Acute Chagas disease (ACD) has a distinct epidemiological profile in the Amazon Region, with cases and outbreaks of Trypanosoma cruzi infection being possibly related to the ingestion of contaminated food. Data on ACD in the state of Pará retrieved from 2000 to 2016 from the Brazilian Notifiable Diseases Information System (SINAN) were evaluated. During this period, 2,030 of the 16,807 reported cases were confirmed, with a higher incidence between the months of August and December, thus characterising a seasonal pattern of acute infection, and coinciding with the higher production of “açaí”, one fruit likely involved in the oral transmission of the disease. Evaluation of the absolute numbers of confirmed ACD cases secondary to oral infection suggests that infection through this route increased during the 2010-2016 period, differing from what was recorded in terms of vectorial or other infection routes. These findings point to the need of intensifying strategies to prevent or substantially reduce oral transmission.

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Metabolic syndrome (MS) plays a key role in the origin of cardiovascular diseases. Studies on the MS in Brazil are recent, and its epidemiology in more isolated regions such as the Amazon is still unknown. The study aimed to estimate the prevalence of MS and associated factors in adults of the Brazilian Amazon. This study was conducted in 2012–2013. It is a cross-sectional population-based study, involving 787 adults randomly selected from the urban area of four cities in the state of Pará, in the Brazilian Eastern Amazon. The participants underwent anthropometric measurements, laboratory examination, and were questioned about their lifestyle. MS was defined by the Joint Interim Statement criteria, using the multiple logistic regression to investigate the potential association of risk factors with the presence of MS. The overall prevalence of MS was 34.1% (95% CI = 30.8–37.4), increasing linearly with the increasing body mass index and age. From 40–49 years of age, MS was observed in about half of the women (46.0%), while men only experienced a high prevalence in the fifth decade of life (43.3%). The low HDL-c (64.4%) and abdominal obesity (58.9%) were higher in women (p < 0.001), while for men, high blood pressure was significantly higher (p < 0.001). Individuals aged 40–59 years old (odds ratio [OR] = 3.35 [95% CI = 2.30–4.90]), ≥ 60 years old (OR = 5.80 [3.63–9.27]), overweight (OR = 4.17 [2.77–6.29]), and obese (OR = 8.82 [5.56–13.98]) were more likely to have MS. The study population experienced high cardiometabolic risk, requiring government efforts to control MS and related risk factors, especially obesity.

Background While still controversial, it has been demonstrated that vascular defects can precede the onset of other AD hallmarks features, making it an important therapeutic target. Given that the protein transthyretin (TTR) has been established as neuroprotective in AD, here we investigated the influence of TTR in the vasculature. Methods We evaluated the thickness of the basement membrane and the length of brain microvessels, by immunohistochemistry, in AβPPswe/PS1A246E (AD) transgenic mice and non-transgenic mice (NT) bearing one (TTR+/−) or two (TTR+/+) copies of the TTR gene. The angiogenic potential of TTR was evaluated in vitro using the tube formation assay, and in vivo using the chick chorioallantoic membrane (CAM) assay. Results AD transgenic mice with TTR genetic reduction, AD/TTR+/−, exhibited a thicker BM in brain microvessels and decreased vessel length than animals with normal TTR levels, AD/TTR+/+. Further in vivo investigation, using the CAM assay, revealed that TTR is a pro-angiogenic molecule, and the neovessels formed are functional. Also, TTR increased the expression of key angiogenic molecules such as proteins interleukins 6 and 8, angiopoietin 2, and vascular endothelial growth factor, by endothelial cells, in vitro, under tube formation conditions. We showed that while TTR reduction also leads to a thicker BM in NT mice, this effect is more pronounced in AD mice than in NT animals, strengthening the idea that TTR is a neuroprotective protein. We also studied the effect of TTR tetrameric stabilization on BM thickness, showing that AD mice treated with the TTR tetrameric stabilizer iododiflunisal (IDIF) displayed a significant reduction of BM thickness and increased vessel length, when compared to non-treated littermates. Conclusion Our in vivo results demonstrate the involvement of TTR in angiogenesis, particularly as a modulator of vascular alterations occurring in AD. Since TTR is decreased early in AD, its tetrameric stabilization can represent a therapeutic avenue for the early treatment of AD through the maintenance of the vascular structure.