Key points Therapeutic hypothermia (HT) to 33.0–34.0°C for 72 h provides optimal therapy for infants with neonatal encephalopathy (NE) in high‐resource settings. HT is not universally implemented in low‐ and middle‐income countries as a result of both limited resources and evidence. Facilitated passive cooling, comprising infants being allowed to passively lower their body temperature in the days after birth, is an emerging practice in some West African neonatal units. In this observational study, we demonstrate that infants undergoing facilitated passive cooling in a neonatal unit in Accra, Ghana, achieve temperatures within the HT target range ∼20% of the 72 h. Depth of HT fluctuates and can be excessive, as well as not maintained, especially after 24 h. Sustained and deeper passive cooling was evident for severe NE and for those that died. It is important to prevent excessive cooling, to understand that severe NE babies cool more and to be aware of facilitated passive cooling with respect to the design of clinical trials in low‐ and mid‐resource settings. Abstract Neonatal encephalopathy (NE) is a significant worldwide problem with the greatest burden in sub‐Saharan Africa. Therapeutic hypothermia (HT), comprising the standard of care for infants with moderate‐to‐severe NE in settings with sophisticated intensive care, is not available to infants in many sub‐Saharan African countries, including Ghana. We prospectively assessed the temperature response in relation to outcome in the 80 h after birth in a cohort of babies with NE undergoing ‘facilitated passive cooling’ at Korle Bu Teaching Hospital, Accra, Ghana. We hypothesized that NE infants demonstrate passive cooling. Thirteen infants (69% male) ≥36 weeks with moderate‐to‐severe NE were enrolled. Ambient mean ± SD temperature was 28.3 ± 0.7°C. Infant core temperature was 34.2 ± 1.2°C over the first 24 h and 35.0 ± 1.0°C over 80 h. Nadir mean temperature occurred at 15 h. Temperatures were within target range for HT with respect to 18 ± 14% of measurements within the first 72 h. Axillary temperature was 0.5 ± 0.2°C below core. Three infants died before discharge. Core temperature over 80 h for surviving infants was 35.3 ± 0.9°C and 33.96 ± 0.7°C for those that died (P = 0.043). Temperature profile negatively correlated with Thompson NE score on day 4 (r2 = 0.66): infants with a Thompson score of 0–6 had higher temperatures than those with a score of 7–15 (P = 0.021) and a score of 16+/deceased (P = 0.007). More severe NE was associated with lower core temperatures. Passive cooling is a physiological response after hypoxia–ischaemia; however, the potential neuroprotective effect of facilitated passive cooling is unknown. An awareness of facilitated passive cooling in babies with NE is important for the design of clinical trials of neuroprotection in low and mid resource settings.
Alzheimer's disease is the sixth leading cause of death in the United States. The leading hypothesis to explain the prevalence of the disease in the brain is the aggregation of Amyloid Beta peptides in the brain, which form senile plaques and suppress neuronal function. Selective estrogen receptor modulators (SERMs) have been found to provide protective effects against the neurotoxic effects of Amyloid Beta. This experiment was conducted in two distinct phases: the experimental phase and the literature review phase. The experimental phase sought to determine if Amyloid Beta was neurotoxic to SH-SY5Y neuroblastoma cells, and if STX-an SERM-was able to rescue cell viability after exposure to Amyloid Beta toxicity. During the literature review phase, potential pathways already described in the literature were identified, which might be able to account for how STX was able to rescue cell viability after exposure to Amyloid Beta toxicity. Amyloid Beta was found to have a significant toxic effect on cell viability when compared to a control assay of cells grown in DMSO. STX, however, was not found to have a significant rescue effect against Amyloid Beta toxicity. The literature review identified several pathways that were likely candidates for neuroprotection, including MAPK, ERK1, ERK2, and PI3K. The future direction of this experiment would be to determine if STX is as effective at providing neuroprotection against Amyloid Beta as previously suggested by similar experiments. the next stage of investigation would then be to inhibit different pathways that have been identified as possible pathways for neuroprotection.
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