Myelodysplastic syndrome accompanied by basophilia and eosinophilia with t(5;12)(q31;p13)

The t(5;12)(q31not, vert, similar35;p12not, vert, similar13) is rare among cytogenetically categorized myeloid diseases. Here we describe a case of myelodysplastic syndrome (MDS) with basophilia followed by leukocytosis, basophilia, and eosinophilia with t(5;12)(q31;p13).A 44-year-old man was referred to Tsukuba University Hospital in August 2005, due to severe anemia and thrombocytopenia. Peripheral blood examination showed hemoglobin 4.5 g/dL, with mean corpuscular volume 109 fL, platelets 73 × 109/L, and white blood cells 4.9 × 109/L with 23% basophils, 3% eosinophils, and 0% blasts. Bone marrow was slightly hypocellular, with trilineage dysplasia. Cytogenetic examination of the bone marrow cells revealed a normal karyotype, 46,XY. A diagnosis of myelodysplastic syndrome–refractory anemia with excess blasts type 2 (MDS-RAEB2) was made according to the WHO classification

Impact of combined pulmonary fibrosis and emphysema on lung cancer risk and mortality in rheumatoid arthritis: A multicenter retrospective cohort study.

ObjectiveCombined pulmonary fibrosis and emphysema (CPFE) is a syndrome characterized by the coexistence of emphysema and fibrotic interstitial lung disease (ILD). The aim of this study was to examine the effect of CPFE on lung cancer risk and lung cancer-related mortality in patients with rheumatoid arthritis (RA).MethodsWe conducted a multicenter retrospective cohort study of patients newly diagnosed with lung cancer at five community hospitals between June 2006 and December 2021. Patients were followed until lung cancer-related death, other-cause death, loss to follow-up, or the end of the study. We used the cumulative incidence function with Gray's test and Fine-Gray regression analysis for survival analysis.ResultsA total of 563 patients with biopsy-proven lung cancer were included (82 RA patients and 481 non-RA patients). The prevalence of CPFE was higher in RA patients than in non-RA patients (40.2% vs.10.0%) at lung cancer diagnosis. During follow-up, the crude incidence rate of lung cancer-related death was 0.29 and 0.10 per patient-year (PY) in RA and non-RA patients, and 0.32 and 0.07 per PY in patients with CPFE and patients without ILD or emphysema, respectively. The estimated death probability at 5 years differed between RA and non-RA patients (66% vs. 32%, pConclusionsRA patients with lung cancer had a higher prevalence of CPFE and increased cancer-related mortality compared with non-RA patients. Close monitoring and optimal treatment strategies tailored to RA patients with CPFE are important to improve the poor prognosis of lung cancer

ELISA using absorbed antisera and whole-cell sonicates as antigen.

<p>Whole-cell sonicates were coated on ELISA plates as antigens. Antisera from mice immunized with each pure genotype fimbriae were used after absorption with the fimbria-deficient mutant 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster. “Non” indicates non-immunized mouse sera. W83 rarely produces FimA protein and fimbriae. Data show mean ± SD. Asterisks indicate statistical significance compared with Non (* <i>p</i><0.05, ** <i>p</i><0.01). Note that scales of Y axes are adjusted in order to compare titers clearly.</p

Immunoblot analysis for PgmA using whole-cell sonicates.

<p>Whole-cell sonicates (W) were fractionated into soluble (Sol), envelope (Env), inner membrane (IM) and outer membrane (OM) fractions. Samples were denatured in an SDS-containing buffer with 2-mercaptoethanol by heating at 100°C for 10 min, then subjected to SDS-PAGE and immunoblot analysis. Emp denotes 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster/pT-COW::<i>ragAP</i>, carrying empty vector, used as a negative control; 33277 denotes the wild-type strain; Complement denotes 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster carrying pT-COW::<i>ragAP</i>::<i>fimX-pgmA-fimA</i>. An arrow indicates PgmA as a 60-kDa protein. Degradation bands (below the 60-kDa) were also visualized because PgmA was highly sensitive to intrinsic proteases of this bacterium <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0043722#pone.0043722-Hongo1" target="_blank">[13]</a>.</p

ELISA using absorbed antisera and purified FimA fimbriae as antigen.

<p>Pure FimA fimbriae, derived from each <i>fimA</i> gene, were coated on ELISA plates as antigens. Antisera from mice immunized with each pure genotype fimbriae were used after absorption with the fimbria-deficient mutant 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster. “Non” indicates non-immunized mouse sera. Data show mean ± SD. Asterisks indicate statistical significance compared with Non (* <i>p</i><0.05, ** <i>p</i><0.01). Note that scales of Y axes are adjusted as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0043722#pone-0043722-g006" target="_blank">Fig. 6</a>.</p

Immunoblot analysis using whole-cell sonicates partially denatured.

<p>Whole-cell sonicates were denatured in an SDS-containing buffer with 2-mercaptoethanol by heating at 70°C for 10 min, and subjected to SDS-PAGE and immunoblot analysis by using antisera, 1,000-fold dilution, from mice immunized with purified FimA fimbriae. Antigen samples were as follows: <i>P. gingivalis</i> ATCC 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster (FimA deficient, lane 1), and the wild-type strains of ATCC 33277 (lane 2), TDC60 (lane 3), 6/26 (lane 4), W83 (lane 5), HG564 (lane 6), and HNA99 (lane 7). M denotes a standard marker. W83 rarely produces FimA protein and fimbriae. Note that ladder bands are specific for FimA fimbriae whereas smear bands between 40–80 kDa are nonspecific. Arrows with dotted lines are placed in order to clearly discriminate each lane.</p

SDS-PAGE and CBB staining using purified FimA fimbriae.

<p>Purified FimA fimbriae were denatured in an SDS-containing buffer with 2-mercaptoethanol by heating at 60 to 100°C for 10 min, then subjected to SDS-PAGE and CBB staining. Samples were as follows: purified from <i>P. gingivalis</i> ATCC 33277 Δ<i>mfa1</i> (native 33277 FimA fimbriae, lane 1), <i>P. gingivalis</i> ATCC 33277 Δ<i>mfa1</i> Δ<i>fim</i> cluster with <i>fimA</i> of ATCC 33277 (I) (lane 2), TDC60 (II) (lane 3), 6/26 (III) (lane 4), W83 (IV) (lane 5), HG564 (IV) (lane 6), and HNA99 (V) (lane 7) introduced. Note that CBB staining did not visualize a ladder band as seen in immunoblot analysis in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0043722#pone-0043722-g002" target="_blank">Fig. 2</a>.</p