Ação da luz visível na oxidação da melanina e no descolorimento do cabelo / Action of the visible on the melanin oxidation and hair discoloration

O dano capilar causado pelo descolorimento oxidativo é muito intenso, sendo que dois fatores são responsáveis por essa ação: primeiro, a ação direta e danosa do oxidante em diversas estruturas capilares e segundo, o dano oxidativo primário facilita o dano causado por outros agentes físicos (luz, temperatura) e químicos (tensoativos), que comumente tem ação nos cabelos. Desenvolver conceitos e tecnologias que possam tornar o oxidante específico para a melanina e por conseguinte efetuando o descolorimento sem causar danos ao fio é extremamente desejável. Neste trabalho buscaremos entender de que forma a luz visível pode aumentar a ação do oxidante sem danificar o fio colateralmente. O objetivo principal deste trabalho é demonstrar que é possível utilizar a luz visível, que é absorvida pela melanina, para tornar esse pigmento mais suscetível ao agente oxidante e desta forma, permitir que o descolorimento seja realizado com concentrações pequenas de oxidante. Também almejamos desenvolver métodos de análises por microscopia ótica de fluorescência e de reflexão para mensurar o dano nas estruturas dos fios processados com oxidante e na presença ou ausência da luz

The capillary damage caused by oxidative discoloration is very intense, and two factors are responsible for this action: first, the direct and harmful action of the oxidant on several capillary structures and second, the primary oxidative damage facilitates the damage caused by other physical agents (light, temperature) and chemicals (surfactants), which commonly have action on the hair. Developing concepts and technologies that can make the oxidant specific to melanin and therefore discoloring without causing damage to the hair is extremely desirable. In this work we will try to understand how visible light can increase the oxidant's action without damaging the wire collaterally. The main objective of this work is to demonstrate that it is possible to use visible light, which is absorbed by melanin, to make this pigment more susceptible to the oxidizing agent and, thus, to allow the discoloration to be carried out with small concentrations of oxidizer. We also aim to develop methods of analysis by optical fluorescence and reflection microscopy to measure the damage to the structures of the threads processed with oxidizer and in the presence or absence of light

Cerebral Hypoperfusion and the Energy Deficit in Alzheimer's Disease.

There is a perfusion deficit in Alzheimer's disease (AD), commencing in the precuneus and spreading to other parts of the cerebral cortex. The deficit anticipates the development of dementia, contributes to brain damage, and is caused by both functional and structural abnormalities of the cerebral vasculature. Most of the abnormalities are probably secondary to the accumulation of Aß but the consequent hypoperfusion may, in turn, increase Aß production. In the early stages of disease, abnormalities that cause vasoconstriction predominate. These include cholinergic vascular denervation, inhibition of endothelial nitric oxide synthase, increased production of endothelin-1 production and possibly also of angiotensin II. Patients with AD also have an increased prevalence of structural disease of cerebral microvessels, particularly CAA and capillary damage, and particularly in the later stages of disease these are likely to make an important contribution to the cerebral hypoperfusion. The metabolic abnormalities that cause early vascular dysfunction offer several targets for therapeutic intervention. However, for intervention to be effective it probably needs to be early. Prolonged cerebral hypoperfusion may induce compensatory circulatory changes that are themselves damaging, including hypertension and small vessel disease. This has implications for the use of antihypertensive drugs once there is accumulation of Aß within the brain.

Autosplenectomy in severity of sickle cell diseases.

BACKGROUND: We tried to understand whether or not there is an association between prevalence of autosplenectomy and severity of sickle cell diseases (SCDs). METHODS: All SCDs patients with red blood cell (RBC) transfusions of less than 50 units in their lives were put into the first group and 50 units or higher were put into the second group. RESULTS: The study included 316 patients (155 females). There were 224 cases (70.8%) in the first group and 92 cases (29.1%) in the second group (p<0.001). The male ratio was significantly higher in the second group (64.1% versus 45.5%, p<0.001). Although both the white blood cell and platelet counts were higher in the second group, there was a significant difference in platelet counts (p=0.005), and this was probably due to the small sample sizes. Although the prevalence of autosplenectomy was significantly higher in the first group (56.2% versus 45.6%, p<0.05), the mean number of painful crises per year, digital clubbing, chronic obstructive pulmonary disease (COPD), leg ulcers, stroke, chronic renal disease (CRD) and coronary heart disease (CHD) were significantly higher in the second groups (p<0.05 for all). CONCLUSION: In contrast to the lower prevalence of autosplenectomy, the mean number of painful crises per year, digital clubbing, COPD, leg ulcers, stroke, CRD, and CHD were significantly higher in the second group. So there may be an inverse relationship between prevalence of autosplenectomy and severity of SCDs, and spleen may act as a chronic inflammatory focus as a filter of blood for these abnormally hard RBCs.

Acute chest syndrome in severity of sickle cell diseases.

BACKGROUND: Sickle cell diseases (SCDs) are chronic inflammatory processes on capillary level. We tried to understand whether or not there are some positive correlations between acute chest syndrome (ACS) and severity of SCDs. METHODS: All patients with the SCDs were taken into the study. RESULTS: The study included 337 cases (167 females). There were 15 patients (4.4%) with the ACS. The mean ages were similar in both groups (29.4 versus 29.7 years in the ACS group and other, respectively, P > 0.05). The female ratios were similar in both groups, too (60.0% versus 49.0%, respectively, P > 0.05). Additionally, prevalences of associated thalassemia minors were similar in them (66.6% versus 65.5%, respectively, P > 0.05). Smoking was higher in the ACS group (20.0% versus 13.9%), but the difference was nonsignificant (P > 0.05). Although the mean white blood cell count and hematocrit value of peripheric blood were higher in the ACS group, the mean platelet count was lower in them, but the differences were nonsignificant again (P > 0.05 for all). On the other hand, although the painful crises per year, tonsilectomy, priapism, ileus, digital clubbing, pulmonary hypertension, rheumatic heart disease, cirrhosis, stroke, and mortality were higher in the ACS group, the difference was only significant for the stroke (P < 0.05), probably due to the small sample size of the ACS group. CONCLUSION: SCDs are chronic destructive processes on capillaries iniatiating at birth, and terminate with early organ failures in life. Probably ACS is one of the terminal consequences of the inflammatory processes that may indicate shortened survival in such patients.

A microcirculação coronária na reperfusäo miocárdica. O fenômeno da näo reperfusão / Coronary microcirculation in myocardial reperfusion. The phenomenon of no-flow

Objetivo - Estudo da ultraestrutura dos capilares do coração, na reperfusão que sucede ao infarto do miocárdio. Material e Métodos - Cinco cães de ambos os sexos, pesando de 12 a 17,5 kg, anestesiados com pentobarbital, na dose de 30 mg/kg, de peso e ventilados com ar atmosférico, tiveram aberto o tórax e a artéria descendente anterior (DA) isolada, antes da emergência dos ramos septais. As pressões de aorta e átrio direito, eletrocardiograma e o fluxo coronário foram medidos para análise da relação pressão fluxo, objetivo de outro estudo. A DA foi ocluída por 90 min. após o que, procedeu-se à reperfusão por 20 min. Imediatamente, a DA foi canulada, injetou-se Nankin, o coração retirado, colocado em salina gelada, e em seguida fatiado, retirando-se fragmentos para estudo à microscopia eletrônica, na área marcada pelo nankin, desde o endocárdio até o epicárdio. Foi retirado um fragmento da região dorsal do coração, para estudo controle. As fatias do coração foram incubadas com TTC a 1%, a 37ºC, durante 10 min. Resultados - Na área infartada observaram-se alterações dos capilares, com edema da célula endotelial e desaparecimento das vesículas de pinocitose. Verificou-se a presença de "blebs", hemácias e neutrófilos no volume vascular. Os miócitos apresentavam desarranjo e ruptura dos miofilamentos, critólise e ruptura da membrana mitocondrial com intenso edema celular. No mesocárdio, próximo à área de não reperfusão, observaram-se capilares, com grau de lesão semelhante aos da área infartada. Os miócitos, entretanto, mostraram-se pouco alterados

Purpose - The study of the ultrastructural features of the coronary microvessels in postischemic reperfusion. Material and Methods - Five mongrel dogs of either sex, weighing 2 to 17 kg were studied Each dog was anesthesiated with 30 mg. of pentobarbital and ventilated with room air. A thoracotomy was done and the left descendent coronary artery was isolated. Aorta and right atria pressures, eletrocardiogram and coronary blood flow was measured. After 90 minutes of coronary occlusion and 20 minutes of reperfusion carbon black was injected into the anterior descending coronary artery to identify the area of impaired perfusion. The heart was excised and placed in a ice-cold saline. The left ventricle was curt transversely in six slices of 1 cm thickness parallel to the atrioventricular sulcus. Tissue specimens were taken from the subendocardial, mid-myocardial (in the non reperfused area) subepicardial and control layers for electron microscopic examination. Each slice was then incubated in a 1% solution of triphenyltetrazolium chloride (TTC) at 37ºC for 10 minutes. Results - The infarcted areas showed widespread tissue damage with relazed myofibrils cellular edema, swollen mitocondria with fractured cristae and nuclear changes. The vascular endothelium demonstrated severe injury with edema, cytoplasmic clearing, loss of pinocytotic vesicles, nuclear changes, formation of blebs into the vascular lumen and intravascular neutrophil. In the mid-myocardial layer, near the non reperfused vessels, a striking contrast was observed beetween the vessel and myocardium cells patterns. The usual picture was a severe vascular damage without myocyte injury