Transcutaneous pacing is commonly performed in emergency departments to treat patients with cardiac dysrhythmias. Although emergency nurses are required to complete a standardized course that reviews components of transcutaneous pacing, such as Advanced Cardiac Life Support, performing transcutaneous pacing on patients may be done infrequently in some facilities and can lead to anxiety and fear for bedside emergency nurses, especially novice emergency nurses and nurses who infrequently care for patients requiring external pacing. This manuscript provides a practical guide for emergency nurses to care for patients who require transcutaneous pacing. Key information found in this manuscript includes indications for transcutaneous pacing, the nurse's role when performing transcutaneous pacing, and transcutaneous pacing troubleshooting information.Outcome after failure of initial therapy in younger adult patients with acute myeloid leukaemia (AML) is highly variable. Cytogenetics, length of first remission (CR1) before relapse, and allogeneic transplantation are known prognostic factors, but the contribution of leukaemic genotype is less clear, particularly in resistant disease. Of 5,651 younger adult patients entered into UK MRC/NCRI AML trials between 1988 and 2014 with available FLT3ITD and NPM1 genotype, 326 (6%) had resistant disease and 2338 (41 %) relapsed after achieving CR1. Bufalin Overall survival (OS) was significantly higher in relapsed compared to resistant disease (p = 0·03). Independent favourable prognostic factors for OS in resistant disease included lower blast cell percentage after two courses of induction therapy (p = 0.0006) and NPM1 mutant (NPM1MUT) (p = 0.04). In relapsed disease, longer CR1 was a favourable independent factor for attainment of CR2 (p  less then  0.0001) and OS from time of relapse (p  less then  0.0001), but CR2 rate and OS from relapse were significantly worse in those who had received an allograft in CR1 (respectively p  less then  0.05, p  less then  0·002). NPM1MUT was marginally beneficial for OS (p = 0.04). FLT3ITD and DNMT3AMUT were adverse factors for OS (respectively p  less then  0.0001, p = 0.02). Mutational analysis adds additional independent prognostic information to demographic features and previous therapy in patients with resistant and relapsed disease.Fluctuations in luteinizing hormone (LH) release contribute to the development and maintenance of the reproductive system and become dysregulated during aging. Of note, increasing evidence supports extra-gonadal roles for LH within the CNS, particularly as it relates to cognition and plasticity in aging and age-related degenerative diseases such as Alzheimer's disease (AD). However, despite increasing evidence that supports a link between this hormone and CNS function, the mechanisms underlying LH action within the brain and how they influence cognition and plasticity during the lifespan is poorly understood and, in fact, often in conflict. This chapter aims to provide an up-to-date review of the literature addressing the role of LH signaling in the context of CNS aging and disease and put forward a unifying hypothesis that may explain currently conflicting theories regarding the role of LHCGR signaling in CNS function and dysfunction in aging and disease.Preservation of a robust circadian rhythmicity (particulsarly of the sleep/wake cycle), a proper nutrition and adequate physical exercise are key elements for healthy aging. Aging comes along with circadian alteration, e.g. a disrupted sleep and inflammation, that leads to metabolic disorders. In turn, sleep cycle disturbances cause numerous pathophysiological changes that accelerates the aging process. In the central nervous system, sleep disruption impairs several functions, among them, the clearance of waste molecules. The decrease of plasma melatonin, a molecule of unusual phylogenetic conservation present in all known aerobic organisms, plays a particular role as far as the endocrine sequels of aging. Every day, the late afternoon/nocturnal increase of melatonin synchronizes both the central circadian pacemaker located in the hypothalamic suprachiasmatic nuclei as well as myriads of peripheral cellular circadian clocks. This is called the "chronobiotic effect" of melatonin, the methoxyindole being the pr studies the cytoprotective effects of melatonin need higher doses to become apparent (i.e. in the 100mg/day range). Hence, controlled studies employing melatonin doses in this range are urgently needed.Aging undergoes serious worsening of peripheral organs and vital physiological processes including reproductive performances. Altered white adipose tissue and adipocyte functioning during aging results in ectopic lipid storage/obesity or metabolic derangements, leading to insulin resistance state. Eventually, accelerating cellular senescence thereby enhancing the high risk of age-associated metabolic alterations. Such alterations may cause derangement of numerous physiologically active obesity hormones, known as "adipokines." Specifically, adiponectin exhibits insulin sensitizing action causing anti-aging and anti-obesity effects via activation of adiponectin receptors (AdipoRs). The male reproductive physiology from reproductive mature stage to advanced senescent stage undergoes insidious detrimental changes. The mechanisms by which testicular functions decline with aging remain largely speculative. Adiponectin has also recently been shown to regulate metabolism and longevity signaling thus prolonging lifespan. Therefore, the strategy for activating adiponectin/AdipoRs signaling pathways are expected to provide a solid basis for the prevention and treatment of aging and obesity-associated reproductive dysfunctions, as well as for ensuring healthy reproductive longevity in humans.Late-onset hypogonadism, resulting from deficiency in serum testosterone (T), affects the health and quality of life of millions of aging men. T is synthesized by Leydig cells (LCs) in response to luteinizing hormone (LH). LH binds LC plasma membrane receptors, inducing the formation of a supramolecular complex of cytosolic and mitochondrial proteins, the Steroidogenic InteracTomE (SITE). SITE proteins are involved in targeting cholesterol to CYP11A1 in the mitochondria, the first enzyme of the steroidogenic cascade. Cholesterol translocation is the rate-determining step in T formation. With aging, LC defects occur that include changes in SITE, an increasingly oxidative intracellular environment, and reduced androgen formation and serum T levels. T replacement therapy (TRT) will restore T levels, but reported side effects make it desirable to develop additional strategies for increasing T. One approach is to target LC protein-protein interactions and thus increase T production by the hypofunctional Leydig cells themselves.