Morsinghalvorsen4280

030). Peak torque of the eccKF was significantly reduced from pre- to post-exercise at 60 (-7.7%; p = .018), 180 (-10.5%; p = .042), and 270 deg∙s-1 (-7.5%; p = .034). A main effect for time was identified for PL-T (p less then .010), PL-V (p = .033), and PL-AP (p less then .010). Conclusions These findings suggest that muscle excitation of the rectus femoris is reduced during ET, accompanied with a deficit in the torque generation of the knee flexors following 120 min of soccer-specific activity. Practitioners should adequately condition players for the additional ET period by incorporating exercises into training schedules that develop fatigue-resistant eccentric hamstring strength to minimize injury risk.

Tissue resident memory T cells play a critical role in the defense against inhaled pathogens. The isolation and study of human lung tissue resident memory T cells and lung resident macrophages is limited by experimental constraints.

To characterize the spatial and functional relationship between lung resident macrophages and human lung tissue resident memory T cells using ex-vivo lung perfusion.

Tissue resident memory T cells and lung resident macrophages were isolated using ex-vivo lung perfusion and intra-perfusate labeled CD45 antibody. Cells isolated after 6 hours of ex-vivo lung perfusion were analyzed using spectral flow cytometry. Spatial relationships between CD3+ and CD68+ cells were explored with multiplexed immunohistochemistry (IHC). Functional relationships were determined by co-culture and T cell receptor complex signal transduction.

Lungs from 8 research-consented organ donors underwent ex-vivo lung perfusion for 6 hours. We show that human lung TRM and MLR co-localize within the human lung, preferentially around the airways. Furthermore, we found that human lung CD8+ TRM are composed of two functionally distinct populations based on PD1 and ZNF683 (HOBIT) protein expression. We show that MLR provide co-stimulatory signaling to PD1hi CD4+ and CD8+ lung TRM, augmenting TRM effector cytokine production and degranulation.

Ex-vivo lung perfusion provides an innovative technique to study resident immune populations in humans. Human lung resident macrophages co-localize with and provide co-stimulation signaling to tissue resident memory T cells, augmenting their effector function.

Ex-vivo lung perfusion provides an innovative technique to study resident immune populations in humans. Human lung resident macrophages co-localize with and provide co-stimulation signaling to tissue resident memory T cells, augmenting their effector function.

Approximately 40% of people worldwide are exposed to household air pollution (HAP) from the burning of biomass fuels. Previous efforts to document health benefits of HAP mitigation have been stymied by an inability to lower emissions to target levels.

We sought to determine if a cleaner energy intervention improved cardiopulmonary health outcomes in adult women living in a resource-poor setting in Peru.

We conducted a randomized controlled field trial in 180 women aged 25-64 years living in rural Puno, Peru. Intervention women received a liquefied petroleum gas (LPG) stove, continuous fuel delivery for one year, education and behavioral messaging, whereas control women were asked to continue their usual cooking practices. We assessed for stove use adherence using temperature loggers installed in both LPG and biomass stoves of intervention households.

At baseline and at 3-4 visits post-randomization, we measured blood pressure, peak expiratory flow (PEF) and respiratory symptoms using the St. George's Respiratory Questionnaire (SGRQ). Intervention women used their LPG stove exclusively for 98% of days. We did not find average differences in post-randomization systolic (intervention - control 0.7 mmHg, 95% CI -2.1 to 3.4) or diastolic blood pressure (0.3 mmHg, -1.5 to 2.0), pre- (0.14 L/sec/m2, -0.02 to 0.29) or post-bronchodilator PEF/height2 (0.11 L/sec/m2, -0.05 to 0.27), or SGRQ total score (-1.4, -3.9 to 1.2) in intention-to-treat analysis. There were no reported harms related to the intervention.

We did not find evidence of a difference in blood pressure, lung function or respiratory symptoms during the year-long cleaner energy intervention. Clinical trial registration available at www.clinicaltrials.gov, ID NCT02994680.

We did not find evidence of a difference in blood pressure, lung function or respiratory symptoms during the year-long cleaner energy intervention. Clinical trial registration available at www.clinicaltrials.gov, ID NCT02994680.

Cigarette smoke is considered the chief leading cause of chronic obstructive pulmonary disease (COPD). Its impact on the progressive deterioration of the airways has been extensively studied, but its direct effects on pulmonary vasculature are less known.

We aim to prove that pulmonary arterial remodeling in COPD patients is not just a consequence of alveolar hypoxia, but it is also due to direct effects of cigarette smoke on the pulmonary vascular bed.

We have used different molecular and cell biology approaches, as well as traction force microscopy, wire myography and patch-clamp techniques in human cells and freshly isolated pulmonary arteries. Additionally, we relied on in vivo models and human samples to analyze the effects of cigarette smoke on pulmonary vascular tone alterations.

Cigarette smoke extract (CSE) exposure directly promoted a hypertrophic, senescent phenotype that in turn contributed, through the secretion of inflammatory molecules, to increase the proliferative potential of non-exposed cells. Interestingly, these effects were significantly reversed by antioxidants. Furthermore, CSE affected cell contractility and dysregulated the expression and activity of the voltage-gated K+ channel Kv7.4. This contributed to impair vasoconstriction and vasodilation responses. Most importantly, the levels of this channel were diminished in the lungs of smoke-exposed mice, smokers and COPD patients.

Cigarette smoke directly contributes to pulmonary arterial remodeling through increased cell senescence, as well as vascular tone alterations due to diminished levels and function of the Kv7.4 channel. Strategies targeting these pathways may lead to novel therapies for COPD.

Cigarette smoke directly contributes to pulmonary arterial remodeling through increased cell senescence, as well as vascular tone alterations due to diminished levels and function of the Kv7.4 channel. AS601245 in vivo Strategies targeting these pathways may lead to novel therapies for COPD.