Nutritional value of Pleurotus (Flabellatus) Djamor (R-22) cultivated on sawdusts of different woods

The sawdust of different woods were investigat ed for the cultivation of exotic strain of Pleurotus (flabellatus) djamor (R-22) to find out the efficiency of different nutrients including protein, fat, crude fiber, ash, dry matter and moisture. Among all type of nutrients, protein, fat, cr ude fiber, ash, dry matter and moisture of Pleurotus ostreatus on sawdust of different woods were observed. Protein was observed on cont rol treatment (cotton waste, kikar, mango, mixed sawdust, simbal and kail (21.89), (21.64), (21.34), (21.16), (21.03) and (20.75) % respectively. Fat was observed on control treatment (cotton waste, kikar, mango, mi xed sawdust, simbal and kail (0.80), (0.53), (0 .41), (0.33), (0.24) and (0.11)% respectively. Crude fiber was observed on control treatment (cotton waste, kikar, mango, mixed sawdust, simbal and kail (8.92), (8.45), (8.17), (7.96), (7.70) and (7.32) % respectively. Ash was observ ed on control treatment (cotton waste, kikar, mango, mixed sawdust, simbal and kail (7.65), (6.75), (6 .47), (6.39), (6.33) and (6.23%) respectively. Dry matter was observed on control treatment (cotton waste, kikar, mango, mixed sawdust, simbal and kail (6.47), (6.27), (6.13), (6.01), (5.87) and (5.67) % respectively. Moisture was observed on control treatment (c otton waste, kikar, mango, mixed sawdust, simbal and kail (84.55), (81.20), (79.85), (76.26), (74.35) and (71.14) % respectively. Oyster mushroom showed relatively more contents on control treatment cotton waste as compared to other substrates. The maximum protein, fat, crude fiber, ash, dry matter and moisture contents in Pleurotus (flabellatus) djamor (R-22) was obtained on Kikar sawdust .The lowest contents was obtained on kail sawdust

Adenoviral delivery of angiotensin-(1-7) or angiotensin-(1-9) inhibits cardiomyocyte hypertrophy via the mas or angiotensin Type 2 receptor

The counter-regulatory axis of the renin angiotensin system peptide angiotensin-(1-7) [Ang-(1-7)] has been identified as a potential therapeutic target in cardiac remodelling, acting via the mas receptor. Furthermore, we recently reported that an alternative peptide, Ang-(1-9) also counteracts cardiac remodelling via the angiotensin type 2 receptor (AT(2)R). Here, we have engineered adenoviral vectors expressing fusion proteins which release Ang-(1-7) [RAdAng-(1-7)] or Ang-(1-9) [RAdAng-(1-9)] and compared their effects on cardiomyocyte hypertrophy in rat H9c2 cardiomyocytes or primary adult rabbit cardiomyocytes, stimulated with angiotensin II, isoproterenol or arg-vasopressin. RAdAng-(1-7) and RAdAng-(1-9) efficiently transduced cardiomyocytes, expressed fusion proteins and secreted peptides, as demonstrated by western immunoblotting and conditioned media assays. Furthermore, secreted Ang-(1-7) and Ang-(1-9) inhibited cardiomyocyte hypertrophy (Control = 168.7±8.4 µm; AngII = 232.1±10.7 µm; AngII+RAdAng-(1-7) = 186±9.1 µm, RAdAng-(1-9) = 180.5±9 µm; P<0.05) and these effects were selectively reversed by inhibitors of their cognate receptors, the mas antagonist A779 for RAdAng-(1-7) and the AT(2)R antagonist PD123,319 for RAdAng-(1-9). Thus gene transfer of Ang-(1-7) and Ang-(1-9) produces receptor-specific effects equivalent to those observed with addition of exogenous peptides. These data highlight that Ang-(1-7) and Ang-(1-9) can be expressed via gene transfer and inhibit cardiomyocyte hypertrophy via their respective receptors. This supports applications for this approach for sustained peptide delivery to study molecular effects and potential gene therapeutic actions

Antimicrobial activity of potato Rhizospheric Pseudomonas chlororaphis subsp. aureofaciens from Sétif Algeria

Aims: This study was assessed to demonstrate the antimicrobial activity in vitro of an identified fluorescent Pseudomonas strain characterized for its capacity to produce phenazine compounds. Methodology: First Pseudomonas chlororaphis subsp aureofaciens was inoculated on Nutrient Broth supplemented with Yeast Extract (NBY) and with glucose at a final concentration of 2%, after incubation the filtered culture was acidified with HCl to pH 2. The solution was extracted twice with the same volume of ethyl-acetate. The organic supernatants were combined, dried over anhydrous Na2SO4, and evaporated to dryness. The crude extract was resuspended in methanol and tested for antimicrobial activity. Antimicrobial activity was determined (i) by disc diffusion technique for bacteria and (ii) using serial dilution technique in soft PDA for fungi. Secondly the antifungal activity of the bacterial strain was tested against several phytopathogenic fungi in dual culture. Results: The studied strain has an important activity against the phytopathogenic bacteria and fungi tested. Among the tested fungi Fusarium oxysporum f. sp. albedinis is the most sensitive to the actions of this Pseudomonas, where the inhibition rate reached 77.78%. The less sensitive one was Pythium ultimum with a rate of 55.56%. While for pathogenic bacteria only Salmonella enteridis was sensitive to the tested strain. Conclusion: Pseudomonas chlororaphis subsp aureofaciens showed appreciable antagonistic activity, in vitro, against special forms of Fusarium oxysporum and the tested phytopathogenic bacteria

Cloning, sequencing, and characterization of the hexahydro-1,3,5-trinitro-1,3,5-triazine degradation gene cluster from Rhodococcus rhodochrous

Hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) is a high explosive which presents an environmental hazard as a major land and groundwater contaminant. Rhodococcus rhodochrous strain 11Y was isolated from explosive contaminated land and is capable of degrading RDX when provided as the sole source of nitrogen for growth. Products of RDX degradation in resting-cell incubations were analyzed and found to include nitrite, formaldehyde, and formate. No ammonium was excreted into the medium, and no dead-end metabolites were observed. The gene responsible for the degradation of RDX in strain 11Y is a constitutively expressed cytochrome P450-like gene, xpLA, which is found in a gene cluster with an adrenodoxin reductase homologue, xplB. The cytochrome P450 also has a flavodoxin domain at the N terminus. This study is the first to present a gene which has been identified as being responsible for RDX biodegradation. The mechanism of action of XplA on RDX is thought to involve initial denitration followed by spontaneous ring cleavage and mineralization

Bacteriocins contributing in Rhizospheric competition among Fluorescent Pseudomonads

Aims: To examine the production of bacteriocins through the study of a group of rhizospheric Pseudomonas isolates already known to produce metabolites that are antagonistic to fungi. Methodology: Fourteen rhizospheric strains of fluorescent Pseudomonads spp., were tested as well as two referenced strains Pseudomonas protogens CHA0 and Pseudomonas aureofaciens 30-84, for their ability to produce induced bacteriocins. The induction is carried out first by UV light, and secondly by mitomycin C. Results: In addition to the reference strains, six isolates were found to produce bactericidal substances after UV light induction against Pseudomonas target bacteria but also against other genera (Escherichia and Staphylococcus). Producing strains were treated with mitomycin C, and then lysed with chloroform. Analysis of the lysates by trypsin and freezing treatments, suggests that the active compounds are of high molecular weight. Conclusion: It is therefore suggested that these bacteria could be good competitors for their introduction as biocontrol agents

Manipulating adenovirus hexon hypervariable loops dictates immune neutralisation and coagulation factor X-dependent cell interaction in vitro and in vivo

Adenoviruses are common pathogens, mostly targeting ocular, gastrointestinal and respiratory cells, but in some cases infection disseminates, presenting in severe clinical outcomes. Upon dissemination and contact with blood, coagulation factor X (FX) interacts directly with the adenovirus type 5 (Ad5) hexon. FX can act as a bridge to bind heparan sulphate proteoglycans, leading to substantial Ad5 hepatocyte uptake. FX “coating” also protects the virus from host IgM and complement-mediated neutralisation. However, the contribution of FX in determining Ad liver transduction whilst simultaneously shielding the virus from immune attack remains unclear. In this study, we demonstrate that the FX protection mechanism is not conserved amongst Ad types, and identify the hexon hypervariable regions (HVR) of Ad5 as the capsid proteins targeted by this host defense pathway. Using genetic and pharmacological approaches, we manipulate Ad5 HVR interactions to interrogate the interplay between viral cell transduction and immune neutralisation. We show that FX and inhibitory serum components can co-compete and virus neutralisation is influenced by both the location and extent of modifications to the Ad5 HVRs. We engineered Ad5-derived HVRs into the rare, native non FX-binding Ad26 to create Ad26.HVR5C. This enabled the virus to interact with FX at high affinity, as quantified by surface plasmon resonance, FX-mediated cell binding and transduction assays. Concomitantly, Ad26.HVR5C was also sensitised to immune attack in the absence of FX, a direct consequence of the engineered HVRs from Ad5. In both immune competent and deficient animals, Ad26.HVR5C hepatic gene transfer was mediated by FX following intravenous delivery. This study gives mechanistic insight into the pivotal role of the Ad5 HVRs in conferring sensitivity to virus neutralisation by IgM and classical complement-mediated attack. Furthermore, through this gain-of-function approach we demonstrate the dual functionality of FX in protecting Ad26.HVR5C against innate immune factors whilst determining liver targeting

Gene therapy with Angiotensin-(1-9) preserves left ventricular systolic function after myocardial infarction

BACKGROUND: Angiotensin-(1-9) [Ang-(1-9)] is a novel peptide of the counter-regulatory axis of the renin angiotensin system previously demonstrated to have therapeutic potential in hypertensive cardiomyopathy when administered via osmotic minipump in mice. Here, we investigate whether gene transfer of Ang-(1-9) is cardioprotective in a murine model of myocardial infarction (MI). OBJECTIVES: To evaluate effects of Ang-(1-9) gene therapy on myocardial structural and functional remodeling post infarction. METHODS: C57BL/6 mice underwent permanent left anterior descending coronary artery ligation and cardiac function was assessed using echocardiography for 8 weeks followed by a terminal measurement of left ventricular (LV) pressure-volume loops. Ang-(1-9) was delivered by adeno-associated viral vector via single tail vein injection immediately following induction of MI. Direct effects of Ang-(1-9) on cardiomyocyte excitation–contraction coupling and cardiac contraction were evaluated in isolated mouse and human cardiomyocytes and in an ex vivo Langendorff perfused whole heart model. RESULTS: Gene delivery of Ang-(1-9) significantly reduced sudden cardiac death post-MI. Pressure–volume measurements revealed complete restoration of end systolic pressure, ejection fraction, end systolic volume and the end diastolic pressure–volume relationship by Ang-(1-9) treatment. Stroke volume and cardiac output were significantly increased versus sham. Histological analysis revealed only mild effects on cardiac hypertrophy and fibrosis, but a significant increase in scar thickness. Direct assessment of Ang-(1-9) on isolated cardiomyocytes demonstrated a positive inotropic effect via increasing calcium transient amplitude and increasing contractility. Ang-(1-9) increased contraction in the Langendorff model through a protein kinase A-dependent mechanism. CONCLUSIONS: Our novel findings show that Ang-(1-9) gene therapy preserves LV systolic function post-MI, restoring cardiac function. Furthermore, Ang-(1-9) has a direct effect on cardiomyocyte 3 calcium handling through a protein kinase A-dependent mechanism. These data highlight Ang-(1-9) gene therapy as a potential new strategy in the context of MI

A light-activated antimicrobial surface is active against bacterial, viral and fungal organisms

Evidence has shown that environmental surfaces play an important role in the transmission of nosocomial pathogens. Deploying antimicrobial surfaces in hospital wards could reduce the role environmental surfaces play as reservoirs for pathogens. Herein we show a significant reduction in viable counts of Staphylococcus epidermidis, Saccharomyces cerevisiae, and MS2 Bacteriophage after light treatment of a medical grade silicone incorporating crystal violet, methylene blue and 2 nm gold nanoparticles. Furthermore, a migration assay demonstrated that in the presence of light, growth of the fungus-like organism Pythium ultimum and the filamentous fungus Botrytis cinerea was inhibited. Atomic Force Microscopy showed significant alterations to the surface of S. epidermidis, and electron microscopy showed cellular aggregates connected by discrete surface linkages. We have therefore demonstrated that the embedded surface has a broad antimicrobial activity under white light and that the surface treatment causes bacterial envelope damage and cell aggregation

Elevated levels of inflammatory cytokines predict survival in idiopathic and familial pulmonary arterial hypertension

BACKGROUND: Inflammation is a feature of pulmonary arterial hypertension (PAH), and increased circulating levels of cytokines are reported in patients with PAH. However, to date, no information exists on the significance of elevated cytokines or their potential as biomarkers. We sought to determine the levels of a range of cytokines in PAH and to examine their impact on survival and relationship to hemodynamic indexes. METHODS AND RESULTS: We measured levels of serum cytokines (tumor necrosis factor-alpha, interferon-gamma and interleukin-1beta, -2, -4, -5, -6, -8, -10, -12p70, and -13) using ELISAs in idiopathic and heritable PAH patients (n=60). Concurrent clinical data included hemodynamics, 6-minute walk distance, and survival time from sampling to death or transplantation. Healthy volunteers served as control subjects (n=21). PAH patients had significantly higher levels of interleukin-1beta, -2, -4, -6, -8, -10, and -12p70 and tumor necrosis factor-alpha compared with healthy control subjects. Kaplan-Meier analysis showed that levels of interleukin-6, 8, 10, and 12p70 predicted survival in patients. For example, 5-year survival with interleukin-6 levels of >9 pg/mL was 30% compared with 63% for patients with levels < or = 9 pg/mL (P=0.008). In this PAH cohort, cytokine levels were superior to traditional markers of prognosis such as 6-minute walk distance and hemodynamics. CONCLUSIONS: This study illustrates dysregulation of a broad range of inflammatory mediators in idiopathic and familial PAH and demonstrates that cytokine levels have a previously unrecognized impact on patient survival. They may prove to be useful biomarkers and provide insight into the contribution of inflammation in PAH

Onset of experimental severe cardiac fibrosis is mediated by overexpression of angiotensin-converting enzyme 2

Angiotensin-converting enzyme (ACE) 2 is a recently identified homologue of ACE. There is great interest in the therapeutic benefit for ACE2 overexpression in the heart. However, the role of ACE2 in the regulation of cardiac structure and function, as well as maintenance of systemic blood pressure, remains poorly understood. In cell culture, ACE2 overexpression led to markedly increased myocyte volume, assessed in primary rabbit myocytes. To assess ACE2 function in vivo, we used a recombinant adeno-associated virus 6 delivery system to provide 11-week overexpression of ACE2 in the myocardium of stroke-prone spontaneously hypertensive rats. ACE2, as well as the ACE inhibitor enalapril, significantly reduced systolic blood pressure. However, in the heart, ACE2 overexpression resulted in cardiac fibrosis, as assessed by histological analysis with concomitant deficits in ejection fraction and fractional shortening measured by echocardiography. Furthermore, global gene expression profiling demonstrated the activation of profibrotic pathways in the heart mediated by ACE2 gene delivery. This study demonstrates that sustained overexpression of ACE2 in the heart in vivo leads to the onset of severe fibrosis