3 ± 5.7 (range, 19.0–52.0) years (Figure 2, C), and the mean gestational age was 13.3 ± 4.1 (range, 9.0–38.0) weeks (Figure 2, D). While the majority of NIPT samples were from women at early gestational ages, samples were received up to 40 weeks’ gestation (Figure 3); 2% (658/30,795) of samples were from women in their third trimester. Karyotype or ultrasound confirmation (karyotype for singleton pregnancies,

ultrasound for multifetal pregnancies) was available for 76 (58.5%) of the 130 cases identified with additional parental haplotypes. This included 32 (42.1%) vanishing twin, 37 (48.7%) viable twin, 4 (5.3%) triploid pregnancies, and 3 (3.9%) nontriploid pregnancies that lacked evidence of co-twin demise (Table 1). For the 3 nontriploid pregnancies, 2 had euploid karyotypes, and 1 was shown to be a trisomy 18 fetus (Appendix; Supplementary Z-VAD-FMK ic50 Table). Vanishing twin cases had a significantly higher median maternal age than twin cases, 37.5 and 33.0 years, respectively (P < .001). The median gestational age was slightly lower in vanishing twin cases than in twin cases, 12.1 and 13.0 weeks, respectively (P = .018). There was no significant difference

(P = .686) between the average fetal fraction of vanished twin (11.0 ± 3.8%) and twin (11.4 PD0332991 ic50 ± 4.3%) pregnancies. Of the 32 vanishing twin cases, 25 (78.1%) were in the first trimester and 7 (21.9%) were in the second trimester at the time of NIPT sampling. Five cases reported an estimated date of fetal demise: demise occurred in the first trimester in all 5 cases ( Figure 3). The time between demise and NIPT sampling ranged from 2-8 weeks ( Table 2). All triploidy cases in this cohort were determined no to be diandric (Table 3), indicating that in each case the additional fetal haplotype was paternal in origin. Fetal sex was determined for all triploidy cases by analysis of fetal sex chromosome copy numbers; the fetal karyotype matched the fetal sex determined by NIPT for all 3 triploidy cases where karyotype

specifics were communicated during follow-up (Table 3). For triploidy cases 1, 2, and 4 detailed in Table 3, the pregnancies spontaneously aborted and karyotype confirmation was obtained from the POC; during clinical follow-up, 2 of these cases were reported as partial mole pregnancies. For triploidy cases 3 and 5 (Table 3), clinical evaluation identified large placentas and oligohydramnios in both cases. This SNP-based NIPT approach identified previously undetected twin and triploid pregnancies in women undergoing routine prenatal screening. This method was previously validated for detecting fetal trisomy 21, trisomy 18, trisomy 13, monosomy X, and sex chromosome trisomies in singleton pregnancies, as well as additional fetal haplotypes indicating twin or triploid pregnancies.

We have been unable to find

other population-based published GSK1210151A mouse data on duration with visual disability in glaucoma. Thus, we found that approximately 1 out of 6 glaucoma patients was bilaterally blind at the last visit, while more than 40% were blind in at least 1 eye. Blindness mostly occurred at late ages, and the great majority of bilaterally blind patients were older than 80 years when the best eye became blind. Life expectancy has increased considerably during the last 50 years, by 10 years in the United States, and is expected to increase further. With longer life expectancy, glaucoma patients will have the disease for a longer time and it is possible that the lifetime risk of glaucoma blindness may increase even further. All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Heijl is a consultant to Carl Zeiss Meditec, Allergan, and Alcon; receives lecture fees and payment for development of educational presentations from Allergan; and receives patent royalties from Carl Zeiss Meditec. Dr Bengtsson is a consultant to Carl Zeiss Meditec. This study was supported by the Swedish Research Council (grant K2011-63X-10426-19-3), the Herman

Järnhardt Foundation, the Foundation for Visually Impaired in Former Malmöhus County, and Crown Princess Margareta’s Foundation. Contribution of authors: design of the study (A.H., B.B., D.P.); conduct of the study (A.H., B.B., D.P.); collection of data (D.P.); analysis and interpretation of the data (A.H., B.B., D.P.); preparation of the data (B.B., NVP-AUY922 mouse D.P.); and review and approval of the manuscript (A.H., D.P., B.B.). “
“Giani A, Cigada M, Choudhry N, Deiro AP, Oldani M, Pellegrini

M, Invernizzi A, Duca P, Miller JW, Staurenghi G. Reproducibility of retinal thickness measurements on normal and pathologic eyes by different optical coherence tomography instruments. Am J Ophthalmol 2010;150(6):815–824. In the December 2010 issue, two errors occur in Figure 5: 1 In the first part of the figure (Whole Sample), row 4, column 5, the value was incorrectly stated with a minus sign as Spectralis = Stratus x1−83. The correct value should be Spectralis = Stratus PAK6 x1+83 (with a plus sign). The authors regret these errors. “
“Macular edema is the leading cause of decreased visual acuity in patients with diabetic retinopathy.1 and 2 Laser photocoagulation has been the standard-of-care treatment for diabetic macular edema (DME) for decades, based on the Early Treatment Diabetic Retinopathy Study (ETDRS) and other more recent clinical trials.3, 4, 5 and 6 However, because visual acuity improvement post laser is observed infrequently, and because of the frequent recurrence or persistence of DME after laser treatment, there is a need for better treatments for the management of DME (especially for diffuse DME involving the foveal center, since focal DME not involving the foveal center may have a good prognosis after focal laser treatment).

This booklet provided detailed shoulder and thoracic exercises that incorporated all functional and anatomical shoulder movements and advice regarding progression of ambulation after discharge. The physiotherapist coached each experimental

group participant individually regarding post-discharge exercise frequency, duration, and progression. At discharge, an exercise diary was given to experimental group participants with instructions to complete it daily and return it at their final assessment three months postoperatively. In order to maintain concealment ALK inhibitor of group allocation, the exercise diary was returned to the principal investigator (JR) in a reply-paid envelope. Control group participants received no postoperative physiotherapy intervention. Participant-rated outcomes (pain, shoulder

function, and health-related quality of life) were measured on all participants up to three months postoperatively. Following hospital discharge, the scales and Stem Cells inhibitor questionnaires with which these were measured were mailed to participants for completion and return in a reply-paid envelope. Therapistrated outcomes (shoulder range of motion, muscle strength) were assessed in participants who lived within 60 kilometres of the hospital and indicated that they would be able to attend outpatient assessments after hospital discharge. All outcome measures were recorded at baseline, 1, and 3 months postoperatively. Additionally, pain and

range of motion were measured at discharge from hospital. Pain was measured by asking participants to shade areas on a body chart where they had experienced pain or discomfort on the day of assessment and to rate the intensity of their pain in each area using a numerical rating scale (from 0 = no pain to 10 = pain as bad as you can imagine). Three pain regions were identified: incisional (along the incision or within two intercostal spaces above or below), thoracic cage (apart from too incisional), and the shoulder joint complex (upper limb proximal to the mid-humerus, including the clavicular and scapular areas and the trapezius muscle). Pain that was superior to the cervical spine, inferior to the umbilicus, or distal to the mid-humerus was excluded from analysis. The pain scores reported were for the shoulder region (out of 10) and for total pain (out of 30, calculated by adding together the pain scores for the three regions). Active shoulder range of motion was measured with digital inclinometrya using a standard protocol. Total shoulder motion allowing movement of all joints in the shoulder complex was measured, not isolated glenohumeral movement. Shoulder flexion, elevation through abduction, and external rotation were measured as these movements elongate the muscles divided during open thoracotomy.

À l’inverse la substitution androgénique d’un hypogonadisme l’améliore [64]. Sur la base de résultats obtenus dans des modèles animaux, il n’est par ailleurs pas exclu que la testostérone puisse également exercer un effet protecteur direct sur la cellule β des îlots de Langherans [65]. De façon attendue, le risque d’association au DT2 d’une diminution de la testostéronémie s’élève avec l’âge et le surpoids comme chez le patient non diabétique. Dhindsa et al. [2] ont constaté 24 % d’hypogonadiques chez les diabétiques de type

2 cinquantenaires contre 55 % après 70 ans. Pasquali Enzalutamide cell line et al. [17] ont montré que l’obésité, plus fréquemment observée chez les patients DT2, était un facteur majeur de réduction des taux de testostérone totale et libre calculée et d’augmentation de l’insulinémie par rapport aux patients de poids normal. Les autres mécanismes physiopathologiques de l’hypogonadisme associé au DT2 sont nombreux et en partie communs avec ceux retrouvés pour le tandem testostéronémie-obésité. C’est notamment le cas de l’influence inhibitrice de l’insulino-résistance http://www.selleckchem.com/products/epz-6438.html et de certaines cytokines (TNFα,

IL-1β) sur la sécrétion gonadotrope. L’insulino-résistance intervient également par le biais d’une réduction de la synthèse hépatique de SHBG. Cette conséquence, qui expose plus aisément à la survenue d’un DT2 [47] and [48], peut en outre se trouver majorée par la présence de certains polymorphismes de la SHBG responsables par eux-mêmes d’un abaissement du taux plasmatique de cette protéine de transport. La concentration plasmatique de CRP est par ailleurs nettement plus élevée chez l’homme

lorsque le DT2 s’associe à un hypogonadisme [66]. La présence de médiateurs de l’inflammation, susceptibles d’interférer avec les voies de transduction de l’insuline, peut ainsi contribuer à l’insulino-résistance [67]. A contrario de ce qui peut être observé dans l’obésité simple, et bien que le taux d’œstradiol plasmatique soit positivement lié à la masse de graisse viscérale [68] l’œstradiolémie MycoClean Mycoplasma Removal Kit n’est pas élevée, ce qui suggère que l’œstradiol ne joue pas de rôle physiopathologique notable dans la genèse de l’hypogonadisme hypogonadotrope du patient atteint de DT2 [2] and [69]. Si l’hypogonadisme est le plus souvent observé au cours du DT2, il est également susceptible de s’associer au diabète de type I. Avec le critère fourni par le calcul de la testostérone plasmatique libre, un hypogonadisme est retrouvé chez 20 % des patients atteints d’un diabète de type I [19]. Cette réduction de la fraction biologiquement active de la testostérone, contraste avec une testostéronémie totale normale dans la majorité des études menées dans le diabète de type I. Cette apparente discordance est liée à une élévation du taux plasmatique de SHBG [70].

It was 100% soluble in range of solvents like alcohol and chloroform. The solubility was less in distilled water but solubility tremendously increased in aqueous solutions like normal saline, dextrose solution, glycerol, propylene glycol. Ninety eight percent drug was soluble in 0.1 N HCl, and alcohol

containing HCl solution. Drug had fairer solubility in phosphate buffer saline of basic range. As the pH of buffer saline increased the solubility decreased (Table 2). selleck screening library Solid state stability of AS was conducted, maximum stability was found at 2–8 °C, 60% RH in 24 h. On increasing the temperature and % relative humidity drug degradation was noted (Table 3). The drug was stored at temperature 2–8 °C, 25 °C, 40 °C and 50 °C with humidity 60% RH, 65% RH, 70% RH, buy VE-822 75% RH and 60% RH respectively. As temperature was increased humidity was also increased up to 40 °C. With storage temperature 50 °C humidity was kept 60% RH so as to distinguish the

degradative effect of temperature in comparison to humidity. Drug had maximum stability at storage temperature 2–8 °C with 60% RH up to 3 weeks. Storage at 25 °C and 65% RH showed fairer stability up to 24 h only. Storage time of 1st week, 3rd weeks, 5th weeks at 25 °C temperature and 65% RH showed 92 ± 0.54%, 90 ± 0.24% and 90 ± 0.38%, drug was remaining. Hence the degradation rate seems to be slow. However storage of AS at temperature 40 °C along with humidity 75% RH, the drug was not stable as it degraded and amount of drug remaining was found to be: 90 ± 0.68%, 86 ± 0.04%, 80 ± 0.88%, 78 ± 0.06% at 24 h, one week, three week and five week of storage timing respectively. These data suggests drug’s instability at 40 °C temperature (Table 3). The degradation pattern at storage 50 °C temperature and humidity 60% RH reveals that less amount of drug was degraded as compared

to storage temperature 40 °C and 75% RH. Hence degradation of drug was more moisture related i.e. increment in temperature have very little effect on the same. It may thus be concluded that AS in solid state until is quite stable in refrigerated storage. Hydrolytic degradation studies for AS were performed at different pH in pharmaceutical buffers. As the pH decreased i.e. acidity increased, the degradation of AS increased. The drug was most stable at pH 8 at both temperatures of storage temperature i.e. 2–8 °C and 25 °C (Table 4). Ageing increased degradation of HCQ drug as 88.07 ± 0.5% drug was remaining at storage temperature 2–8 °C for 3 weeks as compared to 94 ± 0.2% drug remaining when stored for one week. HCQ Sulphate was found to be stable at room temperature. Increment in temperature up to 25 °C only 1% drug was degrades after storage of 24 h (Table 5). The photo reactivity screening of HCQ gave idea of packaging the formulation in light resistant container as after 5th week of storage at 25 °C only 80 ± 0.38% HCQ was remaining.

Consequently, differences between StreptInCor and the M protein sequences do not affect opsonization of the target strain, indicating that StreptInCor have broad capacity of coverage against the diverse M-types around the world. Previously we showed

that StreptIncor can be recognized by several HLA class II molecules, making it a candidate vaccine with broad capacity of coverage. The binding prediction of the C-terminal selleck kinase inhibitor amino acid sequences of the M1, M5, M6, M12 and M87 proteins with different HLA class II molecules shows that the possibility of recognition/processing of M proteins and peptides in the pockets (P1, P4, P6 and P9) of different HLA class II molecules agree with previous human studies from our group [26]. Another important data present here is that the anti-StreptInCor opsonizing and neutralizing antibodies did not induce cross-reactivity with human valve protein extracts, indicating the absence of cross-reactive antibodies. These results agrees with previous studies with HLA class II transgenic mice, in which no cross reactivity against heart-tissue derived proteins and

no tissue lesions were observed in several organs up to one year post-vaccination [29]. The present work reinforces the safety of and strong immune response triggered by the StreptInCor mice vaccination. Productions of antibodies that opsonize and neutralize a broad range of S. pyogenes this website strains indicate

the potential of StreptInCor to prevent streptococcal infections without causing deleterious reactions. The authors declare that there is no conflict of interest. StreptInCor intellectual properties are in the names of Luiza Guilherme and Jorge Kalil. This work was supported by grants from “Fundação de Amparo à Pesquisa do Estado de Sao Paulo (FAPESP)” and “Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)”. Karine De Amicis’s benefits were supported by “Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)”. Sitaxentan “
“Global molecular analyses are exploited to enhance our understanding of novel vaccination strategies. High-throughput technologies, including microarray analyses and RNA deep sequencing, allow genome-wide profiling of gene expression within different study groups. Similarly, targeted assays enable study of the expression of a dedicated number of genes [e.g. dual colour reverse transcription multiplex ligation-dependent probe amplification (dcRT-MLPA) assay], cell-expressed molecules (e.g. flow cytometry) or secreted molecules (multiplex assays). Expectations of data output from these analyses in vaccine trials are high, and it is hoped that through the systematic analysis of biomarkers using modern bioassays, predictive biomarkers, which can be used as (surrogate) markers of clinical endpoints or of adverse events, can be identified.

These findings therefore complement the conclusion made

in the primary analysis of the clinical trial that the two-dose schedule was immunologically non-inferior to the three-dose schedule [6]. This study also supports the use of this simple modified ELISA approach to monitor avidities for vaccine and non-vaccine specific antibodies in future HPV vaccine studies. This work was funded by GlaxoSmithKline Biologicals SA. The costs associated with the development and publishing of the manuscript, including scientific writing assistance and statistical advice were also covered Lapatinib nmr by GlaxoSmithKline Biologicals SA. SG, LL, MB and CL developed and designed the study. LL, MB, CL and MF acquired the data. LL, MB, CL and MF performed and supervised the analysis. SG, LL, MB, CL, MF and FT were involved in the interpretation of the data. All authors were involved in the drafting of the manuscript or revising it critically for important intellectual content. All authors approved the manuscript before it was submitted by the corresponding author. All authors had full access to the data and had final responsibility to submit for publication. All authors completed the ICMJE Form for disclosure of potential conflicts of interest and declared that MEK inhibitor the following interests are relevant to the submitted work. All authors are employees

of the GlaxoSmithKline group of companies. Sandra Giannini, Clarisse Lorin and Florence Thomas report ownership of GSK stock options. The authors thank the study participants and their families, the study investigators and their staff members as well as the central and local teams of

GSK Vaccines for their participation in the clinical studies HPV-013 (NCT00196924), HPV-014 (NCT00196937), and HPV-048 (NCT00541970). Mehdi Hamrouni, Laurent Renquin and Annie Leroy (all GSK Vaccines) provided technical support. Frédéric Renaud (GSK Vaccines) and Marie-Pierre Malice (StatAdvice) performed the statistical analyses. Matthew Morgan (MG Science Communications) provided science and writing advice in the manuscript’s development. Ulrike Krause (GSK Vaccines) provided editorial advice and coordinated the manuscript’s development. “
“Influenza A viruses cause annual seasonal epidemics, sporadic avian influenza virus infections and influenza through pandemics such as the H1N1 pandemic virus of 2009–2010 [1]. Seasonal influenza A virus infections cause substantial mortality and morbidity, particularly in high risk groups, such as children younger than age 5, elderly, people with certain chronic medical conditions and immune-compromised individuals [2]. Active immunization is the most cost effective way of limiting influenza related morbidity and mortality. Current split-virion or subunit seasonal influenza vaccines, of which hemagglutinin (HA) is considered the major immunogenic component, are effective against circulating homologous virus strains [3].

When, a few months ago, I received his e-mail informing me that he was recently diagnosed with pancreatic cancer in advanced stage, we were shocked. He said, “I have an Angel to look after me through this coming process. He was a great cardiovascular pathologist and an extremely good, generous and naïve person. God takes the best people to heaven earlier. “
“Figure options Download full-size 3-MA order image Download high-quality image (641 K) Download as PowerPoint slide

Professor Alan Rose was a graduate of the University of Cape Town, qualifying first as a medical doctor and then, in 1968, as an anatomical pathologist. At that time, he was a pathologist involved with cardiac research in association with the Barnard brothers. This research culminated in the world’s first Selleck Tyrosine Kinase Inhibitor Library heart transplant, and Alan Rose ultimately conducted the autopsy on the recipient. So a famous and productive career in cardiovascular pathology was launched. His interest and contributions to the field of cardiovascular pathology grew exponentially and in a short time he was recognized as a pioneer, innovator, and major player in this area. His international reputation burgeoned, and he was invited to speak at several meetings

overseas. His international prominence and scholarly academic contributions and his potential as a leader were recognized by the University of Cape Town who appointed him as the Wernher Beit Chair and Head of Pathology in 1988. It was during this time that it was my infinite good fortune to work under his stewardship and tutelage. I was impressed immediately by this intellect, knowledge, approachability and easy-going manner. He had a relaxed disarming demeanor that made him hugely popular and served as a role model and mentor Carnitine dehydrogenase to several. The department under his vibrant leadership grew, flourished and became an extremely invigorating environment. His international reputation and expertise led to him being invited in 1994 to head the Jesse E. Edwards Heart Registry, a collection of about 15,000 hearts at the United Hospital in St. Paul, MN,

USA. He subsequently joined the University of Minnesota Medical School in 1998, where in due course, he became the Director of the Residency Program and played a major role in the autopsy service. He continued to make major and seminal contributions in the field and was an active member of the Society for Cardiovascular Pathology of the United States and Canadian Academy of Pathology, where he presented short courses and at other fora. He published numerous papers in peer-reviewed journals and was the author of two books. His passing is a great loss to the pathology community at large for he was a true expert in his field and an excellent pathologist in general. I would like also to convey condolences to his family and share in their great loss.

Such antibodies may be effectors, or their detection may have utility as a correlate or surrogate of vaccine-induced cross-protection [21]. The development of potential next generation vaccines to improve the breadth of genotype coverage [1] and [22]

is based upon two approaches: improving the immunogenicity of a conserved region of the minor capsid protein (L2) to generate broadly neutralizing antibodies [23], and using a multivalent L1 VLP-based vaccine that induces type-specific antibodies against a wider array of HPV genotypes (HPV6, HPV11, HPV16, HPV18, HPV31, HPV33, HPV45, HPV52, HPV58; V503, Merck Research Laboratories). The latter approach is the most advanced selleck inhibitor and early clinical trial data show promising immunogenicity and efficacy profiles [24], whereas L2-based candidate vaccines are currently in pre-clinical development [23]. Reduced dosing schedules for the current HPV vaccines are also being investigated with data suggesting non-inferiority of type-specific antibody responses, although there is an impact on the development of cross-neutralizing Dasatinib cell line antibodies [10], [25], [26] and [27]. Early pre-clinical immunogenicity [28], [29] and [30] and MAb reactivity [17] data suggest a degree of inter-genotype antigenic similarity within the Alpha-7 and Alpha-9 species

groups. The extent of this antibody cross-reactivity is unclear as only a limited number of immunogens and target antigens have been used. Some of these

data have been generated using L1-based targets [28], rather than pseudovirus targets bearing both the L1 and L2 proteins, with both proteins being necessary for efficient infectivity and the appropriate presentation of L1 conformational epitopes [23], [31] and [32]. We carried out a comprehensive pre-clinical evaluation of the immunogenicity of L1 VLP derived from multiple HPV genotypes within the Alpha-7 and Alpha-9 species groups and used L1L2 pseudoviruses, representing these same genotypes, as the target antigens in neutralization assays. Such data should improve our understanding of the antigenic the diversity of the L1 protein per se and may inform the design of a next generation vaccine formulation that encompasses a limited number of antigens based upon empirical data. Cervarix® was obtained through the National Vaccine Evaluation Consortium, UK. L1 VLP representing Alpha-7 and Alpha-9 HPV genotypes and control Bovine Papillomavirus (BPV) were expressed using the Bac-to-Bac® Baculovirus System (Life Technologies), as previously described [33] and [34], wherein the L1 genes shared 100% amino acid sequence identity with the L1 genes of the pseudovirus clones [20] used for the neutralization assay (see Section 2.3). Five week old female BALB/c mice were immunized with saline (naïve) or 1/10th (2 μg each HPV16 and HPV18 VLP) the human dose equivalent of Cervarix®[35] by the intramuscular (IM) or sub-cutaneous (SC) routes.

The three atp mutants showed little net bacterial growth between days 1 and 3 postinfection whereas bacterial loads in mice infected with SL1344 increased by nearly 3 logs over the same period. By day 7 the various atp mutants showed no significant bacterial growth, with counts similar to those at day 3, whereas mice infected with SL1344 would have been dead by this time point. Following immunisation with the three atp mutants, mice were re-challenged intravenously with SL1344 ( Fig. 2). The wild type infection grew rapidly as expected in unimmunised control mice whereas mice immunised with the

click here atp mutants had significantly lower bacterial counts in spleens and livers at days 1 and 4 postinfection. Bacterial counts were comparable between the animals immunised with the

different atp mutants and with mice immunised with the well-characterised aroA mutant vaccine strain, SL3261. Therefore SL1344 F0, SL1344 F1 and SL1344 atp were all protective against subsequent challenge. Since all three atp mutants behaved the same in terms of attenuated growth in vivo and protection against subsequent infection, SL1344 atp was selected for further characterisation. To confirm that the attenuation of SL1344 atp was specifically due to the deletion of the atp operon, SL1344 atp was complemented by find more insertion of the whole atp operon fused to a chloramphenicol resistance cassette

into the malXY pseudogene region to generate strain SL1344 atp (malXYatp operon+). BALB/c mice were infected intravenously with 105 CFU of SL1344, SL1344 atp, SL1344 atp (malXYatp operon+) and SL1344 atp (malXY CmR). The complemented strain, SL1344 atp (malXY atp operon+) displayed a wild type-like phenotype with increased bacterial loads in livers and spleens relative to SL1344 atp at days 1, 2 and 3 postinfection ( Fig. 3). Insertion of the chloramphenicol resistance cassette into the malXY region in strain SL1344 atp (malXY CmR) had Sodium butyrate no effect on bacterial counts compared to SL1344 atp ( Fig. 3). Survival and replication of SL1344 and SL1344 atp were assessed in the RAW 264.7 murine macrophage-like cell line. Host cells were infected at MOIs of 1 and 10 and intracellular bacterial counts and macrophage survival were determined at 3 and 24 h postinfection. At both MOIs and at both time points intracellular bacterial viable counts and macrophage survival were similar after infection with SL1344 or SL1344 atp with no statistically significant difference between the two strains ( Fig. 4). To begin to define the immunological components required to control infection with SL1344 atp and to assess the potential use of SL1344 atp immunisation in immunocompromised individuals, two gene knock-out mouse strains and their respective wild types were infected with SL1344 atp.