143 research outputs found
The Maximal Intensity Period: Rationalising its Use in Team Sports Practice
Quantifying the highest intensity of competition (the maximal intensity period [MIP]) for varying durations in team sports has been used to identify training targets to inform the preparation of players. However, its usefulness has recently been questioned since it may still underestimate the training intensity required to produce specific physiological adaptations. Within this conceptual review, we aimed to: (i) describe the methods used to determine the MIP" (ii) compare the data obtained using MIP or whole-match analysis, considering the influence of different contextual factors" (iii) rationalise the use of the MIP in team sports practice and (iv) provide limitations and future directions in the area. Different methods are used to determine the MIP, with MIP values far greater than those derived from averaging across the whole match, although they could be affected by contextual factors that should be considered in practice. Additionally, while the MIP might be utilised during sport-specific drills, it is inappropriate to inform the intensity of interval-based, repeated sprint and linear speed training modes. Lastly, MIP does not consider any variable of internal load, a major limitation when informing training practice. In conclusion, practitioners should be aware of the potential use or misuse of the MIP
Near-field speckle imaging of light localization in disordered photonic
Optical localization in strongly disordered photonic media is an attractive topic for proposing novel cavity-like structures. Light interference can produce random modes confined within small volumes, whose spatial distribution in the near-field is predicted to show hot spots at the nanoscale. However, these near-field speckles have not yet been experimentally investigated due to the lack of a high spatial resolution imaging techniques. Here, we study a system where the disorder is induced by random drilling air holes in a GaAs suspended membrane with internal InAs quantum dots. We perform deep-subwavelength near-field experiments in the telecom window to directly image the spatial distribution of the electric field intensity of disordered-induced localized optical modes. We retrieve the near-field speckle patterns that extend over few micrometers and show several single speckles of the order of λ/10 size. The results are compared with the numerical calculations and with the recent findings in the literature of disordered media. Notably, the hot spots of random modes are found in proximity of the air holes of the disordered system
Tuning of photonic crystal cavities by controlled removal of locally infiltrated water
We present a spectral tuning mechanism of photonic crystal microcavities based on microfluidics. The microinfiltration with water of one or few cavity holes and its subsequent controlled evaporation allow us to tune the cavity resonances in a spectral range larger than 20 nm, with subnanometer accuracy, and we also observe that the addition of water in the microcavity region improves its quality factor Q. (C) 2009 American Institute of Physics. [doi:10.1063/1.3247894
Nonlinear optical tuning of photonic crystal microcavities by near-field probe
We report on a nonlinear way to control and tune the dielectric environment of photonic crystal microcavities exploiting the local heating induced by near-field laser excitation at different excitation powers. The temperature gradient due to the optical absorption results in an index of refraction gradient which modifies the dielectric surroundings of the cavity and shifts the optical modes. Reversible tuning can be obtained either by changing the excitation power density or by exciting in different points of the photonic crystal microcavity. (C) 2008 American Institute of Physics
Spectral tuning and near-field imaging of photonic crystal microcavities
We experimentally observe a sizable and reversible spectral tuning of the resonances of a two-dimensional photonic crystal microcavity induced by the introduction of a subwavelength size glass tip. The comparison between experimental near-field data, collected with lambda/6 spatial resolution, and results of numerical calculations shows that the spectral shift induced by the tip is proportional to the local electric field intensity of the cavity mode. This observation proves that the electromagnetic local density of states in a microcavity can be directly measured by mapping the tip-induced spectral shift with a scanning near-field optical microscope
BRCA2 polymorphic stop codon K3326X and the risk of breast, prostate, and ovarian cancers
Background: The K3326X variant in BRCA2 (BRCA2*c.9976A>T; p.Lys3326*; rs11571833) has been found to be associated with small increased risks of breast cancer. However, it is not clear to what extent linkage disequilibrium with fully pathogenic mutations might account for this association. There is scant information about the effect of K3326X in other hormone-related cancers.
Methods: Using weighted logistic regression, we analyzed data from the large iCOGS study including 76 637 cancer case patients and 83 796 control patients to estimate odds ratios (ORw) and 95% confidence intervals (CIs) for K3326X variant carriers in relation to breast, ovarian, and prostate cancer risks, with weights defined as probability of not having a pathogenic BRCA2 variant. Using Cox proportional hazards modeling, we also examined the associations of K3326X with breast and ovarian cancer risks among 7183 BRCA1 variant carriers. All statistical tests were two-sided.
Results: The K3326X variant was associated with breast (ORw = 1.28, 95% CI = 1.17 to 1.40, P = 5.9x10- 6) and invasive ovarian cancer (ORw = 1.26, 95% CI = 1.10 to 1.43, P = 3.8x10-3). These associations were stronger for serous ovarian cancer and for estrogen receptor–negative breast cancer (ORw = 1.46, 95% CI = 1.2 to 1.70, P = 3.4x10-5 and ORw = 1.50, 95% CI = 1.28 to 1.76, P = 4.1x10-5, respectively). For BRCA1 mutation carriers, there was a statistically significant inverse association of the K3326X variant with risk of ovarian cancer (HR = 0.43, 95% CI = 0.22 to 0.84, P = .013) but no association with breast cancer. No association with prostate cancer was observed.
Conclusions: Our study provides evidence that the K3326X variant is associated with risk of developing breast and ovarian cancers independent of other pathogenic variants in BRCA2. Further studies are needed to determine the biological mechanism of action responsible for these associations
Circulating Levels of Insulin-like Growth Factor 1 and Insulin-like Growth Factor Binding Protein 3 Associate With Risk of Colorectal Cancer Based on Serologic and Mendelian Randomization Analyses
BACKGROUND & AIMS: Human studies examining associations between circulating levels of insulin-like growth factor 1 (IGF1) and insulin-like growth factor binding protein 3 (IGFBP3) and colorectal cancer risk have reported inconsistent results. We conducted complementary serologic and Mendelian randomization (MR) analyses to determine whether alterations in circulating levels of IGF1 or IGFBP3 are associated with colorectal cancer development. METHODS: Serum levels of IGF1 and other proteins were measured in blood samples collected from 397,380 participants from the UK Biobank, from 2006 through 2010. Incident cancer cases and cancer cases recorded first in death certificates were identified through linkage to national cancer and death registries. Complete follow-up was available through March 31, 2016. For the MR analyses, we identified genetic variants associated with circulating levels of IGF1 and IGFBP3. The association of these genetic variants with colorectal cancer was examined with 2-sample MR methods using genome-wide association study consortia data (52,865 cases with colorectal cancer and 46,287 individuals without [controls]) RESULTS: After a median follow-up period of 7.1 years, 2665 cases of colorectal cancer were recorded. In a multivariable-adjusted model, circulating level of IGF1 level associated with colorectal cancer risk (hazard ratio per 1 standard deviation increment of IGF1, 1.11; 95% confidence interval [CI] 1.05-1.17). Similar associations were found by sex, follow-up time, and tumor subsite. In the MR analyses, a 1 standard deviation increment in IGF1 level, predicted based on genetic factors, was associated with a higher risk of colorectal cancer risk (odds ratio 1.08; 95% CI 1.03-1.12; P = 3.3 × 10-4). Level of IGFBP3, predicted based on genetic factors, was associated with colorectal cancer risk (odds ratio per 1 standard deviation increment, 1.12; 95% CI 1.06-1.18; P = 4.2 × 10-5). Colorectal cancer risk was associated with only 1 variant in IGFBP3 (rs11977526), which also associated with anthropometric traits and circulating level of IGF2. CONCLUSIONS: In an analysis of blood samples from almost 400,000 participants in the UK Biobank, we found an association between circulating level of IGF1 and colorectal cancer. Using genetic data from 52,865 cases with colorectal cancer and 46,287 controls, a higher level of IGF1, determined by genetic factors, was associated with colorectal cancer. Further studies are needed to determine how this signaling pathway might contribute to colorectal carcinogenesis
Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer
We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 x 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 x 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 x 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 x 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 x 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 x 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies
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