Effect of resistant and susceptible soybean cultivars on the nymphal development, fecundity and mortality of Euschistus heros (Hemiptera:pentatomidae).

The association of resistant varieties and biological control has great interest and potential to be used for pest management. lhe aims of this work were to evaluate the effect of cultivars Silvânia (susceptible to stink bug attack), Dowling e IACI00 (resistant) on E. heras nymph development and to investigate the influence of the flavonoids on the resistance [1]. Nymphs of stink bug were placed in Petri dishes on a diet of soybean pods and observed daily. After adult emergence, they were weight and then put in pairs for mating. lhe nymph mortality, the adult longevity, fecundity and the eggs fertility were evaluated for each cultivar. To quantify the flavonoid compounds, extracts of immature seeds (cv Silvânia and Dowling) undamaged and damage by herbivory, were analysed using high performance liquid chromatography (HPLC). lhe nymphs reared on cv Dowling did not complete their biological cycle. Survivorship curves of immatures in cv. Sylvania and IAClOO, analysed by Kaplan-Meier Survival Distribution, did not show significant difference. lhe medium weight of adults on others cultivars was not different. lhe medium male longevity on cv IAClOOwas 11.0 days, while on cv Silvânia was 35.8 days; for females was 13.4 days on cv IAClOOand 40.6 days on cv Silvânia. lhe female fecundity (105.7 eggs/female) and egg fertility (66.3 nymphs) on cv Silvânia were higher than on cv IACI00 (10.2 eggs/female e 5.8 nymphs). Total amount of flavonoids compounds was higher in cv Silvânia than in cv Dowling, but did not differ when compared between herbivory damage and undamaged plants in the same cultivar. These results suggest that the cv IACI00 and Dowling present direct defense (constitutive) against E. heras, and that the herbivory damage did not induce flavonoids production

Vitamin D3 as adjuvant in the treatment of type 2 diabetes mellitus: modulation of genomic and biochemical instability

Erratum in - Corrigendum: Vitamin D3 as adjuvant in the treatment of type 2 diabetes mellitus: modulation of genomic and biochemical instability. Fagundes GE, Macan TP, Rohr P, Damiani AP, Da Rocha FR, Pereira M, Longaretti LM, Vilela TC, Ceretta LB, Mendes C, Silveira PCL, Teixeira JPF, de Andrade VM. Mutagenesis. 2019 May 29;34(2):215. doi: 10.1093/mutage/gez006.Type 2 diabetes mellitus has undergone a worldwide growth in incidence in the world and has now acquired epidemic status. There is a strong link between type 2 diabetes and vitamin D deficiency. Because vitamin D has beneficial effects on glucose homeostasis, the aim of this study was to evaluate the influence of vitamin D3 supplementation on the modulation of glycaemic control and other metabolic effects, as well as modulation of genomic instability in patients with type 2 diabetes. We evaluated 75 patients with type 2 diabetes, registered in the Integrated Clinics of the University of Southern Santa Catarina. Participants received 4000 IU of vitamin D3 (25(OH)D) supplementation daily for 8 weeks. Blood samples were collected at the beginning and at the end of the supplementation, and 4 weeks after the end of supplementation. The glycidic and lipid profiles [total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein and triglycerides], oxidative stress, DNA damage and 25(OH)D levels were evaluated. Vitamin D3 supplementation for 8 weeks showed enough to significantly increase blood levels of 25(OH)D. A significant difference in lipid profile was observed only in non-HDL cholesterol. Significant changes were observed in glucose homeostasis (fasting glucose and serum insulin) and, in addition, a reduction in the parameters of oxidative stress and DNA damage. There was a significant reduction in the values of 25(OH)D 4 weeks after the end of the supplementation, but levels still remained above baseline. Use of vitamin D supplementation can be an ally in the health modulation of patients with type 2 diabetes mellitusThis work was supported by grants from Conselho Nacional de Pesquisa e Desenvolvimento (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), Fundação de Amparo à Pesquisa e Inovação do Estado de Santa Catarina (FAPESC) and Programa de Pós-Graduação em Ciências da Saúde/ Universidade do Extremo Sul Catarinense.info:eu-repo/semantics/publishedVersio

Genome of the Avirulent Human-Infective Trypanosome—Trypanosoma rangeli

Background: Trypanosoma rangeli is a hemoflagellate protozoan parasite infecting humans and other wild and domestic mammals across Central and South America. It does not cause human disease, but it can be mistaken for the etiologic agent of Chagas disease, Trypanosoma cruzi. We have sequenced the T. rangeli genome to provide new tools for elucidating the distinct and intriguing biology of this species and the key pathways related to interaction with its arthropod and mammalian hosts.  Methodology/Principal Findings: The T. rangeli haploid genome is ,24 Mb in length, and is the smallest and least repetitive trypanosomatid genome sequenced thus far. This parasite genome has shorter subtelomeric sequences compared to those of T. cruzi and T. brucei; displays intraspecific karyotype variability and lacks minichromosomes. Of the predicted 7,613 protein coding sequences, functional annotations could be determined for 2,415, while 5,043 are hypothetical proteins, some with evidence of protein expression. 7,101 genes (93%) are shared with other trypanosomatids that infect humans. An ortholog of the dcl2 gene involved in the T. brucei RNAi pathway was found in T. rangeli, but the RNAi machinery is non-functional since the other genes in this pathway are pseudogenized. T. rangeli is highly susceptible to oxidative stress, a phenotype that may be explained by a smaller number of anti-oxidant defense enzymes and heatshock proteins.  Conclusions/Significance: Phylogenetic comparison of nuclear and mitochondrial genes indicates that T. rangeli and T. cruzi are equidistant from T. brucei. In addition to revealing new aspects of trypanosome co-evolution within the vertebrate and invertebrate hosts, comparative genomic analysis with pathogenic trypanosomatids provides valuable new information that can be further explored with the aim of developing better diagnostic tools and/or therapeutic targets