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Landscape-level variation inside British telecom plant life anticipate Helicoverpa zea (Lepidoptera: Noctuidae) weight within organic cotton agroecosystems.
34), sedatives (0.48) and hospital death (0.14). It increased the OR for home care (3.27), general practitioner contact (4.65), palliative care unit admission (2.61), non-IV (2.65), gastric tube (2.15), oxygen (2.22) and opioids (4.04) (p less then 0.001). Mean total healthcare costs were €1569 lower for using PHC. All PHC timing categories showed a benefit in medical resource use and costs. However, we observed the largest benefit in the category PHC 90-31 DBD. CONCLUSION Health policy and services should focus on increasing PHC access, while research should further explore early PHC initiation for COPD. Funding SBO IWT nr. 140009. Copyright ©ERS 2020.Rhinovirus infections are the main cause of asthma exacerbations. As Natural Killer (NK) cells are important actors of the antiviral innate response, we aimed at evaluating the functions of NK cells from severe asthma patients in response to rhinovirus-like molecules or rhinoviruses. Peripheral blood mononuclear cells from patients with severe asthma and healthy donors were stimulated with pathogen-like molecules or with the rhinoviruses (RV)-A9 and RV-2. NK cell activation, degranulation and IFN-γ expression were analysed. NK cells from severe asthma patients were less cytotoxic than those from healthy donors in response to TLR3, TLR7/8 or RV-A9 but not in response to RV-2 stimulation. Furthermore, when cultured with IL-12+IL-15, cytokines which are produced during viral infections, NK cells from patients with severe asthma were less cytotoxic and expressed less IFN-γ than NK cells from healthy donors. NK cells from severe asthmatics exhibited an exhausted phenotype, with an increased expression of the checkpoint molecule Tim-3. Together, our findings indicate that the activation of NK cells from patients with severe asthma may be insufficient during some but not all respiratory infections. The exhausted phenotype may participate in NK cell impairment and aggravation of viral-induced asthma exacerbation in these patients. Copyright ©ERS 2020.There are limited published data defining survival and treatment response in patients with mild lung disease and/or reduced gas transfer who fulfil diagnostic criteria for idiopathic pulmonary arterial hypertension (IPAH).Patients diagnosed with IPAH between 2001-19 were identified in the ASPIRE registry. Using pre-specified criteria based on CT imaging and spirometry, patients with a diagnosis of IPAH and no lung disease were termed IPAHno-LD (n=303), and those with minor-mild emphysema or fibrosis were described as IPAHmild-LD (n=190).Survival was significantly better in IPAHno-LD than in IPAHmild-LD (1 and 5-year survival 95% and 70% versus 78% and 22% respectively, p less then 0.0001). In the combined group of IPAHno-LD and IPAHmild-LD, independent predictors of higher mortality were increasing age, lower DLCO, lower exercise capacity and a diagnosis of IPAHmild-LD (p all less then 0.05). Exercise capacity and quality of life improved (p both less then 0.0001) following treatment in patients with IPAHno-LD but not IPAHmild-LD A proportion of patients with IPAHno-LD had a DLCO less then 45%; these patients had poorer survival than patients with DLCO ≥45% although demonstrated improved exercise capacity following treatment.The presence of even mild parenchymal lung disease in patients who would be classified as IPAH according to current recommendations has a significant adverse effect on outcomes. This phenotype can be identified using lung function testing and clinical CT reports. Patients with IPAH, no lung disease and severely reduced DLCO may represent a further distinct phenotype. These data suggest that RCTs of targeted therapies in patients with these phenotypes are required. Copyright ©ERS 2020.There is an emerging role for blood eosinophil count (EOS) as a biomarker to guide inhaled corticosteroid (ICS) therapy in COPD. Since ICS administration could influence EOS, we hypothesised that change in EOS following treatment with ICS may predict outcomes of long-term therapy.In a post-hoc analysis of ISOLDE, a three-year, double-blind trial comparing 500 µg fluticasone propionate BID with placebo in 751 patients with moderate-to-severe COPD, we evaluated whether the initial changes in EOS during ICS treatment were predictive of ICS treatment response.EOS change within 1 year after the introduction of ICS was strongly predictive of treatment response. A suppressed EOS was associated with treatment effect. Characteristically, in patients with EOS suppression of ≥200 EOS·μL-1, ICS use was associated with a decelerated FEV1 decline rate, by 32 mLs·year-1, and 30% reduction in the exacerbation rate. In contrast, in patients experiencing an increase in EOS of ≥200 EOS·μL-1, ICS use was associated with an accelerated FEV1 decline rate by 37 mLs·year-1 and an increased exacerbation rate by 80% (p less then 0.0001). EOS change was not predictive of clinical response with regards to health status evaluated using Saint George Respiratory Questionnaire.These findings suggest EOS change after ICS administration may predict clinical response to ICS therapy in patients with moderate-to-severe COPD at risk of exacerbations. ICS administration may be associated with more frequent exacerbations and an accelerated lung function decline in the 20% of patients where EOS increases after the administration of ICS. These hypothesis-generating observations will need validation in prospectively designed studies. Copyright ©ERS 2020.BACKGROUND/AIM This study aimed to identify the genes that cause biochemical recurrence (BCR) following radical prostatectomy (RP) in men with localized prostate cancer. PATIENTS AND METHODS A two-stage genetic association study of 19 single-nucleotide polymorphisms in 11 key cell cycle regulation genes was carried out. BCR-free survival after RP was evaluated in a discovery cohort of 458 patients with prostate cancer, and replication was investigated in another cohort of 185 patients. RESULTS A consistent association was found between BCR and rs2290291 (discovery p=0.008; replication p=0.029). rs2290291 is located in the tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta (YWHAZ), and was predicted to possess a regulatory function that affected YWHAZ expression. Furthermore, YWHAZ expression was frequently up-regulated in advanced tumours, and associated with poorer survival in patients with prostate cancer. CONCLUSION YWHAZ rs2290291 was found to be associated with BCR. YWHAZ may function as a putative oncogene during prostate cancer progression. BACKGROUND/AIM Prostate cancer (PCa) is the most frequent cancer found in males worldwide, and its mortality rate is increasing every year. However, there are no known molecular markers for advanced or aggressive PCa, and there is an urgent clinical need for biomarkers that can be used for prognosis and prediction of PCa. MATERIALS AND METHODS Mass spectrometry-based proteomics was used to identify new biomarkers in tissues obtained from patients with PCa who were diagnosed with T2, T3, or metastatic PCa in regional lymph nodes. RESULTS Among 1,904 proteins identified in the prostate tissues, 344 differentially expressed proteins were defined, of which 124 were up-regulated and 216 were down-regulated. Subsequently, based on the results of partial least squares discriminant analysis and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses, we proposed that spermidine synthase (SRM), nucleolar and coiled-body phosphoprotein 1 (NOLC1), and prostacyclin synthase (PTGIS) represent new protein biomarkers for diagnosis of advanced PCa. These proteomics results were verified by immunoblot assays in metastatic PCa cell lines and by indirect enzyme-linked immunosorbent assay in prostate specimens. CONCLUSION SRM was significantly increased depending on the cancer stage, confirming the possibility of using SRM as a biomarker for prognosis and prediction of advanced PCa. BLZ945 BACKGROUND/AIM Age may pertain to different tumor genotype characteristics which may interfere with treatment efficacy and prognosis. We investigated the distribution and prognostic effect of mutations and tumor infiltrating lymphocyte (stromal TIL density) in young (≤35 years) and elderly (>65 years) early breast cancer patients. MATERIALS AND METHODS Paraffin tumor genotypes of all clinical subtypes from 345 patients were examined. RESULTS A total of 638 mutations were detected in 221 patients (64.1%). Compared to young, elderly patients presented with lower TIL density (p less then 0.001) but more TILs in TP53 mutated tumors (p=0.042). Mutation in one, rather than in 2 or more genes, conferred better outcome (DFS HR=0.51, p=0.016; OS HR=0.47, p=0.015) but the effect was age-independent. CONCLUSION There are fewer TILs and different mutations patterns in tumors from elderly patients compared to young. Age and TIL-independent gene agnostic co-mutations affect patient outcome. BACKGROUND/AIM Mounting evidence has shown that miRNAs play a critical role in the regulation of hematopoiesis of cell proliferation and apoptosis as well as in tumorigenesis. The miR146a rs2910164 polymorphism, which is closely responsive for its expression, has been reported to associate with the risk of several solid cancers. The study aimed at examining the association of the it with susceptibility to childhood acute lymphoblastic leukemia (ALL) in Taiwan. MATERIALS AND METHODS We recruited 266 patients with childhood ALL and 266 healthy controls, and rs2910164 genotypes were determined by the polymerase chain reaction-restriction fragment length polymorphism methodology. RESULTS The allele G was associated with decreased childhood ALL risk (OR=0.66, 95%CI=0.52-0.85, p=0.0011). Consistently, the GG genotype was associated with a decreased susceptibility (OR=0.40, 95%CI=0.23-0.67, p=0.0004). Patients with CG and GG genotypes were of earlier onset than those with CC genotype (p=0.0255 and p=0.0001). CONCLUSION MiR146a rs2910164 G allele serves as a protective marker for childhood ALL in Taiwan. BACKGROUND/AIM In this study, we aimed to investigate the prognostic role of a previously identified panel of 10 stem cell markers stratified against the catalytic subunit of telomerase (hTERT) in human breast cancer. MATERIALS AND METHODS The mRNA copy numbers of these genes were determined using real time quantitative PCR in 124 breast cancer tissues and adjacent non-cancerous tissues. Relations between mRNA levels and survival were analysed using Kaplan-Meier plots and Cox regression analysis. RESULTS Five genes (BMI1, NES, POU5F1, ALDH1A2 and CDKN1A) correlated with survival when stratified with hTERT and predicted overall (Wilcoxon p=0.004; Cox p=0.006) and disease-free (Wilcoxon p less then 0.000; Cox p=0.000) survival. CONCLUSION This panel of genes stratified by hTERT could open new avenues for the development of new prognostic tools, as well as for the identification of new research directions regarding breast oncogenesis. BACKGROUND/AIM Osteoblastoma is a rare benign tumor of the bones in which recurrent rearrangements of FOS have been found. Our aim was to investigate two osteoblastomas for possible genetic aberrations. MATERIALS AND METHODS Cytogenetic, RNA sequencing, and molecular analyses were performed. RESULTS A FOS-ANKH transcript was found in the first tumor, whereas a FOS-RUNX2 was detected in the second. Exon 4 of FOS fused with sequences either from intron 1 of ANKH or intron 5 of RUNX2. The fusion events introduced a stop codon and removed sequences involved in the regulation of FOS. CONCLUSION Rearrangements and fusions of FOS show similarities with those of HMGA2 (a feature of leiomyomas and lipomas) and CSF1 (tenosynovial giant cell tumors). The replacement of a 3'-untranslated region, controlling the gene's expression, by a new sequence is thus a common pathogenetic theme shared by FOS, HMGA2, and CSF1 in many benign connective tissue tumors.
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