Examining the profound effects of COVID19 on mental health: A comprehensive systematic review on anxiety and depression

The COVID-19 pandemic has presented challenges to humanity, economically and in health and wellbeing. The associated limited social isolation and lifestyle changes has increased the risk for mental health services, especially among vulnerable people. This highlights the need for mental health services, burden that already stretch the health systems. This review presents an exposition on COVID-19 and mental health, and ways to minimise, and possibly prevent, their effect on the psychological well-being of those people. We searched four databases (Academic Search Complete, CINAHL Plus, PsycINFO and PsycARTICLES) using specific search terms and eligibility criteria. Of the 33 included studies, 31 were quantitative, and one qualitative and mixed method each. The studies were analysed using thematic narrative synthesis that resulted in three main themes: (a) the internal and external influences on COVID-19 behaviour, (b) the impact of COVID-19 on health and well-being and (c) the coping strategies used. Since COVID-19 will exist for the foreseeable future, understanding its impact on health and mental well-being and the coping techniques to be adopted are important now than ever. This study contributes to such an understanding along with suggestions regarding ways to minimise the impact of COVID-19 on mental health using context-appropriate strategies

Development and Characterization of Thirteen Microsatellite Markers for the Longbill Spearfish (Tetrapturus pfluegeri)

The longbill spearfish (Tetrapturus pfluegeri; Istiophoridae) is an epipelagic billfish species broadly distributed in the Atlantic Ocean and exploited by multinational fisheries. No data exist on the population structure or genetic diversity of this apex predator, despite a strong need for this information to inform international conservation and management efforts. Thirteen microsatellite loci, comprising mostly tri- and tetra-nucleotide repeats, were isolated and characterized for this species by genotyping individuals (n = 29–42) obtained from western North and South Atlantic fisheries. The average number of alleles ranged from 3 to 16 and the expected heterozygosity ranged from 0.35 to 0.86. This suite of markers provides the first population genetic nuclear resources for the longbill spearfish, allowing initiation of studies for assessing the population structure and demography of this poorly understood species

Genetic and Biophysical Modelling Evidence of Generational Connectivity in the Intensively Exploited, Western North Atlantic Red Grouper (Epinephelus morio)

Understanding the connectivity of reef organisms is important to assist in the conservation of biological diversity and to facilitate sustainable fisheries in these ecosystems. Common methods to assess reef connectivity include both population genetics and biophysical modelling. Individually, these techniques can offer insight into population structure; however, the information acquired by any singular analysis is often subject to limitations, underscoring the need for a multi-faceted approach. To assess the connectivity dynamics of the red grouper (Epinephelus morio), an economically important reef fish species found throughout the Gulf of Mexico and USA western Atlantic, we utilized two sets of genetic markers (12 microsatellite loci and 632 single nucleotide polymorphisms) to resolve this species’ population genetic structure, along with biophysical modelling to deliver a spatial forecast of potential larval “sources” and “sinks” across these same regions and spatial scale. Our genetic survey indicates little, if any, evidence of population genetic structure and modelling efforts indicate the potential for ecological connectivity between sampled regions over multiple generations. We offer that using a dual empirical and theoretical approach lessens the error associated with the use of any single method and provides an important step towards the validation of either of these methodologies

High-Performance Capillary Electrophoresis for Determining HIV-1 Tat Protein in Neurons

The HIV-1 protein, Tat has been implicated in AIDS pathogenesis however, the amount of circulating Tat is believed to be very low and its quantification has been difficult. We performed the quantification of Tat released from infected cells and taken up by neurons using high performance capillary electrophoresis. This is the first report to successfully measure the amount of Tat in neurons and places Tat as a key player involved in HIV-associated neurocognitive disorders

Tourism, inclusive growth and decent work: a political economy critique

This paper interrogates the ideas of ‘sustained’ and ‘inclusive’ growth that are intrinsic to one of three UN Sustainable Development Goals (SDG 8 - Decent Work and Growth) adopted by the UN World Tourism Organisation’s (UNWTO) 2030 sustainable tourism agenda. It provides a Marxian-inspired political economy critique of the UNWTO’s embrace of SDG8 and highlights the blind spot within the UNWTO’s inclusive growth-led SDG agenda with respect to questions of equity and social justice. The paper contends that the UNWTO’s SDG-led agenda is contradicted by the logics of growth, competitiveness and profit-making that drive the continued expansion and development of tourism. Rather than addressing the structural injustices that entrench inequalities and reproduce exploitative labour practices, the notion of sustained and inclusive growth reinforces the primacy of capital and market notions of justice and continues to perpetuate a growth driven tourism development model. The paper contributes to a critical theorization of sustainable tourism and offers an informed critique of the current political agenda for sustainable tourism and its potential outcomes

Convergence of marine megafauna movement patterns in coastal and open oceans

The extent of increasing anthropogenic impacts on large marine vertebrates partly depends on the animals’ movement patterns. Effective conservation requires identification of the key drivers of movement including intrinsic properties and extrinsic constraints associated with the dynamic nature of the environments the animals inhabit. However, the relative importance of intrinsic versus extrinsic factors remains elusive. We analyze a global dataset of ∼2.8 million locations from >2,600 tracked individuals across 50 marine vertebrates evolutionarily separated by millions of years and using different locomotion modes (fly, swim, walk/paddle). Strikingly, movement patterns show a remarkable convergence, being strongly conserved across species and independent of body length and mass, despite these traits ranging over 10 orders of magnitude among the species studied. This represents a fundamental difference between marine and terrestrial vertebrates not previously identified, likely linked to the reduced costs of locomotion in water. Movement patterns were primarily explained by the interaction between species-specific traits and the habitat(s) they move through, resulting in complex movement patterns when moving close to coasts compared with more predictable patterns when moving in open oceans. This distinct difference may be associated with greater complexity within coastal microhabitats, highlighting a critical role of preferred habitat in shaping marine vertebrate global movements. Efforts to develop understanding of the characteristics of vertebrate movement should consider the habitat(s) through which they move to identify how movement patterns will alter with forecasted severe ocean changes, such as reduced Arctic sea ice cover, sea level rise, and declining oxygen content

Mislocalization of XPF-ERCC1 Nuclease Contributes to Reduced DNA Repair in XP-F Patients

Xeroderma pigmentosum (XP) is caused by defects in the nucleotide excision repair (NER) pathway. NER removes helix-distorting DNA lesions, such as UV–induced photodimers, from the genome. Patients suffering from XP exhibit exquisite sun sensitivity, high incidence of skin cancer, and in some cases neurodegeneration. The severity of XP varies tremendously depending upon which NER gene is mutated and how severely the mutation affects DNA repair capacity. XPF-ERCC1 is a structure-specific endonuclease essential for incising the damaged strand of DNA in NER. Missense mutations in XPF can result not only in XP, but also XPF-ERCC1 (XFE) progeroid syndrome, a disease of accelerated aging. In an attempt to determine how mutations in XPF can lead to such diverse symptoms, the effects of a progeria-causing mutation (XPFR153P) were compared to an XP–causing mutation (XPFR799W) in vitro and in vivo. Recombinant XPF harboring either mutation was purified in a complex with ERCC1 and tested for its ability to incise a stem-loop structure in vitro. Both mutant complexes nicked the substrate indicating that neither mutation obviates catalytic activity of the nuclease. Surprisingly, differential immunostaining and fractionation of cells from an XFE progeroid patient revealed that XPF-ERCC1 is abundant in the cytoplasm. This was confirmed by fluorescent detection of XPFR153P-YFP expressed in Xpf mutant cells. In addition, microinjection of XPFR153P-ERCC1 into the nucleus of XPF–deficient human cells restored nucleotide excision repair of UV–induced DNA damage. Intriguingly, in all XPF mutant cell lines examined, XPF-ERCC1 was detected in the cytoplasm of a fraction of cells. This demonstrates that at least part of the DNA repair defect and symptoms associated with mutations in XPF are due to mislocalization of XPF-ERCC1 into the cytoplasm of cells, likely due to protein misfolding. Analysis of these patient cells therefore reveals a novel mechanism to potentially regulate a cell's capacity for DNA repair: by manipulating nuclear localization of XPF-ERCC1

The Epistatic Relationship between BRCA2 and the Other RAD51 Mediators in Homologous Recombination

RAD51 recombinase polymerizes at the site of double-strand breaks (DSBs) where it performs DSB repair. The loss of RAD51 causes extensive chromosomal breaks, leading to apoptosis. The polymerization of RAD51 is regulated by a number of RAD51 mediators, such as BRCA1, BRCA2, RAD52, SFR1, SWS1, and the five RAD51 paralogs, including XRCC3. We here show that brca2-null mutant cells were able to proliferate, indicating that RAD51 can perform DSB repair in the absence of BRCA2. We disrupted the BRCA1, RAD52, SFR1, SWS1, and XRCC3 genes in the brca2-null cells. All the resulting double-mutant cells displayed a phenotype that was very similar to that of the brca2-null cells. We suggest that BRCA2 might thus serve as a platform to recruit various RAD51 mediators at the appropriate position at the DNA–damage site

Rad51 Inhibits Translocation Formation by Non-Conservative Homologous Recombination in Saccharomyces cerevisiae

Chromosomal translocations are a primary biological response to ionizing radiation (IR) exposure, and are likely to result from the inappropriate repair of the DNA double-strand breaks (DSBs) that are created. An abundance of repetitive sequences in eukaryotic genomes provides ample opportunity for such breaks to be repaired by homologous recombination (HR) between non-allelic repeats. Interestingly, in the budding yeast, Saccharomyces cerevisiae the central strand exchange protein, Rad51 that is required for DSB repair by gene conversion between unlinked repeats that conserves genomic structure also suppresses translocation formation by several HR mechanisms. In particular, Rad51 suppresses translocation formation by single-strand annealing (SSA), perhaps the most efficient mechanism for translocation formation by HR in both yeast and mammalian cells. Further, the enhanced translocation formation that emerges in the absence of Rad51 displays a distinct pattern of genetic control, suggesting that this occurs by a separate mechanism. Since hypomorphic mutations in RAD51 in mammalian cells also reduce DSB repair by conservative gene conversion and stimulate non-conservative repair by SSA, this mechanism may also operate in humans and, perhaps contribute to the genome instability that propels the development of cancer