Bacillus thuringiensis C25 suppresses popcorn disease caused by Ciboria shiraiana in mulberry (Morus australis L.)

The mulberry tree is an important crop for silkworm farming and for the health care industry. In Asia, the annual productivity of mulberry fruits is greatly reduced due to popcorn disease mainly caused by Ciboria shiraiana, a sclerotia-forming fungal pathogen. To date, the development of efficient biocontrol agents (BCAs) against this disease has been hampered by the recalcitrance of C. shiraiana to in vitro culturing methods. Here, we established alternative in vitro antifungal assays that directly monitored the effects of BCAs on the growth of C. shiraiana apothecia and further reported that Bacillus thuringiensis C25 suppressed popcorn disease in field conditions. Initially, from mulberry drupelets showing the popcorn disease symptoms, we confirmed the infection of C. shiraiana and observed its morphology in asexual stage. Then, apothecia of C. shiraiana were induced from the sclerotia collected from the disease-infested orchard. Two bacterial isolates, Enterobacter sp. C5 and B. thuringiensis C25, strongly suppressed the elongation and fresh weight accumulation of apothecia stalks, the width of hymenium, and ascus and ascospore formation of C. shiraiana. In addition, both bacterial isolates degraded the ultrastructure of hymenium cells in C. shiraiana apothecia. Ultimately, treatment of mulberry trees with B. thuringiensis C25 mitigated the incidence of popcorn mulberry disease under field conditions. In conclusion, B. thuringiensis C25 is the first reported BCA shown to efficiently control mulberry popcorn disease. Our results also support that B. thuringiensis exerts diverse biocontrol roles in addition to insecticidal behaviour.     

Biochemical and morphological attributes of broiler kidney in response to dietary glucocorticoid,dexamethasone

Glucocorticoids (GCs) initiate oxidative stress and cause renal damage which lead to hypertension, heart failure and ultimately death. The current study aimed to investigate the alterations in serum biochemical parameters i.e. HDL and LDL; gross anatomy, histomorphology and histomorphometry of broiler kidney in response to dietary GC, dexamethasone (DEX). Day old chicks (DOCs) were randomly assigned into four groups: control and three treatment groups (T1, T2 and T3). The control group was fed commercial broiler type ration and the treated groups were fed commercial broiler type ration containing GC (Dexamethasone @ 3, 5 and 7 mg/kg in T1, T2 and T3 group respectively). To measure the biochemical parameters, blood samples were collected on days 7, 14, 21, and 28 of the experiment. For histological investigation, kidney (left) samples were collected from the individual birds after sacrificing on days 7, 14, 21, and 28 of the experiment. Histomorphological alterations of the kidney were assessed by routine hematoxylin and eosin (H&E) staining. Biochemical analysis showed significantly increased serum HDL and LDL level compared to the control. In gross study, dark congested kidney was found with significantly decreased weight, length and width. Treatment with DEX augmented congestion, inflammation and fibrosis in kidney, as evidence by histomorphometric study. Extensively degenerated and atrophied glomeruli, degenerated tubular epithelium with distorted tubules and inter tubular empty spaces were seen. Percentage of atrophied glomeruli increased significantly and maximum percentage of glomerular atrophy was seen at day 28. These changes were found more explicitly in the higher dose group. Histomorphometric study also revealed significant decrease in the diameter of glomerulus. The findings of this study suggest that DEX may alter the serum biochemical parameters as well as kidney gross and histomorphology.     

Role of ethylene signalling in growth and systemic resistance induction by the plant growth‐promoting fungus Penicillium viridicatum in Arabidopsis

The plant growth‐promoting fungi (PGPF) have long been known to improve plant growth and suppress plant diseases. The PGPF Penicillium viridicatum GP15‐1 elicited plant growth and induced systemic resistance (ISR) in Arabidopsis thaliana against Pseudomonas syringae pv. tomato DC3000 (Pst), leading to a restriction of pathogen growth and disease development. Examination of local and systemic genes indicated that GP15‐1 did not modulate the expression of any of the tested defence‐related marker genes involved in salicylic acid (SA), jasmonic acid (JA) and ethylene signalling pathways. Subsequent challenge of GP15‐1‐colonized plants with Pst bacterium primed Arabidopsis plants for enhanced activation of the JA‐inducible Atvsp (vegetative storage protein) gene at a later stage of infection. To assess the contribution of different signalling pathways in GP15‐1‐elicited plant growth and ISR, Arabidopsis genotypes implicated in SA signalling expressing the nahG transgene (NahG) or carrying disruption in NPR1 (npr1), JA signalling (jar1) and ethylene signalling (ein2) were tested. The GP15‐1‐induced plant growth and ISR were fully compromised in an ein2 mutation. Root colonization assay revealed that the inability of the ein2 mutant to express GP15‐1‐induced plant growth and ISR was not associated with reduced root colonization by GP15‐1. In conclusion, our results demonstrate the ethylene signalling pathway is involved in plant growth promotion and ISR elicitation by the PGPF P. viridicatum GP15‐1 in Arabidopsis. These results provide evidence that ethylene signalling has a substantial role in plant growth and disease resistance.     

The relationship between trace elements and cardiac markers in acute coronary syndromes

Previous studies have demonstrated increased serum copper and iron levels and decreased selenium and zinc levels in patients with myocardial infarction. Furthermore, the prognostic value of the levels of trace elements in myocardial infarction has been stressed. We examined serum levels of Cu, Fe, Zn and Se, as well as glutathione peroxidase (GPx), a selenoenzyme with antioxidant properties, and C-reactive protein (CRP), a marker of inflammation, in acute coronary syndromes (ACS) regarding their relationship to cardiac troponins and creatine kinase-MB mass (CK-MBm), important prognostic markers. Serum trace elements, GPx activity and CRP were determined in 70 patients with ACS who were admitted within 12 h after the onset. Differences in these parameters were evaluated in three groups of patients divided according to the levels of cardiac markers: group III consisted of patients with high increases in cTnT, cTnI and CK-MBm (> or =0.9 ng/mL, > or =1.0 ng/mL, > or =30 ng/mL, respectively), patients with milder increases in these markers were included in groups II and I consisted of patients with values just above the upper reference limits. Serum Fe levels increased significantly in group II and even more prominently in group III compared to group I (p = 0.04, 0.002, respectively). There was no significant difference between groups II and III. The increase in serum Cu was significant in group III compared to both groups II and I (p = 0.04, 0.001, respectively). There was no significant difference between groups I and II regarding Cu and Zn. The decrease in serum Se and GPx levels was significant only between groups III and I (p = 0.004 for Se and p = 0.0001 for GPx). CRP levels showed a significant increase in group III compared to groups II and I (p = 0.03 and 0.001). CRP showed a significant positive and GPx a significant negative correlation to the cardiac markers cTnT, cTnI and CK-MBm. Cu was positively correlated to all cardiac markers, while the positive correlation between Fe and cardiac markers was significant only for cTnI. Both Zn and Se were negatively correlated to cTnT, and Se was also to cTnI. In conclusion, the increase in serum levels of Cu and Fe and the decrease in serum levels of Zn and Se in patients with higher levels of troponins and CK-MBm imply that trace element levels are related to the degree of myocardial damage and thus may play a role in the pathogenesis of ischemic heart disease. The strong correlations between cardiac markers and both CRP and GPx suggest that these parameters are promising prognostic factors in acute coronary syndromes.     

The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak

Aberrant wound-healing responses to injury have been implicated in the development of pulmonary fibrosis, but the mediators directing these pathologic responses have yet to be fully identified. We show that lysophosphatidic acid levels increase in bronchoalveolar lavage fluid following lung injury in the bleomycin model of pulmonary fibrosis, and that mice lacking one of its receptors, LPA1, are markedly protected from fibrosis and mortality in this model. The absence of LPA1 led to reduced fibroblast recruitment and vascular leak, two responses that may be excessive when injury leads to fibrosis rather than to repair, whereas leukocyte recruitment was preserved during the first week after injury. In persons with idiopathic pulmonary fibrosis, lysophosphatidic acid levels in bronchoalveolar lavage fluid were also increased, and inhibition of LPA1 markedly reduced fibroblast responses to the chemotactic activity of this fluid. LPA1 therefore represents a new therapeutic target for diseases in which aberrant responses to injury contribute to fibrosis, such as idiopathic pulmonary fibrosis.     

Determination of HER-2/Neu status in hepatocellular carcinoma cases

Specific chromosome abnormalities and genetic changes in hepatocellular carcinoma (HCC) have been demonstrated by conventional cytogenetic studies or molecular cytogenetic approaches like comparative genomic hybridization and loss of heterozygosity analyses. HER-2/Neu amplification and expression has been studied as a molecular target for treatment of HCC, and there are conflicting results. We aimed to determine HER-2/Neu status in archive materials of HCC patients by fluorescence in situ hybridization (FISH). Among the 35 patients, 2 had HER-2/Neu amplification and 3 had increased chromosome 17 copy number. All these patients had grade 2 or 3 tumor with a diameter of 3-12 cm. We conclude that although HER-2/Neu amplification is not the primary mechanism in the development of liver tumors, it might play a role in one of the steps of multistage carcinogenesis.