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Pulmonary oedema (PED) is an accumulation of fluid in the lung interstitium and alveoli. PED is typically divided into cardiogenic and non-cardiogenic mechanisms. Cardiogenic PED, or congestive heart failure, occurs when the heart is unable to pump the blood returning from the lungs to the body effectively, either as a result of intrinsic heart dysfunction or external effects such as hypertension causing increased afterload. Non-cardiogenic PED, also known as acute respiratory distress syndrome (ARDS), occurs due to changes in capillary membrane permeability, resulting in the accumulation of fluid in the alveoli and interstitium. PED complicates between 0.08% and 0.5% of pregnancies.
Molecular pathways underlying carcinogenesis: nuclear receptors
Nicole L. Moore, Dame Roma Mitchell Cancer Research Laboratories, Adelaide University/Hanson Institute, Adelaide, South Australia,
Margaret M. Centenera, Dame Roma Mitchell Cancer Research Laboratories, Adelaide University/Hanson Institute, Adelaide, South Australia,
Lisa M. Butler, Dame Roma Mitchell Cancer Research Laboratories, Adelaide University/Hanson Institute, Adelaide, South Australia,
Theresa E. Hickey, Dame Roma Mitchell Cancer Research Laboratories, Adelaide University/Hanson Institute, Adelaide, South Australia,
Wayne D. Tilley, Dame Roma Mitchell Cancer Research Laboratories, Adelaide University/Hanson Institute, Adelaide, South Australia
Androgens are sex steroid hormones that are produced in both males and females, albeit in different amounts. Androgens are essential for development and maintenance of the male phenotype (1), and are also important in females, where they can either act directly via the androgen receptor (AR) or indirectly as metabolic precursors for estrogen biosynthesis (2). The majority of circulating androgens in males and females are produced by the gonads, under hypothalamic–pituitary regulation, and adrenal glands. The major circulating androgens are dehydroepiandrosterone, DHEA sulfate, androstenedione, and testosterone, which can all be metabolized to other androgens or to estrogens. Testosterone and its intracrine metabolite, 5α-dihydrotestosterone (DHT), are the most potent androgenic hormones, as they bind with high affinity to the AR. Many organs in both males and females are sensitive to androgen action and, depending on the tissue-specific context, androgens regulate multiple cellular processes, including proliferation, differentiation, apoptosis, metabolism, secretory responses, and the synthesis of lipids and fatty acids (3). Accordingly, deregulation of AR expression and/or function is associated with a diverse range of clinical conditions, including androgen insensitivity syndrome (AIS), a form of motor neuron disease known as Kennedy's disease, male and female pattern baldness, hirsutism, acne, male infertility, polycystic ovary syndrome, benign prostatic hyperplasia, and breast and prostate cancer. In particular, the AR is considered an oncogene in the prostate as it plays a critical role at all stages of prostate carcinogenesis, and consequently, inhibition or abrogation of androgen signaling is the goal of hormonal therapies for this disease. In contrast, androgens predominantly have a growth inhibitory role in the breast, consistent with an emerging view of the AR playing a tumor-suppressive role in breast tumorigenesis.
This chapter reviews the major physiological adaptations during pregnancy and also highlights changes in the reference ranges of common laboratory values encountered in pregnancy. Pregnancy induces a myriad of changes involving the cardiovascular system, respiratory system, gastrointestinal and hepatobiliary systems and genitourinary system. Pregnancy is associated with an overall increase in the serum concentrations of total cortisol, free cortisol, aldosterone, deoxycorticosterone, corticosteroid binding globulin, and adrenocorticotropic hormone. Pituitary enlargement occurs in pregnancy by estrogen mediated proliferation of prolactin-producing cells. During the first trimester of pregnancy, total thyroxine and total tri iodothyronine concentrations begin to increase and peak at mid-gestation, primarily as a result of increased production of thyroid-binding globulin. The immunological adaptations of pregnancy, particularly at the maternal-fetal interface, comprise complex mechanisms that enable the fetus to grow while preventing the mother from rejecting the fetus.