A Thermoelectric Energy Harvester Based on Microstructured Quasicrystalline Solar Absorber.

As solar radiation is the most plentiful energy source on earth, thermoelectric energy harvesting emerges as an interesting solution for the Internet of Things (IoTs) in outdoor applications, particularly using semiconductor thermoelectric generators (TEGs) to power IoT devices. However, when a TEG is under solar radiation, the temperature gradient through TEG is minor, meaning that the TEG is useless. A method to keep a significant temperature gradient on a TEG is by using a solar absorber on one side for heating and a heat sink on the other side. In this paper, a compact TEG-based energy harvester that features a solar absorber based on a new class of solid matter, the so-called quasicrystal (QC), is presented. In addition, a water-cooled heat sink to improve the temperature gradient on the TEG is also proposed. The harvester is connected to a power management circuit that can provide an output voltage of 3 V and store up to 1.38 J in a supercapacitor per day. An experimental evaluation was carried out to compare the performance of the proposed QC-based harvester with another similar harvester but with a solar absorber based on conventional black paint. As a result, the QC-based harvester achieved 28.6% more efficient energy generation and achieved full charge of a supercapacitor around two hours earlier. At last, a study on how much the harvested energy can supply power to a sensor node for Smart agriculture during a day while considering a trade-off between the maximum number of measurements and the maximum number of transmission per day is presented.

Report of envenomation in humans by handling a dyeing poison frog Dendrobates tinctorius (SCHNEIDER, 1799) (Anura: Dendrobatidae) in the Amazon, Brazil

Abstract We report a case of envenomation by Dendrobates tinctorius in the northwest of the Amazon Forest. The patients were two men, who presented with numbness in the right arm and slight numbness in the lower lip, respectively. Dendrobates tinctorius secretions contain pumiliotoxin, one of several toxins found in the dendrobatidis skin, which interferes with muscle contraction and causes locomotor difficulties. Although Dendrobatidae is a family of anurans known for their venom, few studies describe the symptoms of envenomation in humans.

Report of envenomation in humans by handling a dyeing poison frog Dendrobates tinctorius (SCHNEIDER, 1799) (Anura: Dendrobatidae) in the Amazon, Brazil.

We report a case of envenomation by Dendrobates tinctorius in the northwest of the Amazon Forest. The patients were two men, who presented with numbness in the right arm and slight numbness in the lower lip, respectively. Dendrobates tinctorius secretions contain pumiliotoxin, one of several toxins found in the dendrobatidis skin, which interferes with muscle contraction and causes locomotor difficulties. Although Dendrobatidae is a family of anurans known for their venom, few studies describe the symptoms of envenomation in humans.

Thickness and nanomechanical properties of protective layer formed by TiF4 varnish on enamel after erosion.

The layer formed by fluoride compounds on tooth surface is important to protect the underlying enamel from erosion. However, there is no investigation into the properties of protective layer formed by NaF and TiF4 varnishes on eroded enamel. This study aimed to evaluate the thickness, topography, nanohardness, and elastic modulus of the protective layer formed by NaF and TiF4 varnishes on enamel after erosion using nanoindentation and atomic force microscopy (AFM). Human enamel specimens were sorted into control, NaF, and TiF4 varnish groups (n = 10). The initial nanohardness and elastic modulus values were obtained and varnishes were applied to the enamel and submitted to erosive challenge (10 cycles: 5 s cola drink/5 s artificial saliva). Thereafter, nanohardness and elastic modulus were measured. Both topography and thickness were evaluated by AFM. The data were subjected to ANOVA, Tukey's test and Student's t test (α = 0.05). After erosion, TiF4 showed a thicker protective layer compared to the NaF group and nanohardness and elastic modulus values were significantly lower than those of the control group. It was not possible to measure nanohardness and elastic modulus in the NaF group due to the thin protective layer formed. AFM showed globular deposits, which completely covered the eroded surface in the TiF4 group. After erosive challenge, the protective layer formed by TiF4 varnish showed significant properties and it was thicker than the layer formed by NaF varnish.

Thickness and nanomechanical properties of protective layer formed by TiF4 varnish on enamel after erosion

Abstract The layer formed by fluoride compounds on tooth surface is important to protect the underlying enamel from erosion. However, there is no investigation into the properties of protective layer formed by NaF and TiF4 varnishes on eroded enamel. This study aimed to evaluate the thickness, topography, nanohardness, and elastic modulus of the protective layer formed by NaF and TiF4 varnishes on enamel after erosion using nanoindentation and atomic force microscopy (AFM). Human enamel specimens were sorted into control, NaF, and TiF4 varnish groups (n = 10). The initial nanohardness and elastic modulus values were obtained and varnishes were applied to the enamel and submitted to erosive challenge (10 cycles: 5 s cola drink/5 s artificial saliva). Thereafter, nanohardness and elastic modulus were measured. Both topography and thickness were evaluated by AFM. The data were subjected to ANOVA, Tukey's test and Student's t test (α = 0.05). After erosion, TiF4 showed a thicker protective layer compared to the NaF group and nanohardness and elastic modulus values were significantly lower than those of the control group. It was not possible to measure nanohardness and elastic modulus in the NaF group due to the thin protective layer formed. AFM showed globular deposits, which completely covered the eroded surface in the TiF4 group. After erosive challenge, the protective layer formed by TiF4 varnish showed significant properties and it was thicker than the layer formed by NaF varnish.

Effect of time and pH on physical-chemical properties of orthodontic brackets and wires.

OBJECTIVE: To test the hypothesis that treatment time, debris/biofilm, and oral pH have an influence on the physical-chemical properties of orthodontic brackets and arch wires. MATERIALS AND METHODS: One hundred twenty metal brackets were evaluated. They were divided into four groups (n  =  30) according to treatment time: group C (control) and groups T12, T24, and T36 (brackets recovered after 12, 24, and 36 months of treatment, respectively). Rectangular stainless-steel arch wires that remained in the oral cavity for 12 to 24 months were also analyzed. Dimensional stability, surface morphology, composition of brackets, resistance to sliding of the bracket-wire set, surface roughness of wires, and oral pH were analyzed. One-way analysis of variance, followed by a Tukey multiple comparisons test, was used for statistical analysis (P < .05). RESULTS: Carbon and oxygen were shown to be elements that increased expressively and in direct proportion to time, and there was a progressive increase in the coefficient of friction and roughness of wires as a function of time of clinical use after 36 months. Oral pH showed a significant difference between group T36 and its control (P  =  .014). CONCLUSIONS: The hypothesis was partially accepted: treatment time and biofilm and debris accumulation in bracket slots were shown to have more influence on the degradation process and frictional force of these devices than did oral pH.

In vitro effects of nano-hydroxyapatite paste on initial enamel carious lesions.

PURPOSE: The purpose of this study was to analyze the protective effect of remineralizing agents on enamel caries lesions using surface Knoop microhardness testing (KHN) and atomic force microscopy (AFM). METHODS: Forty-eight human enamel blocks were assigned to four groups (N=12): (1) control (without agent); (2) fluoride varnish (Duraphat); (3) nano-HAP paste (Desensibilize Nano P); and (4) casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) paste (MI Paste Plus). Incipient caries-like lesions were artificially developed. Cariogenic challenge (pH-cycling) was performed for seven days. The pastes were applied before each immersion in demineralization solution, and the varnish was applied only once. KHN values were obtained at baseline, after incipient enamel lesion, and after challenge. The percentage of surface hardness recovery (%SMHR) was performed, and the surface morphology was evaluated by atomic force microscopy (AFM). ANOVA, Tukey's, and student paired t tests were applied at P<.05. RESULTS: After the cariogenic challenge, the nano-HAP group showed significantly higher KHN and %SMHR values than varnish. The CPP-ACP group showed no increase in KHN. The nano-HAP group showed, via AFM, a protective layer formation with globular deposits on the surface. CONCLUSION: SMHR and AFM morphology revealed that nano-hydroxyapatite paste showed a protective effect against in vitro enamel caries development.

In vitro effect of calcium nanophosphate and high-concentrated fluoride agents on enamel erosion: an AFM study.

BACKGROUND: Calcium nanophosphate paste can provide ions to remineralize enamel. There are, however, no data available about the remineralizing effect of this paste on the prevention of enamel erosion, when compared with highly concentrated fluoride agents. AIM: To analyze the effect of calcium nanophosphate paste, fluoride gel, and varnish to protect against enamel erosion using surface Knoop hardness (KNH) and atomic force microscopy (AFM). DESIGN: Forty enamel blocks (4 × 4 mm) of third molars were used for 4 groups (n = 10): 1.23% fluoride gel (Fluorgel-DFL(®) ); calcium nanophosphate paste (Desensibilize NanoP-FGM(®) ); fluoride varnish (Duraphat-Colgate(®) ) and control (without agent). The specimens were immersed in cola drink for 5 min and 2 h in artificial saliva, 4× per day for 5 days. The agents were applied before the first erosive cycle. KNH values were obtained before and after the erosive challenge. The surface morphology was evaluated by AFM. anova, Tukey's, and T-Student tests were applied. RESULTS: After erosion, no significant difference was found for KNH among gel, nanophosphate, and varnish groups; however, they showed higher KNH than control group. Gel and nanophosphate paste showed a protective layer formation on enamel surface by AFM. CONCLUSIONS: The calcium nanophosphate paste showed similar protection against enamel erosion compared with high-concentrated fluoride agents, even containing lower fluoride concentration.

In Vitro Effects of Nano-hydroxyapatite Paste on Initial Enamel Carious Lesions.

PURPOSE: The purpose of this study was to analyze the protective effect of remineralizing agents on enamel caries lesions using surface Knoop microhardness testing (KHN) and atomic force microscopy (AFM). METHODS: Forty-eight human enamel blocks were assigned to four groups (N=12): (1) control (without agent); (2) fluoride varnish (Duraphat); (3) nano-HAP paste (Desensibilize Nano P); and (4) casein phosphopeptide-amorphous calcium phosphate (CPP-ACP) paste (MI Paste Plus). Incipient caries-like lesions were artificially developed. Cariogenic challenge (pH-cycling) was performed for seven days. The pastes were applied before each immersion in demineralization solution, and the varnish was applied only once. KHN values were obtained at baseline, after incipient enamel lesion, and after challenge. The percentage of surface hardness recovery (%SMHR) was performed, and the surface morphology was evaluated by atomic force microscopy (AFM). ANOVA, Tukey's, and student paired t tests were applied at P<.05. RESULTS: After the cariogenic challenge, the nano-HAP group showed significantly higher KHN and %SMHR values than varnish. The CPP-ACP group showed no increase in KHN. The nano-HAP group showed, via AFM, a protective layer formation with globular deposits on the surface. CONCLUSION: SMHR and AFM morphology revealed that nano-hydroxyapatite paste showed a protective effect against in vitro enamel caries development.

Protective effect of calcium nanophosphate and CPP-ACP agents on enamel erosion.

The aim of this study was to assess the effect of different remineralizing agents on enamel microhardness (KHN) and surface topography after an erosive challenge. Forty-eight human enamel specimens (4 × 4 mm) were randomly assigned to 4 groups: control (no treatment), fluoride varnish, calcium nanophosphate paste and casein phosphopeptide-amorphous calcium phosphate paste (CPP-ACP). Both pastes were applied for 5 minutes, and fluoride varnish, for 24 h. Four daily erosive cycles of 5 minutes of immersion in a cola drink and 2 h in artificial saliva were conducted for 5 days. KHN readings were performed at baseline and after 5 days. The percentage of enamel hardness change (%KHN) was obtained after erosion. The surface topography was evaluated by atomic force microscopy (AFM). The data were tested using ANOVA, Tukey's and paired-T tests (p < 0.05). After an erosive challenge, there was no statistically significant difference between the control (96.8 ± 11.4 KHN / 72.4 ± 3.0%KHN) and the varnish (91.7 ± 14.1 KHN / 73.4 ± 5.5%KHN) groups. The nanophosphate group showed lower enamel hardness loss (187.2 ± 27.9 / 49.0 ± 7.9%KHN), compared with the CPP-ACP group (141.8 ± 16.5 / 60.6 ± 4.0%KHN), and both were statistically different from the varnish and the control groups. AFM images showed a rough surface for the control and the varnish groups, a non-homogeneous layer with globular irregularities for CPP-ACP, and a thick homogeneous layer for the nanophosphate group. None of the agents provided protection against the development of erosion; however, nanophosphate paste was able to reduce enamel surface softening after the erosive challenge.

Protective effect of calcium nanophosphate and CPP-ACP agents on enamel erosion

The aim of this study was to assess the effect of different remineralizing agents on enamel microhardness (KHN) and surface topography after an erosive challenge. Forty-eight human enamel specimens (4 × 4 mm) were randomly assigned to 4 groups: control (no treatment), fluoride varnish, calcium nanophosphate paste and casein phosphopeptide-amorphous calcium phosphate paste (CPP-ACP). Both pastes were applied for 5 minutes, and fluoride varnish, for 24 h. Four daily erosive cycles of 5 minutes of immersion in a cola drink and 2 h in artificial saliva were conducted for 5 days. KHN readings were performed at baseline and after 5 days. The percentage of enamel hardness change (%KHN) was obtained after erosion. The surface topography was evaluated by atomic force microscopy (AFM). The data were tested using ANOVA, Tukey's and paired-T tests (p < 0.05). After an erosive challenge, there was no statistically significant difference between the control (96.8 ± 11.4 KHN / 72.4 ± 3.0 %KHN) and the varnish (91.7 ± 14.1 KHN / 73.4 ± 5.5 %KHN) groups. The nanophosphate group showed lower enamel hardness loss (187.2 ± 27.9 / 49.0 ± 7.9 %KHN), compared with the CPP-ACP group (141.8 ± 16.5 / 60.6 ± 4.0 %KHN), and both were statistically different from the varnish and the control groups. AFM images showed a rough surface for the control and the varnish groups, a non-homogeneous layer with globular irregularities for CPP-ACP, and a thick homogeneous layer for the nanophosphate group. None of the agents provided protection against the development of erosion; however, nanophosphate paste was able to reduce enamel surface softening after the erosive challenge.

Disfunção miocárdica e alterações no trânsito de cálcio intracelular em ratos obesos / Myocardial dysfunction and abnormalities in intracellular calcium handling in obese rats

FUNDAMENTO: Vários mecanismos têm sido propostos contribuir para a disfunção cardíaca em modelos de obesidade, tais como alterações nas proteínas do trânsito de cálcio (Ca+2) e nos receptores beta-adrenérgicos. Todavia, o papel desses fatores no desenvolvimento da disfunção miocárdica induzida pela obesidade ainda não está claro. OBJETIVO: Este estudo pretende investigar se a obesidade induzida por um ciclo de dieta hipercalóricas resulta em disfunção cardíaca. Além disso, foi avaliado se essa alteração funcional em ratos obesos está relacionada com o prejuízo do trânsito de Ca+2 e do sistema beta-adrenérgico. MÉTODOS: Ratos Wistar machos, 30 dias de idade, foram alimentados com ração padrão (C) e um ciclo de cinco dietas hipercalóricas (Ob) por 15 semanas. A obesidade foi definida pelo aumento da porcentagem de gordura corporal dos ratos. A função cardíaca foi avaliada mediante análise isolada do músculo papilar do ventrículo esquerdo em condições basais e após manobras inotrópicas e lusitrópicas. RESULTADOS: Em comparação com o grupo controle, os ratos obesos apresentaram aumento da gordura corporal e intolerância a glicose. Os músculos dos ratos obesos desenvolveram valores basais semelhantes; entretanto, as respostas miocárdicas ao potencial pós-pausa e aumento de Ca+2 extracelular foram comprometidas. Não houve alterações na função cardíaca entre os grupos após a estimulação beta-adrenérgica. CONCLUSÃO: A obesidade promove disfunção cardíaca relacionada com alterações no trânsito de Ca+2 intracelular. Esse prejuízo funcional é provavelmente ocasionado pela redução da atividade da bomba de Ca+2 do retículo sarcoplasmático (SERCA2a) via Ca+2 calmodulina-quinase.

BACKGROUND: Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca2+) handling proteins and β-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear. OBJECTIVE: The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca2+ handling and the β-adrenoceptor system. METHODS: Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers. RESULTS: Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca2+ were compromised. There were no changes in cardiac function between groups after β-adrenergic stimulation. CONCLUSION: Obesity promotes cardiac dysfunction related to changes in intracellular Ca2+ handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca2+ ATPase (SERCA2) activation via Ca2+ calmodulin kinase.

Myocardial dysfunction and abnormalities in intracellular calcium handling in obese rats.

BACKGROUND: Several mechanisms have been proposed to contribute to cardiac dysfunction in obesity models, such as alterations in calcium (Ca²âº) handling proteins and ß-adrenergic receptors. Nevertheless, the role of these factors in the development of myocardial dysfunction induced by obesity is still not clear. OBJECTIVE: The purpose of this study was to investigate whether obesity induced by hypercaloric diets results in cardiac dysfunction. Furthermore, it was evaluated whether this functional abnormality in obese rats is related to abnormal Ca²âº handling and the ß-adrenoceptor system. METHODS: Male 30-day-old Wistar rats were fed with standard food (C) and a cycle of five hypercaloric diets (Ob) for 15 weeks. Obesity was defined as increases in body fat percentage in rats. Cardiac function was evaluated by isolated analysis of the left ventricle papillary muscle under basal conditions and after inotropic and lusitropic maneuvers. RESULTS: Compared with the control group, the obese rats had increased body fat and glucose intolerance. The muscles of obese rats developed similar baseline data, but the myocardial responsiveness to post-rest contraction stimulus and increased extracellular Ca²âº were compromised. There were no changes in cardiac function between groups after ß-adrenergic stimulation. CONCLUSION: Obesity promotes cardiac dysfunction related to changes in intracellular Ca²âº handling. This functional damage is probably caused by reduced cardiac sarcoplasmic reticulum Ca²âº ATPase (SERCA2) activation via Ca²âº calmodulin kinase.

Severe food restriction induces myocardial dysfunction related to SERCA2 activity.

Previous studies have shown that food restriction promotes myocardial dysfunction in rats. However, the molecular mechanisms that are responsible are unclear. We investigated the role of sarcoplasmic reticulum Ca2+-ATPase (SERCA2) on myocardial performance in food-restricted rats. Male Wistar-Kyoto rats, 60 days old, were fed a control or restricted diet (daily energy intake reduced to 50% of the control) for 90 days. Expression of Serca2a, phospholamban (PLB), Na+/Ca2+ exchanger (NCX), and thyroid hormone receptor (TRalpha1, TRbeta1) mRNA was determined by quantitative PCR. SERCA2 activity was measured by using 20 micromol/L cyclopiazonic acid (CPA) in a left ventricular papillary muscle preparation during isometric contraction in basal conditions and during post-rest contraction. Serum concentrations of thyroxine (T4) and thyrotropin (TSH) were also determined. The 50%-restricted diet reduced body and ventricular weight and serum T4 and TSH levels. The interaction of CPA and food restriction reduced peak developed tension and maximum rate of tension decline (-dT/dt), but increased the resting tension intensity response during post-rest contraction. PLB and NCX mRNA were upregulated and TRalpha1 mRNA was downregulated by food restriction. These results suggest that food restriction promotes myocardial dysfunction related to impairment of sarcoplasmic reticulum Ca2+ uptake as a result of a hypothyroid state.

Food restriction promotes downregulation of myocardial L-type Ca2+ channels.

Food restriction (FR) has been shown to impair myocardial performance. However, the mechanisms behind these changes in myocardial function due to FR remain unknown. Since myocardial L-type Ca2+ channels may contribute to the cardiac dysfunction, we examined the influence of FR on L-type Ca2+ channels. Male 60-day-old Wistar rats were fed a control or a restricted diet (daily intake reduced to 50% of the amount of food consumed by the control group) for 90 days. Myocardial performance was evaluated in isolated left ventricular papillary muscles. The function of myocardial L-type Ca2+ channels was determined by using a pharmacological Ca2+ channel blocker, and changes in the number of channels were evaluated by mRNA and protein expression. FR decreased final body weights, as well as weights of the left and right ventricles. The Ca2+ channel blocker diltiazem promoted a higher blockade on developed tension in FR groups than in controls. The protein content of L-type Ca2+ channels was significantly diminished in FR rats, whereas the mRNA expression was similar between groups. These results suggest that the myocardial dysfunction observed in previous studies with FR animals could be caused by downregulation of L-type Ca2+ channels.

Exercise training increases myocardial inotropic response in food restricted rats.

This study evaluated the effects of exercise training on myocardial function and ultrastructure of rats submitted to different levels of food restriction (FR). Male Wistar-Kyoto rats, 60 days old, were submitted to free access to food, light FR (20%), severe FR (50%) and/or to swimming training (one hour per day with 5% of load, five days per week for 90 days). Myocardial function was evaluated by left ventricular papillary muscle under basal condition (calcium 1.25 mM), and after extracellular calcium elevation to 5.2 mM and isoproterenol (1 microM) addition. The ultrastructure of the myocardium was examined in the papillary muscle. The training effectiveness was verified by improvement of myocardial metabolic enzyme activities. Both 20% and 50% food restriction protocols presented minor body and ventricular weights gain. The 20%-FR, in sedentary or trained rats, did not alter myocardial function or ultrastructure. The 50%-FR, in sedentary rats, caused myocardial dysfunction under basal condition, decreased response to inotropic stimulation, and promoted myocardial ultrastructural damage. The 50%-FR, in exercised rats, increased myocardial dysfunction under basal condition but increased response to inotropic stimulation although there was myocardial ultrastructural damage. In conclusion, the exercise training in severe restriction caused marked myocardial dysfunction at basal condition but increased myocardial response to inotropic stimulation.