Increased awareness of the service within secondary care is essential for its continual provision. To further optimise the quality of the service provided, training on drugs and conditions covered need to be provided especially for antiplatelets/anticoagulants as none of the Z-VAD-FMK chemical structure surveyed pharmacists provided the NMS for patients who were newly prescribed these medications. Oladapo Ogunbayo, Ellen Schafheutle, Christopher Cutts, Peter Noyce The University of Manchester, Manchester, UK The purpose of the study was to explore community pharmacy’s contributions

in supporting self-care of people with LTCs Current services to support self-care are fragmented and product-centred, and may not fully engage the whole pharmacy team There is a need for more integrated and coherent approaches to delivering support services to people with long term conditions in the community pharmacy Self-care support has emerged as a holistic approach of supporting people with long-term conditions (LTCs) and reducing its burden on healthcare professionals (HCPs)1. Community pharmacy currently provides essential, advanced and enhanced services to support people with LTCs. Community pharmacy’s role in supporting self-care of LTCs is primarily provided through services around medication reviews and medicines management. The overall aim

of this study was to explore the roles and contributions of community pharmacy learn more in supporting self-care for people with LTCs. The study is part of a larger exploratory qualitative research programme involving community pharmacists, primary care doctors and nurses, and people living with LTCs. Community pharmacists were recruited Oxalosuccinic acid by purposive

sampling from England (Greater Manchester) and Scotland (Glasgow, Tayside) between January and March 2013. Participants were selected to allow for maximal variation2 in pharmacy types (multiples and independents), location (urban, rural, supermarket), area (deprived, affluent, mixed) and pharmacist demographics (ethnicity, age, gender). Semi-structured interviews were conducted face-to-face at participants’ places of work or other agreed location. The topic guide evolved iteratively and focused on questions around approaches in managing and supporting people with LTCs, definition/description of self-care, practices and challenges for holistically supporting self-care, and roles of other pharmacy support staff. Interviews were audio-recorded, transcribed verbatim and data were managed using the QSR NVIVO software (version 10). Data analysis was thematic using template analysis technique. NHS Research Ethics and R&D approvals were obtained. Interviews were conducted with 24 community pharmacists (12 in England, 12 in Scotland). All participants gave detailed accounts of how they support people with LTCs, and the roles and contribution of other pharmacy support staff.

Homology searches revealed that the plasmid (designated pMK100) found in S. Infantis (S20) exhibited 100% homology with

qnrB19-carrying plasmids including pSGI15, a Fulvestrant in vivo small ColE plasmid identified recently in S. enterica serovar Typhimurium isolated in Germany (Hammerl et al., 2010), and a qnrB19-containing plasmid pPAB19 from an S. Infantis clinical isolate recovered in Argentina (GenBank accession number GQ412195). The plasmid purified from isolate S75 (designated pMK101) was found to be 97% similar to these latter plasmids. The dissimilarity noted was mapped to an insertion located between nucleotide positions 896 and 957. Remarkably, the latter DNA sequence was identical to one found in a pBC633 from a K. pneumoniae strain KN633 (accession number EU176012), a urinary isolate from Colombia displaying carbapenem resistance and reported in 2005. This plasmid of approximately 15.5 kb carried a blaKPC−2 gene encoding a class A carbapenemase (Villegas et

al., 2006). The additional check details DNA sequence contained in the plasmid from the isolate S75 was located between the qnrB19 gene and orf2, and was found to be homologous with a region of pBC633. Furthermore, nucleotide sequence similarity was observed in the region upstream of the inserted fragment, possibly facilitating the incorporation of the new DNA fragment. The fact that pBC633 was found only in Colombia indicates that the homology found here may not be coincidental. It is interesting to speculate that pMK101 (the plasmid from isolate S75) is chimeric and may have emerged as a result of a recombination event that led to the horizontal acquisition of a fragment from another plasmid containing blaKPC−2. The process is likely to have occurred in a bacterium simultaneously hosting Amobarbital a plasmid similar to or identical to pBC633, as well as a small ColE-like plasmid such as pMK100. While blaKPC−2 genes are frequent in K. pneumoniae and only sporadic in other Enterobacteriaceae, there are insufficient data to conclude what species was the primary host of the new plasmid structure (Villegas et al., 2006; Pournaras et al., 2009). In addition, it is noteworthy

that pBC633 containing a blaKPC−2 gene was found on a transposon Tn4401 with multiple insertion sequence (IS) elements that have likely contributed to its emergence (Naas et al., 2008). Of particular concern is the possibility of the emergence of chimeric plasmids carrying both qnr genes and blaKPC−2 that could compromise the clinical value of fluoroquinolones and virtually all β-lactams. In view of this, monitoring of phenotypic resistance as well as associated mechanisms and mobility is essential. Furthermore, the occurrence of both blaKPC−2 and qnr in Colombia and their associated plasmids is likely to be under-reported as a result of poor surveillance as well as diagnostic challenges associated with the low-level resistance conferred (Villegas et al., 2006).

4%) did not restart HAART, but did not die, with evidence of further programme

contact by later VL or CD4 test result; 63 (10.1%) did not restart ART, but did not die, without evidence of further programme contact; 260 (41.7%) restarted ART with further interruptions; and 164 (26.3%) restarted ART without further interruptions. An additional 24 (3.9%) restarted ART within 3 months prior to the end of follow-up and could not be assessed with respect to further TIs. Cox proportional hazards modelling Alectinib nmr indicated that male patients (AHR=1.39; 95% CI 1.10–1.76) and those who developed an AIDS-defining illness prior to their TI (AHR=1.54; 95% CI 1.14–2.09) were more likely to restart HAART. Higher CD4 cell counts at the time of TI (AHR=0.89; 95% CI 0.84–0.94) and unknown hepatitis C status (AHR=0.68; 95% CI 0.50–0.92) were associated with a reduced likelihood of restarting HAART (Table 3). Participants whose last regimen prior to the TI-included lopinavir (AHR=1.57; 95% CI 1.15–2.13) were more likely to restart HAART than those who were receiving NVP. Participants whose nucleoside reverse transcriptase inhibitor (NRTI) regimens at the time of TI

were not 3TC/stavudine, 3TC/ZDV or abacavir (ABC)/3TC were less likely to restart HAART (AHR=0.63; 95% CI 0.43–0.93) in comparison to those receiving tenofovir/3TC. Participants who did not restart therapy were at higher risk of mortality in comparison to those who interrupted treatment for <230 days (the median duration of all TIs) (AHR=5.51; 95% CI 3.34–9.07) (Table 4). However, individuals who restarted therapy after a TI of more than 230 days were selleck chemicals not at a significantly higher risk

of mortality (AHR=1.39; 95% CI 0.90–2.16) than those with shorter interruptions. In addition, mortality was associated with increasing age (AHR=1.04; 95% CI 1.02–1.06), physician experience (AHR=0.81; 95% CI 0.67–0.97), CD4 cell count at the time of TI (AHR=0.75 per 100 cell increase; 95% CI 0.67–0.85) and either positive (AHR=2.10; 95% CI 1.19–3.71) or unknown hepatitis C antibody status (AHR=2.24; 95% CI 1.20–4.18). Participants who had a TI within the first AMP deaminase year of HAART were at a greater risk of mortality than those who interrupted treatment later in the course of their therapy in univariate analyses, but not in multivariate models, even when duration of interruption was excluded (data not shown). Our results demonstrate that interruption of HAART treatment is a relatively common phenomenon in the BC DTP with nearly 40% of individuals having at least one TI in a median of 3.3 years of follow-up. Most participants with interruptions remained alive and eventually restarted HAART, although the majority of these individuals experienced further TIs. Individuals who had TIs were more likely to be female, less immunosuppressed and more likely to have a history of IDU.

055 in shell) individually. Reward.  Selleck Ipilimumab Selective reward encoding was seen in 56% of core and 38% of shell neurons, although there was only a trend towards a statistical difference between regions (χ2 = 3.0, P = 0.08). Phasic responses developed shortly after the rewarded lever press. An example of a representative neuron that showed reward-related firing is shown in Fig. 3A. Previous studies have shown that cells that encode information about both cues and outcomes may be particularly

important for supporting normal goal-directed behavior (Schoenbaum et al., 2003a). Given this, it was possible that there would be a population of reward-encoding neurons that also expressed cue selectivity. Overall, there were significantly more neurons encoding this conjunction in the core (28%) than in the shell (5%) (χ2 = 8.04, P < 0.005) (Fig. 3B). Thus, despite similar rates of cue and outcome encoding separately in both regions,

core neurons were more likely to encode more explicit stimulus–outcome representations than shell neurons. Instrumental responding.  Next, the neural correlates of lever-pressing behavior were investigated. mTOR inhibitor In the first analysis, active lever presses were examined regardless of whether there was a cue present or not. A large percentage of neurons were involved in encoding some aspect of lever-pressing behavior. Specifically, 72% (36/50) of core neurons were phasic around the press, whereas 85% (34/40) of shell neurons were phasic. As in previous work, some cells were phasic

prior to the press (e.g. Fig. 4A), some following the press (e.g. Fig. 4B) and some encoded both approach and response (not shown). The majority of phasic neurons encoded both approach and response in both regions (55% in core; 58% in shell). A much smaller proportion in both regions (14% core; 18% shell) was only active during the approach, and a slightly larger proportion was selectively phasic following the response (31% core; 24% shell). Next, lever pressing between the active and inactive lever was assessed. Although Cell Penetrating Peptide the majority of cells recorded showed some form of phasic press-related activity, there was little evidence that these same neurons showed similar phasic firing on the inactive lever (Fig. 4C). Both core and shell neurons showed significantly greater phasic activity for the active compared with the inactive press, but there were no reliable differences between the core and shell in the percentage of phasic neurons encoding active and inactive lever presses (χ2 = 1.01, P = 0.31) (Fig. 4C). Further, whereas the population for active lever pressing was inhibitory and locked to the time of press, there was no such general pattern for the population of inactive presses (Fig. 4D). These findings together suggest that phasic press-related activity is related to tracking the goal instead of merely encoding the motor response alone. Pavlovian-to-instrumental transfer-modulated lever pressing.

In Canada, Worthington et al. [29] found that employment status and the presence of symptoms were independent predictive factors of poorer quality of life scores in MOS-HIV questionnaire regression models. Similarly, in a group of Italian patients, Murri et al. [25] found that PARP activity the factors associated with poor PHS were low CD4 cell count, having been hospitalized, and the presence of symptoms, while a low level of satisfaction with information received, having been hospitalized and the

presence of symptoms were predictive factors of poor MHS. The findings of our study highlight the importance of evaluation of HRQL and related factors in HIV-infected patients. Further investigation is warranted to verify our findings in greater numbers of patients and in studies with a prospective design, in which the significance of associations could be determined over time, which may allow more definitive conclusions to be reached regarding efficient health care for HIV-infected patients. “
“Knowledge about advanced chronic kidney disease (CKD) and end-stage renal

disease (ESRD) in HIV-positive BAY 80-6946 in vitro persons is limited. The aim of this study was to investigate incidence, predictors and outcomes for advanced CKD/ESRD and renal death. Advanced CKD was defined as confirmed (two consecutive measurements ≥ 3 months apart) estimated glomerular filtration rate (eGFR) ≤ 30 mL/min/1.73 m2 using Cockcroft−Gault, and ESRD as haemodialysis or peritoneal dialysis for ≥ 1 month or renal transplant. Renal death was death with renal disease as the underlying cause, using Coding Causes of Death in HIV (CoDe) methodology. Follow-up was from 1 January 2004 until last eGFR measurement, advanced CKD, ESRD or renal death, whichever occurred first. Poisson regression was used to identify predictors. Of 9044 individuals included in the study, 58 (0.64%) experienced Chlormezanone advanced CKD/ESRD/renal death [incidence rate 1.32/1000 person-years of follow-up (PYFU); 95% confidence interval (CI) 0.98–1.66]; 52% of those who experienced the endpoint had a baseline eGFR ≤ 60 mL/min/1.73 m2

compared with 3% of those who did not. Using Kaplan−Meier methods, at 6 years from baseline, 0.83% (95% CI 0.59–1.07%) were estimated to have experienced the endpoint overall and 11.26% (95% CI 6.75–15.78%) among those with baseline eGFR ≤ 60 mL/min/1.73 m2. Independent predictors of the endpoint included any cardiovascular event [incidence rate ratio (IRR) 2.16; 95% CI 1.24–3.77], lower eGFR (IRR 0.64 per 5 mL/min/1.73 m2; 95% CI 0.59–0.70) and lower CD4 count (IRR 0.77 per doubling; 95% CI 0.62–0.95). One year after experiencing advanced CKD or ESRD, an estimated 19.21% (95% CI 7.84–30.58%) of patients had died, mostly from extra-renal causes. The incidence of advanced CKD/ESRD/renal death was low and predictors included traditional renal risk factors, HIV-related factors and pre-existing renal impairment.

Fig. S1. SEM of MDCK cells treated with AZA (5 μM) for 24 h at 37 °C Fig. S2. TEM of MDCK cells treated with AZA (5 μM) for 24 h at 37 °C. Fig. S3. MDCK cells treated with 5 μM AZA (a) or 10 μM EIL (b) for 24 h. Please note: Wiley-Blackwell is not responsible for the content or functionality

INK 128 datasheet of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Microcins are low-molecular-weight proteins secreted by certain bacteria that act by limiting the growth of other bacteria that share the same ecological niche. In the present work, the previous microcin 24 system was resequenced. We detected three nucleotide differences in the microcin-coding gene that partially change the amino acid sequence. According to the present microcin nomenclature, we renamed the five genes

constituting this microcin system (mcnRINAB), which are arranged in an operon-like structure: mcnR codes for a putative histone-like nucleoid protein regulator; mcnI codes for the immunity protein; mcnN encodes microcin N; and mcnA and mcnB correspond to an ATP-binding cassette transporter system. Purified microcin N has a molecular weight of 7274.23 Da, as determined by MS. This peptide was stable up to 100 °C, resistant to treatment with lipase, lysozyme, trypsin, and chymotrypsin, and susceptible to degradation by proteinase K. Microcins are a family Selleck Caspase inhibitor of antimicrobial peptides produced principally by bacteria of the Enterobacteriaceae

family. These bacteriocins have a bacteriostatic or bactericidal activity against species closely related to the bacteria that produce them (Riley, 1998). In contrast to the majority of colicins, microcins cAMP have a low molecular weight (<10 000 Da), are resistant to the action of some proteases and to extreme conditions of pH and temperature, are soluble in methanol, and are not inducible by the SOS system (Kolter & Moreno, 1992). Microcin N (also known previously as microcin or colicin 24) is a bacteriocin produced by the uropathogenic strain Escherichia coli 2424. The genetic determinants involved in the production of microcin N are contained in a 5.25-kb DNA fragment, originally located in a 43-kb conjugative plasmid and afterward cloned into pBR322 (O’Brien & Mahanty, 1994). According to Mahanty and O’Brien’s initial annotation, this region contains five ORFs: mdbA, mtfI, mtfS, mtfA, and mtfB (GenBank accession numberU47048). mtfS codes for microcin, a polypeptide of 90 amino acids that has a signal peptide of 16 residues with a double-glycine motif typical of proteins secreted into the extracellular space by ATP-binding cassette (ABC)-type transporters.

This notion supports the emerging theory that the functional consequences of the distal effects of lesions go beyond simple deafferentation. Specifically, some frontal cortical regions exhibit hypersensitivity to deafferentation that is only detected during behavioral and/or

physiological demand. “
“Cholinergic, GABAergic and glutamatergic projection neurons of the basal forebrain (BF) innervate widespread regions of the neocortex and are thought to modulate learning and attentional processes. Although it is known that neuronal cell types E7080 concentration in the BF exhibit oscillatory firing patterns, whether the BF as a whole shows oscillatory field potential activity, and whether such neuronal patterns relate to components of cognitive tasks, has yet to be determined. To this end, local field potentials (LFPs) were recorded from the BF of rats performing an associative

learning task wherein neutral objects were paired with differently valued reinforcers (pellets). Over time, rats developed preferences for the different objects based on pellet-value, indicating that the pairings had been well learned. LFPs from all rats revealed robust, short-lived bursts of beta-frequency oscillations (∼25 Hz) around the time of object encounter. Beta-frequency LFP events were found to be learning-dependent, with beta-frequency peak amplitudes significantly greater on the first day of the task when ERK inhibitor object–reinforcement pairings were novel than on the last day when pairings were well learned. The findings indicate that oscillatory bursting field potential activity occurs in the BF in freely behaving animals. Furthermore, the temporal distribution of these bursts suggests that they are probably relevant to associative learning. “
“We have shown that delta opioid receptor (DOPR)-mediated analgesia was enhanced in the complete Freund’s adjuvant (CFA) model of inflammation. This effect is thought to originate from translocation of DOPR in the plasma membrane

of dorsal root ganglia and spinal cord neurons. Among the putative mechanisms involved in the regulation of DOPR trafficking, an interaction with substance P (SP) in large dense-core vesicles has been described as an essential event for the externalization of DOPR. As we have previously observed that membrane find more DOPRs were upregulated in small- and medium-sized neurons under inflammatory pain conditions (whereas SP is mainly expressed by small dorsal root ganglia neurons), we raised the hypothesis that an SP-independent mechanism mediates DOPR trafficking and functional emergence in the CFA model. Therefore, we investigated the role of SP in DOPR-mediated analgesia by using preprotachykinin A (precursor of SP) knockout mice (PPTA−/−) in the CFA model of inflammation. First, we confirmed that PPTA−/− mice are not expressing SP and have a similar level of CFA-induced inflammation as wildtype mice.

These results provide the first evidence that NMDARs and LTCCs interact to permit calcium-dependent mitral cell plasticity during early odor preference learning. “
“What are the neuroplastic mechanisms that allow some stroke patients to regain high-quality control of their paretic leg, when others do not? One theory implicates ipsilateral corticospinal pathways projecting from the non-lesioned hemisphere. We devised a new transcranial magnetic stimulation protocol to identify ipsilateral corticospinal tract conductivity from the non-lesioned hemisphere to the paretic limb in chronic stroke patients. We also assessed

corticospinal tract degeneration by diffusion GDC 941 tensor imaging, and used an ankle tracking task to assess lower limb motor control. We found greater tracking error during antiphase bilateral ankle movement for patients with strong conductivity from the non-lesioned hemisphere to the paretic ankle than for those with weak or no conductivity. These findings suggest that, instead of assisting

motor control, contributions to lower limb motor control from the non-lesioned hemisphere of some stroke survivors may be maladaptive. “
“The interactions between inhibitory fast-spiking (FS) interneurons and excitatory pyramidal neurons contribute to the fundamental properties of cortical networks. An important role for FS interneurons in mediating Regorafenib chemical structure rapid inhibition in local sensory and motor cortex microcircuits and processing thalamic inputs to the cortex has been shown in multiple reports; Endonuclease however, studies in the prefrontal cortex, a

key neocortical region supporting working memory, are less numerous. In the present work, connections between layer 2/3 pyramidal cells and FS interneurons were studied with paired whole-cell recordings in acute neocortical slices of the medial prefrontal cortex from juvenile rats. The connection rate between FS interneurons and pyramidal neurons was about 40% in each direction with 16% of pairs connected reciprocally. Excitatory and inhibitory connections had a high efficacy and a low neurotransmission failure rate. Sustained presynaptic activity decreased the amplitude of responses and increased the failure rate more in excitatory connections than in inhibitory connections. In the reciprocal connections between the FS and pyramidal neurons, inhibitory and excitatory neurotransmission was more efficient and had a lower failure rate than in the unidirectional connections; the differences increased during the train stimulation. These results suggest the presence of distinct preferential subnetworks between FS interneurons and pyramidal cells in the rat prefrontal cortex that might be specific for this cortical area. “
“Serotonin-6 (5-HT6) receptors are densely expressed in the dorsolateral striatum (DLS), a brain region linked to habits.

The demographics of persons missing Epacadostat a CD4 count did not differ from those with a CD4 count available within 3 months of diagnosis (data not shown). The proportion of late diagnoses varied by demographic characteristics and exposure category. The proportion of older adults diagnosed late (64% among those aged 50 years and over) was significantly higher compared with younger adults (31% among those aged 15–24 years). Overall, 57% of men were diagnosed

late compared with 46% of women (P < 0.01); among men, a higher proportion of late diagnoses was observed among heterosexuals compared with MSM (67% vs. 36%, respectively) (P < 0.01). The proportion of late diagnoses was lower in London compared with elsewhere in the UK (P < 0.01) PI3K assay (Fig. 1a). Rates of late diagnosis were highest among black African adults (66%) compared with other ethnicities, with a greater proportion of black African men diagnosed late compared with women (70% vs. 63%, respectively). The majority (96%) of persons of black ethnicity diagnosed late were born abroad. One in ten (10.9%) persons presenting late had an AIDS-defining illness at HIV

diagnosis compared with less than one in 200 (0.4%) among those diagnosed with a CD4 count > 350 cells/μL. In 2011, 82% (5087/6219) of persons had a CD4 count available within 12 months of diagnosis. The proportion of patients linked to care within 1 and 3 months of diagnosis was 88% and 97%, respectively. There was little variation by gender, age, ethnicity, exposure category and geography, particularly for the latter indicator (Fig. 1b). Of the 5833 persons diagnosed in 2010 and not reported to Diflunisal have died, 85% were seen for HIV care in 2011. There

was little variation in retention rates by demographic characteristics (Fig. 1c). Among the 2264 patients who were diagnosed late in 2010 and therefore required treatment, ART coverage was 92% by the end of 2011. Treatment coverage increased with age: it was 82% at date last seen among those diagnosed late aged 15-24 years and 95% in those aged 50 and over (Fig. 1d). There were 199 deaths reported within 1 year among the 6299 adults diagnosed in 2010, representing a crude 1-year mortality rate of 31.6 per 1000 of population. The 1-year mortality rate increased with age, reaching a rate of 92.8/1000 of population among persons aged 50 and over. The 1-year mortality rate was higher among injecting drug users (48.6/1000) compared with other risk groups; however, this was based on only seven of 144 new diagnoses in this group. Nearly nine in ten deaths occurred among those diagnosed late (107 of 121). Consequently, the 1-year mortality rate was higher among persons diagnosed late (40.3/1000) compared with those diagnosed promptly (5.2/1000). The increasing trend in mortality rate associated with age at diagnosis was particularly striking among those diagnosed late (5.6/1000 among 15–24-year-olds versus 107.4 among those aged 50 and over) (Fig. 2).

However, the protective efficacy of the selleckchem protein remained to be evaluated. SS2 strain ZYS was isolated from the brain of a diseased piglet and expressed muramidase-released protein, extracellular protein factor and suilysin (Tang et al., 2006). All the field strains used in this study were derived from samples of different tissues (lung, brain, joint, heart and blood) of diseased pigs with pneumonia and systemic infection (meningitis, arthritis, endocarditis or septicaemia) from 16 provinces (municipalities) of China. All S. suis strains were maintained on tripticase soy agar (Difco Laboratories, Detroit, MI)

plus 10% bovine serum or cultured in Todd–Hewitt broth medium (THB) (Oxoid, Wesel, Germany) plus 10% bovine serum to mid-log phase (OD600 nm of 0.4) at 37 °C under aerobic conditions. Laboratory Escherichia coli strains DH5α and BL21 were used as nonadherent and noninvasive recipients of recombinant protein-containing plasmids pET-28a (+). The purified recombinant HP0272 (accession no. YP_001197640) was performed as described previously (Zhang et al., 2008) and then was resolved on a 10% v/v polyacrylamide vertical slab gel with a 4% v/v stacking gel. After electrophoresis, the gel was visualized by being stained with CBB R-250 and the band of interest was picked, digested with trypsin and then subjected to matrix-assisted laser desorption/ionization-time

of flight MS analysis as described (Fountoulakis & Langen, 1997; Kussmann et al., 1997). Peptide selleck chemicals llc masses were searched against however the NCBI database using the mascot program (http://www.matrixscience.com). All experimental protocols were approved by the Laboratory Animal Monitoring Committee of Hubei Province and were performed accordingly. Thirty-two 4–6-week-old female BALB/c mice were randomly assigned to four groups of eight each. The purified recombinant HP0272 (100 μg) was emulsified with Marcol 52 (ESSO)-based adjuvant and then applied to immunized mice in group 1 intraperitoneally.

Subsequent booster injections were given on the 14th day with the same antigen. Mice in group 2 immunized with commercially SS2-inactive vaccine (China) served as positive controls. Mice in group 3 were inoculated with phosphate-buffered saline (PBS) emulsified in the same adjuvant served as negative controls, and mice in group 4 were inoculated with PBS alone as blank controls. On the 10th day after the booster immunization, sera were obtained from each group by tail vein bleeding. All mice were then challenged with a lethal dose of 2 × 109 CFU of log-phase SS2 ZYS in 0.5 mL PBS. All mice were observed for 10 days for morbidity and mortality. Microtitre plates were coated overnight at 4 °C with 200 ng 100 μL−1 of purified recombinant HP0272 diluted in sodium carbonate buffer (pH 9.6). Having been treated with washing buffer (PBS, pH 7.2, containing 0.