Genetic parameters for weight, morphometry and oviposition of Africanized honeybee queens using simulated data / [Parâmetros genéticos para peso, morfometria e oviposição de abelhas rainhas africanizadas sob simulação]

This study aimed to estimate genetic parameters for simulated data of body weight (BW), abdominal width (AW), abdominal length (AL), and oviposition. Simulation was performed based on real data collected at apiaries in the region of Campo das Vertentes, Minas Gerais, Brazil. Genetic evaluations were performed using single- and two-trait models and (co)variance components were estimated by the restricted maximum likelihood method. The heritability for BW, AW, AL and oviposition were 0.54, 0.47, 0.31 and 0.66, respectively. Positive genetic correlations of high magnitude were obtained between BW and AW (0.80), BW and oviposition (0.69), AW and oviposition (0.82), and AL and oviposition (0.96). The genetic correlations between BW and AL (0.11) and between AW and AL (0.26) were considered moderate and low. In contrast, the phenotypic correlations were positive and high between BW and AW (0.97), BW and AL (0.96), and AW and AL (0.98). Phenotypic correlations of low magnitude and close to zero were obtained for oviposition with AL (0.02), AW (-0.02), and BW (-0.03). New studies involving these characteristics should be conducted on populations with biological data in order to evaluate the impact of selection on traits of economic interest.(AU)

Objetivou-se estimar parâmetros genéticos para dados simulados de peso corporal (PC), largura abdominal (LA), comprimento abdominal (CA) e oviposição (OV). A simulação foi conduzida com base em dados reais, coletados em apiários da região do Campo das Vertentes, Minas Gerais. As estimativas das análises genéticas foram realizadas por modelos uni e bicaracterísticos, sendo os componentes de (co) variância estimados pelo método da máxima verossimilhança restrita. As herdabilidades para PC, LA, CA e OV foram de 0,54, 0,47, 0,31 e 0,66 respectivamente. As correlações genéticas foram positivas e de alta magnitude para PC e LA (0,80), PC e OV (0,69), LA e OV (0,82) e CA e OV (0,96). Para PC e CA (0,11) e LA e CA (0,26), as correlações genéticas foram moderadas e de baixa magnitude. As correlações fenotípicas foram positivas e de alta magnitude para PC e LA (0,97), PC e CA (0,96) e LA e CA (0,98). Para OV e CA (0,02), OV e LA (-0,02) e OV e PC (-0,03), foram encontradas correlações fenotípicas de magnitude baixa e próximas de zero. Novos estudos devem ser realizados em populações com dados biológicos, a fim de se observar o impacto da seleção em características de interesse econômico.(AU)

Plasma proprotein convertase subtilisin/kexin type 9 inhibitors and cataract risk: A systematic review and meta-analysis. / Inhibidores de la proproteína convertasa plasmática subtilisina kexina tipo 9 y riesgo de cataratas: revisión sistemática y metaanálisis.

BACKGROUND: The marked decrease in LDL-C levels produced by the inhibitors of the plasma proprotein convertase subtilisin/kexin type 9 (iPCSK9) could be associated with an increased risk of cataracts. METHODS: A meta-analysis was performed that included randomised clinical trials controlled with iPCSK9, alone, or in combination with other lipid-lowering drugs, which reported new cases of cataracts, by searching PubMed/Medline, databases of EMBASE and Cochrane Clinical Trials. A fixed-effect model was used, and a meta-regression was carried out evaluating the relationship between intra-treatment LDL-C and the risk of developing cataracts. RESULTS: Five eligible studies of iPCSK9 including 83,492 patients were taken into account for the analysis, and 531 new cases of cataracts in iPCSK9 group vs. 532 in placebo group were diagnosed. The iPCSK9 therapy was not associated with an increased risk of cataracts [OR: 0.96, 95% CI: 0.85-1.08; P=.86, I2: 0%]. Likewise, no significant association was found between on-treatment LDL-C levels, differences between study arms, and new cases of cataracts. CONCLUSION: In this analysis, the use of iPCSK9 was not associated with an increased risk of cataracts.

Therapy with cholesteryl ester transfer protein (CETP) inhibitors and diabetes risk.

BACKGROUND: Cholesteryl ester transfer protein (CETP) inhibitors are a class of drugs that targets the CETP enzyme to significantly increase serum high-density lipoprotein cholesterol (HDL-C) and decrease low-density lipoprotein cholesterol (LDL-C) levels. As HDL-C has potential antidiabetic properties, and the beneficial effects of CETP drugs on glucose homoeostasis have not been sufficiently studied, the aims of this study were: (1) to evaluate the effect of CETP inhibitors on the incidence of diabetes; and (2) to assess the association between CETP inhibitor-induced changes in HDL-C levels and incidence of diabetes. METHODS: A meta-analysis was performed of randomized controlled clinical trials of CETP inhibitor therapy, either alone or combined with other lipid-lowering drugs, reporting data from new cases of diabetes with a minimum of 6 months of follow-up, after searching the PubMed/MEDLINE, Embase and Cochrane Controlled Trials databases. A fixed-effects meta-regression model was then applied. RESULTS: Four eligible trials of CETP inhibitors, involving a total of 73,479 patients, were considered for the analyses, including 960 newly diagnosed cases of diabetes in the CTEP inhibitor group vs 1086 in the placebo group. CETP inhibitor therapy was associated with a significant 12% reduction in incidence of diabetes (OR: 0.88, 95% CI: 0.81-0.96; P=0.005). Assessment of the relationship between on-treatment HDL-C and the effect of CETP inhibitors showed a statistically non-significant trend (Z=-1.13, P=0.26). CONCLUSION: CETP inhibitors reduced the incidence of diabetes. The improvement in glucose metabolism may have been related, at least in part, to the increase in HDL-C concentration.

Transthyretin provides trophic support via megalin by promoting neurite outgrowth and neuroprotection in cerebral ischemia.

Transthyretin (TTR) is a protein whose function has been associated to binding and distribution of thyroid hormones in the body and brain. However, little is known regarding the downstream signaling pathways triggered by wild-type TTR in the CNS either in neuroprotection of cerebral ischemia or in physiological conditions. In this study, we investigated how TTR affects hippocampal neurons in physiologic/pathologic conditions. Recombinant TTR significantly boosted neurite outgrowth in mice hippocampal neurons, both in number and length, independently of its ligands. This TTR neuritogenic activity is mediated by the megalin receptor and is lost in megalin-deficient neurons. We also found that TTR activates the mitogen-activated protein kinase (MAPK) pathways (ERK1/2) and Akt through Src, leading to the phosphorylation of transcription factor CREB. In addition, TTR promoted a transient rise in intracellular calcium through NMDA receptors, in a Src/megalin-dependent manner. Moreover, under excitotoxic conditions, TTR stimulation rescued cell death and neurite loss in TTR KO hippocampal neurons, which are more sensitive to excitotoxic degeneration than WT neurons, in a megalin-dependent manner. CREB was also activated by TTR under excitotoxic conditions, contributing to changes in the balance between Bcl2 protein family members, toward anti-apoptotic proteins (Bcl2/BclXL versus Bax). Finally, we clarify that TTR KO mice subjected to pMCAO have larger infarcts than WT mice, because of TTR and megalin neuronal downregulation. Our results indicate that TTR might be regarded as a neurotrophic factor, because it stimulates neurite outgrowth under physiological conditions, and promotes neuroprotection in ischemic conditions.

Specific adipocytokines profiles in patients with hyperactive and/or binge/purge form of anorexia nervosa.

OBJECTIVE: The aim of our study was to determine whether eating behaviors and/or physical activity level may explain contradicting results in adipocytokines levels in anorexia nervosa (AN). SUBJECTS/METHODS: Fasting levels of circulating adipocytokines (adiponectin, resistin and leptin), insulin, glucose, C-reactive protein, cytokines (tumor necrosis factor-alpha and interleukin (IL)-1beta), body composition and resting energy expenditure were measured in 24 women AN patients and 14 women controls. These parameters were compared according to AN subtypes: 15 patients with restrictive (R-AN) form versus 9 patients with binge/purge (BP-AN) form; 15 patients with hyperactive (H-AN) form versus 9 patients with nonhyperactive (NH-AN) form. RESULTS: BP-AN patients had significantly higher serum adiponectin levels compared with R-AN patients (P<0.05), and H-AN patients had higher serum leptin and lower serum resistin levels compared with NH-AN patients (P<0.05 for both). CONCLUSIONS: Our study shows specific adipocytokines profiles depending on the subtype of AN: restrictive versus binge/purge and hyperactive versus Nonhyperactive forms. We suggest that these biological signatures could interfere with the outcome of the disease.

Parallel increase of plasma apoproteins C-II and C-III in Type 2 diabetic patients.

AIMS: To determine plasma levels of apoprotein (apo) C-II and apoprotein C-III in Type 2 diabetic patients and to examine the clinical and biological factors that are associated with elevated apoC concentrations. METHODS: We measured apoC-II and apoC-III in total plasma and in non-high-density lipoprotein fractions by an immunoturbidimetric assay in 88 Caucasian Type 2 diabetic patients and in 138 healthy control subjects. RESULTS: Plasma levels of both apoC-II and apoC-III were increased in Type 2 diabetic patients. The clinical conditions associated with an increase of plasma apoC-II and apoC-III were abdominal obesity, body mass index, poor glycaemic control and lack of insulin treatment. However, when multivariate analysis was used, plasma apoCs levels correlated with triglyceride levels only. The apoC-III/apoC-II ratio was similar in the Type 2 diabetic and control subjects. CONCLUSIONS: Our study shows the parallel increase of apoC-II and C-III in Type 2 diabetic patients. This parallel increase is related to hypertriglyceridaemia only.