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Context: In management of community-acquired pneumonia (CAP), excellent biomarkers for inflammation would be helpful in our practice. Objectives: Kinetics of c-reactive protein (CRP) and serum amyloid A (SAA) was characterized, using their biologic half-life times. Materials and methods: Time course of CRP and SAA levels in the successfully treated 36 CAP patients were investigated and their half-life times were determined and compared. Results & Discussions: SAA and CRP declined in an exponential mean and the biologic half-life times of SAA levels was 34.9 ± 28.7 h, significantly shorter than that of CRP, 46.4 ± 21.7 h (p = 0.0014). Conclusion: The kinetic evidence, presented as biologic half-life times of CRP and SAA, helps us make a clinical assessment of CAP patients.

BackgroundLiquid‐based cytology (LBC) allows immunohistochemistry (IHC), fluorescence in situ hybridization, and molecular testing to be performed in fixed cell materials. We examined the feasibility of subtyping and EGFR mutation testing of bronchoscopic samples from patients with lung cancer using cell blocks (CB) based on LBC fixation (LBC‐CB).MethodsWe included 35 consecutive patients with peripheral lung nodules who underwent endobronchial ultrasonography with a guide sheath in our hospital. Thirty of these patients were diagnosed with lung cancer by obtaining cytological samples. Cytological subtyping was performed with IHC using LBC‐CB, and the Cobas EGFR Mutation Test ver. 2 was performed using extracted genomic DNA from the LBC‐CB, formalin‐fixed paraffin‐embedded (FFPE) tissue, and matched plasma.ResultsOf the 30 cases, 25 were classified cytomorphologically as adenocarcinoma (ADC, n = 17) and squamous‐cell carcinoma (SQCC, n = 8). The remaining five cases were classified by IHC as favor ADC (n = 3) and favor SQCC (n = 2) according to the WHO criteria. In the final ADC group (n = 20), EGFR mutations on the LBC‐CB were identified in eight cases (40%; 1 exon 19 deletion, 6 L858R, and 1 L861Q). Mutations in FFPE samples were identified in seven cases (35%) at the same site in each case. Plasma EGFR mutations were identified in four cases (20%) at the same site. The CB detection rate was higher than for FFPE and plasma.ConclusionLBC‐CB is suitable for subtyping and EGFR mutation testing in lung cancers.

IL-17A in the combination with TNF-α or IL-1β showed a synergistic augmenting effect on IL-8 and GM-CSF production in human airway epithelial cells.

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c Candida glabrata strains sequentially isolated from blood developed resistance to micafungin (MICs from <0.015 to 4 g/ml). A novel mutation identified in micafungin-resistant strains at bp 262 of FKS2 (containing a deletion of F659 [F659del]) was inserted into the homologous region in FKS1. CASE REPORTA 93-year-old man was admitted to our hospital with a diagnosis of pulmonary tuberculosis (day 1). The patient had been receiving treatment for essential hypertension with chronic renal failure for a decade. On admission, the patient's vital signs were normal; however, serum laboratory data showed a marked elevation of creatinine (Cr) (4.7 mg/dl) and blood urea nitrogen (BUN) (74.5 mg/dl). After initiation of antituberculous therapy with oral isoniazid (300 mg/day) plus rifampin (450 mg/day), renal failure progressed (Cr, 7.0 mg/dl) due to drug-induced myoglobinemia (1,000 ng/ml) with uremic symptoms. Although an urgent flexible double lumen (FDL) catheter was introduced into the internal jugular vein, readministration of isoniazid (day 18) caused severe rhabdomyolysis (myoglobinemia, 25,650 ng/ml), with a recurrence of the uremic symptoms.On day 27, the patient suddenly went into a state of shock with high fever and was empirically treated with intravenous meropenem (0.5 g/day), vancomycin (0.5 g, every 48 h [q48h]), and fluconazole (200 mg/day) based on a tentative diagnosis of aspiration pneumonia or catheter-related bloodstream infection complicated by sepsis. On the same day, two sets of blood cultures and serum endotoxin antigen were negative except for an elevation of ␤-D-glucan (133 pg/ml). On day 32, the patient's serum value of ␤-D-glucan rose to 530 pg/ml, and he had a positive result for serum galactomannan (Aspergillus antigen) of 4.5, thrombocytopenia (6.4 ϫ 10 3 platelets/l), and leukocytopenia (2.0 ϫ 10 3 leukocytes/l). Therefore, the fluconazole was changed to voriconazole (6 mg/kg of body weight/day, q12h) with the intent of targeting Aspergillus spp. However, on day 35, a blood culture collected on day 32 (strain NO1) was identified as Candida glabrata; therefore, voriconazole was changed to intravenous micafungin (100 mg/day) according to the Infectious Diseases Society of America (IDSA) 2009 guidelines (1). A blood culture taken on day 34 (NO2) also was positive for C. glabrata; however, after initiation of treatment with micafungin, the persistent fever subsided, and a blood culture taken at day 37 was negative for the yeast. Both strain NO1 and strain NO2 were susceptible to micafungin (MIC, Ͻ0.015 g/ml) but susceptible-dose dependent to fluconazole (MIC Ͻ8 g/ml) by Clinical and Laboratory Standards Institute (CLSI) broth microdilution (BMD) methods (CLSI document M27-S4). With regard to voriconazole, no breakpoint was determined for C. glabrata. In spite of two rounds of replacement of the FDL catheter, the serum value of ␤-D-glucan remained high (Ͼ600 pg/ml), and blood cultures taken on day 48 (NO3) and day 51 (NO4) again yielded C. glabrata. Based on the suspicion of a micafungin-resista...

Circulating microRNAs (miRNAs) are promising markers for cancer diagnosis and prognosis. Numerous studies evaluating miRNAs as markers for non-small cell lung cancer (NSCLC) have been conducted in recent years; however, the majority of candidate markers proposed via individual studies were inconsistent and no marker miRNAs for the diagnosis of early stage NSCLC have been established. In the present study, miR-145, miR-20a, miR-21 and miR-223, which were previously reported as candidate diagnostic markers of NSCLC, were re-evaluated. The serum levels of these miRNAs were quantified in 56 patients with stage I–IV NSCLC using the TaqMan microRNA assays and separately compared the levels at each stage with those in 26 control patients. The level of miR-145 was significantly reduced in patients with NSCLC, regardless of clinical stage, and its level increased following tumor resection in patients with stage I–II disease. These results indicate that miR-145 is relevant as a diagnostic marker for stages I–IV NSCLC. Additionally, the levels of miR-20a and miR-21 demonstrated notable differences among patients at different clinical stages. These miRNAs distinguished patients in a number of, but not all, stages of NSCLC from cancer-free control patients. These results indicated that it is essential to analyze miRNA levels at each stage separately in order to evaluate marker miRNAs for NSCLC diagnosis.