Introduction/PurposeExtreme ultra-endurance races are growing in popularity but their effects on skeletal muscles remain mostly unexplored. This longitudinal study explores physiological changes in mountain ultramarathon (MUM) athletes' quadriceps using quantitative magnetic resonance imaging (qMRI) coupled with serological biomarkers.The study aimed to monitor the longitudinal effect of the race and recovery, and to identify local inflammatory and metabolic muscle responses by codetection of biological markers. MethodsAn automatic image processing framework was designed to extract imaging-based biomarkers from qMRI acquisitions of the upper legs of 20 finishers at three time points.
A research program has been carried out to establish the low-cycle fatigue and creep-fatigue behaviors of Inconel 625 at elevated temperatures (650 and 815°C). The main observations were related to the effect of temperature and of hold times. Under continuous cycling, a temperature increase from 650 to 815°C caused a reduction in the fatigue life by a factor of 2 at a high strain and by a factor of 3 at a low strain. Tension hold times had little detrimental effect on cyclic life at 650°C concerning the life reduction with respect to continuous cycling; at 815°C, on the other hand, this became more significant. Compressive hold times also had a damaging effect on fatigue life, and this was larger than that associated with tensile hold times; in particular, it was very pronounced for low strain levels at 815°C. An analysis of data using a life prediction method previously suggested for creep-fatigue combination loadings has also been carried out. The method takes into account the damaging effect due to a compression hold time separately from that due to a tensile hold time in interspersed creep-fatigue loadings. The overall correlation between theoretical calculations and experimental results is reasonably good, for strain levels ranging from 1.2 to 0.4%.
ObjectivesThe mechanism of raltegravir (RAL)-resistant evolutions has not already been elucidated. Because the emergence of RAL resistance is usually initiated by the N155H mutant, we assessed the role of minor N155H-mutated variants in circulating RNA and archived DNA in five heavily treated patients experiencing long-term RAL therapy failure and harbouring three different resistance profiles determined by standard genotyping. MethodsAllele-specific polymerase chain reaction (AS-PCR) was used to detect N155H mutants in longitudinal stored plasma and whole-blood samples before, during and after RAL-based regimens in five patients infected with the HIV-1 B subtype. ResultsNo minor N155H-mutated variant was found by AS-PCR in either plasma or whole-blood samples collected at baseline and after RAL withdrawal in any of the five patients. During RAL failure, the mutation N155H was detected at different levels in three patients displaying the N155H pathway and gradually declined when the double mutant Q148H+G140S was selected in one patient. In two patients with the Q148H resistance pathway, no N155H variant was identified by AS-PCR in either viral RNA or DNA. ConclusionsThe N155H mutation present at various levels from minority to majority showed no relationship with the three RAL-associated resistance profiles, suggesting that this mutant may not play a role in determining different resistance profiles. Moreover, pre-existing N155H is very infrequent and, if selected during RAL failure, the N155H mutant disappears quickly after RAL withdrawal.Keywords: HIV, mutation, N155H, raltegravir, resistance Patients and methodsThis retrospective study used plasma and whole-blood samples collected at different time-points from five patients infected with HIV-1 subtype B who experienced virological failure with RAL-based salvage regimens at Saint-Louis Hospital, Paris, France. Informed consent was obtained from all five patients before proceeding. As treatment options were limited in these patients, RAL therapy was still administrated for a period of time even when RAL-associated mutations were detected. Plasma viral load was determined using Cobas Ampliprep/Cobas Taqman® HIV-1 (Roche, Meylan, France) and CD4 T-lymphocyte count was measured by flow cytometry using a FACScalibur cytometer (Becton Dickinson, San Jose, CA).Longitudinal stored samples taken before, during and after treatment with the RAL-based regimen were analysed. Plasma samples (1 mL) were ultracentrifuged at 28 100 g for 2 h at 4°C, and then were extracted using the QIAamp viral RNA minikit (Qiagen, Valencia, CA). Total HIV-1 DNA was extracted from whole-blood samples (MagnaPure; Roche, France). For standard genotyping, Agence Nationale de Recherches sur le SIDA et les hépatites virales (ANRS) consensus protocols (http://www.hivfrenchresistance.org) were used to amplify the regions of interest. Amplicons were subjected to purification (QIAquick PCR Purification Kit; Qiagen) prior to sequencing using the BigDye Terminator Kit (Applied Biosystems, Foster City, ...
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