The type and location of the exercise may also influence the benefit obtained. These points BVD523 are important to consider in an elderly population, who may experience limitations in where and how they can exercise. The meta-analysis examined the combined results of different studies to increase the overall statistical power and the precision of estimates while controlling for bias and limiting random error. Nevertheless, several limitations in generalising the findings must be acknowledged. First, a relatively small number of trials, all of which included a relatively small sample size, were examined. Trials reported in languages other than English and Chinese were excluded, as were trials reported only as

abstracts. These exclusions may have led to publication bias. Also, more participants were female, making the observed effects less certain in men. A-1210477 manufacturer In summary, the results of this meta-analysis indicate that participation in exercise training has a moderately beneficial effect on sleep quality and decreases both sleep

latency and use of sleep medication. These findings suggest that physical exercise therapy could be an alternative or complementary approach to existing therapies for sleep problems, especially since exercise is low cost, widely available and generally safe. eAddenda: Figures 3, 5, 7, 9, 10, 11, 12, and 13 available at jop.physiotherapy.asn.au “
“Acute low back pain is defined as pain, increased muscle tonus, and stiffness localised below the costal margin and above the inferior gluteal folds, sometimes accompanied by radiating pain, for up to six weeks. Pain that continues but does not exceed 12 weeks is defined as subacute, becoming chronic thereafter (van Tulder et al 2002, Koes et al 2006). The lifetime prevalence of low back pain Parvulin is greater than 70% in industrialised countries (Airaksinen et al 2006). Several studies have reported that acute low back pain improves within four weeks, with 75–90% recovery and a relapse rate of 60% (Coste et al 2004, Grotle et al 2007). However, a small proportion of people

with acute low back pain progress to have chronic low back pain (Waddell et al 2003, Waddell et al 2004). Low back pain may cause a person to take sick leave or it may cause disability that limits a person’s ability to perform usual work activities. Either of these can contribute to the period absent from usual work. Recall of sick leave is accurate over 2 to 3 months and reliable (Burdorf et al 1996, Severens et al 2000, Frederiksson et al 1998). Some psychosocial factors measured in the acute or subacute stages of low back pain are predictors of progression, with the strength of the prediction being dependent on the time of measurement (Burton et al 2003). One psychosocial factor that we address in this review is the patient’s prediction or expectations, which we define as what patients believe might occur. These expectations may be a prognostic indicator, perhaps by affecting clinical outcomes.

Importantly during persistent infection, the adaptive immune response

is able to control, but not clear infection. The inability to clear the infection is thought to be due to the generation of antigenically variant surface proteins which escape detection and allow for a window of pathogen replication [17]. For example, repeated exposure to Plasmodium falciparum, one of the causative agents of malaria, results in the development of naturally acquired immunity. In both A. marginale and P. falciparum, control of persistent infection is thought to be due in part to antibody directed toward surface learn more expressed variant antigens. In the case of A. marginale, a temporal relationship exists between clearance of an Msp2 variant and development of a variant-specific antibody response [8] and [9]. Similarly, P. falciparum parasites causing clinical disease express a PfEMP1 protein to which the patient has no pre-existing antibody; in response the immune system mounts an antibody response selleck chemicals llc with specificity for the expressed protein [18], [19], [20], [21] and [22]. Thus, it has been suggested that naturally acquired immunity to P. falciparum correlates with gradual acquisition of an entire repertoire of protective PfEMP1 antibody characterized by asymptomatic parasitemia, but does not result in sterile immunity or protection

against re-infection, and requires years to develop [22] and [23]. In contrast Dipeptidyl peptidase to naturally acquired immunity, sterile immunity

can be induced by immunization with irradiated sporozoites in the case of P. falciparum, and outer membrane proteins, in the case of A. marginale [7], [10], [11] and [24]. The data presented in this paper indicate that there is no correlation between the prevention of infection due to immunization and the antibody response to the highly immunogenic hypervariable surface protein responsible for immune evasion. Thus, the difference between the evasion of immunity resulting in persistent infection and the immunization-induced complete clearance is likely due to induction of antibody to conserved proteins that occurs following immunization but does not occur during natural infection. Although antibody to Msp2 is abundantly produced in response to immunization, antibodies targeting a wide variety of conserved proteins have also been identified [25]. Thus, shifting the immune response toward conserved epitopes that are poorly recognized during infection may be the key to effective vaccine development. The excellent technical assistance of Bev Hunter is gratefully acknowledged. This research was supported by NIHR01 AI44005, USDA ARSCRIS5348-32000-027-00D, and USDA-ARS cooperative agreement 58-5348-3-0212. The research reported in this manuscript was supported by the Wellcome Trust (GR075800M). “
“The authors would like to apologies that the first column of the second line of the table should be “Varilrix”. Please see the correct Table 3. “
“Bordetella pertussis (B.

The CAMPRAL® GSK1210151A enteric coated tablets containing 333 mg Acamprosate per tablet, were obtained from Forest pharmaceuticals, INC, USA. The 1200 Series HPLC system (Agilent Technologies, Waldbronn, Germany), Mass spectrometry API 4200 triple quadrupole instrument (ABI-SCIEX, Toronto, Canada) and data processing was performed on Analyst 1.5.1 software package (SCIEX). The mass spectrometer was operated in the multiple reaction monitoring (MRM) mode. Sample introduction and ionization were electrospray

ionization in the negative ion mode. Sources dependent parameters optimized were as follows: nebulizer gas flow: 20 psi; Heatergas flow 40 psi; curtain gas flow: 8 psi; ion spray voltage (ISV): 5500 V; temperature (TEM): 650 °C. The compound dependent parameters such as the declustering potential (DP), focusing potential (FP), entrance potential (EP), collision energy (CE), cell exit potential selleck chemical (CXP) were optimized during tuning as 55, 30, 10, 18, 12 eV for Acamprosate and Acamprosate D12, respectively. The collision activated dissociation (CAD) gas was set at 5 psi using nitrogen gas. Quadrupole 1 and quadrupole 3 were both maintained at a unit resolution and dwell time was set at 600 ms for Acamprosate and Acamprosate D12. The mass transitions were selected as m/z 180.0 → 79.9 for Acamprosate and m/z 186.1→ 79.9 for

Acamprosate D12. The parent and product ion spectra for Acamprosate and Acamprosate D12 are represented in Figs. 2a and b, 3a and b respectively. The data acquisition was ascertained by Analyst 1.5.4software. Waters Atlantis, HILIC, 50 × 2.1 mm, 3 μm, was selected as the analytical column connected with Guard column Waters Atlantis, HILIC, 10 × 2.1 mm, 3 μm. Column temperature was set at 40 °C. Mobile phase composition was 10 mM Ammonium formate pH 3.5: Acetonitrile (10:90 v/v). Source flow rate 250 μL/min without split. Injection volume of 10 μL. Acamprosate and Acamprosate D12 were eluted at 2.1 ± 0.2 min, with a total run time of 3.0 min for each sample. Acamprosate and Acamprosate D12 standard stock solutions 100 μg/mL each were prepared by dissolving the appropriate standard in methanol. From the Acamprosate

stock solution calibration and quality control standards were prepared by using screened human blank plasma as diluent. Calibration standards were prepared at concentration levels of 1.00, Astemizole 2.00, 5.00, 25.00, 50.00, 100.00, 150.00, 200.00 and 250.00 ng/mL. Quality control standards were prepared at concentration levels of 1.00, 3.00, 125.00 and 175.00 ng/mL for Acamprosate. Internal standard spiking solution at 50 ng/mL concentration was prepared by using 50% methanol solution from Acamprosate D12 standard stock solution. Calibration and quality control standards were prepared from two separate stock solutions of Acamprosate and stored at −30 °C. Internal standard spiking solution was stored in refrigerator conditions at 2–8 °C until analysis.

1% Tween 20 (v/v) (PBST) and 3% (w/v) non-fat dry milk powder. After three washes with PBST, the blots were incubated for 3 h with convalescent serum obtained from mice sublethally infected with SH1 at a dilution of 1:1000. Membranes were washed three times with PBST and incubated for

1 h at room temperature with a horseradish-peroxidase-conjugated goat anti-mouse IgG (H + L) secondary antibody (Santa Cruz Biotechnology, Inc., Dallas, TX) at a dilution of 1:2000. Then, membranes were rinsed again and protein bands were visualised using the two-component Western Lightning® Plus-ECL selleck chemical enhanced chemiluminescence substrate kit (PerkinElmer, Inc., Waltham, MA) and Ultra Cruz™ Autoradiography Blue Films (Santa Cruz Biotechnology, Inc., Dallas, TX). Radiographs were Selleck PD0325901 developed on a SRX-101A processor (Konica Minolta, Osaka, Japan). HA content of the VLP samples was determined densitometrically against known concentrations of the SH1-HA protein using ImageJ (National Institutes of Health). Two-fold serial dilutions of PR8:AH1, PR8:SH1, PR8:malNL00, PR8:malAlb01 and PR8:chickJal12 recombinant reassortant virus strains in PBS (50 μL) were prepared in Nunc® 96-well polystyrene

V-bottom microwell plates (Thermo Fisher Scientific, Waltham, MA), followed by the addition of 50 μL 0.5% (v/v) chicken or turkey red blood cells (RBCs) (Lampire Biological Laboratory, Pipersville, PA) in PBS into each well. RBCs were allowed to settle for 45–60 min at 4 °C and the HA titre was determined by visual inspection. Hemagglutination units (HAU) are read as the reciprocal of the last dilution, giving rise to hemagglutination of red blood cells. Baculovirus titres in the VLP vaccine doses were determined by plaque assay on Sf9 cells with minor modifications as described in [24]. Briefly, the assay was carried out in 6-well plates in duplicates. After seeding 1 × 106 cells per well, the cells were allowed to attach to the

surface, because medium was removed and 200 μL of the diluted VLP vaccine formulations (10-fold dilutions in TNM-FH unsupplemented) were added and incubated for 1 h at 27 °C with periodic shaking. After infection, the samples were removed and cells were overlaid with 2 mL of a solution containing 1% agarose in TNM-FH, 10% (v/v) foetal bovine serum, Penicillin–Streptomycin antibiotic mixture pre-warmed to 37 °C. The plates were incubated at 27 °C for 6 days and plaques were counted after live-cell staining with 200 μL of 5 mg/mL Thiazolyl blue formazan MTT (Sigma, St. Louis, MO) for 3–4 h. SH1-VLPs were prepared in three different concentrations in PBS as per HA content (3 μg, 0.3 μg and 0.03 μg SH1-HA per 50 μL vaccine dose). The AH1-VLP vaccine was prepared at a single concentration (0.3 μg AH1-HA per 50 μL). M1-VLPs served as a negative control and were adjusted to a total protein concentration equal to that of SH1-VLP (0.

, California, USA) at 1/500. Slides were mounted in selleck inhibitor Vectashield mounting medium with 4′,6′-diamidino-2-phenylindole (DAPI) (Vector Laboratories, Inc., California, USA) and examined with a Nikon eclipse E600 fluorescence microscope with 100× oil immersion objective and 10× eyepiece. Endpoint titre for each serum was defined as the highest dilution that resulted in bright and clear schizont-specific fluorescence. Sera from immunized mice and rabbits were assayed for reactivity to recombinant GST-fusion proteins previously described [23] representing each of the three MSP1 block 2 allelic types, 3D7 (K1-like), Wellcome (MAD20-like),

and R033 by ELISA following methods previously outlined in detail [15] and [24]. Briefly, Immulon 4HBX flat bottomed plates (Dynex Technologies inc.) were coated with 50 ng/well of each recombinant protein in 100 μl of coating buffer (15 mM Na2CO3, 35 mM NaHCO3; pH 9.3). Plates were incubated overnight at 4 °C, washed with PBS-T (PBS with 0.05% Tween), blocked (1% skimmed milk in PBS-T) for 5 h and washed again. Sera were diluted (1/1000 for murine sera and 1/2000 for rabbit sera) in blocking buffer, and 100 μl volumes were aliquoted in duplicate into antigen coated wells and incubated overnight at 4 °C. Plates were washed and wells incubated with either rabbit anti-mouse (P0260, Dako UK) (1/5000 Vorinostat cell line dilution) or swine anti-rabbit HRP-conjugated

IgG (P0399, Dako UK) (1/4000 dilution) for 3 h at room temperature. Plates were washed and developed with O-phenylenediamine dihydochloride (OPD) using SigmaFast OPD tablets (Sigma, UK). Detection of mouse IgG subclasses followed the same protocol, except biotin-conjugated polyclonal goat anti-mouse antibodies to murine else IgG subclasses were used as the secondary antibody (Cambridge Bioscience, UK), followed by detection with HRP-conjugated streptavidin (Sigma, UK). All six new recombinant proteins (Fig. 1A) were expressed as soluble products that appeared as single

bands on SDS-PAGE gels (Fig. 1B), and Western blots were probed with specific polyclonal sera previously raised to GST-expressed proteins expressing the K1 Super Repeat [15] and individual block 2 alleles [23] (Fig. 1C). The individual sera reacted with predicted specificity against the different hybrid antigens, verifying the modular antigenic composition of each hybrid construct. The yield for the full polyvalent hybrid protein (antigen 6) averaged ∼13 mg/l of culture, and the lyophilized product was stable at temperatures ranging from −20 to 56 °C for at least 3 weeks. CD-1 outbred mice were immunized with each of the 6 hybrid constructs (antigens 1–6, Fig. 1A) in Alum. ELISAs were performed to determine IgG antibody reactivities against different GST-fusion proteins (MSP1 block 2 of 3D7, R033 and Wellcome alleles) [11] in sera collected from the mice at days 0, 14, 42 and 70 post immunization.

In addition, the more stringent Center for Biologics Evaluation and Research (CBER) criteria [lower limits of 95% CI for SPR ≥70% and SCR ≥40%] [26] were met for all study vaccines at Day 21. Six months after the first vaccine dose and prior to the booster dose, the CHMP criteria were still met for all study vaccines, with the highest HI antibody SPRs and GMTs in subjects who received two primary doses of the AS03B-adjuvanted 1.9 μg HA H1N1/2009 vaccine. At this time point,

the CBER criteria were not met for the single dose regimen of the 1.9 μg HA AS03B-adjuvanted HA H1N1/2009 vaccine but were met for all other formulations. The HI antibody SPRs observed following one dose of the AS03-adjuvanted H1N1/2009 vaccines in the current study (98.5–100.0%) are consistent with previously observed SPRs (96.7–100.0%) for similar vaccines in children between high throughput screening assay 6 months and 17 years old [21], [22] and [27]. The observations in the current study are consistent with published literature that one dose of non-adjuvanted H1N1/2009 vaccines can elicit putatively protective levels of HI antibodies in adolescents 10 to 17 years old, 21 days after vaccination [22], [28], [29], [30], [31] and [32], although two doses may be required in younger children [29], [30], [31], [32] and [33].

Previous studies have reported that two doses of AS03B-adjuvanted 1.9 μg HA or 3.75 μg HA H1N1/2009 vaccines induced persistence of HI antibody responses (SPR: >98.0%; SCR: >89.0%) in children through 6 months after vaccination [22] and [23]. In one Venetoclax in vivo of these studies [22], enrolling healthy children

from 6 months to 9 years of age, the parallel study arm with non-adjuvanted 15 μg HA H1N1/2009 vaccine (but not 7.5 μg HA) also elicited long-term persistence of HI antibody response (SPR: 91.5%; SCR: 74.5%), although the HI antibody GMTs (122.7) were lower than that observed for the AS03-adjuvanted vaccines (267.9–296.2). Nassim et al. reported from a dose-ranging study that only the MF59-adjuvanted vaccines with 3.75–15 μg HA antigen doses, but not the non-adjuvanted vaccines with 7.5–30 μg HA antigen doses, met the regulatory criteria through one year after vaccination mafosfamide [34]. This is the first study to assess the concept of priming for immunological memory with AS03-adjuvanted H1N1/2009 vaccines in children 10–17 years old. A rapid increase in HI antibody titers after the booster dose administered at month 6 was observed for all study vaccines, suggesting effective priming irrespective of the one- or two-dose priming regimens. The HI antibody SPRs 7 days after the booster dose were comparable across the treatment groups (97.2–100.0%), although the HI antibody GMTs were higher for the AS03-adjuvanted vaccines (416.7–589.4) compared with those for the non-adjuvanted vaccine (273.4).

Stretch alone may be ineffective for the treatment and prevention of contracture because it does not address possible underlying causes of contracture, namely muscle weakness and spasticity (Ada et al 2006). Weakness and spasticity buy Onalespib are common impairments after acquired brain injury. They immobilise joints in stereotypical postures predisposing them to contracture (Ada et al 2006, Fergusson et al 2007). Stretch provided in conjunction with interventions

addressing weakness and spasticity may be more effective than stretch alone. Electrical stimulation is increasingly used to increase strength and reduce spasticity in people with GS-7340 ic50 acquired brain injury. A systematic review concluded that electrical stimulation has a modest beneficial effect on muscle strength after stroke (Glinsky et al 2007). Two of the What is already known on this topic: Stretch alone may not affect contracture, perhaps because it does not address underlying muscle weakness and spasticity. Electrical stimulation can increase strength and reduce spasticity in some patients at risk of contracture. What this study adds: The effect of electrical stimulation for contracture management was not clear. While further research is needed to clarify the effectiveness of electrical stimulation, it may be reasonable

to use electrical stimulation in conjunction with splinting because it is inexpensive and not associated with discomfort or pain. It may be appropriate to use stronger doses of electrical stimulation than that used in the study. The possible therapeutic effect of electrical stimulation for contracture management is supported by a trial in people with stroke (Bakhtiary and Fatemy 2008), which reported a small treatment effect of electrical stimulation on passive ankle dorsiflexion range of motion (mean between-group difference 5 degrees, 95% CI 2 to 7). While this trial suggests that Resminostat electrical stimulation is therapeutic,

supramaximal levels of electrical stimulation for 9 minutes a day were applied (ie, the intensity was set at 25% over the intensity needed to produce a maximum contraction). Supramaximal doses are not commonly used clinically because of the associated discomfort. It is not clear how Bakhtiary and Fatemy overcame this problem. We were interested in whether we could replicate these results using a similar protocol of electrical stimulation but with a lower and more readily tolerated intensity of electrical stimulation applied for 1 hour a day rather than 9 minutes a day. We were also interested in combining electrical stimulation with stretch as this has not been investigated previously.

The highest serum dilution that reduced in at least 50% the number of plaques was considered the final neutralization titer. Lymphoid spleen cells from immunized and control mice were collected, washed twice in RPMI 1640 containing 10% heat-inactivated FBS. After wash, the cells were resuspended at a final concentration of 1 × 106 cells/ml with RPMI 1640 and 100 μl aliquots were plated into 96-well culture plates. Then we added different stimuli to the culture, 1 × 106 PFU of DENV-4 (heat inactivated) as specific stimulus or concanavalin http://www.selleckchem.com/products/isrib-trans-isomer.html A 2 μg/ml (Sigma–Aldrich) as mitogenic stimulus, the plates were covered and incubated at 37 °C in a 5%

CO2 atmosphere. After 48 h of stimulation, aliquots of supernatants were removed and stored at −70 °C for subsequent analysis. Sandwich-type ELISAs (DuoSet™, R&D Systems) were used to estimate the IFN-γ, IL-2 and IL-10 levels in virus-stimulated and control cell supernatants, according to the manufacturer’s instructions. Briefly, serial dilutions of cytokine standards, samples and controls were added to 96-well ELISA microplates coated with specific monoclonal antibody and incubated for 2 h at room temperature. Plates were then washed five times with PBS/T (PBS/0.5% Tween) and 100 μl of horseradish peroxidase-linked polyclonal anti-mouse

antibody was added. After 2 h at room temperature, the plates were washed five times and 100 μl of a substrate solution were added to each well. The plates were incubated for 30 min at room temperature, MK0683 concentration and then read at 450 nm. The levels of cytokines in the supernatants were calculated by comparing their O.D. to a standard calibration curve. The DENV-4 specific lymphoproliferative

responses from vaccine and control immunized mice were determined by standard CFSE staining in two different experiments. Spleens were harvested from the same mice (4 mice per group) inoculated with recombinant DENV-4-DNAv, inactivated DENV-4, and pCI, as previously described in the Imunization of mice heading. Spleen cell suspensions were treated with Tris-buffered ammonium chloride to eliminate the red blood cells, washed, and resuspended in RPMI 1640 supplemented with 5% FBS, HEPES buffer, l-glutamine, penicillin and streptomycin. Cells mafosfamide were cultured in triplicate in 96-well microtiter plates (1 × 105 cells/well) in the presence of heat inactivated DENV-4 (1 × 105 PFU), control RPMI medium, or ConA 2 μg/ml. Specific T cell proliferation of DENV-4-DNAv-immunized mice and control groups were evaluated by staining the cells with 5-(and-6) carboxy-fluorescein diacetate, succinimidyl ester (CFSE) (Molecular Probes, Oregon, USA). The reading was performed after 3 days of stimulus in a flow cytometry (FACscan) with software Cellquest (both from Becton-Dickinson Immunocytometry Systems Inc., San Jose, CA), and the statistical analysis was accomplished using the program WinMDI version 2.8.

We chose to keep the concentration of LOX-1 vector the same (1×1010 pfu/ml) and supplement it with an equal concentration of LOXIN vector. As the total concentration of virus was double, a separate control group was used with 2×1010 pfu/ml RAd66 (Fig. 2). Carotid arteries

transduced by LOX-1 and LOXIN together show no difference in plaque coverage compared to the high-dose RAd66 control (62% vs. 60%). Hence co-expression of LOXIN with LOX-1 abolishes its atherogenic effect. Again, a trend towards greater plaque coverage was observed in the high-dose RAd66 group compared to vehicle alone (30% vs. 60%; P=.09), presumably due to adenovirus-induced inflammation of the vessel wall. The higher dose of RAd66 produced a small nonsignificant increase in atherogenic effect Obeticholic Acid chemical structure compared to the lower dose (60% vs. 50%). We demonstrated here for the first time the ability

of endothelial LOX-1 overexpression to promote atherogenesis in the common carotid artery of hyperlipidemic ApoE−/− mice. This amplifies the conclusions from LOX-1-null mice where the function of LOX-1 is deleted in other cell types, including macrophage and smooth muscle cells. LOX-1 is MAPK Inhibitor Library up-regulated in nondiseased but atheroprone arterial sites in hyperlipidemic rabbits, in addition to early atherosclerotic lesions in rabbits and humans [2] and [19]. The experiments performed here suggest that endothelial LOX-1 expression may have pathological consequences and is not simply a passive marker of disturbed flow in atheroprone vascular sites. We have also demonstrated experimentally for Calpain the first time in an in vivo model that LOXIN is capable of inhibiting the development of atherosclerosis that is induced by LOX-1 overexpression.

This is in keeping with the human data, which shows that SNPs that increase LOXIN expression are linked to a lower event rate of acute coronary syndromes [14]. The interpretation of the LOXIN-alone group is difficult, as the overexpression of LOXIN in the absence of LOX-1 is an unphysiological situation. LOXIN naturally occurs at a roughly equivalent level compared to LOX-1 in humans [14] and is able to inhibit LOX-1 cell surface expression [14] and [15]; however, the effect of overexpressing LOXIN in the absence of LOX-1 overexpression is unknown and unphysiological. Mouse LOX-1 contains an exon not present in humans; thus it is unclear whether human LOXIN is able to interact with murine LOX-1. The presence of an equivalent murine LOXIN splice variant in the mouse has not been described. The expression and action of LOX-1 have been widely investigated and are the subject of many publications (reviewed in Refs. [6] and [10]). One of the key mediators of LOX-1 signalling is the activation and nuclear localization of the transcription factor NFκB [9].

05 were considered statistically significant. Results were expressed as mean levels and standard deviations (SD) or as median and interquartile range as appropriate. χ2 was used to assess group differences in categorical variables. Odd ratio (OR) and 95% confidence limits (95% CL), when possible, were calculated. For continuous variables, the t-test was used with Logarithmic transformation of non-normal distributed variables. In the study period, 136

buy INCB024360 cases of invasive meningococcal B disease were reported. The mean age was 5.0 years, median 2.7 years, interquartile range 10.2 months–6.4 years. Among these, 96/136 (70.6%) patients were between 0 and 5 years, 61/136 (45.2%) patients were between 0 and 2 years. Among cases under 2 years of age, 39/61 (63.9%) occurred during the first year of life. Distribution of cases according to age is shown in Fig. 1. Within the first year of age the highest incidence was observed between the 4th and the 8th month of age, where 20/39 (51.3%) cases occurred. Case distribution according buy Gemcitabine to months of age is shown in Fig. 2. Fifty-two blood samples

were tested both by culture and RT-PCR. MenB was found in 43/52 (82.7%); the 9 (17.3%) patients who were negative for both tests in blood were positive by RT-PCR in CSF. MenB was identified by RT-PCR alone in 32/43 (74.4%) patients and by both RT-PCR and culture in 11/43 (25.6%) patients (McNemar’s p < 10−3); no sample was identified by culture alone. Fifty-nine CSF samples were tested both by culture and RT-PCR. MenB was found in 57/59 (96.6%); the 2 (3.4%) patients who were negative for both tests in CSF were positive by RT-PCR

in blood. MenB was identified by RT-PCR alone in 35/57 (61.4%) patients; by culture alone in 1/57 (1.8%) and by both RT-PCR and culture in 21/57 (36.8%) patients (McNemar’s p < 10−3). Overall, 82 patients were tested at the same time by both molecular and cultural tests either in blood or in CSF or in both and a Neisseria meningitidis infection was found by RT-PCR in blood or CSF in 81/82 cases (98.8%). Astemizole In the same patients culture could identify 27/82 (32.9%) infections. RT-PCR was significantly more sensitive than culture in achieving laboratory diagnosis of meningococcal infection (Cohen’s Kappa: 0.3; McNemar p < 10−5). Sensitivity according to clinical presentation was evaluated. In 44 patients who were admitted to hospital with the diagnosis of sepsis with or without meningitis, RT-PCR was performed in the blood of 29/44 and in CSF of 15/44 and was positive in 29/29 (100%) blood and in 13/15 (86.7%) CSF. Culture was performed in the blood of 24/44 and in the CSF of 10/44 and was positive in 6/24 blood (25.0%) and in 2/10 (20.0%) CSF. As for meningitis, in 90 patients with the diagnosis of meningitis with no sign of sepsis, RT-PCR was performed in 39 blood samples and in 61 CSF samples and was positive in 29/39 (74.4%) blood samples and 60/61 (98.4%) CSF samples.