Condição e práticas de saúde bucal do deficiente visual

A deficiência visual é uma limitação sensorial com alteração da capacidade funcional da visão. O Deficiente Visual (DV) pode ser mais suscetível ao desenvolvimento de doenças bucais devido à limitação na identificação visual de sinais iniciais e na capacidade de remoção da placa. O presente estudo teve como objetivo descrever as condições de saúde bucal, bem como a abordagem mais adequada de educação em saúde. O estudo foi conduzido por meio de busca nos bancos de dados eletrônicos Scielo, Bireme e Pubmed, e sites de busca na internet, com artigos publicados em inglês e português entre os anos de 2008 a 2019.   O DV apresenta dificuldade em alcançar uma higiene bucal adequada devido à impossibilidade da detecção precoce das doenças bucais. Métodos tradicionais de ensino de higiene oral não são eficientes para o DV, sendo que as instruções verbais, texto em braille, demonstração tátil, material lúdico-pedagógico e palestras com orientações podem ser uma maneira eficaz de fornecer educação em saúde bucal. O DV possui maior acúmulo de biofilme dental, pior índice em higiene oral, doença periodontal, cárie e traumatismo. O Cirurgião-Dentista (CD) deve adotar um foco na prevenção e implantação de estratégias diferenciadas na abordagem e comunicação com esse público

Protective effect of ions against cell death induced by acid stress in Saccharomyces

Saccharomyces boulardii is a probiotic used to prevent or treat antibiotic-induced gastrointestinal disorders and acute enteritis. For probiotics to be effective they must first be able to survive the harsh gastrointestinal environment. In this work, we show that S. boulardii displayed the greatest tolerance to simulated gastric environments compared with several Saccharomyces cerevisiae strains tested. Under these conditions, a pH 2.0 was the main factor responsible for decreased cell viability. Importantly, the addition of low concentrations of sodium chloride (NaCl) protected cells in acidic conditions more effectively than other salts. In the absence of S. boulardii mutants, the protective effects of Na 1 in yeast viability in acidic conditions was tested using S. cerevisiae Na 1 -ATPases (ena1-4), Na 1 /H 1 antiporter (nha1D) and Na 1 /H 1 antiporter prevacuolar (nhx1D) null mutants, respectively. Moreover, we provide evidence suggesting that this protection is determined by the plasma membrane potential, once altered by low pH and low NaCl concentrations. Additionally, the absence or low expression/activity of Ena proteins seems to be closely related to the basal membrane potential of the cells

Osteomalacia: The Missing Link in the Pathogenesis of Bisphosphonate-Related Osteonecrosis of the Jaws?

Background. Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is a well-documented adverse event from treatment with nitrogen-containing bisphosphonates (NBPs). During a preliminary histomorphometric study aimed at assessing the rate of bone remodeling in the jaws of patient with surgically resected BRONJ, we found a defect of bone mineralization (unpublished data). We hypothesized that osteomalacia could be a risk factor for BRONJ in patients taking NBPs. Therefore, we looked for static and dynamic histomorphometric evidence of osteomalacia in biopsies from subjects with and without BRONJ.Methods. This case-control study used histomorphometric analysis of bone specimens of patients using NBPs (22 patients with BRONJ and 21 patients without BRONJ) who required oral surgical interventions for the treatment/prevention of osteonecrosis. Patients were given tetracycline hydrochloride according to a standardized protocol before taking bone biopsies from their jaws. Biopsies with evidence of osteomyelitis or necrosis at histology were excluded from the study. Osteomalacia was defined as a mineralization lag time >100 days, a corrected mean osteoid thickness >12.5 mm, and an osteoid volume >10%.Results. In all, 77% of patients with BRONJ were osteomalacic compared with 5% of patients without BRONJ, according to histomorphometry. Because osteomalacia was found almost exclusively in NBP users with BRONJ, this is likely to be a generalized process in which the use of NBPs further deteriorates mechanisms of bone repair.Conclusions. Osteomalacia represents a new and previously unreported risk factor for disease development. This finding may contribute to a better understanding of the pathogenesis of this disease and help with the development of strategies to increase the safety of NBP administration

The ventrolateral medulla and medullary raphe in sudden unexpected death in epilepsy

Sudden unexpected death in epilepsy (SUDEP) is a leading cause of premature death in patients with epilepsy. One hypothesis proposes that sudden death is mediated by post-ictal central respiratory depression, which could relate to underlying pathology in key respiratory nuclei and/or their neuromodulators. Our aim was to investigate neuronal populations in the ventrolateral medulla (which includes the putative human pre-Bötzinger complex) and the medullary raphe. Forty brainstems were studied comprising four groups: 14 SUDEP, six epilepsy controls, seven Dravet syndrome cases and 13 non-epilepsy controls. Serial sections through the medulla (from obex 1 to 10 mm) were stained for Nissl, somatostatin, neurokinin 1 receptor (for pre-Bötzinger complex neurons) and galanin, tryptophan hydroxylase and serotonin transporter (neuromodulatory systems). Using stereology total neuronal number and densities, with respect to obex level, were measured. Whole slide scanning image analysis was used to quantify immunolabelling indices as well as co-localization between markers. Significant findings included reduction in somatostatin neurons and neurokinin 1 receptor labelling in the ventrolateral medulla in sudden death in epilepsy compared to controls (P < 0.05). Galanin and tryptophan hydroxylase labelling was also reduced in sudden death cases and more significantly in the ventrolateral medulla region than the raphe (P < 0.005 and P < 0.05). With serotonin transporter, reduction in labelling in cases of sudden death in epilepsy was noted only in the raphe (P ≤ 0.01); however, co-localization with tryptophan hydroxylase was significantly reduced in the ventrolateral medulla. Epilepsy controls and cases with Dravet syndrome showed less significant alterations with differences from non-epilepsy controls noted only for somatostatin in the ventrolateral medulla (P < 0.05). Variations in labelling with respect to obex level were noted of potential relevance to the rostro-caudal organization of respiratory nuclear groups, including tryptophan hydroxylase, where the greatest statistical difference noted between all epilepsy cases and controls was at obex 9-10 mm (P = 0.034), the putative level of the pre-Bötzinger complex. Furthermore, there was evidence for variation with duration of epilepsy for somatostatin and neurokinin 1 receptor. Our findings suggest alteration to neuronal populations in the medulla in SUDEP with evidence for greater reduction in neuromodulatory neuropeptidergic and mono-aminergic systems, including for galanin, and serotonin. Other nuclei need to be investigated to evaluate if this is part of more widespread brainstem pathology. Our findings could be a result of previous seizures and may represent a pathological risk factor for SUDEP through impaired respiratory homeostasis during a seizure

Biologically regulated nutrient supply systems: compost and arbuscular mycorrhizas - a review

To achieve global food security, we will need to produce more food, and do so in an environmentally sustainable manner. Inorganic fertilizers have been instrumental in increasing food production, but with some fertilizers becoming increasingly scarce and expensive, we also need to consider other options for providing agricultural plants with nutrients. To this end, there has been increased interest in the potential to make better use of the nutrients tied up in organic matter; composts are an example of this, and are the focus of this review. Plant nutrient acquisition can be enhanced through the formation of arbuscular mycorrhizas (AM). The purpose of this review is to explore interactions between compost and AM, with an emphasis on the impacts of compost addition and formation and functioning of AM. Based on available literature, it is clear that the application of compost either has a positive or neutral effect on the formation of the symbiosis, and that dual application of compost and arbuscular mycorrhizal fungi (AMF) provides clear benefits to plants in terms of growth and nutrition. There is also emerging evidence that dual application also provides benefits in terms of soil structure. Taken together, the conclusion of this review is that the biologically regulated nutrient supply systems based on compost and AM are compatible.Timothy R. Cavagnar

Respiratory and anatomical changes within the brainstem in experimental epilepsy models.

A morte súbita inexplicável na epilepsia (SUDEP) ainda está sujeita a várias controvérsias na literatura. No entanto, uma das possíveis causas de óbito são as apnéias observadas durante o sono, promovendo aumento dos níveis de CO2 (hipercapnia) e/ou diminuição dos níveis de O2 (hipoxemia). Tem sido especulado que essas alterações podem estar associadas às disfunções na atividade dos neurônios quimiossensíveis localizados no tronco encefálico. Além disso, é possível que os distúrbios respiratórios poderiam envolver alterações na neurotransmissão serotoninérgica. Os neurônios quimiossensíveis, localizados no núcleo retrotrapezoide (RTN), constituem um dos principais grupamentos responsáveis por controlar a atividade respiratória. O RTN recebe uma densa inervação serotoninérgica dos vários subnúcleos da rafe. Diante das várias lacunas na literatura, sobre as alterações respiratórias como possíveis causadoras de morte inexplicável na epilepsia, o presente estudo procurou entender quais eram as possíveis alterações respiratórias e neuroanatômicas no tronco encefálico observadas em dois modelos experimentais de epilepsia: ratos Wistar audiogênicos (cepa WAR) e animais submetidos à estimulação da amígdala (kindling rápido da amígdala - ARK). Os animais WAR apresentaram uma redução da ventilação (VE) basal (332 ± 105, vs. Wistar: 505 ± 36 ml/kg/min) e uma redução da resposta ventilatória a hipercapnia (7% CO2) (813 ± 341, vs. Wistar: 1661 ± 177 ml/kg/min). No modelo ARK, observamos apenas que a resposta de taquipnéia ao aumento do CO2 foi reduzida (126 ± 6 vs controle: 143 ± 6 rpm) comparado com o grupo controle. Em outro protocolo experimental, os animais WAR foram submetidos à exposição em hipercapnia durante um período de 3 horas para a expressão da proteína fos. Nesses animais, observamos uma redução no número de neurônios imunorreativos para fos na região do RTN e na região da rafe pálido e obscurus. Por outro lado, observamos um aumento do número de neurônios imunorreativos para fos na região do locus coeruleus. Os animais WAR também apresentaram uma redução significante do número de varicosidades serotoninérgicas na superfície ventral da região do RTN, quando comparados com os ratos Wistar. Essa redução foi devida a uma redução no número de neurônios imunorreativos para serotonina na rafe pallidus e obscurus. Por fim, observamos também que aumento da VE produzida pela injeção unilateral de serotonina no RTN foi menor nos animais WAR quando comparado aos animais Wistar. No modelo de epilepsia de ARK quando submetidos à hipercapnia de 3 horas, observamos também uma redução no número de neurônios imunorreativos a expressão de fos na região do RTN e na região do núcleo do trato solitário. Da mesma maneira aos animais WAR, observamos um aumento do número de neurônios imunorreativos para fos na região do locus coeruleus. Considerando estes resultados, sugere-se que nos modelos experimentais de epilepsia utilizados no presente estudo, observamos uma redução da atividade respiratória basal e na resposta ventilatória à hipercapnia, bem como uma alteração neuroanatômica no tronco encefálico. Assim, gostaríamos de sugerir que ambos os modelos experimentais de epilepsia, utilizados no presente estudo, podem ser considerados modelos experimentais de epilepsia com o objetivo de se estudar distúrbios respiratórios e possivelmente correlacionar com mortes súbitas e inexplicáveis na epilepsia.Unexplained sudden death in epilepsy (SUDEP) is still subject to several controversies in the literature. However, one of the possible causes of death are the apneas observed during sleep, promoting an increase in CO2 levels (hypercapnia) and/or a decrease in O2 levels (hypoxemia). It has been speculated that these changes may be associated with dysfunctions in chemosensitive neurons. In addition, it is possible that respiratory disorders may involve changes in serotonergic neurotransmission. The chemosensitive neurons located in the retrotrapezoid nucleus (RTN) are one of the main groups responsible for controlling respiratory activity. The RTN receives a dense serotonergic innervation of the various subnuclei of rafe. The present study sought to understand the possible respiratory alterations observed in two models of epilepsy: audiogenic Wistar rats (WAR strain) and rapid amygdala kindling (ARK). WAR animals showed a reduction in baseline ventilation (332 ± 105, vs. Wistar: 505 ± 36 ml/kg/min) and a reduction in hypercapnic (7% CO2) ventilatory response (813 ± 341, vs. Wistar: 1661 ± 177 ml/kg/min). In the ARK model, we only observed that the tachypnea response to CO2 was reduced (126 ± 6 vs control: 143 ± 6 rpm). In a different experimental protocol, WAR animals were exposed to hypercapnia for a period of 3 hours in order to have the fos protein expression. In these animals, we observed a reduction in the number of fos-immunoreactive neurons in the RTN region and in the raphe pallidus and obscurus. On the other hand, we observed an increase in the number of fos-immunoreactive neurons of the locus coeruleus. WAR animals also showed a significant reduction in the number of serotonergic varicosities of the ventral medullary surface. This reduction was due to a reduction in the number of serotonin-immunoreactive neurons in raphe pallidus and obscurus. Finally, we also observed that the increase in VE produced by the unilateral injection of serotonin in the RTN was lower in the WAR animals when compared to the Wistar rats. In the ARK epilepsy model submitted to 3 hour of hypercapnia, we also observed a reduction in the number of fos-immunoreactive neurons in the RTN region and in the region of the nucleus of the solitary tract. In the same way as WAR animals, we observed an increase in the number of fos-immunoreactive neurons in the locus coeruleus region. Considering these results, it is suggested that in the experimental models of epilepsy used in the present study, we observed a reduction of basal respiratory activity and hypercapnic ventilatory response, as well as a neuroanatomic changes in the brainstem. Thus, we would like to suggest that both experimental models of epilepsy used in the present study can be considered good experimental models of epilepsy in order to study respiratory disorders and possibly correlate with sudden and unexplained deaths in epilepsy

Involvement of the commissural nucleus of the solitary tract in cardiovascular and sympathetic responses elicited by the anti-hypertensive drug moxonidine in rats.

O objetivo central do presente estudo foi avaliar se os agonistas adrenérgicos a2 e imidazólicos, importantes drogas de ação anti-hipertensiva utilizadas na clínica médica, podem atuar também na região comissural do núcleo do trato solitário (NTSc), o qual constituí uma importante região do bulbo envolvida no controle cardiovascular. Em ratos Wistar adultos, observamos que a hipotensão produzida pela injeção de moxonidina no 4º V foi reduzida após a lesão eletrolítica do NTSc. Ademais, a injeção de moxonidina no NTSc reduziu a pressão arterial média (PAM), a frequência cardíaca (FC) e a atividade simpática (AS). A injeção de antagonistas adrenérgicos (ioimbina ou RX821002) no NTSc foi capaz de bloquear as respostas hipotensora e de simpatoinibição produzida pela moxonidina no NTSc. A injeção bilateral de moxonidina na região RVL/C1 reduziu PAM e AS de maneira mais intensa do que as injeções no NTSc. Em concordância com os resultados apresentados, mostramos que a atividade elétrica dos neurônios da região do RVL/C1 foi reduzida após a injeção de moxonidina no NTSc. Concluímos que a moxonidina pode produzir os seus efeitos anti-hipertensivos atuando também sobre o NTSc.The main objective of this study was to evaluate whether the a2 adrenergic and imidazoline agonists, important antihypertensive drugs used in clinical medicine, may also act in the commissural region of the nucleus of the solitary tract (cNTS), which constitutes an important region of brainstem involved in cardiovascular control. In adult rats, the hypotension elicited by central injections of moxonidine was reduced after electrolytic lesion of cNTS. Furthermore, injection of moxonidine into the cNTS reduced mean arterial pressure (MAP), heart rate (HR) and sympathetic activity (SNA). Injection of the a2 adrenergic antagonist (RX821002 or yohimbine) into the cNTS completely blocked the hypotension and sympathoinhibition responses produced by moxonidine into the cNTS. Bilateral injection of moxonidine in the RVLM/C1 produced huge effects on MAP and SNA in comparison of cNTS injections. In agreement with our results, moxonidine-injected into the cNTS also elicited a reduction in the activity of RVLM/C1 neurons. Our conclusion is that moxonidine may produce their antihypertensive effects also acting on cNTS neurons

I nodi economici di una strategia operativa di tutela ambientale

L'ambiente è risorsa fragile e non riproducibile, l'impatto dell'inquinamento può essere lesivo di sviluppo

The "Cultural" Dimension in Tourist Growth: Reference to the Experience of the European Community

La cultura, volano del turismo, si rivela fondamentale per lo sviluppo economico, come indica l'esperienza europea