Building living systematic reviews and reporting standards for comparative microscopic analysis of white diseases in hard corals.

Over the last 4 decades, coral disease research has continued to provide reports of diseases, the occurrence and severity of disease outbreaks and associated disease signs. Histology using systematic protocols is a gold standard for the microscopic assessment of diseases in veterinary and medical research, while also providing valuable information on host condition. However, uptake of histological analysis for coral disease remains limited. Increasing disease outbreaks on coral reefs as human impacts intensify highlights a need to understand the use of histology to date in coral disease research. Here, we apply a systematic approach to collating, mapping and reviewing histological methods used to study coral diseases with 'white' signs (i.e., white diseases) in hard coral taxa and map research effort in this field spanning study design, sample processing and analysis in the 33 publications identified between 1984 and 2022. We find that studies to date have not uniformly detailed methodologies, and terminology associated with reporting and disease description is inconsistent between studies. Combined these limitations reduce study repeatability, limiting the capacity for researchers to compare disease reports. A primary outcome of this study is the provision of transparent and repeatable protocols for systematically reviewing literature associated with white diseases of hard coral taxa, and development of recommendations for standardised reporting procedures with the aim of increasing uptake of histology in addition to allowing for ongoing comparative analysis through living systematic reviews for the coral disease field.

Localising terrestrially derived pollution inputs to threatened near-shore coral reefs through stable isotope, water quality and oceanographic analysis.

Near-shore coral reefs are at high-risk of exposure to pollution from terrestrial activities. Pollution impacts can vary with site-specific factors that span sources, rainfall and oceanographic characteristics. To effectively manage pollution, we need to understand how these factors interact. In this study, we detect terrestrially derived nutrient inputs on near-shore reefs at Norfolk Island, South Pacific by analysis of dissolved inorganic nitrogen (DIN) and stable isotopes. When compared to a reef site with predominantly oceanic inputs, we found that both the lagoon and a small reef adjacent to a catchment have signatures of human-derived DIN shown through depleted δ15N signatures in macroalgae. We find pollution exposure of reef sites is associated with known and unknown sources, rainfall and mixing of water with the open ocean. In characterising exposure of reef sites we highlight the role of site-specific context in influencing pollution exposure for benthic communities even in remote island systems.

High flow conditions mediate damaging impacts of sub-lethal thermal stress on corals' endosymbiotic algae.

The effects of thermal anomalies on tropical coral endosymbiosis can be mediated by a range of environmental factors, which in turn ultimately influence coral health and survival. One such factor is the water flow conditions over coral reefs and corals. Although the physiological benefits of living under high water flow are well known, there remains a lack of conclusive experimental evidence characterizing how flow mitigates thermal stress responses in corals. Here we use in situ measurements of flow in a variety of reef habitats to constrain the importance of flow speeds on the endosymbiosis of an important reef building species under different thermal regimes. Under high flow speeds (0.15 m s-1) and thermal stress, coral endosymbionts retained photosynthetic function and recovery capacity for longer compared to low flow conditions (0.03 m s-1). We hypothesize that this may be due to increased rates of mass transfer of key metabolites under higher flow, putatively allowing corals to maintain photosynthetic efficiency for longer. We also identified a positive interactive effect between high flow and a pre-stress, sub-lethal pulse in temperature. While higher flow may delay the onset of photosynthetic stress, it does not appear to confer long-term protection; sustained exposure to thermal stress (eDHW accumulation equivalent to 4.9°C weeks) eventually overwhelmed the coral meta-organism as evidenced by eventual declines in photo-physiological function and endosymbiont densities. Investigating flow patterns at the scale of metres within the context of these physiological impacts can reveal interesting avenues for coral reef management. This study increases our understanding of the effects of water flow on coral reef health in an era of climate change and highlights the potential to learn from existing beneficial bio-physical interactions for the effective preservation of coral reefs into the future.

Npas4 deficiency interacts with adolescent stress to disrupt prefrontal GABAergic maturation and adult cognitive flexibility.

Healthy cognitive and emotional functioning relies on a balance between excitatory and inhibitory neurotransmission in the prefrontal cortex (PFC). This balance is largely established during early postnatal and adolescent developmental periods by maturation of the γ-aminobutyric acid (GABA) system, including increased density of parvalbumin (PV) cells and perineuronal nets (PNNs). Genetic and/or environmental factors during adolescence can disrupt GABAergic maturation and lead to behavioral dysfunction in adulthood. The present study examined the interaction between chronic mild stress during adolescence and genetic deficiency of neuronal Per-Arnt-Sim domain 4 (Npas4), a brain-specific transcription factor that regulates inhibitory neurotransmission and that contributes to adolescent prefrontal GABAergic maturation. Male Npas4 wild-type (WT) and heterozygous (HET) mice were exposed to adolescent chronic stress and tested in adulthood for cognitive function using the attention set shifting task. When Npas4 deficiency was combined with adolescent stress, mice displayed impaired cognitive flexibility as observed by poor performance on the extra-dimensional set shift task. At the cellular level, adolescent stress increased the percentage of PV cells surrounded by PNNs in the PFC of adult WT animals, an effect that was not observed in HET mice. Additionally, Npas4 deficiency and/or adolescent stress dysregulated expression of certain GABAergic system markers. These results suggest that Npas4 mediates susceptibility to adolescent stress and subsequent cognitive functioning and inhibitory tone in adulthood. This shows a novel gene by environment interaction related to resilience vs vulnerability to stress, with implications for adolescent onset disorders like schizophrenia.

Avalanche deaths in the United States: a 45-year analysis.

OBJECTIVE: To describe the demographic characteristics and patterns of death of persons killed in snow avalanches over a 45-year study period. METHODS: The national avalanche database was the source of data in this retrospective, descriptive study. RESULTS: A total of 440 victims were killed in 324 fatal avalanches, of which 87.7% were fully buried, 4.7% were partially buried, and 7.6% were not buried. The average age was 27.6 +/- 10.6 years, and 87.3% were men. Victims who died included climbers (25.5%), backcountry skiers (22.7%), out-of-bounds skiers (10.0%), snowmobilers (6.8%), in-bounds skiers (5.2%), residents (4.5%), ski patrollers (3.6%), workers (3.6%), and motorists (3.0%). Over the 45-year study period there appear to be decreases in the deaths of in-bounds skiers, highway workers, and motorists. Increasing fatalities were observed among out-of-bounds skiers, snowmobilers, ski patrollers, and backcountry skiers. Most deaths occurred in Colorado (33.0%), Washington (13.2%), and Alaska (12.0%). CONCLUSIONS: Avalanche fatalities have increased over the last 45 years. Climbers, backcountry skiers, out-of-bounds skiers, and more recently snowmobilers constitute the majority of the victims. The decrease in deaths among groups that benefit from avalanche control programs supports the benefit of avalanche prevention strategies. Further study is needed to assess the impact of avalanche safety education for individuals who travel in remote and uncontrolled terrain.

Genetic analysis of three patients with an 18p- syndrome and dystonia.

Some patients with an 18p- syndrome show dystonia, and a focal dystonia gene has been mapped to chromosome 18p. The authors evaluated the extent of the deletion in three patients with an 18p- syndrome and dystonia using 14 DNA markers on 18p. A common deleted area, covering the DYT7 locus, places the putative dystonia gene between the telomere of 18p and D18S1104 (49.6 cM). Dystonia in these patients may be caused by haploinsufficiency of the DYT7 gene, a new dystonia gene on 18p, or may result from developmental brain anomalies.

The TOR1A (DYT1) gene family and its role in early onset torsion dystonia.

Most cases of early onset torsion dystonia are caused by a 3-bp deletion (GAG) in the coding region of the TOR1A gene (alias DYT1, DQ2), resulting in loss of a glutamic acid in the carboxy terminal of the encoded protein, torsin A. TOR1A and its homologue TOR1B (alias DQ1) are located adjacent to each other on human chromosome 9q34. Both genes comprise five similar exons; each gene spans a 10-kb region. Mutational analysis of most of the coding region and splice junctions of TOR1A and TOR1B did not reveal additional mutations in typical early onset cases lacking the GAG deletion (N = 17), in dystonic individuals with apparent homozygosity in the 9q34 chromosomal region (N = 5), or in a representative Ashkenazic Jewish individual with late onset dystonia, who shared a common haplotype in the 9q34 region with other late onset individuals in this ethnic group. A database search revealed a family of nine related genes (50-70% similarity) and their orthologues in species including human, mouse, rat, pig, zebrafish, fruitfly, and nematode. At least four of these genes occur in the human genome. Proteins encoded by this gene family share functional domains with the AAA/HSP/Clp-ATPase superfamily of chaperone-like proteins, but appear to represent a distinct evolutionary branch.

The early-onset torsion dystonia gene (DYT1) encodes an ATP-binding protein.

Early-onset torsion dystonia is a movement disorder, characterized by twisting muscle contractures, that begins in childhood. Symptoms are believed to result from altered neuronal communication in the basal ganglia. This study identifies the DYT1 gene on human chromosome 9q34 as being responsible for this dominant disease. Almost all cases of early-onset dystonia have a unique 3-bp deletion that appears to have arisen idependently in different ethnic populations. This deletion results in loss of one of a pair of glutamic-acid residues in a conserved region of a novel ATP-binding protein, termed torsinA. This protein has homologues in nematode, rat, mouse and humans, with some resemblance to the family of heat-shock proteins and Clp proteases.

False positive results of tests for syphilis and outcome of pregnancy: a retrospective case-control study.

In a retrospective case-control study 64 women yielding a false positive result to a test for syphilis in pregnancy were compared with 128 controls individually matched for age, parity, hospital of delivery, and year of delivery. There were significantly more unsuccessful pregnancies, mainly spontaneous abortions during the first and second trimesters, among women with persistent false positive results. There was no significant difference between groups in the mean birth weights of liveborn infants. The antibodies responsible for the false positive result may indicate the presence of an immunological disturbance. Women who give a false positive result should be carefully managed throughout their pregnancy.