Medical, dental, and dietary histories were obtained. The children were examined for DE using a modified index. Results.  The

prevalence of DE by subject affected was 77% in monozygotic twins (MZ), 74% in dizygotic twins (DZ), and 75% in singleton controls (P > 0.1). Of the teeth scored, 12% had mild, 10% moderate, and 1% severe lesions, and DE was more severe in the older age group (P < 0.05). Concordance rates for erosion lesions in MZ and DZ co-twins were not statistically significant. Conclusions.  The prevalence of DE and the concordance of erosion lesions were similar between MZ and DZ twins and singleton children, suggesting that the contribution of genetic factors to DE is negligible. "
“International Journal of Paediatric Dentistry 2011; Background.  Physiological root resorption differentiates primary from permanent teeth. The understanding of what protects and regulates root resorption might help to develop this website therapies to its control. Aim.  To verify the presence and distribution of ECRM and the expression of CK14, OPG, TRAP and COX-2 in the periodontal ligament (PDL) of

human primary and Buparlisib permanent teeth. Design.  Eight primary teeth undergoing physiological or pathological root resorption and 4 permanent teeth were immunohistochemically processed for CK14, TRAP, COX-2 and OPG expression. Results.  PDL from primary and permanent teeth showed similar morphological features; however, fewer ECRM clusters and higher immunoreactivity to CK14 were found in primary PDL. In permanent teeth, ECRM were distributed along the entire MRIP PDL tissue. Howship′s lacunae were found only in primary teeth, associated with the presence of TRAP-positive cells and increase in COX-2 expression. OPG expression in primary PDL was detected in nonresorptive cervical areas and in lacunae

showing reparative tissue. It was observed higher expression of OPG in all permanent teeth when compared to primary specimens. Conclusions.  It may be concluded that PDL from primary teeth shows less ECRM clusters and lower expression of OPG. These features may be associated with lower protection against root resorption in primary teeth. “
“International Journal of Paediatric Dentistry 2011; 21: 141–150 Objective.  To evaluate the effect of acidic medicines (Klaricid®, Claritin®, and Dimetapp®) on surface enamel in vitro. Methods.  Enamel blocks (n = 104) were randomly distributed into two groups: G1 (pH-cycling simulating physiological oral conditions) and G2 (erosive conditions). Each group was divided into four subgroups, three to be immersed in the medicines and the control in deionized water. Specimen surfaces were evaluated for roughness and hardness at baseline and again after the in vitro experimental phase, which included 30 min immersions in the medicines twice daily for 12 days.

, 2003b; Shinkai, unpublished results). The results of the present study, which employed

both mono- and co-culture studies, strongly support this possibility. None of the S. ruminantium isolates could independently digest fiber as previously reported (Kingsley & Hoeniger, 1973; Scheifinger & Wolin, 1973), whereas the addition of S. ruminantium to a culture of F. succinogenes significantly improved fiber digestion with a concomitant increase in propionate production. This synergy find more could be caused by cross-feeding between the two species. Thus, F. succinogenes degrades cellulose to produce succinate and cello-oligosaccharides, while S. ruminantium decarboxylates succinate to propionate (Scheifinger & Wolin, 1973; Strobel C646 solubility dmso & Russell, 1991) and utilizes cello-oligosaccharides, some of which are known to function as feedback inhibitors of F. succinogenes cellulase (Huang & Forsberg, 1990; Maglione et al., 1997). More importantly, the extent of this synergy between F. succinogenes and S. ruminantium might depend on the phylotype of S. ruminantium, because clade I isolates were found to be more potent than clade II isolates in terms of increasing fiber digestion and propionate production. This result

could be explained by the superior ability of clade I isolates in succinate conversion, cello-oligosaccharide consumption or special niche formation, or by other unknown factors. It is therefore a priority to define the metabolic and ecologic advantages of clade I isolates that lead to their enhanced synergy with F. succinogenes compared with clade II isolates. This synergy between F. succinogenes and S. ruminantium aminophylline for fiber digestion only occurred on orchardgrass hay and rice straw but not on alfalfa. Although the reason for this difference is not apparent, it may depend on structural and chemical differences between fiber sources such as grasses and legumes (Akin et al., 1993). Indeed, S. ruminantium has often been found in bacterial 16S rRNA gene clones retrieved from ruminally incubated orchardgrass hay but has never found in clones

retrieved from ruminally incubated alfalfa hay (Koike et al., 2003b). However, Fibrobacter and Treponema species may synergize for the digestion of alfalfa as described by Stanton & Canale-Parola (1980), because ruminally incubated alfalfa yields several clones that show high similarity with Treponema (Koike et al., 2003b). Overall, clades I may be better symbionts for F. succinogenes in terms of grass fiber digestion. The S137 isolate (clade I) showed the highest synergy with F. succinogenes, which is in good agreement with a previous report regarding combinations of S. ruminantium and R. flavefaciens (Sawanon & Kobayashi, 2006). Active decarboxylation of succinate to produce propionate, which was previously demonstrated for the combination of S. ruminantium and R.

In conclusion, an increase in movement speed changes the power of GPi oscillations by means of a reduction of the activity in the low beta band and an elevation of activity in the gamma band. The current study yields new

insights into the physiological mechanism of GPi during the execution of the motor task at low and high speed. “
“The insular cortex (IC) is involved in the generalization of epileptic discharges in temporal lobe epilepsy (TLE), whereas seizures originating in the IC can mimic the epileptic phenotype seen in some patients with TLE. However, few studies have addressed www.selleckchem.com/products/byl719.html the changes occurring in the IC in TLE animal models. Here, we analyzed the immunohistochemical and electrophysiological see more properties of IC networks in non-epileptic control and pilocarpine-treated epileptic rats. Neurons identified with a neuron-specific nuclear protein antibody showed similar counts in the two types of tissue but parvalbumin- and neuropeptide Y-positive interneurons were significantly decreased (parvalbumin, approximately −35%; neuropeptide Y, approximately −38%; P < 0.01) in the epileptic IC. Non-adapting neurons were seen more frequently in the epileptic IC during intracellular injection of depolarizing current pulses. In addition, single-shock electrical

stimuli elicited network-driven epileptiform responses in 87% of epileptic and 22% of non-epileptic control neurons (P < 0.01) but spontaneous postsynaptic potentials had similar amplitude, duration and intervals of occurrence in the two groups. Finally, pharmacologically isolated, GABAA receptor-mediated inhibitory learn more postsynaptic potentials had more negative reversal potential (P < 0.01) and higher peak conductance (P < 0.05) in epileptic tissue. These data reveal moderate increased network excitability in the IC of pilocarpine-treated epileptic rats. We propose that this limited

degree of hyperexcitability originates from the loss of parvalbumin- and neuropeptide Y-positive interneurons that is compensated by an increased drive for GABAA receptor-mediated inhibition. “
“HPC-1/syntaxin 1A (STX1A) is thought to regulate the exocytosis of synaptic vesicles in neurons. In recent human genetic studies, STX1A has been implicated in neuropsychological disorders. To examine whether STX1A gene ablation is responsible for abnormal neuropsychological profiles observed in human psychiatric patients, we analysed the behavioral phenotype of STX1A knockout mice. Abnormal behavior was observed in both homozygotes (STX1A−/−) and heterozygotes (STX1A+/−) in a social interaction test, a novel object exploring test and a latent inhibition (LI) test, but not in a pre-pulse inhibition test.

There are currently no medical facilities on Mount Kilimanjaro to assist trekkers suffering from mountain sickness. We propose that consideration should be given to use some of the money raised by trekkers entering the National Park to set up a staffed medical help station at the Stella Point (150 m below Uhuru Peak) and part way down to Barafu Camp (4,673 m). These outposts could contain oxygen and a stretcher and would selleck kinase inhibitor only need to be staffed by a trained individual for a few hours each day. Most trekkers summit in the early morning and descend by late morning back to Barafu or Millennium Camp. “
“Persistence of immune response was assessed in adults aged >40 years (N = 596) following primary vaccination with combined hepatitis

A/B vaccine or concomitant 17-AAG nmr monovalent hepatitis A and B vaccines. Anti-hepatitis A virus antibody responses persisted for at least 4 years regardless of the vaccine used, with anti-hepatitis B surface antibody responses higher and more sustained in subjects who received the combined hepatitis A/B vaccine. Response rates to an additional dose of the same vaccine(s) used for priming were high. Travelers to areas

of medium and high endemicity for hepatitis A and B aged >40 years may benefit from combined hepatitis A/B vaccination.1–5 Superior seroprotection rates against HB and similar hepatitis A seropositivity rates have been reported in adults aged >40 years following primary vaccination with a combined hepatitis A/B vaccine compared

with concomitant Histidine ammonia-lyase administration of monovalent hepatitis A and B vaccines.6 This follow-up study assessed persistence of immune response after 4 years. Response to an additional dose of the same vaccine(s) used for priming was also assessed. This was a prospective, multicenter, open-label study. Adults aged >40 years were randomized (1 : 1 : 1) to receive combined hepatitis A/B vaccine [Twinrix; GlaxoSmithKline (GSK) Biologicals, Belgium] at 0, 1, and 6 months (HAB group), hepatitis B vaccine (Engerix-B; GSK Biologicals) at 0, 1, and 6 months co-administered with hepatitis A vaccine (Havrix; GSK Biologicals) at 0 and 6 months (ENG + HAV group), or hepatitis B vaccine (HBVAXPRO; Sanofi Pasteur, Lyon, France) at 0, 1, and 6 months co-administered with hepatitis A vaccine (Vaqta; Merck & Co., NJ, USA) at 0 and 6 months (HBVX + VAQ group). Randomization was stratified by age (41–50 years, 51–60 years, >60 years), gender, and body mass index (BMI) (<25 kg/m2 or lean/healthy, ≥25 and <30 kg/m2 or overweight, ≥30 kg/m2 or obese) as previously described.6 Subjects were followed for up to 4 years to evaluate persistence of immune response. At 4 years, all subjects received an additional dose of the same vaccine(s) used for priming and immune response was assessed after 30 days. Anti-hepatitis A virus (HAV) and anti-hepatitis B surface (HBs) antibody concentrations were measured by enzyme immunoassays, with respective cut-offs of 15 and 3.3 mIU/mL.

In multiple regression analysis, after adjustment for age, BMI and sex, high FABP-4 levels were significantly associated with lipodystrophy [odds ratio (OR) 1.016; 95% confidence interval (CI) 1.01-1.027; P=0.004]. To determine the OR for the presence of lipodystrophy in patients with higher FABP-4 levels, we used tertiles to categorize the FABP-4 level, and carried out a multiple logistic regression analysis (Table 3). Patients in the highest FABP-4 tertile had a higher OR for the presence of lipodystrophy than those in the middle tertile. The OR for those in the highest tertile remained significant after adjustment for sex, BMI and age. In the whole HIV-1-infected cohort, bivariate correlation

analyses showed significant correlations between

circulating FABP-4 level and some clinical and metabolic traits. Correlations were positive with BMI (P<0.001), insulin (P<0.001), VEGFR inhibitor HOMA-IR (P<0.001), total cholesterol (P=0.013), LDL cholesterol (P=0.040) and triglycerides (P<0.001), and negative with HDL selleck screening library cholesterol (P=0.002) (Table 4). Regarding immunological and inflammatory parameters, significant positive correlations were observed between plasma FABP-4 level and sTNF-R1 (P<0.001), leptin (P<0.001) and IL-18 (P=0.034) plasma levels (Table 4), while a negative correlation was observed with adiponectin (P=0.006). When we analysed data for HIV-1-infected patients separately in the LD+ and LD− groups, both subsets showed a positive association between FABP-4 plasma level and BMI, fasting insulin and HOMA-IR index (Table 4). In contrast, triglycerides were only positively correlated with FABP-4 in LD+ patients (P=0.035). Regarding immunological and inflammatory parameters, only leptin was positively correlated with plasma FABP-4 level in both the LD+ and LD− groups. Positive correlations between plasma FABP-4 level and sTNF-R1 (P=0.039), sTNF-R2 (P<0.001) and IL-18 (P=0.029) were also found in the LD+ subset (Table 4). To investigate whether the degree of insulin resistance was independently associated with FABP-4 level, we developed a

stepwise multiple linear regression Acetophenone analysis including HOMA-IR as a dependent variable and serum FABP-4 and other clinical and metabolic variables known to be related to insulin resistance as covariates. FABP-4 was one of the five variables included in the model (P=0.004) (Table 5). The variables excluded (P>0.05) were sex, BMI, leptin, HDL cholesterol, LDL cholesterol, total cholesterol, triglycerides and adiponectin. SAT biopsies from 38 HIV-1-infected patients (25 LD+ and 13 LD−) were available (Tables 6 and 7). The use of NRTIs or NNRTIs did not affect the genetic expression profile. The expression of TNF-R1 and MCP-1 was lower in patients on PI drugs, but no differences in the genetic expression profile according to the antiretroviral agent used were found when the LD+ and LD− groups were considered separately (data not shown).

In multiple regression analysis, after adjustment for age, BMI and sex, high FABP-4 levels were significantly associated with lipodystrophy [odds ratio (OR) 1.016; 95% confidence interval (CI) 1.01-1.027; P=0.004]. To determine the OR for the presence of lipodystrophy in patients with higher FABP-4 levels, we used tertiles to categorize the FABP-4 level, and carried out a multiple logistic regression analysis (Table 3). Patients in the highest FABP-4 tertile had a higher OR for the presence of lipodystrophy than those in the middle tertile. The OR for those in the highest tertile remained significant after adjustment for sex, BMI and age. In the whole HIV-1-infected cohort, bivariate correlation

analyses showed significant correlations between

circulating FABP-4 level and some clinical and metabolic traits. Correlations were positive with BMI (P<0.001), insulin (P<0.001), RAD001 order HOMA-IR (P<0.001), total cholesterol (P=0.013), LDL cholesterol (P=0.040) and triglycerides (P<0.001), and negative with HDL AZD9291 cholesterol (P=0.002) (Table 4). Regarding immunological and inflammatory parameters, significant positive correlations were observed between plasma FABP-4 level and sTNF-R1 (P<0.001), leptin (P<0.001) and IL-18 (P=0.034) plasma levels (Table 4), while a negative correlation was observed with adiponectin (P=0.006). When we analysed data for HIV-1-infected patients separately in the LD+ and LD− groups, both subsets showed a positive association between FABP-4 plasma level and BMI, fasting insulin and HOMA-IR index (Table 4). In contrast, triglycerides were only positively correlated with FABP-4 in LD+ patients (P=0.035). Regarding immunological and inflammatory parameters, only leptin was positively correlated with plasma FABP-4 level in both the LD+ and LD− groups. Positive correlations between plasma FABP-4 level and sTNF-R1 (P=0.039), sTNF-R2 (P<0.001) and IL-18 (P=0.029) were also found in the LD+ subset (Table 4). To investigate whether the degree of insulin resistance was independently associated with FABP-4 level, we developed a

stepwise multiple linear regression C-X-C chemokine receptor type 7 (CXCR-7) analysis including HOMA-IR as a dependent variable and serum FABP-4 and other clinical and metabolic variables known to be related to insulin resistance as covariates. FABP-4 was one of the five variables included in the model (P=0.004) (Table 5). The variables excluded (P>0.05) were sex, BMI, leptin, HDL cholesterol, LDL cholesterol, total cholesterol, triglycerides and adiponectin. SAT biopsies from 38 HIV-1-infected patients (25 LD+ and 13 LD−) were available (Tables 6 and 7). The use of NRTIs or NNRTIs did not affect the genetic expression profile. The expression of TNF-R1 and MCP-1 was lower in patients on PI drugs, but no differences in the genetic expression profile according to the antiretroviral agent used were found when the LD+ and LD− groups were considered separately (data not shown).

“
“Department

of Neuroscience, University of Florida, Gainesville, FL, USA Autophagy is a lysosomal degradative process which recycles cellular waste and eliminates potentially toxic damaged organelles and protein aggregates. The important cytoprotective functions of autophagy are demonstrated by the diverse pathogenic consequences that may stem from autophagy dysregulation in a growing number of neurodegenerative disorders. In many of the diseases associated with autophagy anomalies, it is the final stage of autophagy–lysosomal degradation that is disrupted. In several disorders, including Alzheimer’s disease (AD), defective lysosomal acidification contributes to this proteolytic failure. The complex regulation of lysosomal pH makes this process vulnerable to disruption by many factors, and reliable lysosomal Seliciclib cost pH measurements have become increasingly important in investigations of disease mechanisms. Although various reagents for pH quantification have been developed over several decades, they are not all equally well suited Selleckchem IDH inhibitor for measuring the pH of lysosomes. Here, we evaluate the most commonly used pH probes for sensitivity and localisation,

and identify LysoSensor yellow/blue-dextran, among currently used probes, as having the optimal profile of properties for measuring lysosomal pH. In addition, we review evidence that lysosomal acidification is defective in AD and extend our original findings, of elevated lysosomal pH in presenilin 1 (PS1)-deficient blastocysts and neurons, to additional cell models of PS1 and PS1/2 deficiency, to fibroblasts from AD patients with PS1 mutations, and to neurons in the PS/APP mouse model of AD. “
“Feature-specific enhancement refers to the process by which selectively attending to a particular stimulus feature specifically increases the response in the same region

of the brain that codes that stimulus property. Whereas there are many demonstrations of this mechanism in the visual system, the evidence is less clear in the auditory system. The present functional magnetic resonance imaging (fMRI) study examined this process for two complex sound features, namely frequency modulation (FM) and spatial motion. The experimental design enabled us to investigate whether selectively attending to FM and spatial motion enhanced activity in those auditory cortical areas that were sensitive 3-oxoacyl-(acyl-carrier-protein) reductase to the two features. To control for attentional effort, the difficulty of the target-detection tasks was matched as closely as possible within listeners. Locations of FM-related and motion-related activation were broadly compatible with previous research. The results also confirmed a general enhancement across the auditory cortex when either feature was being attended to, as compared with passive listening. The feature-specific effects of selective attention revealed the novel finding of enhancement for the nonspatial (FM) feature, but not for the spatial (motion) feature.

The combination of tests reported here, with the scoring provided by

the Rasch analysis, provides a quantitative estimate of cognitive ability in the range from ‘mild impairment’ to normal in HIV-positive patients. The test battery could thus be applied to measure an individual’s cognitive ability at a given point in time, and to measure the change in ability longitudinally. A healthy population was not tested here, nor were the comprehensive buy AZD6244 neuropsychological data acquired that would be needed to determine the sensitivity and specificity of this set of tests as a diagnostic tool. Future work with this battery could certainly examine its validity and seek to determine cut-off scores if diagnosis is the goal. The results of our study do suggest that adjustment for second-language testing and educational level, at least for the MoCA, Selleckchem PTC124 would be required in the development of diagnostic cut-off scores. Relating this novel measurement approach to the current diagnostic framework

would be useful for several reasons, including potentially shedding light on the meaning of cognitive ability estimates in absolute terms. However, the clinical meaning of changes in cognitive ability is inherently individual, as it depends on both pre-morbid abilities and on current functional demands. The diagnostic classification of patients thus may be of less relevance to clinical decision-making than the precise tracking of an individual’s cognitive ability over time. For example, cognitive deterioration in spite of an undetectable viral load raises the possibility of viral escape in the CNS, which would have important therapeutic implications [40]. Similarly, while the optimal management of GNA12 individuals with cognitive impairment in the context of good viral control remains to be clarified, clinicians need to be able to track change over time when evaluating the response to treatment interventions. With this in mind, additional work along the lines shown here should aim to incorporate items

that further improve the test–retest reliability of the cognitive ability score. The finding that cognitive ability in general can be measured with a single number advances our understanding of how cognitive impairment manifests in HIV-positive patients. In contrast to what might be expected in a heterogeneous sample of neurologically ‘localized’ conditions, the cognitive deficits associated with HIV infection seem to reflect diffuse brain dysfunction that varies in degree rather than in localization, at least across the cognitive domains and level of resolution assessed by this battery of tests. This interpretation may be relevant for understanding the pathophysiology of these deficits, arguing for causes that degrade brain function generally, rather than injuring some particular brain region or network.

4A). The supernatant was further centrifuged at 10,000 g for 10 min and the pellet was separated on a sucrose density gradient (0.32, 0.8 and 1.2 m sucrose), and the synaptosome Tofacitinib in vitro fraction was obtained between 0.8 and 1.2 m sucrose. For the postsynaptic density (PSD) fraction, the synaptosome sample was further solubilized with 0.5% Triton X-100 and the pellet, after centrifugation at 200 000 g for 1 h, was suspended with 40 mm Tris–HCl pH 8.0 and 1% sodium dodecyl sulfate (SDS). Protein samples from homogenate (20 μg), synaptosome (3 μg) and PSD (2 μg) fractions were loaded onto each lane and subjected to SDS-polyacrylamide gel electrophoresis (SDS-PAGE) for Western blotting

(Fig. 4A). Signal intensities of immunoreacted bands were determined by densitometric measurement using ImageJ software (available from the US National Institutes of Health) and normalized with actin signal intensities. Statistical significance was assessed by two tailed, one-sample t-test using PRISM (GraphPad Software, San Diego,

CA, USA). All results are expressed as mean ± SEM. Under deep pentobarbital anesthesia (100 mg/kg of body weight, i.p.), mice were perfused transcardially with 4% paraformaldehyde RAD001 in 0.1 m sodium phosphate buffer (PB; pH 7.2) for light microscopic immunohistochemistry or with 4% paraformaldehyde and 0.1% glutaraldehyde in 0.1 m PB for postembedding immunogold electron microscopy. Brains to be compared simultaneously were embedded in single paraffin blocks, and paraffin sections (4 μm in thickness) were made using a sliding microtome (SM1000R; Leica, Nussloch, Histone demethylase Germany). Microslicer sections were also used for immunofluorescence (50 μm; VT1000S, Leica) and for postembedding

immunogold (400 μm). All immunohistochemical incubations were done at room temperature. For light microscopic immunohistochemistry, paraffin sections were first subjected to pepsin pretreatment for antigen exposure, i.e., incubation in 1 mg/ml of pepsin (DAKO, Carpinteria, CA, USA) in 0.2 N HCl for 10 min at 37°C. Then sections were incubated successively with 10% normal donkey serum for 20 min, primary antibodies (1 μg/ml) overnight, biotinylated secondary antibodies for 2 h and avidin–biotin–peroxidase complex for 1 h, using a Histofine SAB-PO(R) kit (Nichirei Corp., Tokyo, Japan). Immunoreaction was visualized using the tyramide signal amplification kit (Perkin-Elmer, Boston, MA, USA). To detect nonsynaptic AMPA receptors, double immunofluorescence without pepsin pretreatment was done for GLAST and GluA1 or GluA4 using microslicer sections. Images of whole brain sections were taken with a dissecting microscope, while those of cerebellar cortex were with a confocal laser scanning microscope (FV1000; Olympus). For postembedding immunogold, cerebellar slices were cryoprotected with 30% sucrose in 0.1 m PB, and frozen rapidly with liquid propane in a Leica EM CPC unit.

Although both strains utilized oxalate, the cell selleck yield was lower than those with fumarate, glycolate, lactate or malate. Differential phenotypic characteristics between MY14T and the type strains of the genus Oxalicibacterium are given in Table 1. The major fatty acids of strain MY14T were C16:0 (37.2%) and C17:0 cyclo (41.6%). In addition, C10:0 3-OH (6%) was the only hydroxylated fatty acid detected (Table 2). Furthermore, C16:0 and C17:0 cyclo seem to be present in strain MY14T in a significantly higher proportion than all other Oxalicibacterium type species examined. Strain MY14T could be differentiated from the

type strains of the other Oxalicibacterium type species by its lack of C14:0 and summed feature 7 that comprises 18:1 ω7c, 12t/9t fatty acids (Table 2). The polar lipid profile consists of the predominant compounds phosphatidylethanolamine Akt inhibitor and phosphatidylglycerol, and a small amount of diphosphatidylglycerol and one unknown polar lipid (see Supporting Information, Fig. S1). Strain ND5 has some differences from the type strains of the

four described Herminiimonas species by its C10:0 3-OH fatty acid content being lower than 0.5% and C18:1ω7c fatty acid content being significantly higher than the Herminiimonas-type species examined. The major quinone system is ubiquinone Q-8. The G+C content of DNA is 55.4 mol%. Phylogenetic analyses using the 16S rRNA gene sequences indicated that strain

MY14T belongs to the family Oxalobacteraceae of the Betaproteobacteria. In the 16S rRNA gene sequences based on neighbour-joining tree, strain MY14T clustered with the members of the genus Oxalicibacterium (Fig. 1). The tree constructed based on the maximum-parsimony method showed a similar topology (see Fig. S2). The highest pairwise nucleotide similarity L-NAME HCl for strain MY14T was found with O. flavum (96.8%). Strain MY14T showed below 97.0% 16S rRNA gene and below 92%cpn60 nucleotide sequence similarity with other members of the genus Oxalicibacterium. Phylogenetic analysis of translated cpn60 peptide sequences was consistent with the 16S rRNA gene-based phylogeny and supported the identification of MY14T as a distinct species within the Oxalicibacterium genus (see Fig. S3). The highest pairwise sequence similarities for strain ND5 were found with H. saxobsidens NS11T (99.8%) and H. glaciei UMB49T (99.6%). Strain ND5 also showed 98%, 97.6% and below 94%cpn60 nucleotide sequence similarity with H. saxobsidens NS11T, H. glaciei UMB49T and the rest of the members of the genus Herminiimonas, respectively. Peptide sequence identities for the ND5 cpn60 sequences were >97% to Herminiimonas spp. The G+C content of the 555 bp cpn60 universal target region of ND5 was 52%. The DNA–DNA relatedness studies among strains MY14T and O. flavum TA17T, sharing the highest (96.