Control of S. exigua was greater with M. pallidipes plus SeNPV than with M. pallidipes alone. Microplitis pallidipes preferred healthy hosts to infected hosts. Parasitoids were able to complete their development in virus-infected hosts before the hosts died from the virus infection. The parasitoid ovipositors contaminated with the virus could carry and transmit SeNPV.

No abstract

The relationship between epidermal growth factor receptor (EGFR) mutation status and EGFR-tyrosine kinase inhibitors (TKI) efficacy in non-small cell lung cancer (NSCLC) patients has been well established. However, there is no available standard to define the optimal testing method and specimen type required for the detection of EGFR mutations. In this study, we compare results of ADx-amplification refractory mutation system (ARMS) and direct sequencing for the detection of EGFR mutation and prediction of EGFR-TKI efficacy for surgery and biopsy tumor tissues in 158 NSCLC patients. For 71 surgery samples, there were 13 and 17 positive samples detected by direct sequencing and ARMS, respectively. For 87 biopsy samples, direct sequencing and ADx-ARMS found 15 and 32 positive samples, respectively. For surgery samples, sensitivity of direct sequencing and ARMS was 72.2% (13/18) and 94.4% (17/18), respectively. For the biopsy samples, sensitivity of direct sequencing and ARMS was 44.1% (15/34) and 94.1% (32/34), respectively. For the biopsy and surgery samples, the ORRs for EGFR positive and negative patients detected by direct sequencing were 46.1 versus 16.7 and 66.7 versus 1.1%, respectively. For ADx-ARMS, the ORR for EGFR positive patients was significantly higher than for negative patients (55.6 vs. 5.6%). The median progression-free survival time of patients with EGFR wild type detected by direct sequencing (4.2 months) was significantly longer than that of patients with wild type detected by ARMS (1.7 months). ARMS has a higher sensitivity and specificity than direct sequencing for EGFR detection of mutation in both surgical and biopsy samples, and the results from ARMS are more consistent with the efficacy of EGFR-TKIs treatment.

No abstract

We confirmed that WU polyomavirus had been found and identified in the respiratory secretions in China.

In this study, we isolated an endophytic quinclorac-degrading bacterium strain Q3 from the root of tobacco grown in quinclorac contaminated soil. Based on morphological characteristics, Biolog identification, and 16S rDNA sequence analysis, we identified strain Q3 as Bacillus megaterium. We investigated the effects of temperature, pH, inoculation size, and initial quinclorac concentration on growth and degrading efficiency of Q3. Under the optimal degrading condition, Q3 could degrade 93% of quinclorac from the initial concentration of 20 mg/L in seven days. We analyzed the degradation products of quinclorac using liquid chromatography–tandem mass spectrometry (LC-MS/MS). The major degradation products by Q3 were different from those of previously identified quinclorac degrading strains, which suggests that Q3 may employ new pathways for quinclorac degradation. Our indoor pot experiments demonstrated that Q3 can effectively alleviate the quinclorac phytotoxicity in tobacco. As the first endophytic microbial that is capable of degrading quinclorac, Q3 can be a good bioremediation bacterium for quinclorac phytotoxicity.

EML4-ALK fusion genes have been recognized as novel "driver mutations" in a small subset of non-small cell lung cancers (NSCLC). The frequency of EML4-ALK fusions in NSCLC patients who have clinical characteristics related to EGFR mutation remains unknown. We screened 102 Chinese patients with NSCLC based on one or more of the following characteristics: female, no or light smoking history, and adenocarcinoma histology. EML4-ALK fusion genes were identified by RT-PCR, whereas EGFR (Exons 18-21) and KRAS (Exons 1 and 2) mutations were detected by DNA sequencing. Eight specimens (8%) were positive for EML4-ALK fusions, with seven being Variant 1 and one Variant 2. There were 44 (43%) and 17 (16%) patients harboring EGFR and KRAS mutations, respectively. Thirty-one (31%) cases were wild type for EML4-ALK, EGFR, and KRAS mutations. Of the eight patients with EML4-ALK, none had an EGFR mutation, whereas a KRAS mutation was detected in one patient. Histologically, five of the EML4-ALK positive tumors were adenocarcinoma and two were mixed adenosquamous carcinoma; only one was a squamous carcinoma. Our data support the conclusion that the EML4-ALK fusion gene defines a new molecular subset of NSCLC with distinct pathologic features.

Purpose: Evidence regarding the relationship between albumin-to-alkaline phosphatase ratio (AAPR) and overall survival (OS) in extensive-disease small-cell lung cancer (ED-SCLC) patients is limited. This study aimed to investigate whether AAPR was independently related to OS in ED-SCLC patients after adjusting for potential covariates. Patients and Methods: This was a retrospective cohort study of 224 patients with ED-SCLC. The target independent and dependent variables were pretreatment AAPR and OS, respectively. Covariates included age; sex; Eastern Cooperative Oncology performance status score; smoking history; existence of metastasis to organs such as the bone, lung, liver, brain, malignant plural effusion and others; sum of organ metastasis (≤3, >3), evaluation of firstline treatment; and sum of treatment lines (<2, ≥2). Student's t test or chi-squared test was used to analyze the associations between AAPR and clinical characteristics. Kaplan-Meier survival analysis and Cox's proportional hazards regression model were used to assess the prognostic value of AAPR for OS. Results: The average patient age was 60.51±8.73 years, and 87.95% were men. A non-linear relationship between AAPR and OS was detected, with an inflection point of 0.35. The hazard ratios (HRs) of the left (AAPR <0.35) and right sides (AAPR ≥0.35) of inflection point were 0.04 (95% CI=0.00-0.70, p=0.0268) and 0.52 (95% CI=0.16-1.64, p=0.2659), respectively. Kaplan-Meier analysis showed a median OS of 9.73 months (95% CI=8.6-12.33) for AAPR <0.35 and 13.7 months (95% CI=11.43-16.37) for AAPR ≥0.35 (log-rank p<0.0001). The Cox proportional hazards model showed that AAPR <0.35 increased the risk of death after adjusting for potential confounders (HR=1.65, 95% CI=1.11-2.46). In subgroup analysis, the trends of HRs were increased across all subgroups with AAPR <0.35 after stratification. Conclusion: Pretreatment AAPR might be served as an independent prognostic indicator in ED-SCLC patients. Our findings should be further validated in large-scale and prospective clinical trials.