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Boreal forests play a key role in the global carbon cycle and are facing rapid shifts in nitrogen availability with poorly understood consequences for ecosystem function and global climate. We quantified the effects of nitrogen availability on carbon fluxes from a relatively understudied component of these forests -- understorey vegetation -- at three intervals over the summer growing period in a northern Swedish Scots Pine stand. Nitrogen addition altered both photosynthetic carbon uptake and respiratory release, but the magnitude and direction of this effect depended on the time during the growing season and the amount of nitrogen added. Specifically, nitrogen addition stimulated net ecosystem carbon uptake only in the late growing season. We find evidence for species-specific control of understorey carbon sink strength, as photosynthesis per unit ground area was positively correlated only with the abundance of the vascular plant Vaccinium myrtillus and no others. Comparison of photosynthetic carbon uptake with data on plant carbon dioxide release from the study site, indicate that understorey vegetation photosynthate was mainly supplying respiratory demands for much of the year. Only in the late season with nitrogen addition did understorey vegetation appear to experience a large surplus of carbon in excess of respiratory requirements. Further work, simultaneously comparing all major biomass and respiratory carbon fluxes in understorey and tree vegetation, is required to resolve the likely impacts of environmental changes on whole-ecosystem carbon sequestration in boreal forests. [ABSTRACT FROM AUTHOR]

Yeast alcohol dehydrogenase is inactivated at different rates by the antipodes of α-iodopropionic acid and its amide; the D (+) antipodes react faster. The influence of coenzyme, substrate and pH on the reaction velocity were investigated. Under all conditions second order kinetics have been observed. Activation parameters for the alkylation of the SH groups with the different antipodes were calculated from the temperature dependence of the reaction rates. Large differences in the activation enthalpies (ΔΔH = 6.8 kcal/mole and 2.3 kcal/mole, respectively) were found for the reaction of yeast alcohol dehydrogenase with the different antipodes of α-iodopropionic acid and α-iodopropionamide. These were compensated for by differences in activation entropy of —18.4 and — 5.6 entropy units, respectively. These results are interpreted by assuming highly dissymmetric surroundings of the reacting SH groups favouring the D (+) antipodes in the transition state of the alkylation reaction. The negative activation entropy indicates that this favourable transition state may be attained only by restriction of the degrees of freedom. The relationship between the stereoselective chemical reactivity and the stereospecificity of the enzyme is discussed. [ABSTRACT FROM AUTHOR]

When undergoing nucleophilic reactions with proteins, α-iodopropionic acid and its amide show greater specificity for SH groups than do iodoacetic acid and its amide. The kinetics and stereochemistry of the reactions of the D(+) and L(-) antipodes of α-iodopropionic acid and its amide with both cysteine and papain were investigated. The antipodes of the SH reagents reacted with these asymmetric SH compounds at different rates. In the reaction with papain, the L(-) antipode of the acid reacted faster than the D(+) antipode; the stereochemical preference was inverted when the amide was used, the D(+)antipode reacting faster than the L(-)antipode. Arguing from the differing reactivities of the SH reagents and their antipodes and the pH dependence of the reaction rates, it has been suggested, that L(-)alpha;-iodopropionic acid is specifically oriented onto the reaction center through the concerted attractive and repulsive actions of a cationic and an anionic group in the protein. These have been tentatively identified as a protonated imidazole residue and a carboxylate group respectively. Parallels between these stereospecific alkylations and the catalytic action of the enzyme are discussed. [ABSTRACT FROM AUTHOR]

The bacterium Helicobacter pylori induces gastric inflammation and predisposes to cancer. H. pylori-infected epithelial cells secrete cytokines and chemokines and undergo DNA-damage. We show that the host cell's mitochondrial apoptosis system contributes to cytokine secretion and DNA-damage in the absence of cell death. H. pylori induced secretion of cytokines/chemokines from epithelial cells, dependent on the mitochondrial apoptosis machinery. A signalling step was identified in the release of mitochondrial Smac/DIABLO, which was required for alternative NF-κB-activation and contributed to chemokine secretion. The bacterial cag-pathogenicity island and bacterial muropeptide triggered mitochondrial host cell signals through the pattern recognition receptor NOD1. H. pylori-induced DNA-damage depended on mitochondrial apoptosis signals and the caspase-activated DNAse. In biopsies from H. pylori-positive patients, we observed a correlation of Smac-levels and inflammation. Non-apoptotic cells in these samples showed evidence of caspase-3-activation, correlating with phosphorylation of the DNA-damage response kinase ATM. Thus, H. pylori activates the mitochondrial apoptosis pathway to a sub-lethal level. During infection, Smac has a cytosolic, pro-inflammatory role in the absence of apoptosis. Further, DNA-damage through sub-lethal mitochondrial signals is likely to contribute to mutagenesis and cancer development., (© 2022. The Author(s).)

Background: Antimicrobial therapy is recommended to eradicate Helicobacter (H.) pylori in infected individuals. As first-line treatments are empiric, knowledge of antimicrobial resistance is key to successful eradication., Aims: We investigated primary resistance in an eastern German region to derive recommendations for eradication treatment., Methods: We used molecular genetic methods to examine Helicobacter rapid urease test (RUT) positive gastric specimens of 533 patients from Berlin and the federal state of Brandenburg with allegedly no prior eradication treatment. Tissue samples were removed from RUT and screened by real-time PCR for mutations conferring resistance to clarithromycin. In addition, 182 samples out of 533 were tested for resistance to levofloxacin and tetracycline., Results: Primary resistances were 10.9% (58 out of 533) to clarithromycin; 13.7% (25/182) to levofloxacin; and 2.2% to tetracycline (4/182). Combined resistance to clarithromycin/levofloxacin was low (2.2%, 4/182). Female sex was significantly associated with clarithromycin resistance., Conclusion: Clarithromycin may be a suitable first-line antibiotic for about 90% of outpatients. A simple molecular test may help physicians avoid prescription of an ineffective first-line regimen., (© 2020 John Wiley & Sons Ltd.)

Background : VPM1002BC is a modified mycobacterium Bacillus Calmette Guérin (BCG) for the treatment of non-muscle invasive bladder cancer (NMIBC). The genetic modifications are expected to result in better immunogenicity and less side effects. We report on patient safety and immunology of the first intravesical application of VPM1002BC in human. Methods : Six patients with BCG failure received a treatment of 6 weekly instillations with VPM1002BC. Patients were monitored for adverse events (AE), excretion of VPM1002BC and cytokines, respectively. Results : No DLT (dose limiting toxicity) occurred during the DLT-period. No grade ≥3 AEs occurred. Excretion of VPM1002BC in the urine was limited to less than 24 hours. Plasma levels of TNFα significantly increased after treatment and blood-derived CD4+ T cells stimulated with PPD demonstrated significantly increased intracellular GM-CSF and IFN expression. Conclusion : The intravesical application of VPM1002BC is safe and well tolerated by patients and results in a potential Th1 weighted immune response., (© 2020 The Author(s). Published with license by Taylor & Francis Group, LLC.)