Search for Scutellonema bradys resistance in yams (Dioscorea spp.)

A study to examine variability in susceptibility of yams to Scutellonema bradys and to identify possible sources of resistance in Ghanaian yam germplasm (Dioscorea spp.) for use in yam improvement programmes, particularly, in West Africa was undertaken. Pot and field screening methodologies were used. In general, S. bradys and dry rot of tuber symptoms as well as tuber cracking increased during the storage period. The study showed a positive correlation between visual nematode damage and population densities in yam tubers. There was also a linear relationship between dry rot disease and tuber cracking at harvest and during storage. This confirms that S. bradys causes dry rot of tubers resulting in external cracking of yam tubers. Positive linear relationship was also observed between yam tuber weight loss and dry rot disease indicating that dry rot disease may have contributed to the tuber weight loss. Therefore, tuber dry rot symptoms caused by S. bradys of yams could be used to discard susceptible yams at harvest and after a period of storage. However, there was no linear relationship between nematode population densities in yam tubers and roots, therefore, a root protocol cannot be used for assessing resistance in yams as it could lead to misclassification. The yam germplasm screened, reaffirmed resistance to S. bradys in Dioscorea dumetorum var. Nkanfo and D. cayenensis var. Afun

Rab38 and Rab32 control post-Golgi trafficking of melanogenic enzymes

Amutation in the small GTPase Rab38 gives rise to the mouse coat color phenotype “chocolate” (cht), implicating Rab38 in the regulation of melanogenesis. However, its role remains poorly characterized. We report that cht Rab38G19V is inactive and that the nearly normal pigmentation in cht melanocytes results from functional compensation by the closely related Rab32. In cht cells treated with Rab32-specific small interfering RNA, a dramatic loss of pigmentation is observed. In addition to mature melanosomes, Rab38 and Rab32 localize to perinuclear vesicles carrying tyrosinase and tyrosinase-related protein 1, consistent with a role in the intracellular sorting of these proteins. In Rab38/Rab32-deficient cells, tyrosinase appears to be mistargeted and degraded after exit from the trans-Golgi network (TGN). This suggests that Rab38 and Rab32 regulate a critical step in the trafficking of melanogenic enzymes, in particular, tyrosinase, from the TGN to melanosomes. This work identifies a key role for the Rab38/Rab32 subfamily of Rab proteins in the biogenesis of melanosomes and potentially other lysosome-related organelles

Contact Networks and Mortality Patterns Suggest Pneumonia-Causing Pathogens may Persist in Wild Bighorn Sheep

Efficacy of disease control efforts is often contingent on whether the disease persists locally in the host population or is repeatedly introduced from an alternative host species. Local persistence is partially determined by the interaction between host contact structure and disease transmission rates: relatively isolated host groups facilitate pathogen persistence by slowing the rate at which highly transmissible pathogens access new susceptibles; alternatively, isolated host groups impede persistence for pathogens with low transmission rates by limiting the number of available hosts and forcing premature fade-out. Here, we use long-term data from the Hells Canyon region to investigate whether variable host contact patterns are associated with survival outcomes for 46 cohorts of bighorn sheep (Ovis canadensis) lambs subject to recurrent pneumonia outbreaks. We build social contact networks for each lamb cohort, and quantify variation in lamb mortality attributable to populations, years, and groups. We then refine estimates of chronic carriage rates in ewes, and disease-induced mortality rates in lambs, by finding parameters for the disease process that produce lamb morality rates similar to those observed when simulated on the observed host contact networks. Our results suggest that summer lamb hazards are spatially structured at the subpopulation level: 92.5 percent of the variation in lamb hazards during pneumonia outbreak years was attributable to sub-population-level groups, whereas 1.7 percent and 5.6 percent were attributable to year and population, respectively.  Additionally, the posterior distribution generated by our disease transmission model suggests that pneumonia-causing pathogens may persist locally in bighorn sheep populations, even during apparently healthy years

Disease Introduction Is Associated With a Phase Transition in Bighorn Sheep Demographics

Ecological theory suggests that pathogens are capable of regulating or limiting host population dynamics, and this relationship has been empirically established in several settings. However, although studies of childhood diseases were integral to the development of disease ecology, few studies show population limitation by a disease affecting juveniles. Here, we present empirical evidence that disease in lambs constrains population growth in bighorn sheep (Ovis canadensis) based on 45 years of population‐level and 18 years of individual‐level monitoring across 12 populations. While populations generally increased (λ = 1.11) prior to disease introduction, most of these same populations experienced an abrupt change in trajectory at the time of disease invasion, usually followed by stagnant‐to‐declining growth rates (λ = 0.98) over the next 20 years. Disease‐induced juvenile mortality imposed strong constraints on population growth that were not observed prior to disease introduction, even as adult survival returned to pre‐invasion levels. Simulations suggested that models including persistent disease‐induced mortality in juveniles qualitatively matched observed population trajectories, whereas models that only incorporated all‐age disease events did not. We use these results to argue that pathogen persistence may pose a lasting, but under‐recognized, threat to host populations, particularly in cases where clinical disease manifests primarily in juveniles

Climate Change and Infectious Disease Dynamics

The International Panel on Climate Change has made an unequivocal case that the earth\u27s climate is changing in profound ways, and that human activities are contributing significantly to climate disruption (IPCC 2007). The weight of evidence demonstrates warming global temperatures, changing patterns of precipitation, and increasing climate variability, with more extreme events. Thus, the physical underpinnings of ecology are changing, with pervasive effects on disease dynamics. Interactions among environment, hosts, and pathogens drive disease processes, and climate change will influence every interaction in this triad, directly and indirectly

Μελέτη επιπτώσεων συνδρομολόγησηςεφαρμογών σε πολυπύρηνες αρχιτεκτονικές

Understanding viral transmission dynamics within populations of reservoir hosts can facilitate greater knowledge of the spillover of emerging infectious diseases. While bat-borne viruses are of concern to public health, investigations into their dynamics have been limited by a lack of longitudinal data from individual bats. Here, we examine capture-mark-recapture (CMR) data from a species of Australian bat (Myotis macropus) infected with a putative novel Alphacoronavirus within a Bayesian framework. Then, we developed epidemic models to estimate the effect of persistently infectious individuals (which shed viruses for extensive periods) on the probability of viral maintenance within the study population. We found that the CMR data analysis supported grouping of infectious bats into persistently and transiently infectious bats. Maintenance of coronavirus within the study population was more likely in an epidemic model that included both persistently and transiently infectious bats, compared with the epidemic model with non-grouping of bats. These findings, using rare CMR data from longitudinal samples of individual bats, increase our understanding of transmission dynamics of bat viral infectious diseases

Formation and dynamics of van der Waals molecules in buffer-gas traps

We show that weakly bound He-containing van der Waals molecules can be produced and magnetically trapped in buffer-gas cooling experiments, and provide a general model for the formation and dynamics of these molecules. Our analysis shows that, at typical experimental parameters, thermodynamics favors the formation of van der Waals complexes composed of a helium atom bound to most open-shell atoms and molecules, and that complex formation occurs quickly enough to ensure chemical equilibrium. For molecular pairs composed of a He atom and an S-state atom, the molecular spin is stable during formation, dissociation, and collisions, and thus these molecules can be magnetically trapped. Collisional spin relaxations are too slow to affect trap lifetimes. However, helium-3-containing complexes can change spin due to adiabatic crossings between trapped and untrapped Zeeman states, mediated by the anisotropic hyperfine interaction, causing trap loss. We provide a detailed model for Ag3He molecules, using ab initio calculation of Ag-He interaction potentials and spin interactions, quantum scattering theory, and direct Monte Carlo simulations to describe formation and spin relaxation in this system. The calculated rate of spin-change agrees quantitatively with experimental observations, providing indirect evidence for molecular formation in buffer-gas-cooled magnetic traps.Comment: 20 pages, 13 figure

Malignant Catarrhal Fever Induced by Alcelaphine herpesvirus 1 Is Associated with Proliferation of CD8+ T Cells Supporting a Latent Infection

Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest asymptomatically, causes malignant catarrhal fever (WD-MCF) when cross-species transmitted to a variety of susceptible species of the Artiodactyla order. Experimentally, WD-MCF can be induced in rabbits. The lesions observed are very similar to those described in natural host species. Here, we used the rabbit model and in vivo 5-Bromo-2′-Deoxyuridine (BrdU) incorporation to study WD-MCF pathogenesis. The results obtained can be summarized as follows. (i) AlHV-1 infection induces CD8+ T cell proliferation detectable as early as 15 days post-inoculation. (ii) While the viral load in peripheral blood mononuclear cells remains below the detection level during most of the incubation period, it increases drastically few days before death. At that time, at least 10% of CD8+ cells carry the viral genome; while CD11b+, IgM+ and CD4+ cells do not. (iii) RT-PCR analyses of mononuclear cells isolated from the spleen and the popliteal lymph node of infected rabbits revealed no expression of ORF25 and ORF9, low or no expression of ORF50, and high or no expression of ORF73. Based on these data, we propose a new model for the pathogenesis of WD-MCF. This model relies on proliferation of infected CD8+ cells supporting a predominantly latent infection

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