| 1. |
- Villa, Luisa L., et al.
(författare)
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Quadrivalent vaccine against human papillomavirus to prevent high-grade cervical lesions
- 2007
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Ingår i: New England Journal of Medicine. - 0028-4793 .- 1533-4406. ; 356:19, s. 1915-1927
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Human papillomavirus types 16 (HPV-16) and 18 (HPV-18) cause approximately 70% of cervical cancers worldwide. A phase 3 trial was conducted to evaluate a quadrivalent vaccine against HPV types 6, 11, 16, and 18 (HPV-6/11/16/18) for the prevention of high-grade cervical lesions associated with HPV-16 and HPV-18. METHODS: In this randomized, double-blind trial, we assigned 12,167 women between the ages of 15 and 26 years to receive three doses of either HPV-6/11/16/18 vaccine or placebo, administered at day 1, month 2, and month 6. The primary analysis was performed for a per-protocol susceptible population that included 5305 women in the vaccine group and 5260 in the placebo group who had no virologic evidence of infection with HPV-16 or HPV-18 through 1 month after the third dose (month 7). The primary composite end point was cervical intraepithelial neoplasia grade 2 or 3, adenocarcinoma in situ, or cervical cancer related to HPV-16 or HPV-18. RESULTS: Subjects were followed for an average of 3 years after receiving the first dose of vaccine or placebo. Vaccine efficacy for the prevention of the primary composite end point was 98% (95.89% confidence interval [CI], 86 to 100) in the per-protocol susceptible population and 44% (95% CI, 26 to 58) in an intention-to-treat population of all women who had undergone randomization (those with or without previous infection). The estimated vaccine efficacy against all high-grade cervical lesions, regardless of causal HPV type, in this intention-to-treat population was 17% (95% CI, 1 to 31). CONCLUSIONS: In young women who had not been previously infected with HPV-16 or HPV-18, those in the vaccine group had a significantly lower occurrence of high-grade cervical intraepithelial neoplasia related to HPV-16 or HPV-18 than did those in the placebo group.
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| 2. |
- Klionsky, Daniel J., et al.
(författare)
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
- 2008
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Ingår i: Autophagy. - : Landes Bioscience. - 1554-8627 .- 1554-8635. ; 4:2, s. 151-175
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Forskningsöversikt (refereegranskat)abstract
- Research in autophagy continues to accelerate,1 and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.2,3 There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much confusion regarding acceptable methods to measure macroautophagy in higher eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers of autophagosomes versus those that measure flux through the autophagy pathway; thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from fully functional autophagy that includes delivery to, and degradation within, lysosomes (in most higher eukaryotes) or the vacuole (in plants and fungi). Here, we present a set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes. This set of guidelines is not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response.
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| 3. |
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| 4. |
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| 5. |
- Liang, Y., et al.
(författare)
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Active control of type-I edge localized modes on JET
- 2007
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Ingår i: Plasma Physics and Controlled Fusion. - 0741-3335 .- 1361-6587. ; 49:12B, s. B581-B589
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Tidskriftsartikel (refereegranskat)abstract
- The operational domain for active control of type-I edge localized modes (ELMs) with an n = 1 external magnetic perturbation field induced by the ex-vessel error field correction coils on JET has been developed towards more ITER-relevant regimes with high plasma triangularity, up to 0.45, high normalized beta, up to 3.0, plasma current up to 2.0 MA and q(95) varied between 3.0 and 4.8. The results of ELM mitigation in high triangularity plasmas show that the frequency of type-I ELMs increased by a factor of 4 during the application of the n = 1 fields, while the energy loss per ELM, Delta W/W, decreased from 6% to below the noise level of the diamagnetic measurement (<2%). No reduction of confinement quality (H98Y) during the ELM mitigation phase has been observed. The minimum n = 1 perturbation field amplitude above which the ELMs were mitigated increased with a lower q(95) but always remained below the n = 1 locked mode threshold. The first results of ELM mitigation with n = 2 magnetic perturbations on JET demonstrate that the frequency of ELMs increased from 10 to 35 Hz and a wide operational window of q95 from 4.5 to 3.1 has been found.
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| 6. |
- Liang, Y., et al.
(författare)
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Active control of type-I edge-localized modes with n=1 perturbation fields in the JET tokamak
- 2007
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Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 98:26
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Tidskriftsartikel (refereegranskat)abstract
- Type-I edge-localized modes (ELMs) have been mitigated at the JET tokamak using a static external n=1 perturbation field generated by four error field correction coils located far from the plasma. During the application of the n=1 field the ELM frequency increased by a factor of 4 and the amplitude of the D-alpha signal decreased. The energy loss per ELM normalized to the total stored energy, Delta W/W, dropped to values below 2%. Transport analyses shows no or only a moderate (up to 20%) degradation of energy confinement time during the ELM mitigation phase.
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| 7. |
- Martorell, X, et al.
(författare)
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Blue Gene/L performance tools
- 2005
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Ingår i: IBM Journal of Research and Development. - : IBM. - 0018-8646 .- 2151-8556. ; 49:2-3, s. 407-424
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Tidskriftsartikel (refereegranskat)abstract
- Good performance monitoring is the basis of modern performance aualysis tools for application optimization. We are providing a variety of such performance analysis tools for the new Blue Gene(®)/L supercomputer. Those tools can be divided into two categories: single-node performance tools and multinode performance tools. Front a single-node perspectire, we provide standard interfaces and libraries, such as PAPI and libHPM, that propide access to the hardware performance counters for applications running on the Blue Gene/L compute nodes. From a multinode perspective, we focus on tools that analyze Message Passing Interface (MPI) behavior. Those tools work by first collecting message-passing trace data when a program runs. The trace data is then used by, graphical interface tools that analyze the behavior of applications. Using the current prototype tools, we demonstrate their usefulness and applicability with case studies of application optimization.
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| 9. |
- Moreira, TJTP, et al.
(författare)
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Enhanced cerebral expression of MCT1 and MCT2 in a rat ischemia model occurs in activated microglial cells
- 2009
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Ingår i: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 1559-7016. ; 29:7, s. 1273-1283
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Tidskriftsartikel (refereegranskat)abstract
- Monocarboxylate transporters (MCTs) are essential for the use of lactate, an energy substrate known to be overproduced in brain during an ischemic episode. The expression of MCT1 and MCT2 was investigated at 48 h of reperfusion from focal ischemia induced by unilateral extradural compression in Wistar rats. Increased MCT1 mRNA expression was detected in the injured cortex and hippocampus of compressed animals compared to sham controls. In the contralateral, uncompressed hemisphere, increases in MCT1 mRNA level in the cortex and MCT2 mRNA level in the hippocampus were noted. Interestingly, strong MCT1 and MCT2 protein expression was found in peri-lesional macrophages/microglia and in an isolectin B4+/S100β+ cell population in the corpus callosum. In vitro, MCT1 and MCT2 protein expression was observed in the N11 microglial cell line, whereas an enhancement of MCT1 expression by tumor necrosis factor-α (TNF-α) was shown in these cells. Modulation of MCT expression in microglia suggests that these transporters may help sustain microglial functions during recovery from focal brain ischemia. Overall, our study indicates that changes in MCT expression around and also away from the ischemic area, both at the mRNA and protein levels, are a part of the metabolic adaptations taking place in the brain after ischemia.
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