Biology subjects

Parker, M.

Publications and source records attributed to Parker, M..

17 recordsLinked to original sources

bioRxiv2026

Designing Well-Organized Touch-Spun 3D Scaffolds: The Role of Interfiber Spacing in Cell Proliferation

Three groups of touch-spun 3D scaffolds with uniform fiber diameters and varying interfiber spacing were studied to identify optimal conditions for NIH/3T3-GFP fibroblast growth. All scaffold groups exhibited higher cell viability relative to control levels after 14 days of culture, with the highest viability observed for scaffolds with a 50.61 {+/-} 15.35 m interfiber spacing. Although cell counts indicated comparable cell growth across groups, scaffolds with medium and large interfiber spacing demonstrated an improved capacity to sustain viable cells without necrotic core formation. These findings provide insight into the optimal structural design of touch-spun 3D scaffolds for tissue engineering applications.

bioengineering↗

bioRxiv2025

A Novel Prognostic Metric Resolves the MYCN enigma in Silico and Points to a Biosynthetic Regulatory Shift Driven by MYCN Amplification in Neuroblastoma

Neuroblastoma (NB) is the most common extra-cranial solid tumour in children. Although MYCN amplification is typically indicative of a poor prognosis, the expression level of MYCN has a non-monotonic relationship with the clinical outcome. This paper proposes an explanation for this phenomenon, which is called the MYCN enigma in the literature. The p53/MYCN metric, which is a measure of the p53 protein level relative to the MYCN protein level in a NB tumour, is the key concept. Our hypothesis is that the metric has a positive relationship with the outcome of a patient. It is presented as a binary classification system, where the prognosis is favourable when p53/MYCN>3.5. The mathematical model presented in this paper describes the dynamics between MYCN, p53, ARF, and MDM2; their genes; and their mRNA transcripts. Simulations were carried out by solving the model numerically in a series of initial value problems. The results are aligned with a list of clinical and experimental observations. We extracted association rules with the Apriori algorithm and explored the parametric space stochastically. Assuming that MYCN enables biogenesis in NB tumours, our results support the prediction that MYCN amplification shifts the balance towards producing MYCN. When a wild-type tumour is deficient in MYCN, stress responses may restore biogenesis in general and preferentially produce MYCN in a negative feedback loop. Another prediction is that MYCN - amplified tumours, without treatment, require hard-to-attain biosynthetic rates and stress responses to achieve good outcomes.

systems biology↗

bioRxiv2025

Mechanistic insights and clinical implications of cross-reactive anti-prophage antibodies and bacterial heteroresistance on phage therapeutic failure

Phage therapy is an exciting strategy against antimicrobial-resistant bacterial infections, but critical knowledge gaps regarding its clinical application persist. Studying a patient with a life-threatening, chronic bacterial infection who failed phage therapy, we uncovered important biological concepts with direct translational impact. Using longitudinal clinical samples, we found that patients can harbour pre-existing antibodies against active prophages induced from the genome of the causative pathogen. Notably, these antibodies can contribute to clinical failure by cross-reacting with and effectively neutralising therapeutic phage. We also uncovered bacterial heteroresistance, characterised by bacterial subpopulations from the initial infection with reduced phage susceptibility, as a further contributor to treatment failure. These findings highlight the intricate interplay between host immunology, bacterial genetic diversity and phage biology, bearing broad significance for clinical phage therapy. Future phage therapy patients, especially those with chronic infections, should be screened for antiphage immunity and bacterial heteroresistance prior to phage treatment.

microbiology↗

bioRxiv2025

Genomic and morphological characterisation of a novel iridovirus, bivalve iridovirus 1 (BiIV1), infecting the common cockle (Cerastoderma edule)

1High rates of mortality of the common cockle, Cerastoderma edule, have occurred in the Wash Estuary, UK since 2008. A previous study linked the mortalities to a novel genotype of Marteilia cocosarum, with a strong correlation between cockle moribundity and the presence of M. cocosarum. Here, we characterise a novel iridovirus, identified by chance during metagenomic sequencing of a gradient purification of Marteilia cells, with presence also correlated to cockle moribundity. The novel 179,695 bp iridovirus, bivalve iridovirus 1 (BiIV1), encodes 193 predicted open reading frames and has a 41% G+C content. BiIV1 clusters together with other aquatic invertebrate iridoviruses in phylogenetic analyses and has a similar genome size to other invertebrate iridoviruses. Comparative analysis revealed that BiIV1 has lost three genes that were previously thought to be common amongst all iridoviruses but has also gained genes, potentially from horizontal transfer from its bivalve mollusc host(s). Electron microscopy showed 158 nm icosahedral virions present in the haemocytes of cockles, typical of those observed in host tissues infected with viruses of the family Iridoviridae. Prevalence of BiIV1 in moribund cockles was higher than that in apparently healthy cockles at most sites in the Wash Estuary, with up to 100% PCR prevalence in moribund cockles. Our findings provide the first genome for a bivalve-infecting iridovirus and identify a second bivalve-associated iridovirus in publicly available genomic datasets, adding to the knowledge of invertebrate iridovirus genomics and diversity.

molecular biology↗

bioRxiv2025

Disruption of the mRNA m6A writer complex triggers autoimmunity in Arabidopsis

Distinguishing self from non-self is crucial to direct immune responses against pathogens. Unmodified RNAs stimulate human innate immunity, but RNA modifications suppress this response. mRNA m6A modification is essential for Arabidopsis thaliana viability. However, the molecular basis of the impact of mRNA m6A depletion is poorly understood. Here, we show that disruption of the Arabidopsis mRNA m6A writer complex triggers autoimmunity. Most gene expression changes in m6A writer complex vir-1 mutants grown at 17{degrees}C are explained by defence gene activation and are suppressed at 27{degrees}C, consistent with the frequent temperature sensitivity of Arabidopsis immunity. Accordingly, we found enhanced pathogen resistance and increased premature cell death in vir-1 mutants at 17{degrees}C but not 27{degrees}C. Global temperature-sensitive mRNA poly(A) tail length changes accompany these phenotypes. Our results demonstrate that autoimmunity is a major phenotype of mRNA m6A writer complex mutants, with important implications for interpreting the role of this modification. Furthermore, we open the broader question of whether unmodified RNA triggers immune signalling in plants.

plant biology↗

bioRxiv2025

Generation of C9orf72h370 mice, an intron 1 humanised C9orf72 repeat-expansion knock-in model

An autosomal dominant GGGGCC repeat expansion in intron 1 of the C9orf72 gene is the most common genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Here, we set out to engineer a gene targeted mouse model harbouring a pathogenic length humanised C9orf72 repeat expansion allele, in order to model pathological mechanisms in a physiological context. In human disease, pathogenic repeats typically range from the hundreds to thousands of units in length, representing a considerable challenge for cellular and in vivo model generation given the instability of GC rich and repetitive DNA sequences during molecular cloning. To overcome this challenge, we developed new methodology to synthetically and iteratively build pure GGGGCC repeats within a linear vector system, which we then seamlessly and scarlessly embedded within the native human genomic sequence. This created a gene targeting DNA vector for homologous recombination of the human sequence in mouse embryonic stem cells. We used this novel targeting vector to generate a new gene targeted mouse allele, C9orf72h370, that for the first time has mouse C9orf72 intron 1 scarlessly replaced with human intron 1 including a pure (GGGGCC)370 hexanucleotide repeat expansion. We confirm that the mouse model expresses human intron 1-derived RNA and produces dipeptide repeat proteins derived from the GGGGCC repeat expansion. We now provide this model as a new freely available resource for the field. In addition, we demonstrate the utility of our cloning method for engineering diverse repeat expansion sequences for modelling other disorders, such as Fragile X Syndrome.

molecular biology↗

bioRxiv2024

Rhizobacteria inoculation of plants for reducing insect pests: A meta-analysis on insect behaviour and fitness

Microbial communities in the plant rhizosphere--the soil region closely associated with plant roots-- play critical roles in shaping plant growth, defence, fitness, and ecosystem processes. Inoculation of plants with specific rhizobacteria strains has shown promising potential for increasing crop yields. Rhizobacteria can also induce plant defences, resulting in reduced insect growth and reproduction, and can manipulate plant biochemistry to alter insect host-choice and recruit natural enemies of the insects. We present a meta-analysis examining the impact of rhizobacteria inoculation of plants on insect fitness and behaviour. Our findings indicate that rhizobacteria inoculation generally reduces herbivore fitness and host choice behaviours. However, effect sizes varied significantly depending on type of herbivore (chewing versus sucking), plant host, and rhizobacterial species. Bacillus spp. showed stronger effects than the commonly studied Pseudomonas spp. Rhizobacteria notably reduced traits such as host choice, leaf consumption, survival, and reproduction of chewing herbivores, while primarily impacting sucking herbivores by reducing reproduction. Single-strain inoculants tended to perform better, especially for sucking herbivores, suggesting potential strain incompatibility issues with multi-strain inoculants. Furthermore, field trials showed less impact on insect fitness reduction compared to experiments under controlled conditions, possibly due to soil diversity and environmental factors affecting inoculant persistence. Despite, very limited experimental data, studies observed that rhizobacteria inoculation of plants can attract parasitoid wasps and predators to the plants. These results underscore the need for considering broader environmental interactions when developing effective rhizobacteria-based pest management strategies. Understanding specific and generalist rhizosphere interactions can aid in developing synthetic microbial communities with broad protective functions across various plants and environments.

ecology↗

bioRxiv2024

Evaluation of the accuracy of bacterial genome reconstruction with Oxford Nanopore R10.4.1 long-read-only sequencing

2.Whole genome reconstruction of bacterial pathogens has become an import tool for tracking antimicrobial resistance spread, however accurate and complete assemblies have only been achievable using hybrid long and short-read sequencing. We have previously found the Oxford Nanopore Technologies (ONT) R10.4/kit12 flowcells produced improved assemblies over the R9.4.1/kit10, however they contained too many errors compared to hybrid Illumina-ONT assemblies. ONT have since released the R10.4.1/kit12 flowcells that promises greater accuracy and yield. They have also released newly trained basecallers using native bacterial DNA containing methylation sites intended to fix systematic errors, specifically Adenosine (A) to Guanine (G) and Cytosine (C) to Thymine (T) substitutions. ONT have recommended the use of Bovine Serum Albumin (BSA) during library preparation to improve sequencing yield and accuracy. To evaluate these improvements, we sequenced DNA extracts from four commonly studied bacterial pathogens, namely Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa and Staphylococcus aureus, as well as 12 disparate E. coli clinical samples from different phylogroups and sequence types. These were all sequenced with and without BSA. These sequences were de novo assembled and compared against Illumina-corrected reference genomes. Here we have found the nanopore long read-only R10.4.1 (kit14) assemblies with basecallers trained using native bacterial methylated DNA produce accurate assemblies from 40x depth or higher, sufficient to be cost-effective compared to hybrid long-read (ONT) and short-read (Illumina) sequencing. 3. Impact statementCurrently, the best method of building accurate and complete bacterial genome assemblies is to create a hybrid assembly; combining both long and short DNA sequencing reads. Short reads are more accurate, but can be difficult to assemble into a complete genome. Long reads are generally less accurate, but easier to reconstruct into a complete genome. By combining long and short reads, we get both accuracy and reconstructive power. However, this also involves higher costs and more labour than using a single sequencing platform. In this study, we compare long read only assemblies from Oxford Nanopore Technologys newest iteration of improvements in both chemistry and software to hybrid Illumina-Nanopore assemblies. We sequenced four bacterial pathogens with published reference genomes (Staphylococcus aureus, Klebsiella Pneumoniae, Pseudomonas Aeruginosa, and Escherichia Coli) and twelve bloodstream associated E. coli, and show that assemblies from the newest technology are not only an improvement on the previous iteration, but are able to compete with hybrid Illumina-Nanopore assemblies in their quality, providing a step towards bacterial genome assembly using a single sequencing platform. 4. Data summaryThe authors confirm all supporting data, code and protocols have been provided within the article, through supplementary data files, or in publicly accessible repositories. Nanopore and Illumina fastq data are available in the ENA under project accession: PRJEB51164. Assemblies have been made available at: https://figshare.com/articles/dataset/R10_4_1_KIT14_comparison_assemblies/2497 2954 Code and analysis outputs are available at: https://gitlab.com/ModernisingMedicalMicrobiology/assembly_comparison

microbiology↗

bioRxiv2023

Dysregulated expression of Hoxa1 isoforms in hematopoietic stem and progenitor cells causes myelodysplastic syndromes.

The homeobox gene, Hoxa1, has two different isoforms generated by alternative splicing: a full-length homeodomain-containing Hoxa1 (Hoxa1-FL), and a truncated Hoxa1 (Hoxa1-T), that lacks the homeodomain. The effects of the distinct Hoxa1 isoforms in hematopoiesis have not been investigated. Oncoretroviral studies revealed that Hoxa1-T acts in a dominant negative manner, regulating transcriptionally active Hoxa1. Oncoretroviral overexpression of wildtype Hoxa1 (WT-Hoxa1), which generates both Hoxa1 isoforms, in murine hematopoietic stem and progenitor cells (HSPCs) perturbed hematopoiesis, resulting in transplantable myelodysplastic syndromes (MDS) in mice. Overexpression of a mutated Hoxa1 cDNA (MUT-Hoxa1) that generates Hoxa1-FL, but not Hoxa1-T, led to a more severe MDS that transformed to secondary acute myeloid leukemia (sAML). DNA damage repair pathways were downregulated in Hoxa1-overexpressing hematopoietic progenitor cells, accompanied by increased {gamma}H2AX foci. In silico analyses revealed that CD34+ cells from approximately 50% of patients with MDS had elevated HOXA1-FL expression. Conditional knock-in WT-Hoxa1 and MUT-Hoxa1 mice were generated and had features of pre-MDS, developing altered hematopoiesis within 4 months of Hoxa1 isoform overexpression in HSPCs. HSPCs were significantly reduced in all knock-in mice, accompanied by significantly increased apoptosis in WT-Hoxa1 HSPCs. Healthy wildtype recipients transplanted with bone marrow cells from Hoxa1 knock-in mice developed trilineage MDS, with Hoxa1 isoform and gene dosage dependent phenotypes. Collectively our data identify a role for HOXA1 in the pathogenesis of MDS. Our Hoxa1 mouse models capture different stages of progression of disease from pre-MDS to MDS to sAML and provide novel, clinically relevant tools to study MDS. Key pointsHOXA1 is upregulated in approximately 50% of MDS patient CD34+ BM cells, highlighting a potential role for HOXA1 in the pathogenesis of MDS. Dysregulated expression of Hoxa1 isoforms in murine hematopoietic stem and progenitor cells predisposes mice to pre-MDS and MDS.

cancer biology↗

bioRxiv2022

Transgenerational Effects of Early-Life Stress on Anxiety in Zebrafish (Danio rerio)

Early-life adversity impacts on anxiety-related behaviors in adulthood. The effects of such adversity not only affects the animal itself, but can be passed on transgenerationally. Pervasive effects of experimentally-induced early-life stress (ELS) have been documented in adult zebrafish but it is not clear if this can be passed on via the germline. Here, we investigated the effects of ELS across three generations, by analyzing the responses of adult animals exposed to ELS in two different anxiety-related tasks, as well as in social behavior, memory, and cognition. Animals exposed to ELS (at 7 days-post-fertilization) showed a marked attenuation of specific anxiety-related behaviors (F0) when adults, and these alterations were maintained across two subsequent generations (F1 and F2). These findings suggest that zebrafish may be a useful model organism to study the transgenerational effects of ELS, and how this pertains to (for example) neuropsychiatric disorders. In addition, our data may naturally provoke questions regarding consideration of the environment of laboratory-housed zebrafish at early developmental stages. In particular, more work may be necessary to determine how different environmental stressors could affect data variability across laboratories. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=59 SRC="FIGDIR/small/517541v1_ufig1.gif" ALT="Figure 1"> View larger version (15K): org.highwire.dtl.DTLVardef@c1aac0org.highwire.dtl.DTLVardef@b14684org.highwire.dtl.DTLVardef@8c878aorg.highwire.dtl.DTLVardef@16a68b_HPS_FORMAT_FIGEXP M_FIG Summary of the ELS effects in zebrafish anxiety-like behavior across multiple generations. C_FIG

neuroscience↗

bioRxiv2022

Antigen-dependent inducible T cell reporter system for PET imaging of breast cancer and glioblastoma

For the past several decades, chimeric antigen receptor T cell (CAR T) therapies have shown promise in the treatment of cancers. These treatments would greatly benefit from companion imaging biomarkers to follow the trafficking of T cells in vivo. Using synthetic biology, we engineered T cells with a chimeric receptor SyNthetic Intramembrane Proteolysis Receptor (SNIPR) that induces overexpression of an exogenous reporter gene cassette upon recognition of specific tumor markers. We then applied a SNIPR-based positron emission tomography (PET) reporter system to two cancer-relevant antigens, human epidermal growth factor receptor 2 (HER2) and epidermal growth factor receptor variant III (EGFRvIII), commonly expressed in breast and glial tumors respectively. Antigen-specific reporter induction of the SNIPR-PET T cells was confirmed in vitro using GFP fluorescence, luciferase luminescence, and the HSV-TK PET reporter with [18F]FHBG. T cells associated with their target antigens were successfully imaged using PET in dual xenograft HER2+/HER2- and EGFRvIII+/EGFRvIII-animal models, with > 10-fold higher [18F]FHBG signals seen in antigen-expressing tumors versus the corresponding controls. The main innovation described is therefore PET detection of T cells via specific antigen-induced signals, in contrast to reporter systems relying on constitutive gene expression.

synthetic biology↗

bioRxiv2021

Climate and mountains shaped human ancestral genetic lineages

Extensive sequencing of modern and ancient human genomes has revealed that contemporary populations can be explained as the result of recent mixing of a few distinct ancestral genetic lineages1. But the small number of aDNA samples that predate the Last Glacial Maximum means that the origins of these lineages are not well understood. Here, we circumvent the limited sampling by modelling explicitly the effect of climatic changes and terrain on population demography and migrations through time and space, and show that these factors are sufficient to explain the divergence among ancestral lineages. Our reconstructions show that the sharp separation between African and Eurasian lineages is a consequence of only a few limited periods of connectivity through the arid Arabian peninsula, which acted as the gate out of the Arican continent. The subsequent spread across Eurasia was then mostly shaped by mountain ranges, and to a lesser extent deserts, leading to the split of European and Asians, and the further diversification of these two groups. A high tolerance to cold climates allowed the persistence at high latitudes even during the Last Glacial Maximum, maintaining a pocket in Beringia that led to the later, rapid colonisation of the Americas. The advent of food production was associated with an increase in movement2, but mountains and climate have been shown to still play a major role even in this latter period3,4, affecting the mixing of the ancestral lineages that we have shown to be shaped by those two factors in the first place.

genomics↗

bioRxiv2021

Chromosome evolution and the genetic basis of agronomically important traits in greater yam

The nutrient-rich tubers of the greater yam Dioscorea alata L. provide food and income security for millions of people around the world. Despite its global importance, however, greater yam remains an "orphan crop." Here we address this resource gap by presenting a highly-contiguous chromosome-scale genome assembly of greater yam combined with a dense genetic map derived from African breeding populations. The genome sequence reveals an ancient lineage-specific genome duplication, followed by extensive genome-wide reorganization. Using our new genomic tools we find quantitative trait loci for susceptibility to anthracnose, a damaging fungal pathogen of yam, and several tuber quality traits. Genomic analysis of breeding lines reveals both extensive inbreeding as well as regions of extensive heterozygosity that may represent interspecific introgression during domestication. These tools and insights will enable yam breeders to unlock the potential of this staple crop and take full advantage of its adaptability to varied environments.

genomics↗

bioRxiv2020

Cyclic gallium-68 labeled peptides for specific detection of human angiotensin-converting enzyme 2

In this study, we developed ACE2-specific, peptide-derived 68Ga-labeled radiotracers, motivated by the hypotheses that (1) ACE2 is an important determinant of SARS-CoV-2 susceptibility, and (2) that modulation of ACE2 in COVID-19 drives severe organ injury. MethodsA series of NOTA-conjugated peptides derived from the known ACE2 inhibitor DX600 were synthesized, with variable linker identity. Since DX600 bears two cystine residues, both linear and cyclic peptides were studied. An ACE2 inhibition assay was used to identify lead compounds, which were labeled with 68Ga to generate peptide radiotracers ([68Ga]NOTA-PEP). The aminocaproate-derived radiotracer [68Ga]NOTA-PEP4 was subsequently studied in a humanized ACE2 (hACE2) transgenic model. ResultsCyclic DX-600 derived peptides had markedly lower IC50s than their linear counterparts. The three cyclic peptides with triglycine, aminocaproate, and polyethylene glycol linkers had calculated IC50s similar to, or lower than the parent DX600 molecule. Peptides were readily labeled with 68Ga, and the biodistribution of [68Ga]NOTA-PEP4 was determined in a hACE2 transgenic murine cohort. Pharmacologic concentrations of co-administered NOTA-PEP ("blocking") showed significant reduction of [68Ga]NOTA-PEP4 signals in the in the heart, liver, lungs, and small intestine. Ex vivo hACE2 activity in these organs was confirmed as a correlate to in vivo results. ConclusionsNOTA-conjugated, cyclic peptides derived from the known ACE2 inhibitor DX600 retain their activity when N-conjugated for 68Ga chelation. In vivo studies in a transgenic hACE2 murine model using the lead tracer [68Ga]NOTA-PEP4 showed specific binding in the heart, liver, lungs and intestine - organs known to be affected in SARS-CoV-2 infection. These results suggest that [68Ga]NOTA-PEP4 could be used to detect organ-specific suppression of ACE2 in SARS-CoV-2 infected murine models and COVID-19 patients. TOC figure O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=44 SRC="FIGDIR/small/412809v1_ufig1.gif" ALT="Figure 1"> View larger version (18K): org.highwire.dtl.DTLVardef@f3047org.highwire.dtl.DTLVardef@12ab9a9org.highwire.dtl.DTLVardef@33f43org.highwire.dtl.DTLVardef@12e77ed_HPS_FORMAT_FIGEXP M_FIG For Table of Contents use only C_FIG

biochemistry↗

bioRxiv2020

A Rare Deletion in SARS-CoV-2 ORF6 Dramatically Alters the Predicted Three-Dimensional Structure of the Resultant Protein

The function of the SARS-CoV-2 accessory protein p6, encoded by ORF6, is not fully known. Based upon its similarity to p6 from SARS-CoV, it may play a similar role, namely as an antagonist of type I interferon (IFN) signaling. Here we report the sequencing of a SARS-CoV-2 strain passaged six times after original isolation from a clinical patient in Hong Kong. The genome sequence shows a 27 nt in-frame deletion ({Delta}27,264-27,290) within ORF6, predicted to result in a 9 aa deletion ({Delta}FKVSIWNLD) from the central portion of p6. This deletion is predicted to result in a dramatic alteration in the three-dimensional structure of the resultant protein (p6{Delta}22-30), possibly with significant functional implications. Analysis of the original clinical sample indicates that the deletion was not present, while sequencing of subsequent passages of the strain identifies the deletion as a majority variant. This suggests that the deletion originated ab initio during passaging and subsequently propagated into the majority, possibly due to the removal of selective pressure through the IFN-deficient Vero E6 cell line. The specific function of the SARS-CoV-2 p6 N-terminus, if any, has not yet been determined. However, this deletion is predicted to cause a shift from N-endo to N-ecto in the transmembrane localization of the SARS-CoV-2 p6{Delta}22-30 N-terminus, possibly leading to the ablation of its native function.

genomics↗

bioRxiv2018

Race modifies default mode network connectivity in Alzheimer’s disease

ObjectiveTo determine if resting state functional MRI biomarkers of Alzheimers disease (AD) differ between older African Americans and Caucasians.\n\nMethodsWe analyzed MRI profiles from 78 individuals (31 African Americans, 47 Caucasians) with normal cognition (n=36) or mild cognitive impairment/mild AD dementia (MCI/AD, n=42). We compared AD-associated intra-network functional connectivity of the default mode network (DMN) according to race, and correlated domain-specific cognitive functions with functional connectivity which differed between the racial groups.\n\nResultsWe identified key differences in DMN functional connectivity associated with AD between the races. Whereas MCI/AD was associated with decreased functional connectivity within the midline core DMN subsystem in older Caucasians, MCI/AD was instead associated with increased functional connectivity within the same subsystem of older African Americans. This is despite decreased functional connectivity in the medial temporal lobe DMN subsystem in both races. Memory function was also positively associated with connectivity between the precuneus and the posterior cingulate/inferior parietal lobule within the midline core subsystem, in keeping with a less amnestic-profile in older African Americans with MCI/AD.\n\nConclusionsThese findings provide structural support that race modifies the AD phenotypes downstream from cerebral amyloid deposition, and suggests a rsf-MRI correlate of African Americans less amnestic neuropsychological profile in MCI/AD.

neuroscience↗

bioRxiv2017

Global cropland connectivity: A risk factor for invasion and saturation by emerging pathogens and pests

The geographic pattern of cropland is an important risk factor for invasion and saturation by crop-specific pathogens and arthropods. Understanding cropland networks supports smart pest sampling and mitigation strategies. We evaluate global networks of cropland connectivity for key vegetatively-propagated crops (banana and plantain, cassava, potato, sweetpotato, and yam) important for food security in the tropics. For each crop, potential movement between geographic location pairs was evaluated using a gravity model, with associated uncertainty quantification. The highly-linked hub and bridge locations in cropland connectivity risk maps are likely priorities for surveillance and management, and for tracing intra-region movement of pathogens and pests. Important locations are identified beyond those locations that simply have high crop density. Cropland connectivity risk maps provide a new risk component for integration with other factors - such as climatic suitability, genetic resistance, and trade routes - to inform Pest Risk Assessment and mitigation.

ecology↗