DendroIDH: agrupando cidades por semelhança de indicadores / DendroHDI: clustering cities by similarity indicators / DendroIDH: intercalación de ciudades por indicadores de similitud

OBJETIVO: as cidades inteligentes estão surgindo mediante a necessidade de otimização de recursos e ampliação do bem-estar dos seus habitantes. Atualmente não existem dados claros sobre como comparar cidades inteligentes com base em indicadores que utilizem dados públicos, principalmente na área de Saúde. MÉTODO: este trabalho propõe a utilização de indicadores de IDH para comparar estatisticamente e agrupar cidades com semelhança de indicadores, e assim, oferecer aos seus gestores, a possibilidade de adotar estratégias de gestão baseadas em visualização de dados dispostos em dendrogramas. RESULTADO: foram realizados cálculos com a utilização de uma ferramenta estatística embases de dados públicas para obter dendrogramas de dados. CONCLUSÃO: o agrupamento de cidades por semelhança de indicadores se mostrou promissor para comparar e medir cidades com semelhantes características.

OBJECTIVE: Smart cities are emerging by the need to optimize resources and expansion of the welfare of its inhabitants. Currently there are no clear data on how to compare smart cities based on indicators using public data, especially in the health area. METHOD: this paper proposes the use of HDI indicators to compare statistically and grouptowns with similar indicators, and thus, offer its managers, the possibility of adopting management strategies based on data visualization arranged in dendrograms. RESULT: Calculations were performed using a statistical tool in public databases for dendrograms data. CONCLUSION: the grouping of cities by similarity indicators showed promise to compareand measure cities with similar characteristics.

(Br-SCMM) Brazilian Smart City Maturity Model: A Perspective from the Health Domain.

The term definition "Smart City" still allows various interpretations, and this causes some difficulty in establishing parameters to measure how smart the cities can be. This paper presents a Maturity Model that uses a set of minimum domains and indicators that aim to encourage cities of different sizes to identify their potential and improve processes and public policies.

Loss of postprandial insulin sensitization during aging.

With aging, there is a decrease in parasympathetic nervous activity. Since the hepatic parasympathetic nerves (HPNs) are essential to the disposal of nutrients, through the hepatic insulin sensitizing substance (HISS), we tested the hypothesis that aging leads to a lowering of postprandial glucose disposal by a decrease of the HISS-dependent component of insulin action. Insulin sensitivity was quantified in fed or fasted, male and female Wistar rats (from 6 to 52 weeks), using a euglycemic clamp. The HISS-dependent component was quantified by administration of the muscarinic antagonist atropine. Total insulin action decreased gradually up to 52 weeks of age: The HISS-independent component of insulin action decreased until 9 weeks of age and remained unchanged thereafter; the HISS-dependent component decreased from 9 weeks of age throughout aging. The continuous decrease of HISS action, uncovered by blocking the HPN, is the key phenomenon for the gradual decrease of insulin sensitivity with aging.

Insulin resistance in two animal models of obesity: A comparison of HISS-dependent and HISS-independent insulin action in high-fat diet-fed and Zucker rats.

Normal postprandial insulin sensitivity depends on the action of the hepatic insulin sensitizing substance (HISS), which requires hepatic parasympathetic nerve activation. Since HISS action is impaired in several pathological models, including the genetically-modified obese Zucker rat (OZR), we compared the HISS-dependent and HISS-independent components of insulin action between the OZR model, and the high-fat diet (HFD)-fed rats. We hypothesize that both models present an impaired HISS action, accounting for the decrease in insulin sensitivity. Male Sprague-Dawley rats fed a HFD for 1 week (n = 5) and OZR (n = 5) were used as obese models. Standard diet-fed (STD, n = 5) and lean Zucker rats (LZR, n = 6) were the HFD and OZR non-obese controls, respectively. Rats were 9-weeks-old when tested. Insulin sensitivity was measured in the fed state, before and after atropine blockade of HISS release), using the Rapid Insulin Sensitivity Test (RIST, mg glucose/kg bw). HISS-dependent action was the difference between control and post-atropine RISTs. HISS action was impaired in both the obese groups (HFD vs STD: 40.1 +/- 5.0 vs 117.0 +/- 3.8 mg glucose/kg bw, p < 0.001; OZR vs LZR: 34.4 +/- 12.8 vs 115.9 +/- 19.4 mg glucose/kg bw, p < 0.01), whereas the HISS-independent component (post-atropine RIST), i.e., insulin action per se, was decreased only in the OZR (OZR vs LZR: 39.3 +/- 3.5 vs 173.3 +/- 20.5 mg glucose/kg bw, p < 0.001). According to our data, the insulin resistance mechanisms are different in the two obesity models studied: in the HFD-fed rats, only the HISS-dependent component is impaired, whereas in the OZR both components of nsulin action are equally impaired.

Defective hepatic nitric oxide action results in HISS-dependent insulin resistance in spontaneously hypertensive rats.

Peripheral insulin sensitivity is dependent on the action of Hepatic Insulin Sensitizing Substance (HISS), in which hepatic NO (HNO) plays an important role. Insulin resistance has been associated with hypertension. NO action is known to be impaired in Spontaneously Hypertensive Rat (SHR) hypertension models. We tested the hypothesis that the HNO pathway is compromised in SHR, resulting in HISS-dependent insulin resistance. Wistar rats (Wis) were the normotensive controls. Insulin sensitivity was evaluated through the Rapid Insulin Sensitivity Test (RIST), a modified euglycemic clamp. A clamp was performed in basal state (control RIST), followed by ipv administration of the NO synthase (NOS) competitive antagonist L-NMMA (0.73 mg/kg) and a RIST post L-NMMA. HISS-dependent insulin sensitivity was assessed by subtracting the RIST post-L-NMMA from the control RIST and is represented as the resultant insulin sensitivity inhibition. In SHR ipv L-NMMA induced 26+/-5% insulin sensitivity inhibition (187.5+/-15.3 mg glucose/kg, n=6; P<0.05), whereas in Wis, ipv L-NMMA induced 53.8+/-5.9% insulin sensitivity inhibition (138.2+/-14.7 mg glucose/kg, n=6, P<0.05), significantly higher than in SHR (P<0.01). Our results suggest that functional HNO is essential to achieve maximal insulin sensitivity and that HNO action is compromised in hypertension, resulting in HISS-dependent insulin resistance.