A New Reference Source for Postmortem Body Measurements and Organ Weights in Neonates and Infants

Abstract

Reference charts for body and organ measurements of neonates and infants were derived from data on 900 investigations done by the Office of the Chief Coroner for Ontario. The statistical analyses in this new reference source addressed deficiencies in sources currently available to pathologists.The present study also considered whether organ weights differed based on the classification of infant deaths using the original definition of either sudden infant death syndrome (SIDS) or sudden unexplained death (SUDS) which considers cases occurring in an unsafe sleeping environment or under adverse socioeconomic conditions. Cases of SUDS for both sexes peaked in 5 to 16 weeks of age. The thymus in the SUDS/SIDS age groups less than 25 weeks weighed more than the control group. Adrenal weights in SUDS cases between 9 and 16 weeks weighed less than SIDS cases. This could mean that deaths in unsafe sleep environments are truly sudden in infants who may have a limited adrenal response to acute hypoxia but have been unaffected by preceding chronic stressors.

Deficient pregnenolone synthesis associated with congenital adrenal hyperplasia and organelle dysfunction

“…SCC activity requires interaction with the IMM translocase, Tim50, or possibly the TIM23 complex for appropriate folding and activity. Drosophila expressing a Tim50 mutant had growth defects and reduced mitochondrial membrane potential, which is similar to that seen in zebrafish models (11). These studies suggest that Tim50 needs to interact with SCC to be capable of inducing metabolic activity with the other interacting partners, such as ferrodoxin, ferrodoxin reductase and NADPH for six electron pairs.…”

“…The acute response to stress consists of a relatively stereotyped series of physiological programs to promote survival mediated by the HPA axis, resulting in hypothalamic CRH secretion that stimulates release of ACTH by the pituitary and subsequent adrenal and gonadal glucocorticoid release. Steroid synthesis starts at the mitochondria of adrenals and gonads, and mitochondrial stress may also induce retrograde signaling in mammalian cells (11). Cells can also respond to stress in a way that is specific to individual organelles and propagate to mitochondria.…”

“…Cells can also respond to stress in a way that is specific to individual organelles and propagate to mitochondria. Specifically, the ER stress response or the unfolded protein response (UPR) is activated in response to mild or short-term stress triggers, inducing the expression of a wide range of genes involved in the maintenance of ER function (11). The impaired stress response arises from either primary defects in the adrenal gland or secondary hypothalamic or pituitary defects, resulting in steroidogenesis defects.…”

“…Testes were fixed in zinc formalin, processed and embedded in paraffin for routine light microscopy. Sections of 5–10 µm were obtained from each specimen, floated onto glass slides, stained with hematoxylin and eosin (H&E) and examined by microscopy (11).…”

“…We have performed a detailed analysis of the ultrastructure of the testis of the patient, analyzing the mitochondria and endoplasmic reticulum (ER) structures using light microscopy, electron microscopy (EM) and biochemical experiments since the adrenal glands and gonads are primary steroid-producing organs in which changes in the environment can affect organelle structure. We observed earlier that environmental stress on the ER affected mitochondrial metabolic activity (11), suggesting that these environmental changes can completely alter activity when only minimal changes in activity were detected following protein mutation in non-environmentally stressed conditions. During endogenous and exogenous stress, the HPA axis was activated and included CRH-stimulated ACTH release, affecting organelle architecture and resulting in the disruption of steroid synthesis (Fig.…”