| 1. |
- Beral, V, et al.
(författare)
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Alcohol, tobacco and breast cancer - collaborative reanalysis of individual data from 53 epidemiological studies, including 58515 women with breast cancer and 95067 women without the disease
- 2002
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 87, s. 1234-45
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Tidskriftsartikel (refereegranskat)abstract
- Alcohol and tobacco consumption are closely correlated and published results on their association with breast cancer have not always allowed adequately for confounding between these exposures. Over 80% of the relevant information worldwide on alcohol and tobacco consumption and breast cancer were collated, checked and analysed centrally. Analyses included 58515 women with invasive breast cancer and 95067 controls from 53 studies. Relative risks of breast cancer were estimated, after stratifying by study, age, parity and, where appropriate, women's age when their first child was born and consumption of alcohol and tobacco. The average consumption of alcohol reported by controls from developed countries was 6.0 g per day, i.e. about half a unit/drink of alcohol per day, and was greater in ever-smokers than never-smokers, (8.4 g per day and 5.0 g per day, respectively). Compared with women who reported drinking no alcohol, the relative risk of breast cancer was 1.32 (1.19 - 1.45, P < 0.00001) for an intake of 35 - 44 g per day alcohol, and 1.46 (1.33 - 1.61, P < 0.00001) for greater than or equal to 45 g per day alcohol. The relative risk of breast cancer increased by 7.1% (95% CI 5.5-8.7%; P<0.00001) for each additional 10 g per day intake of alcohol, i.e. for each extra unit or drink of alcohol consumed on a daily basis. This increase was the same in ever-smokers and never-smokers (7.1 % per 10 g per day, P < 0.00001, in each group). By contrast, the relationship between smoking and breast cancer was substantially confounded by the effect of alcohol. When analyses were restricted to 22 255 women with breast cancer and 40 832 controls who reported drinking no alcohol, smoking was not associated with breast cancer (compared to never-smokers, relative risk for ever-smokers= 1.03, 95% CI 0.98 - 1.07, and for current smokers=0.99, 0.92 - 1.05). The results for alcohol and for tobacco did not vary substantially across studies, study designs, or according to 15 personal characteristics of the women; nor were the findings materially confounded by any of these factors. If the observed relationship for alcohol is causal, these results suggest that about 4% of the breast cancers in developed countries are attributable to alcohol. In developing countries, where alcohol consumption among controls averaged only 0.4 g per day, alcohol would have a negligible effect on the incidence of breast cancer. In conclusion, smoking has little or no independent effect on the risk of developing breast cancer; the effect of alcohol on breast cancer needs to be interpreted in the context of its beneficial effects, in moderation, on cardiovascular disease and its harmful effects on cirrhosis and cancers of the mouth, larynx, oesophagus and liver. (C) 2002 Cancer Research UK.
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| 2. |
- Akerman, J. J., et al.
(författare)
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Dislocation-mediated creep of highly separated vortices in a-axis-oriented HgBa2CaCu2O6+delta thin films
- 2001
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Ingår i: Physical Review B Condensed Matter. - 0163-1829 .- 1095-3795. ; 64:2
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Tidskriftsartikel (refereegranskat)abstract
- Using ac susceptibility, we determine the critical current density J(c) and the flux creep activation energy U of an a-axis-oriented HgBa2CaCu2O6+delta thin film. The critical current density at helium temperatures is found to be 4.6 x 10(4) A/cm(2), i.e., about two orders of magnitude smaller than for corresponding films with c-axis orientation. The temperature and ac field dependent activation energy is consistent with dislocation-mediated flux creep and well described by U(T,H-ac)=U-o(1-t(4))H-ac(-1/2) with t=T/T-c, T-c=120K, and U-o = 0.77 eV Oe(1/2) for temperatures T>45 K and in the field range studied. The activation energy is of the same order as that found in c-axis-oriented films. Below T = 45 K the activation energy is observed to decrease as thermally assisted quantum creep becomes increasingly important.
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| 3. |
- Akerman, J. J., et al.
(författare)
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Two-stage crossover from thermal to quantum flux creep of dilute vortex ensembles in various high-T-c superconducting thin films
- 2001
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Ingår i: Physical Review B Condensed Matter. - 0163-1829 .- 1095-3795. ; 64:9
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Tidskriftsartikel (refereegranskat)abstract
- The thermal-to-quantum flux creep crossover at low vortex densities has been studied in YBa2Cu3O7, TlBa2CaCu2O7-delta, and HgBa2CaCu2O6+delta thin films using ac susceptibility. The crossover temperatures T-cr are 10-11, 17, and 30 K, respectively. Both thermal and quantum flux creep is suppressed as the vortex density is decreased. We observe a two-stage nature in the crossover behavior which appears to be a general property of all the three materials studied.
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| 4. |
- Chen, Yun, 1966, et al.
(författare)
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Neonatal losartan treatment suppresses renal expression of molecules involved in cell-cell and cell-matrix interactions
- 2004
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Ingår i: Journal of the American Society of Nephrology. - : Lippincott Williams & Wilkins. - 1046-6673 .- 1533-3450. ; 15:5, s. 1232-43
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Tidskriftsartikel (refereegranskat)abstract
- Lack of neonatal angiotensin II type 1 receptor (AT(1)) stimulation produces renal abnormalities characterized by papillary atrophy and impaired urinary concentrating ability, but the mechanisms involved are still unclear. DNA microarray was used to identify genes that are differentially expressed in renal medulla in response to neonatal treatment with AT(1) receptor antagonist losartan (30 mg/kg per d), which commenced within 24 h after birth. The data showed that losartan treatment for 48 h downregulated 68 genes, approximately 30% of which encode various components of cytoskeleton and cytoskeleton-associated proteins, extracellular matrix, and enzymes involved in extracellular matrix maturation or turnover. With the use of immunohistochemistry and Western immunoblot, the microarray data were confirmed and it was demonstrated that losartan suppressed renal expression of syndecan 2, alpha-smooth muscle actin, MHC class II, and leukocyte type 12-lipoxygenase by day 4. In addition, losartan inhibited medullary expression of integrin alpha6 and caused relocalization of integrins alpha6 and alpha3. Moreover, losartan inhibited cell proliferation in medullary tubules by day 9, as detected by Ki-67 immunostaining. This study provides new data supporting the contention that a lack of AT(1) receptor stimulation results in abnormal matrix assembly, disturbed cell-cell and cell-matrix interactions, and subsequent abnormal tubular maturation. Moreover, regulation of the expression of leukocyte type 12-lipoxygenase and alpha-smooth muscle actin by the renin-angiotensin system in the immature kidney adds new knowledge toward the understanding of renal vascular development.
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| 5. |
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| 6. |
- Nilsson, A B, et al.
(författare)
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IGF-I treatment attenuates renal abnormalities induced by neonatal ACE inhibition.
- 2000
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Ingår i: American journal of physiology. Regulatory, integrative and comparative physiology. - 0363-6119. ; 279:3
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Tidskriftsartikel (refereegranskat)abstract
- An intact renin-angiotensin system (RAS) during nephrogenesis is essential for normal renal development. We have shown previously that neonatal inhibition of the RAS, either with ANG II type 1-receptor blockade or angiotensin-converting enzyme (ACE) inhibition, induces irreversible renal abnormalities. The aim of the present study was to investigate whether an interrupted RAS can be compensated for by exogenous administration of another important renal growth-promoting factor, the insulin-like growth factor-I (IGF-I). Rats were treated daily with either the ACE inhibitor enalapril (10 mg/kg), recombinant human IGF-I (3 mg/kg), or the combination enalapril + IGF-I from perinatal day 3 to 13. Urinary concentrating ability, renal function, and renal morphology were assessed at adult age. The gene expression and localization of IGF-I, its receptor, and the growth hormone receptor (GHR) were investigated during ongoing ACE inhibition. The present study demonstrates normalized renal function and histology in enalapril + IGF-I-treated animals. Ongoing ACE inhibition suppressed the medullary IGF-I mRNA expression and altered the local distribution of both IGF-I and GHR. Thus the present study provides evidence for an interaction between the RAS and GH/IGF-I axis in renal development.
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| 8. |
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| 9. |
- Åkerman, Johan, et al.
(författare)
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Re-entrant behavior of low-field flux creep in c-axis-oriented HgBa2CaCu2O6+delta thin films
- 2001
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Ingår i: Physical Review B Condensed Matter. - 0163-1829 .- 1095-3795. ; 6418:18
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Tidskriftsartikel (refereegranskat)abstract
- The temperature, ac and dc field, and current dependent activation energy U(T,H)[(J(c0)/J(c))(mu)-1]/mu governing low-field flux creep in epitaxial c-axis-oriented HgBa2CaCu2O6+delta thin films has been determined from measurements of the frequency-dependent in-phase ac susceptibility. Above 35 K three different thermally activated flux creep regimes can be identified: (i) dislocation-mediated plastic flux creep, described by U(T,H) = U-0(1 - t(4))H-1/2 and mu = 0, (ii) elastic collective flux creep which decreases with temperature and has a weaker field dependence of H-0.22 above a field-dependent temperature Tc.(H) where A acquires finite values, and (iii) reappearance of dislocation-mediated plastic flux creep which rapidly increases as T-c is approached. It is argued that the re-entrant plastic-elastic-plastic vortex creep behavior is driven by the underlying temperature and field dependence of the shear modulus c(66). T-cm(H) marks a line in the H-T plane where the increasing c(66) promotes long-range correlations in the dilute vortex phase and creep becomes collective. At high H and T, c(66) again decreases and plastic creep reappears as the ordered phase starts to melt. Evidence for thermally assisted quantum creep is observed up to temperatures as high as T-0 = 35 K.
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