Zika virus (ZIKV) is a flavivirus that has recently been associated with an increased incidence of neonatal microcephaly and other neurological disorders. The virus is primarily transmitted by mosquito bite, although other routes of infection have been implicated in some cases. The Aedes aegypti mosquito is considered to be the main vector to humans worldwide; however, there is evidence that other mosquito species, including Culex quinquefasciatus, transmit the virus. To test the potential of Cx. quinquefasciatus to transmit ZIKV, we experimentally compared the vector competence of laboratory-reared Ae. aegypti and Cx. quinquefasciatus. Interestingly, we were able to detect the presence of ZIKV in the midgut, salivary glands and saliva of artificially fed Cx. quinquefasciatus. In addition, we collected ZIKV-infected Cx. quinquefasciatus from urban areas with high microcephaly incidence in Recife, Brazil. Corroborating our experimental data from artificially fed mosquitoes, ZIKV was isolated from field-caught Cx. quinquefasciatus, and its genome was partially sequenced. Collectively, these findings indicate that there may be a wider range of ZIKV vectors than anticipated.

No abstract

The aim of the present study was to analyze the action of metformin on short-term memory, glial cell activation and neuroinflammation caused by experimental diabetic encephalopathy in C57BL/6 mice. Diabetes was induced by the intraperitoneal injection of a dose of 90mg/kg of streptozotocin on two successive days. Mice with blood glucose levels ≥200dl/ml were considered diabetic and were given metformin hydrochloride at doses of 100mg/kg and 200mg/kg (by gavage, twice daily) for 21 days. On the final day of treatment, the mice underwent a T-maze test. On the 22nd day of treatment all the animals were anesthetized and euthanized. Diabetic animals treated with metformin had a higher spatial memory score. The hippocampus of the diabetic animals presented reactive gliosis, neuronal loss, NF-kB signaling activation, and high levels of IL-1 and VEGF. In addition, the T-maze test scores of these animals were low. Treatment with metformin reduced the expression of GFAP, Iba-1 (astrocyte and microglial markers) and the inflammation markers (p-IKB, IL-1 and VEGF), while enhancing p-AMPK and eNOS levels and increasing neuronal survival (Fox-1 and NeuN). Treatment with metformin also improved the spatial memory scores of diabetic animals. In conclusion, the present study showed that metformin can significantly reduce neuroinflammation and can decrease the loss of neurons in the hippocampus of diabetic animals, which can subsequently promote improvements in spatial memory.

The absence of histone variant macroH2A1 confers a CSC-like phenotype to HCC cells in vitro and in vivo that depends on Ser536 phosphorylation of nuclear factor kappa B p65; this pathway may hold valuable targets for the development of CSC-focused treatments for HCC. (Hepatology 2017).

Phosphodiesterase type 5 inhibitors (PDE5-Is) have recently emerged as a potential therapeutic strategy for neuroinflammatory, neurodegenerative, and memory loss diseases. Mechanistically, PDE5-Is produce an anti-inflammatory and neuroprotection effect by increasing expression of nitric oxide synthases and accumulation of cGMP and activating protein kinase G (PKG), the signaling pathway of which is thought to play an important role in the development of several neurodiseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). The aim of this paper was to review present knowledge of the signaling pathways that underlie the use of PDE5-Is in neuroinflammation, neurogenesis, learning, and memory.

These authors contributed equally to this work. Abstract:Zika virus (ZIKV) is a flavivirus that has recently been associated with increased incidence of neonatal microcephaly and other neurological disorders. The virus is primarily transmitted by mosquito bite, although other routes of infection have been implicated in some cases. The Aedes aegypti mosquito is considered to be the main vector to humans worldwide, but there is evidence of other mosquito species, including Culex quinquefasciatus, playing a role in the Brazilian outbreak. To test this hypothesis, we experimentally compared the vectorial competence of laboratory-reared A. aegypti and C. quinquefasciatus. We found ZIKV in the not peer-reviewed) is the author/funder. All rights reserved. No reuse allowed without permission.The copyright holder for this preprint (which was . http://dx.doi.org/10.1101/073197 doi: bioRxiv preprint first posted online Sep. 2, 2016; 2 midgut, salivary glands, and saliva of artificially fed C. quinquefasciatus. Additionally, we collected ZIKV-infected C. quinquefasciatus from urban areas of high microcephaly incidence in Recife, Brazil. Take into account; these findings indicate that there may be a wider range of vectors for ZIKV than anticipated.Keywords: Zika, microcephaly, Culex, Aedes, vectorial competence, vector control.Zika is classically considered a mild disease whose symptoms include fever, joint pain, rash and, in some cases, conjunctivitis (1). However, the Zika outbreak in Brazil has been associated with an increased incidence of neonatal microcephaly and neurological disorders (2, 3). Zika virus (ZIKV) is a poorly known, small, enveloped RNA virus with ssRNA (+) belonging to the Family Flaviviridae. It was first isolated in April 1947 from a rhesus monkey and in January 1948 from the mosquito species Aedes africanus (4). Since then, several ZIKV strains have been isolated from many samples, mostly mosquitoes, including species from the genera Aedes, Mansonia, Anopheles and Culex (5).The first known Zika epidemic in an urban environment occurred in Micronesia in 2007, with approximately 73% of the human population on Yap island becoming infected (6).Intriguingly, although many Aedes mosquitoes were collected in the field and evaluated for virus detection, no samples were found to be positive for ZIKV (6). Additionally, it is important to highlight that Aedes aegypti (A. aegypti) is absent from most islands in the Micronesia archipelago and is very rare on the islands where it is present (6, 7).There is a global consensus among scientists and health agencies that Aedes spp. are the main ZIKV vector in urban areas (WHO, 2016). This is in part because vector competence experiments for ZIKV have been conducted exclusively for species of this genus, mainly A.aegypti (8, 9). Previous laboratory studies (8, 10) suggested that A. aegypti is a ZIKV vector. not peer-reviewed) is the author/funder. All rights reserved. No reuse allowed without permission.The copyright holder for this preprint (which was . http://dx.doi...

The aim of the present study was to evaluate the in vitro and in vivo effect of the addition of superoxide dismutase (SOD) and reduced glutathione (GSH) to ram semen freezing extender. Significant differences (p < 0.05) were detected between groups regarding total motility (TM), straightness (STR) and wobble (WOB), for which the GSH 7 mM group had lesser TM and better STR than the other groups and the GSH 5 and 7 mM groups had higher wobble values than the control, SOD 25 and 100 U/ml groups. The ultrastructural analysis revealed that the acrosome was better preserved after freezing in the SOD 100 U/ml and GSH 2 and 5 mM (p < 0.05) groups than the other groups, whereas mitochondria in both the control group and the 7 mM GSH group suffered the greatest damage. The plasma membrane remained preserved after freezing, regardless of the group. For in vivo fertilization, the SOD group achieved better results than the GSH group (p > 0.05). It can therefore be concluded that the addition of SOD 100 U/ml and GSH 2 and 5 mM preserves the acrosome integrity of frozen ram spermatozoa, while the addition of SOD 100 U/ml to Tris egg-yolk extender offers protection to the membranes of sperm cells after thawing.

Overweight and obesity have been identified as the most important risk factors for many diseases, including cardiovascular disease, type 2 diabetes and lipid disorders, such as non-alcoholic fatty liver disease (NAFLD). The metabolic changes associated with obesity are grouped to define metabolic syndrome, which is one of the main causes of morbidity and mortality in industrialized countries. NAFLD is considered to be the hepatic manifestation of metabolic syndrome and is one of the most prevalent liver diseases worldwide. Inflammation plays an important role in the development of numerous liver diseases, contributing to the progression to more severe stages, such as non-alcoholic steatohepatitis and hepatocellular carcinoma. Peroxisome proliferator-activated receptors (PPARs) are binder-activated nuclear receptors that are involved in the transcriptional regulation of lipid metabolism, energy balance, inflammation and atherosclerosis. Three isotypes are known: PPAR-α, PPARδ/β and PPAR-γ. These isotypes play different roles in diverse tissues and cells, including the inflammatory process. In this review, we discuss current knowledge on the role PPARs in the hepatic inflammatory process involved in NAFLD as well as new pharmacological strategies that target PPARs.