Ground-truthing daily and lunar patterns of coral reef fish call rates on a US Virgin Island reef

© The Author(s), 2022. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Ferguson, S., Jensen, F., Hyer, M., Noble, A., Apprill, A., & Mooney, T. Ground-truthing daily and lunar patterns of coral reef fish call rates on a US Virgin Island reef. Aquatic Biology, 31, (2022): 77–87, https://doi.org/10.3354/ab00755.Coral reefs comprise some of the most biodiverse habitats on the planet. These ecosystems face a range of stressors, making quantifying community assemblages and potential changes vital to effective management. To understand short- and long-term changes in biodiversity and detect early warning signals of decline, new methods for quantifying biodiversity at scale are necessary. Acoustic monitoring techniques have proven useful in observing species activities and biodiversity on coral reefs through aggregate approaches (i.e. energy as a proxy). However, few studies have ground-truthed these acoustic analyses with human-based observations. In this study, we sought to expand these passive acoustic methods by investigating biological sounds and fish call rates on a healthy reef, providing a unique set of human-confirmed, labeled acoustic observations. We analyzed acoustic data from Tektite Reef, St. John, US Virgin Islands, over a 2 mo period. A subset of acoustic files was manually inspected to identify recurring biotic sounds and quantify reef activity throughout the day. We found a high variety of acoustic signals in this soundscape. General patterns of call rates across time conformed to expectations, with dusk and dawn showing important and significantly elevated peaks in soniferous fish activity. The data reflected high variability in call rates across days and lunar phases. Call rates did not correspond to sound pressure levels, suggesting that certain call types may drive crepuscular trends in sound levels while lower-level critical calls, likely key for estimating biodiversity and behavior, may be missed by gross sound level analyses.This research was funded by the National Science Foundation Biological Oceanography award 1536782. The experiments were conducted under National Park Service Scientific Research and Collecting Permits VIIS-2016-SCI-0017-20, and we thank the Park staff for their support

RNA expression profiling in brains of familial hemiplegic migraine type 1 knock-in mice

Background Various CACNA1A missense mutations cause familial hemiplegic migraine type 1 (FHM1), a rare monogenic subtype of migraine with aura. FHM1 mutation R192Q is associated with pure hemiplegic migraine, whereas the S218L mutation causes hemiplegic migraine, cerebellar ataxia, seizures, and mild head trauma-induced brain edema. Transgenic knock-in (KI) migraine mouse models were generated that carried either the FHM1 R192Q or the S218L mutation and were shown to exhibit increased CaV2.1 channel activity. Here we investigated their cerebellar and caudal cortical transcriptome. Methods Caudal cortical and cerebellar RNA expression profiles from mutant and wild-type mice were studied using microarrays. Respective brain regions were selected based on their relevance to migraine aura and ataxia. Relevant expression changes were further investigated at RNA and protein level by quantitative polymerase chain reaction (qPCR) and/or immunohistochemistry, respectively. Results Expression differences in the cerebellum were most pronounced in S218L mice. Particularly, tyrosine hydroxylase, a marker of delayed cerebellar maturation, appeared strongly upregulated in S218L cerebella. In contrast, only minimal expression differences were observed in the caudal cortex of either mutant mice strain. Conclusion Despite pronounced consequences of migraine gene mutations at the neurobiological level, changes in cortical RNA expression in FHM1 migraine mice compared to wild-type are modest. In contrast, pronounced RNA expression changes are seen in the cerebellum of S218L mice and may explain their cerebellar ataxia phenotyp

High levels of dietary stearate promote adiposity and deteriorate hepatic insulin sensitivity

<p>Abstract</p> <p>Background</p> <p>Relatively little is known about the role of specific saturated fatty acids in the development of high fat diet induced obesity and insulin resistance. Here, we have studied the effect of stearate in high fat diets (45% energy as fat) on whole body energy metabolism and tissue specific insulin sensitivity.</p> <p>Methods</p> <p>C57Bl/6 mice were fed a low stearate diet based on palm oil or one of two stearate rich diets, one diet based on lard and one diet based on palm oil supplemented with tristearin (to the stearate level of the lard based diet), for a period of 5 weeks. <it>Ad libitum </it>fed Oxidative metabolism was assessed by indirect calorimetry at week 5. Changes in body mass and composition was assessed by DEXA scan analysis. Tissue specific insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp analysis and Western blot at the end of week 5.</p> <p>Results</p> <p>Indirect calorimetry analysis revealed that high levels of dietary stearate resulted in lower caloric energy expenditure characterized by lower oxidation of fatty acids. In agreement with this metabolic phenotype, mice on the stearate rich diets gained more adipose tissue mass. Whole body and tissue specific insulin sensitivity was assessed by hyperinsulinemic-euglycemic clamp and analysis of insulin induced PKB^ser473phosphorylation. Whole body insulin sensitivity was decreased by all high fat diets. However, while insulin-stimulated glucose uptake by peripheral tissues was impaired by all high fat diets, hepatic insulin sensitivity was affected only by the stearate rich diets. This tissue-specific pattern of reduced insulin sensitivity was confirmed by similar impairment in insulin-induced phosphorylation of PKB^ser473in both liver and skeletal muscle.</p> <p>Conclusion</p> <p>In C57Bl/6 mice, 5 weeks of a high fat diet rich in stearate induces a metabolic state favoring low oxidative metabolism, increased adiposity and whole body insulin resistance characterized by severe hepatic insulin resistance. These results indicate that dietary fatty acid composition <it>per sé </it>rather than dietary fat content determines insulin sensitivity in liver of high fat fed C57Bl/6 mice.</p

The human amylase-encoding genes amy2 and amy3 are identical to AMY2A and AMY2B

Inspetion of the published nucleotide sequences reveals that the human amylase-encoding genes, amy2 and amy3, must be identical to the genes AMY2A and AMY2B, respectively.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/27629/1/0000005.pd

Purkinje cell-specific ablation of CaV2.1 Channels is sufficient to cause cerebellar ataxia in mice

The Cacna1a gene encodes the α1A subunit of voltage-gated CaV2.1 Ca2+ channels that are involved in neurotransmission at central synapses. CaV2.1-α1- knockout (α1KO) mice, which lack CaV2.1 channels in all neurons, have a very severe phenotype of cerebellar ataxia and dystonia, and usually die around postnatal day 20. This early lethality, combined with the wide expression of CaV2.1 channels throughout the cerebellar cortex and nuclei, prohibited determination of the contribution of particular cerebellar cell types to the development of the severe neurobiological phenotype in Cacna1a mutant mice. Here, we crossed conditional Cacna1a mice with transgenic mice expressing Cre recombinase, driven by the Purkinje cell-specific Pcp2 promoter, to specifically ablate the CaV2.1- α1A subunit and thereby CaV2.1 channels in Purkinje cells. Purkinje cell CaV2.1-α1A-knockout (PCα1KO) mice aged without difficulties, rescuing the lethal phenotype seen in α1KO mice. PCα1KO mice exhibited cerebellar ataxia starting around P12, much earlier than the first signs of progressive Purkinje cell loss, which appears in these mice between P30 and P45. Secondary cell loss was observed in the granular and molecular layers of the cerebellum and the volume of all individual cerebellar nuclei was reduced. In this mouse model with a cell type-specific ablation of CaV2.1 channels, we show that ablation of CaV2.1 channels restricted to Purkinje cells is sufficient to cause cerebellar ataxia. We demonstrate that spatial ablation of CaV2.1 channels may help in unraveling mechanisms of human disease

Familial hemiplegic migraine locus on 19p13 is involved in the common forms of migraine with and without aura

Migraine is a common neurological disease of two main types: migraine with aura and migraine without aura. Familial clustering suggests that genetic factors are involved in the etiology of migraine. Recently, a gene for familial hemiplegic migraine, a rare autosomal dominant subtype of migraine with aura, was mapped to chromosome 19p13. We tested the involvement of this chromosomal region in 28 unrelated families with the common forms of migraine with and without aura, by following the transmission of the highly informative marker D19S394. Sibpair analysis showed that affected sibs shared the same marker allele more frequently than expected by chance. Our findings thus also suggest the involvement of a gene on 19p13 in the etiology of the common forms of migraine