Calosphaeria canker of almond caused by Calosphaeria pulchella in Iran

Trunk diseases are a potential threat for the almond industry in Northern Iran. In a survey on fungal agents associated with almond die back and decline in East Azerbaijan province, located in Northwest of Iran, acremonium-like hyphomycete isolates with hyaline and simple conidiophores and hyaline cylindrical phialides with a finely pigmented apical region and deep, flaring collarettes were repeatedly recovered from symptomatic tissues. Fungal isolates were identified as Calosphaeria pulchella based on cultural and morphological characteristics. The identity of the species was further confirmed based on the sequence data from LSU and ITS rDNA regions. A phylogeny inferred using ITS sequence data, clustered the Calosphaeria isolates together with Calosphaeria pulchella isolates in GenBank known from Prunus persica and Prunus avium. The results of pathogenicity assay using an excised shoot method showed that Calosphaeria pulchella is highly pathogenic on almond. The distribution and host range of this new pathogen on almond and the impact of the disease on almond industry in this region remain to be studied.     

Production of a recombinant cholera toxin B subunit-insulin B chain peptide hybrid protein by Brevibacillus choshinensis expression system as a nasal vaccine against autoimmune diabetes

Mucosally induced tolerance is an attractive strategy for preventing or reducing autoimmune diseases. Here, we produced a recombinant CTB fusion protein linked with autoantigen T cell epitope of insulin B chain peptide 9-23 (C19S) at levels up to 200 mg/L culture media in Brevibacillus choshinensis secretion-expression system. Receptor-competitive assay showed that the CTB-insulin peptide binds to GM1 receptor almost equivalent degree as the native form of CTB. Non-obese diabetes (NOD) mice that spontaneously develop an insulin-dependent diabetes were nasally immunized with CTB-insulin peptide (5 microg) for three times. The nasal treatment significantly reduced the development of insulin-dependent diabetes and peptide specific DTH responses after systemic immunization with the insulin peptide B 9-23(C19S) in CFA. Nasal administration of as high as 50 microg of the peptide alone demonstrated a similar level of the disease inhibition. In contrast, all mice given 5 microg of the insulin peptide alone or 5 microg of insulin peptide with 25 microg of the free form of CTB did not lead to the suppression of diabetes development and DTH responses. Because molecular weight of the insulin peptide is about one tenth of that of the CTB-insulin peptide, the results demonstrate that the recombinant hybrid of autoantigen and CTB increased its tolerogenic potential for nasal administration by up 100-fold on molar base of autoantigen peptide. Taken together, nasally-induced tolerance by administration of the recombinant B. choshinensis-derived hybrid protein of CTB and autoantigen T cell-epitope peptide could be useful mucosal immunetherapy for the control of T cell-mediated autoimmune diseases.     

芒果、香蕉采后病害生物防治的研究进展

芒果、香蕉采后主要病害为炭疽病、蒂腐病、冠腐病、黑腐病、黑星病.生物防治是当前芒果、香蕉采后病害控制的重要研究方向.概述了生物防治芒果、香蕉采后病害的方法,包括诱抗剂、植物提取物、拮抗微生物在芒果、香蕉采后病害防治上的研究与应用.     

Ultrasensitive peroxynitrite-based luminescence with L-012 as a screening system for antioxidative/antinitrating substances, e.g. Tylenol (acetaminophen), 4-OH tempol, quercetin and carboxy-PTIO.

Previously our group developed a water-soluble antioxidant screening system using the luminescence of the reaction of peroxynitrite and luminol. In the present study we replaced luminol with the luminol-like compound L-012. This increases the production of luminescence approximately 100-fold and therefore, with a higher signal:noise ratio, this new system can detect antioxidation and antinitration effects at lower doses of the inhibitor. We studied acetaminophen (Tylenol) and its metabolite 3-nitroacetaminophen, tyrosine and nitrotyrosine and all these substances were inhibitory in a dose-responsive manner and below micromolar amounts. In addition quercetin, a polyphenol, was highly active (below micromolar amounts) as an antioxidant and antinitrating compound. 4-OH tempol, the stable free radical, superoxide dismutase (SOD) mimetic, was inhibitory in a dose-responsive manner and below micromolar amounts. Carboxy-PTIO was inhibitory at 10 times micromolar amount but not below that dose, which may be related to colour quenching, since the drug is deeply blue, or possibly it is an inhibitor with a slow kinetic profile. Finally, the amino acid tyrosine has been found to be inhibitory in micromolar amounts, similar to acetaminophen. This indicates that tyrosine can act as an antioxidant and antinitration target alone or conjugated in protein, e.g. insulin.     

The neuroprotective effect of Activin A and B: implication for neurodegenerative diseases

Activin is a member of the transforming growth factor-beta superfamily which comprises a growing list of multifunctional proteins that function as modulators of cell proliferation, differentiation, hormone secretion and neuronal survival. This study examined the neuroprotective effect of both Activin A and B in serum withdrawal and oxidative stress apoptotic cellular models and investigated the expression of pro- and anti-apoptotic proteins, which may account for the mechanism of Activin-induced neuroprotection. Here, we report that recombinant Activin A and B are neuroprotective against serum deprivation- and toxin- [either the parkinsonism-inducing neurotoxin, 6-hydroxydopamine (6-OHDA) or the peroxynitrite donor, 3-(4-morpholinyl) sydnonimine hydrochloride (SIN-1)] induced neuronal death in human SH-SY5Y neuroblastoma cells. Furthermore, we demonstrate for the first time that transient transfection with Activin betaA or betaB significantly protect SH-SY5Y and rat pheochromocytoma PC12 cells against serum withdrawal-induced apoptosis. This survival effect is mediated by the Bcl-2 family members and involves inhibition of caspase-3 activation; reduction of cleaved poly-ADP ribose polymerase and phosphorylated H2A.X protein levels and elevation of tyrosine hydroxylase expression. These results indicate that both Activin-A and -B share the potential to induce neuroprotective activity and thus may have positive impact on aging and neurodegenerative diseases to retard the accelerated rate of neuronal degeneration.     

Epidemic outbreaks on structured populations

Our chances to halt epidemic outbreaks rely on how accurately we represent the population structure underlying the disease spread. When analysing global epidemics this force us to consider metapopulation models taking into account intra- and inter-community interactions. Here I introduce and analyze a metapopulation model which accounts for several features observed in real outbreaks. First, I demonstrate that depending on the intra-community expected outbreak size and the fraction of social bridges the epidemic outbreaks die out or there is a finite probability to observe a global epidemics. Second, I show that the global scenario is characterized by resurgent epidemics, their number increasing with increasing the intra-community average distance between individuals. Finally, I present empirical data for the AIDS epidemics supporting the model predictions.     

Reservoir interactions and disease emergence

Animal populations act as reservoirs for emerging diseases. In order for transmission to be self-sustaining, a pathogen must have a basic reproduction number R0>1. Following a founding transmission event from an animal reservoir to humans, a pathogen has not yet adapted to its new environment and is likely to have an R0<1. However, subsequent evolution may rescue the pathogen from extinction in its new host. Recent applications of branching process theory investigate how the emergence of a novel pathogen is influenced by the number and rates of intermediate evolutionary steps. In addition, repeated contacts between human and reservoir populations may promote pathogen emergence. This article extends a stepping-stone model of pathogen evolution to include reservoir interactions. We demonstrate that the probability of a founding event culminating in an emerged pathogen can be significantly influenced by ongoing reservoir interactions. While infrequent reservoir interactions do not change the probability of disease emergence, moderately frequent interactions can promote emergence by facilitating adaptation to humans. Frequent reservoir interactions promote emergence even with minimal adaptation to humans. Thus, these results warn against perpetuated interaction between humans and animal reservoirs, as occurs when there are ecological or environmental changes that bring humans into more frequent contact with animal reservoirs.     

Mitochondria: a hub of redox activities and cellular distress control

In their reductionist approach in unraveling phenomena inside the cell, scientists in recent times have focused attention to mitochondria. An organelle with peculiar evolutionary history and organization, it is turning out to be an important cell survival switch. Besides controlling bioenergetics of a cell it also has its own genetic machinery which codes 37 genes. It is a major source of generation of reactive oxygen species, acts as a safety device against toxic increases of cytosolic Ca²⁺ and its membrane permeability transition is a critical control point in cell death. Redox status of mitochondria is important in combating oxidative stress and maintaining membrane permeability. Importance of mitochondria in deciding the response of cell to multiplicity of physiological and genetic stresses, inter-organelle communication, and ultimate cell survival is constantly being unraveled and discussed in this review. Mitochondrial events involved in apoptosis and necrotic cell death, such as activation of Bcl-2 family proteins, formation of permeability transition pore, release of cytochrome c and apoptosis inducing factors, activation of caspase cascade, and ultimate cell death is the focus of attention not only for cell biologists, but also for toxicologists in unraveling stress responses. Mutations caused by ROS to mitochondrial DNA, its inability to repair it completely and creation of a vicious cycle of mutations along with role of Bcl-2 family genes and proteins has been implicated in many diseases where mitochondrial dysfunctions play a key role. New therapeutic approaches toward targeting low molecular weight compounds to mitochondria, including antioxidants is a step toward nipping the stress in the bud.