Slow Wave Sleep and Long Duration Spaceflight

While ground research has clearly shown that preserving adequate quantities of sleep is essential for optimal health and performance, changes in the progression, order and /or duration of specific stages of sleep is also associated with deleterious outcomes. As seen in Figure 1, in healthy individuals, REM and Non-REM sleep alternate cyclically, with stages of Non-REM sleep structured chronologically. In the early parts of the night, for instance, Non-REM stages 3 and 4 (Slow Wave Sleep, or SWS) last longer while REM sleep spans shorter; as night progresses, the length of SWS is reduced as REM sleep lengthens. This process allows for SWS to establish precedence , with increases in SWS seen when recovering from sleep deprivation. SWS is indeed regarded as the most restorative portion of sleep. During SWS, physiological activities such as hormone secretion, muscle recovery, and immune responses are underway, while neurological processes required for long term learning and memory consolidation, also occur. The structure and duration of specific sleep stages may vary independent of total sleep duration, and changes in the structure and duration have been shown to be associated with deleterious outcomes. Individuals with narcolepsy enter sleep through REM as opposed to stage 1 of NREM. Disrupting slow wave sleep for several consecutive nights without reducing total sleep duration or sleep efficiency is associated with decreased pain threshold, increased discomfort, fatigue, and the inflammatory flare response in skin. Depression has been shown to be associated with a reduction of slow wave sleep and increased REM sleep. Given research that shows deleterious outcomes are associated with changes in sleep structure, it is essential to characterize and mitigate not only total sleep duration, but also changes in sleep stages

Hidden giants: The story of Bolbometopon muricatum at ningaloo reef

Bolbometopon muricatum (bumphead parrotfish, Valenciennes, 1839) is a conspicuous, iconic and ecologically important coral reef fish species. B. muricatum plays an important role in the bioerosion of the reef framework and as a result has been described as both an ecosystem engineer and keystone species. Despite the complete absence of B. muricatum from 32 years of scientific surveys across the Ningaloo Reef World Heritage Area, we recorded a total of 155 individuals of B. muricatum across 63.2 ha of reef crest surveys, equating to mean density of 2.38 ind/ha. Our observations represent the first record of this iconic species in scientific surveys at Ningaloo and in combination with qualitative observations of B. muricatum by expert witnesses, indicate B. muricatum is likely to have been present in ecologically relevant densities since 2006. The densities of B. muricatum observed at northern Ningaloo in 2021 suggest this species is removing an estimated 13.42 tonnes/ha or 1.34 kg/m2 of calcium carbonate per year, which is broadly comparable with estimates of total parrotfish bioerosion across many reefs in the central Indian and Pacific Oceans. Although not currently afforded elevated conservation status within management plans, B. muricatum possess many life-history characteristics that make them vulnerable to overfishing and may justify consideration for increased protection within the world heritage listed Ningaloo Reef Marine Park

Potential prognostic marker ubiquitin carboxyl-terminal hydrolase-L1 does not predict patient survival in non-small cell lung carcinoma

<p>Abstract</p> <p>Background</p> <p>Ubiquitin Carboxyl-Terminal Hydrolase-L1 (UCH-L1) is a deubiquitinating enzyme that is highly expressed throughout the central and peripheral nervous system and in cells of the diffuse neuroendocrine system. Aberrant function of UCH-L1 has been associated with neurological disorders such as Parkinson's disease and Alzheimer's disease. Moreover, UCH-L1 exhibits a variable expression pattern in cancer, acting either as a tumour suppressor or promoter, depending on the type of cancer. In non-small cell lung carcinoma primary tumour samples, UCH-L1 is highly expressed and is associated with an advanced tumour stage. This suggests UCH-L1 may be involved in oncogenic transformation and tumour invasion in NSCLC. However, the functional significance of UCH-L1 in the progression of NSCLC is unclear. The aim of this study was to investigate the role of UCH-L1 using NSCLC cell line models and to determine if it is clinically relevant as a prognostic marker for advanced stage disease.</p> <p>Methods</p> <p>UCH-L1 expression in NSCLC cell lines H838 and H157 was modulated by siRNA-knockdown, and the phenotypic changes were assessed by flow cytometry, haematoxylin & eosin (H&E) staining and poly (ADP-ribose) polymerase (PARP) cleavage. Metastatic potential was measured by the presence of phosphorylated myosin light chain (MLC2). Tumour microarrays were examined immunohistochemically for UCH-L1 expression. Kaplan-Meier curves were generated using UCH-L1 expression levels and patient survival data extracted from Gene Expression Omnibus data files.</p> <p>Results</p> <p>Expression of UCH-L1 was decreased by siRNA in both cell lines, resulting in increased cell death in H838 adenocarcinoma cells but not in the H157 squamous cell line. However, metastatic potential was reduced in H157 cells. Immunohistochemical staining of UCH-L1 in patient tumours confirmed it was preferentially expressed in squamous cell carcinoma rather than adenocarcinoma. However the Kaplan-Meier curves generated showed no correlation between UCH-L1 expression levels and patient outcome.</p> <p>Conclusions</p> <p>Although UCH-L1 appears to be involved in carcinogenic processes in NSCLC cell lines, the absence of correlation with patient survival indicates that caution is required in the use of UCH-L1 as a potential prognostic marker for advanced stage and metastasis in lung carcinoma.</p

Coral larval recruitment in north-western Australia predicted by regional and local conditions

Understanding ecological processes that shape contemporary and future communities facilitates knowledge-based environmental management. In marine ecosystems, one of the most important processes is the supply of new recruits into a population. Here, we investigated spatiotemporal variability in coral recruitment at 15 reefs throughout the Dampier Archipelago, north-western Australia between 2015 and 2017 and identified the best environmental predictors for coral recruitment patterns over this period. Large differences in recruitment were observed among years with the average density of recruits increasing by 375% from 0.017 recruits cm−2 in 2015 to 0.059 recruits cm−2 in 2017. Despite differences in recruitment among years, the rank order of coral recruit density among reefs remained similar among years, suggesting that spatial variation in recruitment within the Dampier Archipelago is partly deterministic and predictable. The density of coral recruits was best explained by percent cover of live corals at both local (within 5 m) and meso-scales (within 15 km), water turbidity and an oceanographic model that predicted larval dispersal. The highest density of coral recruits (~0.13 recruits cm−2 or 37 recruits per tile) occurred on reefs within sub-regions (15 km) with greater than 35% coral cover, low to moderate turbidity (KD490 < 0.2) and moderate to high modelled predictions of larval dispersal. Our results demonstrate that broad-scale larval dispersal models, when combined with local metrics of percent hard coral cover and water turbidity, can reliably predict the relative abundance of coral recruits over large geographical areas and thus can identify hotspots of recruit abundance and potential recovery following environmental disturbances; information that is essential for effective management of coral reefs

Lynn Chamber Music Competition 2018

Judges Alfred Gratta Jared Hauser Kevin Robert Orr Winners (New York Prize) The Amadeus Duo: Askar Salimdjanov (violin) and Feruza Dadabaeva (piano) A Fowl Sound: Jon Antisz (clarinet), Melanie Riordan (violin), Michael Puryear (cello), and Kristine Mezines (piano) Winners Concert on May 2, 2019 at Kosciuszko Foundation Winners (Delray Prize) The Peña-Akromova Duo: Jannina Eliana G. Peña (piano) and Robiyakhon Akromova (piano) La Mer Trio: David Brill (violin), Sonya Nanos (cello), and Jiawei Yuan (piano) Winners Concert at St. Paul\u27s Episcopal Church in Delray Beach, FL o La Mer Trio: David Brill (violin), Sonya Nanos (cello), and Jiawei Yuan (piano)https://spiral.lynn.edu/conservatory_chamber-music-competition/1003/thumbnail.jp

Variation in Sexual Behaviors in a Cohort of Adolescent Females: The Role of Personal, Perceived Peer, and Perceived Family Attitudes

Little is known about how adolescent sexual behaviors develop and the influence of personal or perceived social attitudes. We sought to describe how personal, perceived peer and perceived family attitudes towards adolescent sexual activity influences adolescent females’ sexual behaviors over time

Deletion at ITPR1 Underlies Ataxia in Mice and Spinocerebellar Ataxia 15 in Humans

We observed a severe autosomal recessive movement disorder in mice used within our laboratory. We pursued a series of experiments to define the genetic lesion underlying this disorder and to identify a cognate disease in humans with mutation at the same locus. Through linkage and sequence analysis we show here that this disorder is caused by a homozygous in-frame 18-bp deletion in Itpr1 (Itpr1Δ18/Δ18), encoding inositol 1,4,5-triphosphate receptor 1. A previously reported spontaneous Itpr1 mutation in mice causes a phenotype identical to that observed here. In both models in-frame deletion within Itpr1 leads to a decrease in the normally high level of Itpr1 expression in cerebellar Purkinje cells. Spinocerebellar ataxia 15 (SCA15), a human autosomal dominant disorder, maps to the genomic region containing ITPR1; however, to date no causal mutations had been identified. Because ataxia is a prominent feature in Itpr1 mutant mice, we performed a series of experiments to test the hypothesis that mutation at ITPR1 may be the cause of SCA15. We show here that heterozygous deletion of the 5′ part of the ITPR1 gene, encompassing exons 1–10, 1–40, and 1–44 in three studied families, underlies SCA15 in humans

The Access Technology Program of the Indiana Clinical Translational Sciences Institute (CTSI): A model to facilitate access to cutting-edge technologies across a state

Introduction: Access to cutting-edge technologies is essential for investigators to advance translational research. The Indiana Clinical and Translational Sciences Institute (CTSI) spans three major and preeminent universities, four large academic campuses across the state of Indiana, and is mandate to provide best practices to a whole state. Methods: To address the need to facilitate the availability of innovative technologies to its investigators, the Indiana CTSI implemented the Access Technology Program (ATP). The activities of the ATP, or any program of the Indiana CTSI, are challenged to connect technologies and investigators on the multiple Indiana CTSI campuses by the geographical distances between campuses (1–4 hr driving time). Results: Herein, we describe the initiatives developed by the ATP to increase the availability of state-of-the-art technologies to its investigators on all Indiana CTSI campuses, and the methods developed by the ATP to bridge the distance between campuses, technologies, and investigators for the advancement of clinical translational research. Conclusions: The methods and practices described in this publication may inform other approaches to enhance translational research, dissemination, and usage of innovative technologies by translational investigators, especially when distance or multi-campus cultural differences are factors to efficient application

Disrupting LIN28 in atypical teratoid rhabdoid tumors reveals the importance of the mitogen activated protein kinase pathway as a therapeutic target

Atypical teratoid rhabdoid tumor (AT/RT) is among the most fatal of all pediatric brain tumors. Aside from loss of function mutations in the SMARCB1 (BAF47/INI1/SNF5) chromatin remodeling gene, little is known of other molecular drivers of AT/RT. LIN28A and LIN28B are stem cell factors that regulate thousands of RNAs and are expressed in aggressive cancers. We identified high-levels of LIN28A and LIN28B in AT/RT primary tumors and cell lines, with corresponding low levels of the LIN28-regulated microRNAs of the let-7 family. Knockdown of LIN28A by lentiviral shRNA in the AT/RT cell lines CHLA-06-ATRT and BT37 inhibited growth, cell proliferation and colony formation and induced apoptosis. Suppression of LIN28A in orthotopic xenograft models led to a more than doubling of median survival compared to empty vector controls (48 vs 115 days). LIN28A knockdown led to increased expression of let-7b and let-7g microRNAs and a down-regulation of KRAS mRNA. AT/RT primary tumors expressed increased mitogen activated protein (MAP) kinase pathway activity, and the MEK inhibitor selumetinib (AZD6244) decreased AT/RT growth and increased apoptosis. These data implicate LIN28/RAS/MAP kinase as key drivers of AT/RT tumorigenesis and indicate that targeting this pathway may be a therapeutic option in this aggressive pediatric malignancy