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For exercise prescription purposes, it is often assumed that % heart rate reserve (%HRR) provides equivalent intensities to %VO2max. However, a recent study from this laboratory demonstrated that during cycling exercise %HRR is not equivalent to %VO2max, but is instead equivalent to a percentage of the difference between resting and maximal VO2, i.e., % VO2reserve (%VO2R). The current study examined these relationships during treadmill exercise. Fifty adults performed Bruce protocol treadmill tests to exhaustion. For each subject, data obtained at rest, at the end of each stage, and at maximum were used to determine linear regressions of %HRR versus %VO2max, and of %HRR versus %VO2R. For %HRR versus %VO2max the mean intercept and slope were -6.1+/-0.7 and 1.10+/-0.01, respectively, with a mean r of 0.990+/-0.002. For %HRR versus %VO2R, the mean intercept and slope were 1.5+/-0.6 and 1.03+/-0.01, respectively, with a mean r of 0.990+/-0.002. Both regressions differed statistically from the line of identity (i.e., intercept of 0 and slope of 1). However, the regression of %HRR versus %VO2R was significantly closer (P < 0.001 ) to the line of identity than was the regression of %HRR versus %VO2max. We conclude that %HRR should be considered as an indicator of %VO2R, not %VO2max, when prescribing treadmill exercise, as was previously concluded for cycling exercise.

Lymph node (LN) stromal cells, particularly fibroblastic reticular cells (FRCs), provide critical structural support and regulate immunity, tolerance and transport properties of LNs. In many tumors, LN metastasis is predictive of poor prognosis. However, the stromal contribution to the evolving microenvironment of tumor draining LNs (TDLNs) remains poorly understood. Here we show that FRCs specifically of TDLNs proliferate in response to tumor-derived cues and that the network they form is remodeled. Comparative transcriptional analysis of non-draining and TDLN FRCs demonstrated reprogramming of key pathways including matrix remodeling, chemokine/cytokine signaling and immune functions including leukocyte recruitment, migration and activation. In particular, downregulation of FRC-derived CCL21 and IL-7 were accompanied by altered immune composition and aberrant localization. These data imply that stroma of TDLNs adapt on multiple levels, following exposure to tumor-derived factors, to exhibit features typically associated with immune suppression.

European Union policy encourages men and women to share parental leave to balance work and family life and promote gender equality in the labor market. A new directive extends parental leave to four months and introduces a quota, so one month is reserved for each parent. This article explores to what extent government-provided, paid parental leave and quotas for fathers could bring about equality in the division of leave between men and women by focusing on the pioneers in the field, the Nordic countries Á the first nations to offer fathers parental leave and introduce quotas. First, we describe the extent to which parental leave policies have been established and implemented in a way that is likely to promote equal sharing of leave. Next, we evaluate the impact of particular configurations of gender equality incentives in present parental leave policies for the actual division of leave time between men and women. Findings contribute to the conceptual as well as empirical understanding of whether fathers' rights and use of parental leave can help bring about an egalitarian division of leave between mothers and fathers, often thought to be the foundation for gender equality.La politique de l'Union européenne encourage les hommes et les femmes à partager le congé parental, pour mieux balancer le travail et la vie familiale et pour avancer la parité dans le marché du travail. Une nouvelle disposition législative prolonge le congé parental jusqu'à quatre mois et fournit un système de quota, sous forme d'un mois réservé pour chaque parent. Cet article explore dans quelle mesure le congé parental proposé par le gouvernement et les quotas des pères puissent affecter la parité en ce qui concerne la distribution du congé. L'article se concentre sur les pionniers de ce domaine (les pays nordiques)-les premiers pays à offrir aux pères le congé parental et à établir des quotas. D'abord, l'article décrit le contexte dans lequel la politique du congé parental a été établie et les mesures qui ont contribué au progrès de la parité dans la distribution du congé parental. Puis, l'article évalue le vrai impact des configurations spécifiques aux incitations à la parité dans la distribution du congé parental. Le résultat de cette étude contribue à la compréhension conceptuelle et empirique d'une question souvent considerée fondamentale à la parité: Est-ce que les droits des pères et l'utilisation du congé parental pourraient aider à réaliser une distribution égalitaire du congé parental entre mères et pères?

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This study explores fathers' experiences with work-family conflict and their perceptions of how supportive the organizational culture at work is regarding fathers' work-family needs, and whether a family-supportive organizational culture is associated with less work-family conflict. A total of 377 fathers working in private Swedish companies were surveyed. While a modest proportion of fathers experienced high levels of work-tofamily conflict, less family-to-work conflict was reported. Further, fathers perceived little work-family support from top managers, supervisors, and co-workers. Our results indicate that the cultures in the examined companies have norms that separate work and family from each other. Fathers seem likely to experience work-family conflict as long as the familysupportive organizational culture, especially at the work group level, is not well-developed. When fathers experience their work organizations as family-supportive, they are likely to be better able to combine work and family and thus to help Swedes achieve a more gender-equal society.

Angiogenesis is a hallmark of cancer, promoting growth and metastasis. Anti‐angiogenic treatment has limited efficacy due to therapy‐induced blood vessel alterations, often followed by local hypoxia, tumor adaptation, progression, and metastasis. It is therefore paramount to overcome therapy‐induced resistance. We show that Apelin inhibition potently remodels the tumor microenvironment, reducing angiogenesis, and effectively blunting tumor growth. Functionally, targeting Apelin improves vessel function and reduces polymorphonuclear myeloid‐derived suppressor cell infiltration. Importantly, in mammary and lung cancer, Apelin prevents resistance to anti‐angiogenic receptor tyrosine kinase (RTK) inhibitor therapy, reducing growth and angiogenesis in lung and breast cancer models without increased hypoxia in the tumor microenvironment. Apelin blockage also prevents RTK inhibitor‐induced metastases, and high Apelin levels correlate with poor prognosis of anti‐angiogenic therapy patients. These data identify a druggable anti‐angiogenic drug target that reduces tumor blood vessel densities and normalizes the tumor vasculature to decrease metastases.