, 2008a) of potential industrial interest; (2) the mechanism of a

, 2008a) of potential industrial interest; (2) the mechanism of action of the purified bacteriocin on Listeria cells; and (3) some mechanistic aspects of the lytic activity of sakacin A toward Listeria cell walls. Lactobacillus sakei DSMZ 6333 (DSMZ, Braunschweig, Germany) was cultured in an inexpensive culture medium broth (Trinetta et al., 2008a). Listeria ivanovii ATCC BAA-678

grown in Tryptic Soy Agar (Difco Laboratories, Sparks, MD) for 18 h at 37 °C was used as an indicator strain. Stocks were maintained at − 20 °C in appropriate liquid media containing 10% (w/v) selleck chemicals llc glycerol and propagated twice before use. Sakacin A was purified from 1 L cultures of L. sakei, grown at 30 °C for 18 h. Cells were centrifuged (10 000  g , 35 min, 4 °C). The cell-free supernatant was made 50 mM in sodium acetate, and the pH was adjusted to 4.5 with acetic acid/NaOH. The resulting

solution was loaded onto a SP-Sepharose fast flow cation exchange column (4 × 11.3 cm; Whatman). Proteins were eluted stepwise with 0.2 and 1 M NaCl, and fractions selleck chemicals were assayed for antimicrobial activity (Batdorj et al., 2007). The active fraction was applied on a 10 × 250 mm reversed phase (RP) C18 column (300 Â pores, 10 μm, Labservice; Analytica, Milan, Italy) run on a Waters HPLC (625 LC, Toronto, Canada) and equilibrated with 95% (v/v) solvent A [0.1% aqueous trifluoroacetic acid (TFA)] and 5% (v/v) solvent B (0.1% aqueous TFA, 80% acetonitrile). Stepwise elution by increasing acetonitrile

concentration (to 30%, 50% and 80%) was carried out at a flow rate of 1.5 mL min−1. The active Histamine H2 receptor fraction, eluted at 50% acetonitrile, was loaded on a Superdex Peptide column (Amersham Biosciences, Milan, Italy) equilibrated in aqueous 20% (v/v) acetonitrile containing 0.01% (v/v) TFA. The final chromatographic step was carried out on a 4.6 × 250 mm RP Symmetry C18 column (5 μm, 100 Â; Waters, Milan, Italy) equilibrated with 95% (v/v) solvent A and 5% (v/v) solvent B. Sakacin A was eluted with a linear gradient from 20% to 60% of solvent B for 20 min at a flow rate of 0.8 mL min−1. Tricine SDS-PAGE was carried out in precast 12% acrylamide gels (NuPage®; Invitrogen, Milan, Italy). Markers covered the range from 3.5 to 260 kDa (Novex Sharp Pre-Stained Standard; Invitrogen). One half of the gel was stained with Coomassie Blue (Symply-Blue Safestain; Invitrogen), whereas the other half was washed with sterile water and overlaid with soft nutrient agar medium (10 mL) containing the indicator strain. Antimicrobial activity was assessed after incubation at 37 °C (Yamamoto et al., 2003). MALDI-TOF/MS (matrix-assisted laser desorption/ionisation-time of flight mass spectrometry) measurements were carried out on a Voyager DEPRO spectrometer (PerSeptive Biosystems, Framingham, MA) equipped with an N2 laser (337 nm, 3 ns pulse width) operated in the positive reflector ion mode and using delay extraction.


84] It is thus possible that the inflammatory enviro


84] It is thus possible that the inflammatory environment of the rheumatoid synovium can drive Th17 cells to produce IL-17 in a cytokine-dependent manner. Moreover, the concept that CD4+ T cells may not be the only source of IL-17 in the joint is being increasingly Ku-0059436 order recognized. For example, mast cells have recently been identified as a source of IL-17 in RA synovium and are potent producers of IL-17 upon stimulation with TNF-α, immune complexes and LPS.[76, 85] Basically, the high levels of mast cells are observed in avascular, fibrotic regions of RA synovial tissue, without any correlation with lymphocytic infiltration.[86] Several studies have recently proposed neutrophils and Th17 cells as key players in the onset and perpetuation of this disease. The main goal of recent studies was to determine whether cytokines driving neutrophil and Th17 activation are dysregulated in very early RA patients.[87] In addition to inducing a highly find more inflammatory cytokine milieu, IL-17 drives osteoclastogenesis, neoangiogenesis and the subsequent recruitment of innate immune cells that amplify more inflammation in the RA joint.[81, 88] IL-17 as a potent chemoattractant

for pre-committed CD4+ T cells and neutrophils may promote the migration of B cells to lymphoid follicles in the chronic phase of synovial inflammation.[89] It has been identified that Th17 cells are within SF and synovial tissue, and demonstrated that RA synovial fibroblasts treated with IL-17 and TNF-α can promote the survival and functional lifespan of neutrophils, associated with increased number of neutrophils observed in the rheumatoid synovium.[90] As noticed above, IL-17 promotes recruitment of both neutrophils and

monocytes by means of inducing various chemokines. Also preferential recruitment of CCR6-expressing CYTH4 Th17 cells to inflamed joints via CCL20 in RA and its animal model has been shown.[65, 91] Moreover IL-17 exerts an anti-apoptotic effect, mediated by IL-17RA and IL-17RC, associated with increased synoviolin expression. These data suggest that IL-17 contributes to RA chronicity through both synovial inflammation and hyperplasia. The anti-apoptotic role for IL-17 is supported by data in IL-17R knockout mice correlated with markedly reduced synovial hypercellularity.[92, 93] On the other hand, oxygen metabolism has an important role in the pathogenesis of RA. Reactive oxygen species (ROS) are produced in many normal and abnormal processes in patients with atheroma, asthma, joint diseases and cancer.[94] It has been suggested that the level of ROS in patients with RA is higher than in healthy subjects.

056) Cause of death information was available for 1879 deaths: 4

056). Cause of death information was available for 1879 deaths: 452 (84.8%) of 533 deaths in patients infected via IDU and 1427 (90.4%) of 1564 deaths in non-IDU patients. Among these, causes of death could be assigned for 1600 (85%) deaths (379 IDUs and 1221 non-IDUs). Figure 1 shows percentages of deaths from

specific causes in patients who were and were not infected via IDU. The risk of death from each cause was higher in IDUs than non-IDUs, with particularly marked increases in the risks of liver-related deaths, and deaths from violence and non-AIDS infection. Figure 2 shows the estimated cumulative incidence of deaths from GPCR & G Protein inhibitor AIDS, liver-related disease (including hepatitis), violence (including suicide and overdose) and other causes up to 8 years after starting cART, separately for IDUs and non-IDUs. By 8 years after initiation of cART, the cumulative incidence of death was 16.3% in patients infected via IDU, compared with 7.3% in other

patients. By the end of follow-up, the largest differences in the cumulative incidence of cause-specific death between IDUs and non-IDUs were in deaths resulting from hepatitis [0.72 vs. 0.08%, respectively; adjusted hazard ratio (AHR) 8.8; 95% CI 5.0–15.5], liver disease (0.38 vs. 0.09%; AHR 4.6; 95% CI 2.5–8.7) and substance abuse (0.54 vs. 0.04%; AHR 6.7; 95% CI 3.4–13.4). Mortality of unknown cause (1.46 vs. 0.60%; AHR 3.1; 95% CI 2.3–4.1) was also higher in the IDU group than in the non-IDU group. In the subset of patients with information on both HCV coinfection and causes of death (n=13 203), the hazard ratio for death from liver disease was attenuated Selleck PD98059 from 4.08 (95% CI 2.24–7.44) to 1.02 (95% CI 0.50–2.09) on adjustment for coinfection with HCV. In this analysis involving 14 cohort studies and 44 043 participants, individuals infected via IDU experienced higher rates of death and AIDS, compared with other patients, from the time that

they started cART. Although associations for patient characteristics at initiation Sodium butyrate of cART with subsequent disease progression were largely similar between the two groups, the inverse association of baseline CD4 with subsequent disease progression appeared weaker in patients infected via IDU. By contrast, associations of baseline HIV-1 RNA and AIDS diagnosis before baseline with subsequent rates of AIDS appeared stronger in patients infected via IDU. Compared with other patients, those infected via IDU were at greater risk of all of the specific causes of death we examined, with the greatest differences seen for deaths as a result of hepatitis and liver failure and deaths as a result of substance abuse. The differences we observed were not explained by differences in baseline characteristics between IDUs and non-IDUs. However, the association with liver-related death appeared to be explained by coinfection with HCV.

Consistent with the hypothesis that higher levels of cholinergic

Consistent with the hypothesis that higher levels of cholinergic neuromodulatory activity reduce opportunity costs in rats performing an attention task, such levels were found to correlate with the degree of task compliance under taxing conditions (Passetti et al., 2000). Furthermore, this hypothesis also predicts the relatively poor

and fluctuating levels of attentional performance in rats exhibiting relatively low selleck compound levels of cholinergic neuromodulation during such performance (see Paolone et al., 2013). Likewise, this hypothesis predicts that humans who carry a minor allele of the choline transporter gene, which may limit the dynamic range of neuromodulatory cholinergic activation, self-report greater levels of distractibility in situations that readily allow for discontinuation Antiinfection Compound Library of performance and engagement on alternative behavioral

of cognitive activities (e.g. are easily distracted by a TV or radio playing in the next room). In contrast, such vulnerability to distraction may be more difficult to demonstrate in situations that demand high levels of attention but are relatively devoid of competitive alternatives (Berry et al., 2013). In other words, compared with humans expressing the wild-type gene for this transporter, the variant-expressing subjects, assuming that expression of this allele limits the capacity for cholinergic neurotransmission, may experience higher opportunity costs and assign relative greater utility to engaging in alternative mental or behavioral action. As discussed above, the results of our research cumulatively support the hypothesis that increases in cholinergic neuromodulation enhance prefrontal glutamatergic–cholinergic transient interactions (Fig. 1) and that stimulation of nAChRs

‘import’ the neuromodulatory impact on transients. Our studies on the beneficial effects of alpha4beta2* nAChR agonists on cholinergic transients and SAT performance demonstrated that such benefits are restricted to SAT performance Sinomenine that is burdened by the presence of a distractor. Furthermore, nAChR agonist-induced increase in hits was due primarily to an increase in hits on trials where a signal followed extended periods of nonsignal processing, that is, hits for which cholinergic transients are required (Howe et al., 2010). Thus, higher levels of cholinergic neuromodulation increase the probability for cholinergic transients and thus for incongruent hits. These considerations are consistent with the hypothesis that higher levels of cholinergic neuromodulatory activity lower opportunity costs in part by reducing detection uncertainty, thereby stabilising and restoring hit rates and thus performance outcome.

The patient had a history of atopia Treatment with topic clobeta

The patient had a history of atopia. Treatment with topic clobetasol 0.05% in a daily

application was performed for 1 week and intensified by occlusive technique every day for 10 days and to alternate days for 2 more weeks. Cutaneous tests were not realized. The evolution went to the total resolution 5 weeks from the beginning of the symptoms. Which is the reason of the above-mentioned reaction? SOLUTION: Contact dermatitis caused by a temporary tattoo with black henna. The temporary tattoos with henna (powder of greenish color, obtained from Lawsonia inermis’s leaves) are traditionally used as adornment in certain cultures (Muslim and Hindu principally) or ceremonies (weddings, Ferrostatin-1 ic50 pregnancy). The obtained dye can be of different colors: brown, red, purple, black. Its use is habitual in Africa, Asia, and the Middle East and it has spread to Occident at the same time as other procedures like definitive tattoos or piercings. These tattoos are well accepted

by occidental travelers in view of its non-permanent character (2–3 wk of duration) and they Lumacaftor purchase are normally made by “ambulant artists” or in establishments with low sanitary guarantees, since already it had been detected in the destination visited by our patient.1 To improve the quality of the tattoo (color, dried, duration) the henna can be mixed with certain additives, one of them is ρ-phenylenediamine (PPD), a coloring authorized in low concentrations (up to 6%) for cosmetic products like dyes for hair, products that our patient had never used before. PPD is a well-known contact allergen2 being used to obtain the black henna, occasionally in concentrations of up to 15%.

Its use explains the high incidence of contact dermatitis in this type of tattoos.3,4 PPD can cause immediate or late reaction and other problems such as crossed reactivity Benzatropine to dyes used habitually in hairdresser’s shop, clothes, or footwear, even with certain medicaments such as sulfonamides or sulfonylureas. The injuries of our patient suggest a contact dermatitis caused by a delayed-type allergy IV that appeared after a wide lag time of 10 days typical of a first exhibition to the allergen, similar to the two cases described by Laüchl and colleagues.3 Although we believe that PPD is the most probable reason of the reaction we cannot confirm with absolute safety that it should be the responsible allergen given the absence of cutaneous specific tests. The reaction evolved to the complete resolution but permanent injuries have been described as hypo- or hyperpigmentation and cicatrizial queloids.5 In addition, the previous contact with black henna/PPD can cause the permanent sensibilization to commented dyes,6 with the limitation that it can suppose for the affected persons.

The global regulator GlxR,

The global regulator GlxR, check details which controls

expression of some catabolic operons, does not appear to have a binding site in or around the sialic acid cluster (Kohl et al., 2008; Toyoda et al., 2011), making the mechanism of glucose repression unclear. We propose two potential explanations for the ability of C. glutamicum to use sialic acid so well as a nutrient. The first is that these genes are evolutionary remnants of a previous life of this bacterium in close association with a mucosal surface, the type of environments where the vast majority of bacteria that use sialic acids live. We consider this explanation a weak one as unless this association was very recent, the genes would not be intact and would have pseudogenized or been removed from the genome. It is also clear that the clusters in the pathogenic Corynebacteria are slightly differently organized to those in the soil bacterium C. glutamicum, suggesting some active gene transfer within the soil niche and suggesting Doxorubicin cost a positive selection for the retention and regulation of these genes. The second

explanation is that sialic acid is actually an important source of nutrients in the soil. This is supported by the fact that sialidases have in fact been characterized from other nonpathogenic soil Actinobacteria such as Micromonospora viridifaciens and Arthrobacter ureafaciens (Saito et al., 1979; Gaskell et al., 1995), but these have next only been

studied biochemically and structurally with no analysis on their physiological role in these environments. This study demonstrates that a nonpathogenic soil-dwelling, sialidase-positive actinobacterium can use sialic acid efficiently as a nutrient. The soil is a highly variable and complex environment and one could imagine potential sources of sialic acid and other nonulonosinic acids from other organisms in this niche such as Aspergillus sp., which are known to have sialic acids on their surface (Wasylnka et al., 2001) and perhaps other fungi in this niche, and so we favour this explanation being more likely. Also, soil bacteria are likely to encounter patches of rich organic material like decomposing animals, which would also contain sialic acid. We would like to thank Dr Jason Holder for sharing unpublished data and the BBSRC for support on our research on bacterial sialic acid transporters. “
“The Escherichia coli entD gene, which encodes an Sfp-type phosphopantetheinyl transferase (PPTase) that is involved in the biosynthesis of siderophore, is available as a high-expression ASKA clone (pCA24N∷entD) constructed from the E. coli K-12 strain AG1. In E. coli DH5α, pCA24N∷entD complemented a pfaE-deficient clone that comprised pfaA, pfaB, pfaC and pfaD, which are four of the five pfa genes that are responsible for the biosynthesis of eicosapentaenoic acid derived from Shewanella pneumatophori SCRC-2738.

, 2007) As the mechanism of iron acquisition by mycobacteria is

, 2007). As the mechanism of iron acquisition by mycobacteria is unique to these bacteria, this provides a number of possible targets for drug action that will not be found in other microorganisms or, and most importantly, in the host. Such suggestions have already been made on the basis of mutants of

pathogenic mycobacteria losing their virulence in animal models when components of iron acquisition mechanism have been deleted (De Voss et al., 2000; Luo et al., 2005; Somu et al., 2006). The central molecule that is involved in iron acquisition Selleckchem Dorsomorphin in almost all mycobacteria is mycobactin. This is a lipophilic, small-molecular-weight siderophore that is located in the envelope of mycobacteria in close proximity to the cytoplasmic membrane (Ratledge, 1999). Although it has a very high affinity for iron (Ks∼1036), it does not directly sequester iron from the host as it is insufficiently water soluble for

this task and cannot come into direct contact with any iron-containing molecules of the host; instead, a related siderophore, carboxymycobactin, is secreted by pathogenic mycobacteria, which is then the functional extracellular siderophore. Both mycobactin and carboxymycobactin are considered to be synthesized by a common pathway, with divergence to the two siderophores occurring at one of the last stages (Ratledge, 2004). The pathway for mycobactin/carboxymycobactin involves the initial synthesis of salicylic acid via the shikimic acid

pathway; this is then linked to various amino acids or their derivatives to yield the final siderophore (Quadri Ruxolitinib datasheet et al., 1998). Deletion of any one of the three genes (trpE2, entC or entD) that are involved in the biosynthesis of salicylate from chorismic acid in Mycobacterium smegmatis results in the impairment of growth particularly under conditions when iron is at a limiting concentration (Nagachar & Ratledge, 2010). Similar results were reported when salicylate-requiring auxotrophs of M. smegmatis were generated by random mutagenesis (Ratledge & Hall, 1972; Adilakshmi et al., 2000). It is therefore our contention that the antitubercular drug p-aminosalicylate (PAS) acts as an analogue Fossariinae of salicylic acid and either inhibits its synthesis or, more likely, its onward conversion to mycobactin. PAS was one of the first antituberculosis drugs (Lehmann, 1946). As its discovery pre-dated the elucidation of the structure of mycobactin (Snow, 1965), it was suggested both then and later by numerous writers (e.g. Winder, 1964) that its mode of action was that of an antifolate drug as it seemingly could be regarded as an analogue of p-aminobenzoate, the aromatic precursor of folic acid. More recent evidence suggests that the linkage of PAS to folate metabolism could be at the level of thymidylate synthase (ThyA), whose gene, when mutated, leads to PAS resistance in M. tuberculosis (Rengarajan et al., 2004; Mathys et al., 2009).

The direct conversion of H2 (or formate) + CO2 to methane is cata

The direct conversion of H2 (or formate) + CO2 to methane is catalysed by hydrogenotrophic methanogens. The acetate conversion to methane Maraviroc manufacturer and CO2 can be performed through two alternative pathways. The first pathway, catalysed by acetoclastic methanogens (species of Methanosarcina or Methanosaeta), is a cleavage of the methyl and carboxyl groups from acetate producing methane and

CO2, respectively. The second possible pathway relies on the syntrophic association between acetate oxidizing bacteria and hydrogenotrophic methanogens: the formers convert acetate into H2 and CO2, which are then used by the hydrogenotrophic methanogens to produce methane (Schink & Stams, 2006). Regardless of the environmental conditions and of the predominance of either acetoclastic or hydrogenotrophic pathways, methanogenic Archaea, as the terminal oxidizers of the community, play a key role. As a consequence, developing new and rapid methods to elucidate the identity and diversity of methanogens would be useful for the global understanding of the complex

process of methanogenesis. The methyl-coenzyme-M reductase enzyme complex (MCR), composed of two alpha, beta and gamma subunits, catalyses methane formation and is ubiquitous in methanogens (Thauer, 1998). MCR is unique to methanogens, with the exception of the methane-oxidizing Archaea (Hallam et al., 2003). In addition, MycoClean Mycoplasma Removal Kit a few members of the Methanomicrobiales and Methanococcales also possess a type II isoenzyme X-396 mw (Mrt) (Lehmacher & Klenk, 1994). On the basis of the comparison of available 16S rRNA and mcrA gene sequences of methanogens, the mcrA gene was demonstrated to be an alternative phylogenetic marker to the 16S rRNA gene (Luton et al., 2002). T-RFLP fingerprints of the mcrA gene have been used for phylogenetic analysis of methanogen populations (Lueders et al., 2001). Our objective in this study was to develop a novel fingerprinting method that distinguishes the methanogenic groups from environmental or engineered systems that should be

less time-consuming, more cost-effective, but as informative as T-RFLP. This methodology, based on the natural length variations of the mcrA gene, originates from the work of Suzuki et al. (1998), who developed the amplicon length heterogeneity PCR method (LH-PCR) based on the natural length variation of the bacterial 16S rRNA gene. In this study, the new methodology we have developed and named amplicon LH-PCR of the mcrA gene (LH-mcrA) is validated using clones from libraries from a plug flow-type bioreactor (PFBR). The PFBR consisting in eight serially linked compartments was operated at 25 °C and fed with liquid swine manure at a rate of 1–2 g chemical oxygen demand (COD) L−1 day−1 and a hydraulic retention time of 60 days, as described in Roy et al. (2009).

The plasmids pg5′CAoatg1, pg3′downAoatg1, the Entry Clone plasmid

The plasmids pg5′CAoatg1, pg3′downAoatg1, the Entry Clone plasmid containing the A. oryzae adeA gene as a selective marker (constructed in our laboratory),

and the destination vector pDEST™R4-R3 (Invitrogen) were then subjected to the Gateway LR reaction using the Gateway LR Clonase Reaction Mix (Invitrogen) to generate plasmid pgA1EG. Using plasmid pgΔAoatg1 as a template, the sequence containing the deletion cassette, which consisted of the C-terminal region of Aoatg1 (0.8 kb), egfp and adeA genes (2.9 kb), and 1.5-kb downstream region of Aoatg1, was amplified by PCR with the primers pg5′aoatg1locusF and pg3′aoatg1-locusdownR, and then transformed into A. oryzae

NSRku70-1-1. selleck products The recombination of the Aoatg1 and egfp genes was confirmed by Southern blotting using a 2.0-kb fragment of the region downstream of Aoatg1 MAPK inhibitor as a probe, which was generated by PCR with the primers downAoatg1-F and downAoatg1-R. The plasmid pgaA1, which harbored the amyB promoter, Aoatg1 gene, and selection marker niaD, was constructed to overexpress AoAtg1 under control of the amyB promoter using the Multisite Gateway cloning system. The pgaA1 plasmid was transformed into A. oryzae niaD300. We first identified an A. oryzae ATG1 homolog, Aoatg1, in the A. oryzae genome database (http://www.bio.nite.go.jp/dogan/project/view/AO) using the BLAST algorithm. 5′-and 3′-RACE analyses revealed that Aoatg1 contained one intron and two exons, and encoded a predicted polypeptide of 986 amino acids with a calculated molecular mass of 107 kDa. AoAtg1 displayed 25% identity to Atg1 of S. cerevisiae and, as determined from the Pfam database, had an Atg1 kinase domain identified in the Pfam database (http://pfam.sanger.ac.uk/) (Supporting Information, Fig. S1). To determine the localization of AoAtg1, we constructed strain A1EG, which expressed the fusion protein AoAtg1–EGFP under control of the native promoter. After culturing A1EG for 24 h at 30 °C in CD + m medium to promote growth, the

strain was transferred (-)-p-Bromotetramisole Oxalate to nitrogen-deprived medium (CD − N) and further cultured for 4 h to induce autophagy. In CD + m medium, AoAtg1–EGFP localized to PAS-like structures and in the cytoplasm (Fig. 1, left). After starvation in CD − N medium, the number of punctate fluorescent spots had clearly increased (Fig. 1, right). These results were consistent with the reported localization of Atg1–GFP in S. cerevisiae, in which the number of the PAS increased after the induction of autophagy (Cheong et al., 2008). To investigate the function of AoAtg1, we disrupted Aoatg1 by the replacement with the selective marker adeA and confirmed the mutation by Southern blot analysis (Fig. S2).

Previous works stated that only two membranes were

Previous works stated that only two membranes were Panobinostat cost present, the vacuolar membrane and one of the two bacterial membranes. The absence of the cell wall was related to the special vertical transmission of the endosymbionts in whiteflies. In this work,

we present electron microscopic studies showing a complete cell envelope in ‘Ca. Portiera aleyrodidarum’ from the whitefly Bemisia tabaci. Additionally, comparison of the inferred metabolism from the gene content did not show any difference in cell envelope biogenesis compared with the closely related three-membrane endosymbionts ‘Candidatus Carsonella ruddii’ and ‘Candidatus Evansia muelleri’ Xc1. Our results rule out the proposal that ‘Ca. Portiera aleyrodidarum’ is an exception to the three-membrane

system. “
“Kosakonia radicincitans (formerly known as Enterobacter radicincitans), an endophytic bacterium was isolated from the symptomatic tissues of bacterial wilt diseased banana (Musa spp.) plant in Malaysia. The total genome size of K. radicincitans UMEnt01/12 is 5 783 769 bp with 5463 coding sequences (CDS), 75 tRNAs, and 9 rRNAs. The annotated draft genome of the K. radicincitans UMEnt01/12 strain might shed light on its role as a bacterial wilt-associated bacterium. “
” Gerd Döring, Professor of Medical Microbiology and Hygiene at the AZD3965 nmr University of Tübingen (Germany), was very much looking forward to attending the 14th International Conference on Pseudomonas, to which he had been invited and where he was going to chair a session on cystic

fibrosis (CF) and lead a discussion on antibiotic therapy against Pseudomonas aeruginosa infections, in September 2013. But fate had it otherwise. Gerd died on 2 July 2013, after a malignant melanoma had spread to his lung with uncanny speed. Gerd Döring was born in Nürnberg on 30 acetylcholine August 1948, and studied chemistry at the University of Tübingen, where he obtained a PhD for his work on transition metal complexes in 1978. From 1977 to his death, Gerd mostly worked at the Hygiene Institute in Tübingen, only interrupted by scientific visits to Niels Høiby’s laboratory in Copenhagen in the 1980s and 1990s and by a study leave in Lyon in 1992. Under the guidance of the former director of the Hygiene Institute, Konrad Botzenhart, Gerd Döring developed a keen interest in P. aeruginosa and in the chronic infections that this bacterium causes in the lung of CF patients. His post doctoral ‘habilitation’ thesis published in 1986 dealt with pathogenic mechanisms of P. aeruginosa (in particular, proteases), their regulation, and consequences for inflammation. In the same year, one of us (DH) met Gerd for the first time at a symposium that he organized on ‘Basic research and clinical aspects of P. aeruginosa’ in Tübingen. At that time, Gerd was intrigued by observations indicating that P. aeruginosa must be well adapted to hypoxic conditions, in particular in the CF lung, and so we decided to test whether the ability of P.