the colorectal cancer cases, no difference in mutation frequency was seen between the two different homozygotes, 40 TP53 mutations in 97 Arg72 homozygous cases (41.2%) versus 7 in 16 Pro72 homozygous cases (43.8%). These results suggest a selective growth advantage for cells carrying a type of TP53 mutation seen in breast carcinomas when the mutation resides on an Arg72 allele. 相似文献
183.
Hildegunn Berntsen Per Eystein Lønning Dagfinn Ekse Bjørn Netteland Dag Clement Johannessen Rolf Berge Asbjørn Svardal 《Cancer chemotherapy and pharmacology》1998,42(1):46-52
Purpose: Elevated cellular glutathione has been associated with resistance to cancer chemotherapy. Treatment with the aromatase inhibitor
aminoglutethimide increases the concentration of γ-glutamyl transpeptidase (γ-GT) in breast cancer patients. This enzyme catalyzes
the first step in the degradation of extracellular glutathione, and the products formed may act as precursors for intracellular
glutathione synthesis. Methods: Plasma and red-blood-cell glutathione levels were determined in 26 patients suffering from advanced breast cancer before
and during treatment with aminoglutethimide (n=16) or the steroidal aromatase inhibitors exemestane or formestane (n=10) and in 5 cancer patients receiving dexamethasone. Results: Pretreatment values for γ-GT in the total patient group (n=31) correlated negatively with the level of reduced (P<0.0001), oxidized (P<0.025), and total glutathione (P<0.005) in plasma. Plasma γ-GT levels increased by a mean value of 249% during treatment with aminoglutethimide. The concentration
of reduced and oxidized glutathione in plasma decreased to 42.7% (P<0.0005) and 80.6% (P < 0.005) of their pretreatment levels, respectively. This fall in reduced plasma glutathione correlated negatively with the
increase in -GT (P<0.001). The ratio of oxidized to reduced glutathione increased by 88.9% (P<0.005), and this increase correlated positively with the increase in γ-GT (P<0.005). Treatment with the steroidal aromatase inhibitors (exemestane and formestane) or dexamethasone did not influence
the plasma thiol status. Conclusions: We conclude that aminoglutethimide influences plasma glutathione disposition by mechanisms not related to estrogen suppression
or due to glucocorticoids given in concert.
Received: 13 July 1997 / Accepted: 27 October 1997 相似文献
184.
185.
ObjectiveFor long-term stability the adhering interfaces of an implant-retained supraconstruction of titanium/carbon–graphite fiber-reinforced (CGFR) polymer/opaquer layer/denture base polymer/denture teeth must function as a unity. The aim was to evaluate adhesion of CGFR polymer to a titanium surface or CGFR polymer to two different opaquer layers/with two denture base polymers.Materials and methodsTitanium plates were surface-treated and silanized and combined with a bolt of CGFR polymer or denture base polymer (Probase Hot). Heat-polymerized plates of CGFR polymer (47 wt% fiber) based on poly(methyl methacrylate) and a copolymer matrix were treated with an opaquer (Sinfony or Ropak) before a denture base polymer bolt was attached (Probase Hot or Lucitone 199). All specimens were heat-polymerized, water saturated (200 days) and thermally cycled (5000 cycles, 5/55 °C) before shear bond testing.ResultsSilicatized titanium surfaces gave higher bond strength to CGFR polymer (16.2 ± 2.34 and 18.6 ± 1.32) MPa and cohesive fracture than a sandblasted surface (5.9 ± 2.11) MPa where the fracture was adhesive. The opaquer Sinfony gave higher adhesion values and mainly cohesive fractures than the opaquer Ropak. Different surface treatments (roughened or polished) of the CGFR polymer had no effect on bond strength.SignificanceThe fracture surfaces of silicatized titanium/CGFR polymer/opaquer layer (Sinfony)/denture base polymers were mainly cohesive. A combination of these materials in an implant-retained supraconstruction is promising for in vivo evaluation. 相似文献
186.
The objective of this work was to examine the impact of subclinical coccidial infection on commercial performance, expressed as a modified European Production Index, in broilers. Performance data, and litter and faecal samples, were collected from two independent observational surveys of Norwegian broilers receiving in-feed narasin during 2000 to 2004. Numbers of oocysts per gram (OPG) of litter collected during rearing (Study 1) or faecal samples collected at slaughter (both studies), and relative frequencies of Eimeria species categories (both studies) were calculated. Polymerase chain reaction-based identification of Eimeria species was performed in Study 2. A definition of flocks at risk of impaired performance associated with coccidia (“risk flock”), using the predominant species and OPG level as criteria, was tested. Coccidia had a significant effect on performance in the first, but not the second study. In Study 1 the following coccidia variables were found to be associated with impaired performance in multivariate models: OPG at slaughter (ordinal), mean OPG during rearing (ordinal) and “risk flock” (binomial). The European Production Index was ~9% lower in flocks with infection levels >50 000 OPG at slaughter in Study 1. The composition of coccidial populations shifted between Study 1 and Study 2, from a dominance of medium and large oocysts to a dominance of small oocysts. There was a substantial increase in prevalence of coccidial infection from Study 1 to Study 2, but mean infection levels were similar in the two surveys. The “risk flock” definition was useful as an indicator of coccidia-associated performance loss in Study 1, where subclinical coccidiosis was an important factor. The results suggest that the economic importance of subclinical coccidiosis may vary substantially with time, and they emphasize the need for population studies on the importance and dynamics of specific coccidial infections under different field conditions. 相似文献
187.
OBJECTIVES: Silica-glass fiber reinforced polymers can be used for many kinds of dental applications. The fiber reinforcement enhances the mechanical properties of the polymers, and they have good esthetic attributes. There is good initial bonding of glass fibers to polymers via an interface made from silane coupling agents. The aim of this in vitro study was to determine the cytotoxicity of two polymers reinforced with two differently sized silica-glass fibers before and after thermal cycling. Cytotoxicity of the polymers without fibers was also evaluated. METHODS: Two different resin mixtures (A and B) were prepared from poly(vinyl chloridecovinylacetate) powder and poly(methyl methacrylate) (PMMA) dissolved in methyl methacrylate and mixed with different cross-linking agents. The resin A contained the cross-linking agents ethylene glycol dimethacrylate and 1,4-butanediol dimethacrylate, and for resin B diethylene glycol dimethacrylate was used. Woven silica-glass fibers were used for reinforcement. The fibers were sized with either linear poly(butyl methacrylate)-sizing or cross-linking PMMA-sizing. Cytotoxicity was evaluated by filter diffusion test (ISO 7405:1997) of newly made and thermocycled test specimens. Extracts were prepared according to ISO 10993-12 from newly made and from thermocycled specimens and tested by the MTT assay. The results from the experiments were statistically analyzed by one-way ANOVA and Tukey's test (rho<0.05). RESULTS: The filter diffusion test disclosed no change in staining intensity at the cell-test sample contact area indicating non-cytotoxicity in all experimental groups. Cell viability assessed by MTT assay was more than 90% in all experimental groups. All are non-cytotoxic. SIGNIFICANCE: It can be concluded that correctly processed heat polymerized silica-glass fiber reinforced polymers induced no cytotoxicity and that thermocycling did not alter this property. 相似文献
188.
N I Landr? B R Rund A Lund K Sundet N Mjellem A Asbj?rnsen T Thomsen L Ersland A Lundervold A I Smievoll J Egeland K Stordal A Roness H Sundberg K Hugdahl 《Neuroreport》2001,12(18):4047-4054
The present study investigated changes in neuronal activation with fMRI related to Honig's model of working memory, which is much less studied compared with other working memory models. In contrast to other studies which have applied recognition procedures, the primary aim with the present study was to examine brain activation when subjects had to continuously recall and forget items held in working memory. The results showed that the mid-ventrolateral frontal cortex was particularly activated in the left hemisphere, whereas the mid-dorsolateral frontal cortex was particularly activated in the right hemisphere during execution of the working memory task. The findings are discussed in relation to process- and domain-specific accounts of working memory. 相似文献
189.
Yael Goldfarb Tal Givony Noam Kadouri Jan Dobe Cristina Peligero-Cruz Itay Zalayat Golda Damari Bareket Dassa Shifra Ben-Dor Yael Gruper Bergithe E. Oftedal Eirik Bratland Martina M. Erichsen Amund Berger Ayelet Avin Shir Nevo Uku Haljasorg Yael Kuperman Adi Ulman Rebecca Haffner-Krausz Ziv Porat Ulus Atasoy Dena Leshkowitz Eystein S. Husebye Jakub Abramson 《The Journal of experimental medicine》2021,218(11)
The autoimmune regulator (AIRE) is essential for the establishment of central tolerance and prevention of autoimmunity. Interestingly, different AIRE mutations cause autoimmunity in either recessive or dominant-negative manners. Using engineered mouse models, we establish that some monoallelic mutants, including C311Y and C446G, cause breakdown of central tolerance. By using RNAseq, ATACseq, ChIPseq, and protein analyses, we dissect the underlying mechanisms for their dominancy. Specifically, we show that recessive mutations result in a lack of AIRE protein expression, while the dominant mutations in both PHD domains augment the expression of dysfunctional AIRE with altered capacity to bind chromatin and induce gene expression. Finally, we demonstrate that enhanced AIRE expression is partially due to increased chromatin accessibility of the AIRE proximal enhancer, which serves as a docking site for AIRE binding. Therefore, our data not only elucidate why some AIRE mutations are recessive while others dominant, but also identify an autoregulatory mechanism by which AIRE negatively modulates its own expression. 相似文献
190.