Since silence implies compliance with the status quo, the authors encourage occupational therapists to develop their own dialogue about occupational injustices in order to address them openly with others. Dialogue about occupational justice is timely as occupational therapists around the world articulate what distinguishes this numerically small, rather invisible profession and its contributions to individuals, populations, and societies.

Sex differences in the biology of different organ systems and the influence of sex hormones in modulating health and disease are increasingly relevant in clinical and research areas. Although work has focused on sex differences and sex hormones in cardiovascular, musculoskeletal, and neuronal systems, there is now increasing clinical evidence for sex differences in incidence, morbidity, and mortality of lung diseases including allergic diseases (such as asthma), chronic obstructive pulmonary disease, pulmonary fibrosis, lung cancer, as well as pulmonary hypertension. Whether such differences are inherent and/or whether sex steroids play a role in modulating these differences is currently under investigation. The purpose of this review is to define sex differences in lung structure/function under normal and specific disease states, with exploration of whether and how sex hormone signaling mechanisms may explain these clinical observations. Focusing on adult age groups, the review addresses the following: 1) inherent sex differences in lung anatomy and physiology; 2) the importance of certain time points in life such as puberty, pregnancy, menopause, and aging; 3) expression and signaling of sex steroid receptors under normal vs. disease states; 4) potential interplay between different sex steroids; 5) the question of whether sex steroids are beneficial or detrimental to the lung; and 6) the potential use of sex steroid signaling as biomarkers and therapeutic avenues in lung diseases. The importance of focusing on sex differences and sex steroids in the lung lies in the increasing incidence of lung diseases in women and the need to address lung diseases across the life span.

LEO is a leadership tool to extend all occupational therapists' strategic use of scholarship, new accountability approaches, existing and new funding, and workforce planning to improve access to occupational therapy.

No abstract

The severity of asthma, a disease characterized by airway hyperresponsiveness and inflammation, is enhanced in some women during the menstrual cycle and during pregnancy but relieved in others. These clinical findings suggest that sex steroids modulate airway tone. Based on well-known relaxant effects of estrogens on vascular smooth muscle, we hypothesized that estrogens relax airway smooth muscle (ASM), thus facilitating bronchodilation. In ASM tissues from female patients, Western and immunocytochemical analyses confirmed the presence of both estrogen receptor (ER) isoforms, ERalpha and ERbeta. In fura 2-loaded, dissociated ASM cells maintained in culture, acute exposure to physiological concentrations of 17beta-estradiol (E(2); 100 pM to 10 nM) decreased the intracellular Ca(2+) ([Ca(2+)](i)) response to 1 muM histamine, an effect reversed by the ER antagonist ICI-182,780. The ERalpha-selective agonist (R,R)-THC had a greater reducing effect on [Ca(2+)](i) responses to histamine and 1 muM ACh compared with the ERbeta-selective agonist (DPN). The effects of E(2) on [Ca(2+)](i) were mediated, at least in part, via decreased Ca(2+) influx through l-type channels and store-operated Ca(2+) entry but not via Ca(2+)-activated K(+) channels, receptor-operated entry, or sarcoplasmic reticulum reuptake. Overall, these data support our hypothesis that estrogens relax ASM and suggest a potentially novel therapeutic target in airway hyperresponsiveness.