Corelease of Genotoxic Polycyclic Aromatic Hydrocarbons and Nanoparticles from a Commercial Aircraft Jet Engine - Dependence on Fuel and Thrust.

Jet engines are important contributors to global CO2 emissions and release enormous numbers of ultrafine particles into different layers of the atmosphere. As a result, aviation emissions are affecting atmospheric chemistry and promote contrail and cloud formation with impacts on earth's radiative balance and climate. Furthermore, the corelease of nanoparticles together with carcinogenic polycyclic aromatic hydrocarbons (PAHs) affects air quality at airports. We studied exhausts of a widely used turbofan engine (CFM56-7B26) operated at five static thrust levels (idle, 7, 30, 65, and 85%) with conventional Jet A-1 fuel and a biofuel blend composed of hydro-processed esters and fatty acids (HEFA). The particles released, the chemical composition of condensable material, and the genotoxic potential of these exhausts were studied. At ground operation, particle number emissions of 3.5 and 0.5 × 1014 particles/kg fuel were observed with highest genotoxic potentials of 41300 and 8800 ng toxicity equivalents (TEQ)/kg fuel at idle and 7% thrust, respectively. Blending jet fuel with HEFA lowered PAH and particle emissions by 7-34% and 65-67% at idle and 7% thrust, respectively, indicating that the use of paraffin-rich biofuels is an effective measure to reduce the exposure of airport personnel to nanoparticles coated with genotoxic PAHs (Trojan horse effect).

Recent advances in one-stage conversion of lipid-based biomass-derived oils into fuel components - aromatics and isomerized alkanes.

Nowadays, production of biofuels is a rather hot topic due to depleting of conventional fossil fuel feedstocks and a number of other factors. Plant lipid-based feedstocks are very important for production of diesel-, kerosene-, and gasoline-like hydrocarbons. Usually, (hydro)deoxygenation processes are aimed at obtaining of linear hydrocarbons known to have poor fuel characteristics compared to the branched ones. Thus, further hydroisomerization is required to improve their properties as motor fuel components. This review article is focused on conversion of lipid-based feedstocks and model compounds into high-quality fuel components for a single step - direct cracking into aromatics and merged hydrodeoxygenation-hydroisomerization to obtain isoparaffins. The second process is quite novel and a number of the research articles presented in the literature is relatively low. As auxiliary subsections, hydroisomerization of straight hydrocarbons and techno-economic analysis of renewable diesel-like fuel production are briefly reviewed as well.

rdxA, frxA, and efflux pump in metronidazole-resistant Helicobacter pylori: Their relation to clinical outcomes.

BACKGROUND AND AIM: rdxA and frxA mutations and enhancement of efflux pump have been suggested as the cause of metronidazole resistance in Helicobacter pylori. This study was performed to investigate the resistance mechanisms related to clinical eradication outcome, and to examine direct involvement of hefA in metronidazole-resistant isolates with intact rdxA and frxA. METHODS: A total of 53 H. pylori-positive patients who were treated with metronidazole-containing sequential or quadruple therapy from 2011 to 2015 were enrolled. The metronidazole susceptibility of H. pylori isolates was examined by agar dilution test. Mutations in rdxA and frxA, were analyzed with DNA sequencing, and impact of hefA on metronidazole resistance was examined with quantitative real-time reverse transcription polymerase chain reaction, knockout and genetic complementation test for hefA. RESULTS: Seven mutation types of rdxA and/or frxA were found in H. pylori isolated from non-eradicated subjects. rdxA mutation was associated with eradication failure (P = 0.002), and nonsense mutation in rdxA reduced eradication efficacy (P = 0.009). hefA expression was significantly higher in resistant isolates (P < 0.001), especially in rdxA(-)frxA(-) as compared to rdxA(+)frxA(+) (P = 0.027). Resistant isolates with no mutation in rdxA and frxA became susceptible after hefA knockout. Genetic complementation for hefA recovered metronidazole resistance in all of three hefA knockout mutants. CONCLUSIONS: These results suggest that rdxA mutations play a critical role in metronidazole resistance as well as the outcomes of eradication therapy. In addition, hefA seems to be directly involved in metronidazole resistance, which explains the resistance in clinical isolates with intact rdxA and frxA.

Co-administration of amoxicillin-loaded chitosan nanoparticles and inulin: A novel strategy for mitigating antibiotic resistance and preserving microbiota balance in Helicobacter pylori treatment.

Helicobacter pylori (H. pylori) is a causative agent of various gastrointestinal diseases and eradication mainly relies on antibiotic treatment, with (AMX) being a key component. However, rising antibiotic resistance in H. pylori necessitates the use of antibiotics combination therapy, often disrupting gut microbiota equilibrium leading to further health complications. This study investigates a novel strategy utilizing AMX-loaded chitosan nanoparticles (AMX-CS NPs), co-administered with prebiotic inulin to counteract H. pylori infection while preserving microbiota health. Following microbroth dilution method, AMX displayed efficacy against H. pylori, with a MIC50 of 48.34 ± 3.3 ng/mL, albeit with a detrimental impact on Lactobacillus casei (L. casei). The co-administration of inulin (500 µg/mL) with AMX restored L. casei viability while retaining the lethal effect on H. pylori. Encapsulation of AMX in CS-NPs via ionic gelation method, resulted in particles of 157.8 ± 3.85 nm in size and an entrapment efficiency (EE) of 86.44 ± 2.19 %. Moreover, AMX-CS NPs showed a sustained drug release pattern over 72 h with no detectable toxicity on human dermal fibroblasts cell lines. Encapsulation of AMX into CS NPs also reduced its MIC50 against H. pylori, while its co-administration with inulin maintained L. casei viability. Interestingly, treatment with AMX-CS NPs also reduced the expression of the efflux pump gene hefA in H. pylori. This dual treatment strategy offers a promising approach for more selective antimicrobial treatment, minimizing disruption to healthy microbial communities while effectively addressing pathogenic threats.

Aircraft soot from conventional fuels and biofuels during ground idle and climb-out conditions: Electron microscopy and X-ray micro-spectroscopy.

Aircraft soot has a significant impact on global and local air pollution and is of particular concern for the population working at airports and living nearby. The morphology and chemistry of soot are related to its reactivity and depend mainly on engine operating conditions and fuel-type. We investigated the morphology (by transmission electron microscopy) and chemistry (by X-ray micro-spectroscopy) of soot from the exhaust of a CFM 56-7B26 turbofan engine, currently the most common engine in aviation fleet, operated in the test cell of SR Technics, Zurich airport. Standard kerosene (Jet A-1) and a biofuel blend (Jet A-1 with 32% HEFA) were used at ground idle and climb-out engine thrust, as these conditions highly influence air quality at airport areas. The results indicate that soot reactivity decreases from ground idle to climb-out conditions for both fuel types. Nearly one third of the primary soot particles generated by the blended fuel at climb-out engine thrust bear an outer amorphous shell implying higher reactivity. This characteristic referring to soot reactivity needs to be taken into account when evaluating the advantage of HEFA blending at high engine thrust. The soot type that is most prone to react with its surrounding is generated by Jet A-1 fuel at ground idle. Biofuel blending slightly lowers soot reactivity at ground idle but does the opposite at climb-out conditions. As far as soot reactivity is concerned, biofuels can prove beneficial for airports where ground idle is a common situation; the benefit of biofuels for climb-out conditions is uncertain.

Effect of biofilm formation by clinical isolates of Helicobacter pylori on the efflux-mediated resistance to commonly used antibiotics.

AIM: To evaluate the role of biofilm formation on the resistance of Helicobacter pylori (H. pylori) to commonly prescribed antibiotics, the expression rates of resistance genes in biofilm-forming and planktonic cells were compared. METHODS: A collection of 33 H. pylori isolates from children and adult patients with chronic infection were taken for the present study. The isolates were screened for biofilm formation ability, as well as for polymerase chain reaction (PCR) reaction with HP1165 and hp1165 efflux pump genes. Susceptibilities of the selected strains to antibiotic and differences between susceptibilities of planktonic and biofilm-forming cell populations were determined. Quantitative real-time PCR (qPCR) analysis was performed using 16S rRNA gene as a H. pylori-specific primer, and two efflux pumps-specific primers, hp1165 and hefA. RESULTS: The strains were resistant to amoxicillin, metronidazole, and erythromycin, except for one strain, but they were all susceptible to tetracycline. Minimum bactericidal concentrations of antibiotics in the biofilm-forming cells were significantly higher than those of planktonic cells. qPCR demonstrated that the expression of efflux pump genes was significantly higher in the biofilm-forming cells as compared to the planktonic ones. CONCLUSION: The present work demonstrated an association between H. pylori biofilm formation and decreased susceptibility to all the antibiotics tested. This decreased susceptibility to antibiotics was associated with enhanced functional activity of two efflux pumps: hp1165 and hefA.

Inhibitory effects of emodin, baicalin, schizandrin and berberine on hefA gene: treatment of Helicobacter pylori-induced multidrug resistance.

AIM: To investigate the inhibitory effects of emodin, baicalin, etc. on the hefA gene of multidrug resistance (MDR) in Helicobacter pylori (H. pylori). METHODS: The double dilution method was used to screen MDR H. pylori strains and determine the minimum inhibitory concentrations (MICs) of emodin, baicalin, schizandrin, berberine, clarithromycin, metronidazole, tetracycline, amoxicillin and levofloxacin against H. pylori strains. After the screened MDR stains were treated with emodin, baicalin, schizandrin or berberine at a 1/2 MIC concentration for 48 h, changes in MICs of amoxicillin, tetracycline, levofloxacin, metronidazole and clarithromycin were determined. MDR strains with reduced MICs of amoxicillin were selected to detect the hefA mRNA expression by real-time quantitative PCR. RESULTS: A total of four MDR H. pylori strains were screened. Treatment with emodin, baicalin, schizandrin and berberine significantly decreased the MICs of amoxicillin and tetracycline against some strains, decreased by 1 to 2 times, but did not significantly change the MICs of clarithromycin, levofloxacin, and metronidazole against MDR strains. In the majority of strains with reduced MICs of amoxicillin, hefA mRNA expression was decreased; one-way ANOVA (SPSS 12.0) used for comparative analysis, P < 0.05. CONCLUSION: Emodin, baicalin, schizandrin and berberine significantly decreased the MICs of amoxicillin and tetracycline against some H. pylori strains, possibly by mechanisms associated with decreasing hefA mRNA expression.