scholarly journals Phylogeographic parallelism: concordance of patterns in closely related species illuminates underlying mechanisms in the historically glaciated Tasmanian landscape

2019 ◽  
Author(s):  
K. Kreger ◽  
B. Shaban ◽  
E. Wapstra ◽  
C.P. Burridge

AbstractPhylogeography provides a means to understand mechanisms that shaped the distribution and abundance of species, including the role of past climate change. While concordant phylogeographic relationships across diverse taxa suggest shared underlying mechanisms (“phylogeographic parallelism”), it is also possible that similar patterns are the product of different mechanisms (“phylogeographic convergence”), reflecting variation among taxa in factors such as environmental tolerances, life histories, and vagility. Hence, phylogeographic concordance among closely related and ecologically similar species can yield a more confident understanding of the past mechanisms which shaped their distribution and abundance. This study documented mitochondrial and nuclear phylogeographic patterns in the ectotherm skink, Niveoscincus metallicus, which occupies historically glaciated regions of Tasmania, and contrasted these with the closely related and broadly sympatric N. ocellatus. Major phylogeographic breaks were similar in location between the two species, and indicative of isolation caused by retreat from high elevation areas during glaciations, but with long-term persistence at multiple low elevation sites. Hence, Pleistocene glacial refugia were altitudinal rather than latitudinal, a pattern mirrored in other temperate Southern Hemisphere taxa. This study also examined phylogeographic patterns across the intermittently inundated Bassian Isthmus between mainland Australia and the island of Tasmania, and revealed that structuring is similarly maintained when populations were physically isolated during interglacial rather than glacial stages.

Biochar ◽  
2021 ◽  
Author(s):  
Qian Yang ◽  
Yongjie Wang ◽  
Huan Zhong

AbstractThe transformation of mercury (Hg) into the more toxic and bioaccumulative form methylmercury (MeHg) in soils and sediments can lead to the biomagnification of MeHg through the food chain, which poses ecological and health risks. In the last decade, biochar application, an in situ remediation technique, has been shown to be effective in mitigating the risks from Hg in soils and sediments. However, uncertainties associated with biochar use and its underlying mechanisms remain. Here, we summarize recent studies on the effects and advantages of biochar amendment related to Hg biogeochemistry and its bioavailability in soils and sediments and systematically analyze the progress made in understanding the underlying mechanisms responsible for reductions in Hg bioaccumulation. The existing literature indicates (1) that biochar application decreases the mobility of inorganic Hg in soils and sediments and (2) that biochar can reduce the bioavailability of MeHg and its accumulation in crops but has a complex effect on net MeHg production. In this review, two main mechanisms, a direct mechanism (e.g., Hg-biochar binding) and an indirect mechanism (e.g., biochar-impacted sulfur cycling and thus Hg-soil binding), that explain the reduction in Hg bioavailability by biochar amendment based on the interactions among biochar, soil and Hg under redox conditions are highlighted. Furthermore, the existing problems with the use of biochar to treat Hg-contaminated soils and sediments, such as the appropriate dose and the long-term effectiveness of biochar, are discussed. Further research involving laboratory tests and field applications is necessary to obtain a mechanistic understanding of the role of biochar in reducing Hg bioavailability in diverse soil types under varying redox conditions and to develop completely green and sustainable biochar-based functional materials for mitigating Hg-related health risks.


2021 ◽  
Vol 10 (15) ◽  
pp. 3441
Author(s):  
Hashir Ali Awan ◽  
Mufaddal Najmuddin Diwan ◽  
Alifiya Aamir ◽  
Muneeza Ali ◽  
Massimo Di Giannantonio ◽  
...  

The second year of the COVID-19 (coronavirus disease) pandemic has seen the need to identify and assess the long-term consequences of a SARS-CoV-2 infection on an individual’s overall wellbeing, including adequate cognitive functioning. ‘Cognitive COVID’ is an informal term coined to interchangeably refer to acute changes in cognition during COVID-19 and/or cognitive sequelae with various deficits following the infection. These may manifest as altered levels of consciousness, encephalopathy-like symptoms, delirium, and loss of various memory domains. Dysexecutive syndrome is a peculiar manifestation of ‘Cognitive COVID’ as well. In the previous major outbreaks of viruses like SARS-CoV, MERS-CoV and Influenza. There have been attempts to understand the underlying mechanisms describing the causality of similar symptoms following SARS-CoV-2 infection. This review, therefore, is attempting to highlight the current understanding of the various direct and indirect mechanisms, focusing on the role of neurotropism of SARS-CoV-2, the general pro-inflammatory state, and the pandemic-associated psychosocial stressors in the causality of ‘Cognitive COVID.’ Neurotropism is associated with various mechanisms including retrograde neuronal transmission via olfactory pathway, a general hematogenous spread, and the virus using immune cells as vectors. The high amounts of inflammation caused by COVID-19, compounded with potential intubation, are associated with a deleterious effect on the cognition as well. Finally, the pandemic’s unique psychosocial impact has raised alarm due to its possible effect on cognition. Furthermore, with surfacing reports of post-COVID-vaccination cognitive impairments after vaccines containing mRNA encoding for spike glycoprotein of SARS-CoV-2, we hypothesize their causality and ways to mitigate the risk. The potential impact on the quality of life of an individual and the fact that even a minor proportion of COVID-19 cases developing cognitive impairment could be a significant burden on already overwhelmed healthcare systems across the world make it vital to gather further evidence regarding the prevalence, presentation, correlations, and causality of these events and reevaluate our approach to accommodate early identification, management, and rehabilitation of patients exhibiting cognitive symptoms.


2017 ◽  
Vol 284 (1855) ◽  
pp. 20170449 ◽  
Author(s):  
Chloe Bracis ◽  
Thomas Mueller

One of the key questions regarding the underlying mechanisms of mammalian land migrations is how animals select where to go. Most studies assume perception of resources as the navigational mechanism. The possible role of memory that would allow forecasting conditions at distant locations and times based on information about environmental conditions from previous years has been little studied. We study migrating zebra in Botswana using an individual-based simulation model, where perceptually guided individuals use currently sensed resources at different perceptual ranges, while memory-guided individuals use long-term averages of past resources to forecast future conditions. We compare simulated individuals guided by perception or memory on resource landscapes of remotely sensed vegetation data to trajectories of GPS-tagged zebras. Our results show that memory provides a clear signal that best directs migrants to their destination compared to perception at even the largest perceptual ranges. Zebras modelled with memory arrived two to four times, or up to 100 km, closer to the migration destination than those using perception. We suggest that memory in addition to perception is important for directing ungulate migration. Furthermore, our findings are important for the conservation of migratory mammals, as memory informing direction suggests migration routes could be relatively inflexible.


2005 ◽  
Vol 11 (4) ◽  
pp. 319-331 ◽  
Author(s):  
Paul D. Krushelnycky ◽  
Stephanie M. Joe ◽  
Arthur C. Medeiros ◽  
Curtis C. Daehler ◽  
Lloyd L. Loope

2020 ◽  
Vol 22 (10) ◽  
Author(s):  
Domenico D’Amario ◽  
Massimiliano Camilli ◽  
Stefano Migliaro ◽  
Francesco Canonico ◽  
Mattia Galli ◽  
...  

Abstract Purpose of Review The aim of this report is to describe the main aspects of sex-related differences in non-ischemic dilated cardiomyopathies (DCM), focusing on chemotherapy-induced heart failure (HF) and investigating the possible therapeutic implications and clinical management applications in the era of personalized medicine. Recent Findings In cardio-oncology, molecular and multimodality imaging studies confirm that sex differences do exist, affecting the therapeutic cardioprotective strategies and, therefore, the long-term outcomes. Interestingly, compelling evidences suggest that sex-specific characteristics in drug toxicity might predict differences in the therapeutic response, most likely due to the tangled interplay between cancer and HF, which probably share common underlying mechanisms. Summary Cardiovascular diseases show many sex-related differences in prevalence, etiology, phenotype expression, and outcomes. Complex molecular mechanisms underlie this diverse pathological manifestations, from sex-determined differential gene expression to sex hormone interaction with their receptors in the heart. Non-ischemic DCM is an umbrella definition that incorporates several etiologies, including chemotherapy-induced cardiomyopathies. The role of sex as a risk factor for cardiotoxicity is poorly explored. However, understanding the various features of disease manifestation and outcomes is of paramount importance for a prompt and tailored evaluation.


2021 ◽  
Vol 23 (1) ◽  
pp. 474
Author(s):  
Ido Ben-Shalom ◽  
Arnon Karni ◽  
Hadar Kolb

The appearance of new disease-modifying therapies in multiple sclerosis (MS) has revolutionized our ability to fight inflammatory relapses and has immensely improved patients’ quality of life. Although remarkable, this achievement has not carried over into reducing long-term disability. In MS, clinical disability progression can continue relentlessly irrespective of acute inflammation. This “silent” disease progression is the main contributor to long-term clinical disability in MS and results from chronic inflammation, neurodegeneration, and repair failure. Investigating silent disease progression and its underlying mechanisms is a challenge. Standard MRI excels in depicting acute inflammation but lacks the pathophysiological lens required for a more targeted exploration of molecular-based processes. Novel modalities that utilize nuclear magnetic resonance’s ability to display in vivo information on imaging look to bridge this gap. Displaying the CNS through a molecular prism is becoming an undeniable reality. This review will focus on “molecular imaging biomarkers” of disease progression, modalities that can harmoniously depict anatomy and pathophysiology, making them attractive candidates to become the first valid biomarkers of neuroprotection and remyelination.


2002 ◽  
Vol 38 (SI 1 - 6th Conf EFPP 2002) ◽  
pp. S145-S150 ◽  
Author(s):  
J.J. Burdon ◽  
P.H. Thrall

The general outcomes of long-term trajectories of coevolutionary interactions between specific hosts and pathogens are<br />set by the interaction of their life histories. However, within those outcomes the speed of co-evolutionary responses and<br />the extent of their expression in the resistance/virulence structure of wild plant and pathogen populations respectively,<br />are highly variable characters changing from place-to-place and time-to-time as a result of the interaction of host and<br />pathogen with the physical environment. As a consequence, understanding of the role of diseases in the evolution of their<br />hosts requires approaches that simultaneously deal with host and pathogen structures over multiple populations within a<br />metapopulation framework.


2021 ◽  
Vol 14 ◽  
Author(s):  
Vipin V. Dhote ◽  
Muthu Kumaradoss Mohan Maruga Raja ◽  
Prem Samundre ◽  
Supriya Sharma ◽  
Shraddha Anwikar ◽  
...  

: Sports deserve a special place in human life to impart healthy and refreshing wellbeing. However, sports activities, especially contact sports, renders athlete vulnerable to brain injuries. Athletes participating in a contact sport like boxing, rugby, American football, wrestling, and basketball are exposed to traumatic brain injuries (TBI) or concussions. The acute and chronic nature of these heterogeneous injuries provides a spectrum of dysfunctions that alters the neuronal, musculoskeletal, and behavioral responses of an athlete. Many sports-related brain injuries go unreported, but these head impacts trigger neurometabolic disruptions that contribute to long-term neuronal impairment. The pathophysiology of post-concussion and its underlying mechanisms are undergoing intense research. It also shed light on chronic disorders like Parkinson's disease, Alzheimer's disease, and dementia. In this review, we examined post-concussion neurobehavioral changes, tools for early detection of signs, and their impact on the athlete. Further, we discussed the role of nutritional supplements in ameliorating neuropsychiatric diseases in athletes.


2009 ◽  
Vol 191 (7) ◽  
pp. 2060-2068 ◽  
Author(s):  
Jessica K. Kajfasz ◽  
Alaina R. Martinez ◽  
Isamar Rivera-Ramos ◽  
Jacqueline Abranches ◽  
Hyun Koo ◽  
...  

ABSTRACT Mutational analysis revealed that members of the Clp system, specifically the ClpL chaperone and the ClpXP proteolytic complex, modulate the expression of important virulence attributes of Streptococcus mutans. Compared to its parent, the ΔclpL strain displayed an enhanced capacity to form biofilms in the presence of sucrose, had reduced viability, and was more sensitive to acid killing. The ΔclpP and ΔclpX strains displayed several phenotypes in common: slow growth, tendency to aggregate in culture, reduced autolysis, and reduced ability to grow under stress, including acidic pH. Unexpectedly, the ΔclpP and ΔclpX mutants were more resistant to acid killing and demonstrated enhanced viability in long-term survival assays. Biofilm formation by the ΔclpP and ΔclpX strains was impaired when grown in glucose but enhanced in sucrose. In an animal study, the average number of S. mutans colonies recovered from the teeth of rats infected with the ΔclpP or ΔclpX strain was slightly lower than that of the parent strain. In Bacillus subtilis, the accumulation of the Spx global regulator, a substrate of ClpXP, has accounted for the ΔclpXP phenotypes. Searching the S. mutans genome, we identified two putative spx genes, designated spxA and spxB. The inactivation of either of these genes bypassed phenotypes of the clpP and clpX mutants. Western blotting demonstrated that Spx accumulates in the ΔclpP and ΔclpX strains. Our results reveal that the proteolysis of ClpL and ClpXP plays a role in the expression of key virulence traits of S. mutans and indicates that the underlying mechanisms by which ClpXP affect virulence traits are associated with the accumulation of two Spx orthologues.


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