Women are conferred with greater immunologic and survival benefits compared to men. Female sex steroids contribute to this sexual dimorphism. Furthermore, during human pregnancy when female sex hormones are elevated, neutrophil apoptosis is delayed. This study examines the specific effects of estradiol and progesterone on neutrophil apoptosis and function in healthy adult men and women. We also examined the contribution of these hormones to the persistence and resolution of an inflammatory response. Spontaneous apoptosis was significantly decreased in women compared with men. Physiologic doses of estradiol and progesterone caused a further delay in spontaneous apoptosis in both men and women but did not diminish Fas antibody-induced apoptosis. The delay in apoptosis was mediated at the level of the mitochondria with decreased release of cytochrome c, which may alter caspase cleavage and activity. There were no associated alterations in neutrophil CD11b, but production of reactive oxygen intermediates (ROIs) in women was increased. Thus, female sex hormones mediate delayed neutrophil apoptosis in both sexes and enhance female intracellular production of ROIs. Modulating hormonal responses may be an effective therapeutic tool in combating inflammatory diseases. (Blood. 2003;102:2653-2659)

Neutrophils are the most abundant innate immune cell with critical anti-microbial functions. Since the discovery of granulocytes at the end of the nineteenth century, the cells have been given many names including phagocytes, polymorphonuclear neutrophils (PMN), granulocytic myeloid derived suppressor cells (G-MDSC), low density neutrophils (LDN) and tumor associated neutrophils (TANS). This lack of standardized nomenclature for neutrophils suggest that biologically distinct populations of neutrophils exist, particularly in disease, when in fact these may simply be a manifestation of the plasticity of the neutrophil as opposed to unique populations. In this review, we profile the surface markers and granule expression of each stage of granulopoiesis to offer insight into how each stage of maturity may be identified. We also highlight the remarkable surface marker expression profiles between the supposed neutrophil populations.

The Bayley Scales of Infant and Toddler Development—Third Edition (Bayley-III) is a gold standard series of behavioural assessments used by clinicians and researchers to assess the developmental functioning of young children. The rigorous psychometric properties of the tool are attributed to the carefully standardised normative sample and quantitative scoring system. It is a common end-point assessment used in neonatal trials and is routinely used in a clinical setting to assess the development of children at risk of delay. Incidence of developmental delay is higher in clinical populations such as those born preterm or with complications such as neonatal encephalopathy. Early identification of delay is critical as early intervention is most effective in minimising impairment; therefore, routine assessment of developmental outcomes is recommended, particularly among high-risk populations.

Neonatal encephalopathy (NE) is associated with high mortality and morbidity. Factors predisposing to NE can be antenatal, perinatal, or a combination of both. Antenatal maternal factors, familial factors, genetic predisposition, hypoxic ischemic encephalopathy, infections, placental abnormalities, thrombophilia, coagulation defects, and metabolic disorders all have been implicated in the pathogenesis of NE. At present, therapeutic hypothermia is the only treatment available, regardless of etiology. Recognizing the etiology of NE involved can also guide investigations such as metabolic and sepsis workups to ensure optimal management. Understanding the etiology of NE may allow the development of targeted adjunctive therapies related to the underlying mechanism and develop preventative strategies.