12 research outputs found
SipD protein identity sequences for the 4 major <i>Salmonella</i> pathogens of humans.
<p>SipD protein identity sequences for the 4 major <i>Salmonella</i> pathogens of humans.</p
Summary of the antibody responses (IgG and IgA) after the last immunization with PrgI or SipD by the SC, IN and OG routes.
<p>Summary of the antibody responses (IgG and IgA) after the last immunization with PrgI or SipD by the SC, IN and OG routes.</p
Protection efficacy of PrgI and SipD T3SS proteins in mice from lethal challenge with <i>S</i>. Typhimurium.
<p>Protection efficacy of PrgI and SipD T3SS proteins in mice from lethal challenge with <i>S</i>. Typhimurium.</p
Serum Ig(G+M) concentrations of mice immunized with PrgI or SipD (A) and PrgI/SipD (B).
<p>Serum Ig(G+M) antibodies specific for PrgI (left) and SipD (right) were quantified by sandwich ELISA 2 weeks after the last immunization as described in Materials and Methods. Data represent mean concentrations (ng/mL) and the standard errors (SEM) from 14–16 individual mice per group. Asterisks *** indicate <i>P</i> value< 0.001, comparing the antibody responses using different routes versus control mice. No cross-reactions were observed between PrgI and SipD (data not shown). [°: indicates injected immunogen; *: indicates biotinylated recombinant protein].</p
IgA titers of mice immunized with PrgI or SipD (A) or PrgI/SipD (B).
<p>Serum IgA antibodies specific for PrgI (left) and SipD (right) were measured by sandwich ELISA 2 weeks after the last immunization as described in Materials and Methods. Data represent mean titers and the standard errors (SEM) from 14–16 individual mice per group. Asterisks indicate <i>P</i> values: *** <i>p</i> < 0.001, ** 0.001<<i>p <</i>0.01 and * <i>p</i>< 0.05 when comparing mice immunized by the IN or OG route versus mice immunized by the SC route and control mice. No cross-reactions were observed between PrgI and SipD (data not shown). [°: indicates injected immunogen; *: indicates biotinylated recombinant protein].</p
IgG (2a +2b) / IgG 1 ratio after PrgI (left) and SipD (right) immunizations.
<p>Mice immunized with PrgI or SipD separately are represented on panel A and those receiving both PrgI and SipD on panel B. Data represent mean and the standard errors (SEM) from 14–16 mice per group. [°: indicates immunogen injected; *: indicates biotinylated recombinant protein].</p
Summary of the antibody responses (IgG and IgA) after the last immunization with both proteins (PrgI and SipD) by the SC, IN and OG routes.
<p>Summary of the antibody responses (IgG and IgA) after the last immunization with both proteins (PrgI and SipD) by the SC, IN and OG routes.</p
Plasma cell neoplasia after kidney transplantation: French cohort series and review of the literature
<div><p>Although post-transplant lymphoproliferative disorder (PTLD) is the second most common type of cancer in kidney transplantation (KT), plasma cell neoplasia (PCN) occurs only rarely after KT, and little is known about its characteristics and evolution. We included twenty-two cases of post-transplant PCN occurring between 1991 and 2013. These included 12 symptomatic multiple myeloma, eight indolent myeloma and two plasmacytomas. The median age at diagnosis was 56.5 years and the median onset after transplantation was 66.7 months (2–252). Four of the eight indolent myelomas evolved into symptomatic myeloma after a median time of 33 months (6–72). PCN-related kidney graft dysfunction was observed in nine patients, including six cast nephropathies, two light chain deposition disease and one amyloidosis. Serum creatinine was higher at the time of PCN diagnosis than before, increasing from 135.7 (±71.6) to 195.9 (±123.7) μmol/l (p = 0.008). Following transplantation, the annual rate of bacterial infections was significantly higher after the diagnosis of PCN, increasing from 0.16 (±0.37) to 1.09 (±1.30) (p = 0.0005). No difference was found regarding viral infections before and after PCN. Acute rejection risk was decreased after the diagnosis of PCN (36% before versus 0% after, p = 0.004), suggesting a decreased allogeneic response. Thirteen patients (59%) died, including twelve directly related to the hematologic disease. Median graft and patient survival was 31.7 and 49.4 months, respectively. PCN after KT occurs in younger patients compared to the general population, shares the same clinical characteristics, but is associated with frequent bacterial infections and relapses of the hematologic disease that severely impact the survival of grafts and patients.</p></div
Evolution of serum creatinine after kidney transplantation, combined with the occurrence of asymptomatic or symptomatic PCN, hemodialysis and death for each patient.
<p>Evolution of serum creatinine (ÎĽmol/l) over time (in years) after kidney transplantation, for each patient. Patients were classified in six groups, and approximate time of diagnosis of SMM (smoldering multiple myeloma), symptomatic PCN (plasma-cell neoplasia), hemodialysis and death were added. MM: Multiple Myeloma. MGRS: Monoclonal Gammapathy of Renal Significance. LCDD: Light Chain Deposition Disease.</p
Characteristics of plasma-cell neoplasias after kidney transplantation.
<p>Characteristics of plasma-cell neoplasias after kidney transplantation.</p