African cassava mosaic virus (ACMV) and East African cassava mosaic virus (EACMV) are among the major constraints to cassava productivity within tropical and sub-tropical regions, including Ebonyi State, Nigeria. Thus, virus indexing has become imperative to determine the status of cassava mosaic disease (CMD) in Ebonyi State, to implement appropriate preventive and control strategies. Seventy-eight cassava accessions obtained from different locations of Ebonyi State were phenotypically scored, using scales 1–5 depending on CMD symptomatic expressions, followed by multiplex-PCR and sequencing for validation. 11% of cassava accessions cultivated in Afikpo were resistant (RE) to ACMV compared to 8% of moderately-resistant (MR) accessions in Izzi and 55% of tolerant (TO) ACMV accessions in Ebonyi. 100% of cassava accessions in Onicha and 66% in Afikpo South were susceptible (SU) and highly susceptible (HS) to ACMV, respectively. With multiplex-PCR, 97.4% (ACMV) and 2.6% (EACMV) were positive. Dunn’s multiple comparison tests of CMD mean incidence demonstrated differences (P < 0.05), except between RE and MR, and TO and MR. More transitions (A/G, C/T) compared to transversions (A/T, G/T), were detected, with nonsynonymous mutations (Leucine/Isoleucine; Valine/Isoleucine; Arginine/Lysine; Methionine/Isoleucine), and good bit-scores (91.13–99.07% identites; e-values of 7.00e −148 –0.00e +00 ). Phylogeny resolved the sequences into five major groups. DNA sequencing validated the detected ACMV and EACMV species. This study revealed variants of ACMV and low adoption of RE and MR cassava accessions in the farmers’ fields. The findings will guide in getting disease-free and resistant varieties as planting materials to significantly mitigate the CMD spread in Ebonyi State, Nigeria. Supplementary information The online version of this article (10.1007/s11033-020-06039-5) contains supplementary material, which is available to authorized users.

Small vessel disease and/or atherosclerosis produce microvascular and parenchymal inflammation in white matter and results in vascular cognitive impairment (VCI). We have performed bilateral carotid artery stenosis in hypertensive rats (SHR) to better understand disease pathology, targets for intervention and markers. Hypothesis: Complex cognitive deficits and diffuse fiber tract changes relevant to human VCI can be quantified and validated for future use. Methodology: We performed a series of behavioral assays to test declarative memory and executive functioning in stenosis compared to sham surgery SHR. Behavioral assays included T-maze decision making and alternation, novel object recognition (NOR) and active place avoidance (APA). MRI (DTI, DWI, Arterial Spin Labeling; ASL) and FDG-PET imaging was done in Corpus Callosum (CC). Histology-immunohistochemistry included measurements of microglia (Iba-1), astrocytes (GFAP) and Luxol fast blue (for myelin) in CC. Results: Stenosis resulted in consistent executive function decision making (T-maze) deficits (p<0.05) and impaired complex cognitive performance (APA). No significant differences occurred between sham and stenosis animals in NOR and T-maze alternation. DTI analysis indicated significant (p<0.05) changes in the CC of stenosis compared to sham SHR including: (1) decreased fractional anisotropy, (2) increased radial diffusivity, and (3) unchanged axial diffusivity. MRI ASL revealed significant (p<0.05) decreases in white matter perfusion. No significant changes were seen in FDG-PET. In summary, stenosis animals exhibited increased white matter glial cell inflammation related to demyelination and lost cognition. The inflammatory microglia phenotype was verified using TNFα plus Iba-1 double staining. CC changes were significantly (p<0.05) greater in the anterior, periventricular forebrain. Conclusion: We have successfully modeled the behavioral, imaging and histologic profile of human VCI in the rat. Currently pre/mature oligodendrocyte changes are being evaluated. This approach provides future opportunities to localize forebrain white matter changes using MR imaging parameters as markers for monitoring VCI demyelination/pathology and intervention.

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