Validação de método para estudo de deposição de inseticidas biológicos em florestas.

Tem sido dada muito pouca atenção aos estudos da deposição de inseticidas biológicos, os quais tem sido aplicados com equipamento desenvolvido para uso com químicos. O objetivo desta pesquisa foi avaliar um método para a analise da deposição de agrotóxicos em florestas de eucaliptos, caracterizado pelo uso de uma calda de pulverização marcada com traçador e uma técnica especial de amostragem. Empregou-se o cobre como traçador, na forma de fungicida, cuja analise espectrofotométrica e de baixo custo, fácil de execução, alem de possibilitar um excelente nível de recuperação das plantas. Utilizaram-se cartões de papel mata-borrão como alvo artificial para amostrar as gotas. Cartões grampeados em barbantes, em distancias preestabelecidas, foram colocados sobre as plantas, possibilitando uma amostragem estratificada por alturas. Para o solo, os cartões foram colocados em discos de Petri e distribuídos sob a copa das arvores, entre plantas e entre as linhas de plantio. Os resultados indicam que 61% do produto aplicado ficaram retidos nas plantas, 31% atingiram o solo e 8% podem ter sido perdidos através da "exo-deriva".bitstream/item/143340/1/CNPMA-BOLET.-PESQ.-4-99.pd

Aplicação de produtos de proteção fitossanitária via pulverização eletrostática para redução da severidade de doenças foliares em tomateiro tutorado.

o presente trabalho foi realizado com o objetivo de avaliar preliminarmente o potencial da tecnologia no aumento da eficiência de controle da mancha bacteriana e da septoriose em ocorrência simultânea.bitstream/item/221963/1/BPD-213-26-jan-2021.pd

Efficacy and safety of metabolic interventions for the treatment of severe COVID-19: in vitro, observational, and non-randomized open-label interventional study

Background: Viral infection is associated with a significant rewire of the host metabolic pathways, presenting attractive metabolic targets for intervention. Methods: We chart the metabolic response of lung epithelial cells to SARS-CoV-2 infection in primary cultures and COVID-19 patient samples and perform in vitro metabolism-focused drug screen on primary lung epithelial cells infected with different strains of the virus. We perform observational analysis of Israeli patients hospitalized due to COVID-19 and comparative epidemiological analysis from cohorts in Italy and the Veteran's Health Administration in the United States. In addition, we perform a prospective non-randomized interventional open-label study in which 15 patients hospitalized with severe COVID-19 were given 145 mg/day of nanocrystallized fenofibrate added to the standard of care. Results: SARS-CoV-2 infection produced transcriptional changes associated with increased glycolysis and lipid accumulation. Metabolism-focused drug screen showed that fenofibrate reversed lipid accumulation and blocked SARS-CoV-2 replication through a PPARα-dependent mechanism in both alpha and delta variants. Analysis of 3233 Israeli patients hospitalized due to COVID-19 supported in vitro findings. Patients taking fibrates showed significantly lower markers of immunoinflammation and faster recovery. Additional corroboration was received by comparative epidemiological analysis from cohorts in Europe and the United States. A subsequent prospective non-randomized interventional open-label study was carried out on 15 patients hospitalized with severe COVID-19. The patients were treated with 145 mg/day of nanocrystallized fenofibrate in addition to standard-of-care. Patients receiving fenofibrate demonstrated a rapid reduction in inflammation and a significantly faster recovery compared to patients admitted during the same period. Conclusions: Taken together, our data suggest that pharmacological modulation of PPARα should be strongly considered as a potential therapeutic approach for SARS-CoV-2 infection and emphasizes the need to complete the study of fenofibrate in large randomized controlled clinical trials. Funding: Funding was provided by European Research Council Consolidator Grants OCLD (project no. 681870) and generous gifts from the Nikoh Foundation and the Sam and Rina Frankel Foundation (YN). The interventional study was supported by Abbott (project FENOC0003). Clinical trial number: NCT04661930

Risk Alleles for Systemic Lupus Erythematosus in a Large Case-Control Collection and Associations with Clinical Subphenotypes

Systemic lupus erythematosus (SLE) is a genetically complex disease with heterogeneous clinical manifestations. Recent studies have greatly expanded the number of established SLE risk alleles, but the distribution of multiple risk alleles in cases versus controls and their relationship to subphenotypes have not been studied. We studied 22 SLE susceptibility polymorphisms with previous genome-wide evidence of association (p<5×10−8) in 1919 SLE cases from 9 independent Caucasian SLE case series and 4813 independent controls. The mean number of risk alleles in cases was 15.1 (SD 3.1) while the mean in controls was 13.1 (SD 2.8), with trend p = 4×10−128. We defined a genetic risk score (GRS) for SLE as the number of risk alleles with each weighted by the SLE risk odds ratio (OR). The OR for high-low GRS tertiles, adjusted for intra-European ancestry, sex, and parent study, was 4.4 (95% CI 3.8–5.1). We studied associations of individual SNPs and the GRS with clinical manifestations for the cases: age at diagnosis, the 11 American College of Rheumatology classification criteria, and double-stranded DNA antibody (anti-dsDNA) production. Six subphenotypes were significantly associated with the GRS, most notably anti-dsDNA (ORhigh-low = 2.36, p = 9e−9), the immunologic criterion (ORhigh-low = 2.23, p = 3e−7), and age at diagnosis (ORhigh-low = 1.45, p = 0.0060). Finally, we developed a subphenotype-specific GRS (sub-GRS) for each phenotype with more power to detect cumulative genetic associations. The sub-GRS was more strongly associated than any single SNP effect for 5 subphenotypes (the above plus hematologic disorder and oral ulcers), while single loci are more significantly associated with renal disease (HLA-DRB1, OR = 1.37, 95% CI 1.14–1.64) and arthritis (ITGAM, OR = 0.72, 95% CI 0.59–0.88). We did not observe significant associations for other subphenotypes, for individual loci or the sub-GRS. Thus our analysis categorizes SLE subphenotypes into three groups: those having cumulative, single, and no known genetic association with respect to the currently established SLE risk loci

Population mortality during the outbreak of Severe Acute Respiratory Syndrome in Toronto

<p>Abstract</p> <p>Background</p> <p>Extraordinary infection control measures limited access to medical care in the Greater Toronto Area during the 2003 Severe Acute Respiratory Syndrome (SARS) outbreak. The objective of this study was to determine if the period of these infection control measures was associated with changes in overall population mortality due to causes other than SARS.</p> <p>Methods</p> <p>Observational study of death registry data, using Poisson regression and interrupted time-series analysis to examine all-cause mortality rates (excluding deaths due to SARS) before, during, and after the SARS outbreak. The population of Ontario was grouped into the Greater Toronto Area (N = 2.9 million) and the rest of Ontario (N = 9.3 million) based upon the level of restrictions on delivery of clinical services during the SARS outbreak.</p> <p>Results</p> <p>There was no significant change in mortality in the Greater Toronto Area before, during, and after the period of the SARS outbreak in 2003 compared to the corresponding time periods in 2002 and 2001. The rate ratio for all-cause mortality during the SARS outbreak was 0.99 [95% Confidence Interval (CI) 0.93–1.06] compared to 2002 and 0.96 [95% CI 0.90–1.03] compared to 2001. An interrupted time series analysis found no significant change in mortality rates in the Greater Toronto Area associated with the period of the SARS outbreak.</p> <p>Conclusion</p> <p>Limitations on access to medical services during the 2003 SARS outbreak in Toronto had no observable impact on short-term population mortality. Effects on morbidity and long-term mortality were not assessed. Efforts to contain future infectious disease outbreaks due to influenza or other agents must consider effects on access to essential health care services.</p

Association of Communication Between Hospital-based Physicians and Primary Care Providers with Patient Outcomes

Background: Patients admitted to general medicine inpatient services are increasingly cared for by hospital-based physicians rather than their primary care providers (PCPs). This separation of hospital and ambulatory care may result in important care discontinuities after discharge. We sought to determine whether communication between hospital-based physicians and PCPs influences patient outcomes. Methods: We approached consecutive patients admitted to general medicine services at six US academic centers from July 2001 to June 2003. A random sample of the PCPs for consented patients was contacted 2 weeks after patient discharge and surveyed about communication with the hospital medical team. Responses were linked with the 30-day composite patient outcomes of mortality, hospital readmission, and emergency department (ED) visits obtained through follow-up telephone survey and National Death Index search. We used hierarchical multi-variable logistic regression to model whether communication with the patient’s PCP was associated with the 30-day composite outcome. Results: A total of 1,772 PCPs for 2,336 patients were surveyed with 908 PCPs responses and complete patient follow-up available for 1,078 patients. The PCPs for 834 patients (77%) were aware that their patient had been admitted to the hospital. Of these, direct communication between PCPs and inpatient physicians took place for 194 patients (23%), and a discharge summary was available within 2 weeks of discharge for 347 patients (42%). Within 30 days of discharge, 233 (22%) patients died, were readmitted to the hospital, or visited an ED. In adjusted analyses, no relationship was seen between the composite outcome and direct physician communication (adjusted odds ratio 0.87, 95% confidence interval 0.56 – 1.34), the presence of a discharge summary (0.84, 95% CI 0.57–1.22), or PCP awareness of the index hospitalization (1.08, 95% CI 0.73–1.59). Conclusion: Analysis of communication between PCPs and inpatient medical teams revealed much room for improvement. Although communication during handoffs of care is important, we were not able to find a relationship between several aspects of communication and associated adverse clinical outcomes in this multi-center patient sample

The Role of Genetic Variation Near Interferon-Kappa in Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease characterized by increased type I interferons (IFNs) and multiorgan inflammation frequently targeting the skin. IFN-kappa is a type I IFN expressed in skin. A pooled genome-wide scan implicated the IFNK locus in SLE susceptibility. We studied IFNK single nucleotide polymorphisms (SNPs) in 3982 SLE cases and 4275 controls, composed of European (EA), African-American (AA), and Asian ancestry. rs12553951C was associated with SLE in EA males (odds ratio = 1.93, P = 2.5 × 10−4), but not females. Suggestive associations with skin phenotypes in EA and AA females were found, and these were also sex-specific. IFNK SNPs were associated with increased serum type I IFN in EA and AA SLE patients. Our data suggest a sex-dependent association between IFNK SNPs and SLE and skin phenotypes. The serum IFN association suggests that IFNK variants could influence type I IFN producing plasmacytoid dendritic cells in affected skin