Neonatal encephalopathy linked to hypoxia-ischemia (H-I) which is regarded as the most important neurological problem of the newborn, can lead to a spectrum of adverse neurodevelopmental outcomes such as cerebral palsy, epilepsy, hyperactivity, cognitive impairment and learning difficulties. There have been numerous reviews that have focused on the epidemiology, diagnosis and treatment of neonatal H-I; however, a topic that is less often considered is the extent to which the injury might worsen over time, which is the focus of this review. Similarly, there have been numerous reviews that have focused on mechanisms that contribute to the acute or subacute injury; however, there is a tertiary phase of recovery that can be defined by cellular and molecular changes that occur many weeks and months after brain injury and this topic has not been the focus of any review for over a decade. Therefore, in this article we review both the clinical and pre-clinical data that show that tertiary neurodegeneration is a significant contributor to the final outcome, especially after mild to moderate injuries. We discuss the contributing roles of apoptosis, necroptosis, autophagy, protein homeostasis, inflammation, microgliosis and astrogliosis. We also review the limited number of studies that have shown that significant neuroprotection and preservation of neurological function can be achieved administering drugs during the period of tertiary neurodegeneration. As the tertiary phase of neurodegeneration is a stage when interventions are eminently feasible, it is our hope that this review will stimulate a new focus on this stage of recovery towards the goal of producing new treatment options for neonatal hypoxic-ischemic encephalopathy.
Background and objective: While the role of the renin-angiotensin-aldosterone system (RAAS) in the development of hypertension is well known, the significance and contribution of low renin hypertension is often overlooked. RAAS stimulation results in more tubular absorption of sodium and water along the nephron, contributing to a higher circulating vascular volume. In addition, members of the RAAS system, such as angiotensin II, have direct effects on vascular vasoconstriction, the heart, aldosterone synthesis in the adrenal glands, the sympathetic nervous system, and the central nervous system. This has resulted in a line of antihypertensive therapeutics targeting RAAS with angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and renin inhibitors, which prevent conversion of angiotensinogen to angiotensin. While general practitioners and nephrologists are well aware of the causes and the long-term consequences of elevated renin and aldosterone levels, the opposite situation with low renin and/or low aldosterone levels is frequently underappreciated. The objective of this review is to provide insight to the less common forms of hyporeninemic hypertension.
Methods: We searched the PubMed online library for keywords related to hyporeninemic hypertension and focused on the pediatric population. For pathophysiology we focused on literature of the last 5 years.
Key content and findings: The low renin and aldosterone levels may be indicators of inherited (especially when associated with hypokalemia), monogenic forms of hypertension stimulating excessive tubular sodium and water absorption which subsequently results in plasma volume expansion and hypertension. These forms of hypertension require frequently specific forms of therapy. This underlines the importance of the practitioner to be familiar with these rare diseases.
Conclusions: In this review article, we outline the different forms of hypertension characterized by low renin/low aldosterone and low renin/high aldosterone levels, how to diagnose these forms of hypertension, and how to treat them.
Background: Prior data has shown that the home environment impacts child development; however, there remains a paucity of research on how the home environment relates to child and adult words. Therefore, the aim of this prospective and quantitative study was to examine the relationship between the home environment and the quantity of vocalizations or words, and conversational turns produced by infants and parents at 3 and 12 months of age.
Methods: Seventy-two (56% male) full-term infants were assessed at 3 and 12 months of age. The home environment was assessed in person via interview and observation of the child's home using the Infant-Toddler Home Observation for Measurement of the Environment (IT-HOME) Inventory subscales. Vocalizations were measured using the Language Environment Analysis (LENA) device, which measures the adult word count, child vocalization count and conversational turn count. These measures were then averaged for the most voluble, or vocal hour, in the recording period.
Results: At 3 months, IT-HOME Learning Materials scores were significantly associated with a decrease in adult words. We found a statistically significant difference in LENA outcomes between 3 and 12 months when stratified by sex. Specifically, male infants had significantly fewer vocalizations at 12 months when compared to 3 months, whereas females had more vocalizations. There was also a statistically significant difference in IT-HOME Learning Materials, Organization, Responsivity, and Total scores when comparing 3- and 12-month time points.
Conclusions: These findings reveal that the home environment changes significantly over the first year of life. At 3 months, Learning Materials in the home were related to adult words, while between 3 and 12 months, several aspects of the home significantly changed. Male children had reduced vocalizations between 3 and 12 months; whereas, female children had increased vocalizations during the same time points. Future research should focus on examining these outcomes with multiple measures, time points, and patient populations.

