924 resultados para blood vessel prosthesis implantation


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It is known that low level laser therapy is able to improve skin flap viability by increasing angiogenesis. However, the mechanism for new blood vessel formation is not completely understood. Here, we investigated the effects of 660 nm and 780 nm lasers at fluences of 30 and 40 J/cm2 on three important mediators activated during angiogenesis. Sixty male Wistar rats were used and randomly divided into five groups with twelve animals each. Groups were distributed as follows: skin flap surgery non-irradiated group as a control; skin flap surgery irradiated with 660 nm laser at a fluence of 30 or 40 J/cm2 and skin flap surgery irradiated with 780 nm laser at a fluence of 30 or 40 J/cm2. The random skin flap was performed measuring 10 × 4 cm, with a plastic sheet interposed between the flap and the donor site. Laser irradiation was performed on 24 points covering the flap and surrounding skin immediately after the surgery and for 7 consecutive days thereafter. Tissues were collected, and the number of vessels, angiogenesis markers (vascular endothelial growth factor, VEGF and hypoxia inducible factor, HIF-1α) and a tissue remodeling marker (matrix metalloproteinase, MMP-2) were analyzed. LLLT increased an angiogenesis, HIF-1α and VEGF expression and decrease MMP-2 activity. These phenomena were dependent on the fluences, and wavelengths used. In this study we showed that LLLT may improve the healing of skin flaps by enhancing the amount of new vessels formed in the tissue. Both 660 nm and 780 nm lasers were able to modulate VEGF secretion, MMP-2 activity and HIF-1α expression in a dose dependent manner. © 2013 Published by Elsevier B.V.

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PURPOSE: To investigate and compare the biocompatibility of two types of Ferrara intracorneal ring segment: with and without chondroitin sulfate coating by clinical and histopathological evaluation. METHODS: A randomized experimental study was carried out on thirty right-eye corneas from 30 Norfolk albino rabbits allocated into two experimental groups: Group G1 - implanted with Ferrara intracorneal ring segment without coating (FICRS) and Group G2 - implanted with Ferrara intracorneal ring segment with chondroitin sulfate coating (FICRS-CS). Left eyes formed the control group. Clinical parameters analyzed were: presence of edema, vascularization, infection and ring extrusion one, 30, and 60 days after surgery. Histopathological parameters analyzed were: number of corneal epithelial layers over and adjacent to the ring, presence of spongiosis, hydropic degeneration, basement membrane thinning, inflammatory cells, neovascularization and pseudocapsule formation. RESULTS: At clinical examination 60 days after implant, edema, vascularization and extrusion were observed respectively in 20%, 26.7%, 6.7% of FICRS corneas and in 6.7%, 6.7%, and 0% of FICRS-CS corneas. Histopathological evaluation showed epithelial-layer reduction from 5 (5;6) to 3 (3;3) with FICRS and from 5 (5;5) to 4 (3;5) with FICRS-CS in the region over the ring. Epithelial spongiosis, hydropic degeneration, and basement membrane thinning were present in 69.2%, 53.8%, and 69.2% of FICRS and in 73.3%, 73.3%, and 46.7% with FICRS-CS, respectively. Vascularization was present in 38.5% of FICRS and 13.3% with FICRS-CS, inflammatory cells in 75% of FICRS and 33.3% with FICRS-CS, and pseudocapsule in 66.7% of FICRS and 93.3% with FICRS-CS. Giant cells occurred only in the FICRS-CS group (20%). CONCLUSION: Ferrara intracorneal rings coated with chondroitin sulfate (FICRS-CS) caused lower frequency of clinical and histopathological alterations than Ferrara intracorneal rings without the coating (FICRS), demonstrating higher biocompatibility of the FICRS-CS.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Pós-graduação em Pesquisa e Desenvolvimento (Biotecnologia Médica) - FMB

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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O ENH é séria intercorrência aguda ou subaguda que acomete pacientes das formas dimorfa-virchowiana e virchowiana da classificação de Ridley e Jopling. Neste estudo, foi utilizada uma droga imunorreguladora, a ciclosporina A, com o propósito de avaliar a eficácia nesta reação, cujo tratamento depende de medicamentos como a talidomida, que tem contra-indicações formais e corticóides, que provocam dependência, entre outros danos. Foram selecionados dez doentes de ENH com sintomas sistêmicos; todos haviam passado por vários episódios desta reação e faziam uso contínuo e prolongado de prednisona em doses elevadas e ocasionalmente, de talidomida. Os pacientes tomaram ciclosporina A em doses de 3-5 mg/kg/dia durante um período de 90 dias. Realizaram exames laboratoriais nos dias zero, 150 e 600 de uso da ciclosporina A e também o histopatológico das lesões de ENH (antes do tratamento e com 60 dias). Os exames laboratoriais solicitados foram: hemograma e leucograma; TGO; TGP: uréia e creatinina. Detectou-se leucocitose em graus entre moderado e elevado em 70% dos casos, mas evoluiu para leucocitose leve até o término do acompanhamento na mesma percentagem dos doentes. O exame bioquímico não mostrou alterações significantes, com exceção da elevação da TGO em um caso, da TGP em outro, além de dois pacientes que mostraram aumento da uréia e creatinina, mas que posteriormente, normalizaram sem precisar de medidas adicionais. Os achados histológicos encontrados no primeiro exame foram representados em 40% dos doentes, por dermatite granulomatosa e em 30%, por dermatite nodular. Na segunda análise, houve mudança para dermatite perivascular superficial e profunda em 50% dos casos e para paniculite septal em 20%; isto denota melhora histológica compatível com a melhora dos sintomas verificada nos primeiros quinze dias de terapêutica. A ação da ciclosporina A se revelou benéfica, principalmente na sintomatologia sistêmica, com exceção dos casos que se acompanhavam de neurite; desta forma, a ciclosporina A pode ser uma opção para a melhoria clínica das reações hansênicas tipo 11.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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During tooth eruption, structural and functional changes must occur in the lamina propria to establish the eruptive pathway. In this study, we evaluate the structural changes that occur during lamina propria degradation and focus these efforts on apoptosis and microvascular density. Fragments of maxilla containing the first molars from 9-, 11-, 13- and 16-day-old rats were fixed, decalcified and embedded in paraffin. The immunohistochemical detection of vascular endothelial growth factor (VEGF), caspase-3 and MAC387 (macrophage marker), and the TUNEL method were applied to the histological molar sections. The numerical density of TUNEL-positive cells and VEGF-positive blood vessel profiles were also obtained. Data were statistically evaluated using a one-way anova with the post-hoc Kruskal-Wallis or Tukey test and a significance level of P ≤ 0.05. Fragments of maxilla were embedded in Araldite for analysis under transmission electron microscopy (TEM). TUNEL-positive structures, fibroblasts with strongly basophilic nuclei and macrophages were observed in the lamina propria at all ages. Using TEM, we identified processes of fibroblasts or macrophages surrounding partially apoptotic cells. We found a high number of apoptotic cells in 11-, 13- and 16-day-old rats. We observed VEGF-positive blood vessel profiles at all ages, but a significant decrease in the numerical density was found in 13- and 16-day-old rats compared with 9-day-old rats. Therefore, the establishment of the eruptive pathway during the mucosal penetration stage depends on cell death by apoptosis, the phagocytic activity of fibroblasts and macrophages, and a decrease in the microvasculature due to vascular cell death. These data point to the importance of vascular rearrangement and vascular neoformation during tooth eruption and the development of oral mucosa.

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The maxillofacial prosthetic rehabilitation aims of individuals with craniofacial deformities resulting from trauma, congenital malformations or tumors. Many researches have been done to improve the stability and retention of dentures in patients. With the advent of osseointegration, the maxillofacial prosthesis suffered a major advance making possible the realization of prosthetic works with stability, aesthetic quality and predictable results. This paper reviews the literature regarding the use of zygomatic implants in the fixation of maxillofacial prostheses.

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The microvascularization of the collared peccary (Tayassu tajacu) placenta was studied by vascular casts and immunolocalization of alpha-smooth muscle actin and vimentin, to identify the three-dimensional organization and vascular flow interrelation in the microvasculature between the maternal and fetal compartments of the placentae. The immunolocalization of vimentin in the vascular endothelium and in the smooth muscle cells of blood vessels showed indented capillaries along the uterine epithelium and the trophoblast at the sides of complementary maternal and fetal microfolds, or rugae. This confers the three-dimensional structure observed in vascular casts. On the maternal side, casts demonstrated uterine folds coated by with primary and secondary ridges, and by areolae dispersed between these ridges. The arteriole runs through the center/middle of ridges, branching at the top into a microvascular network wall in a basket-like fashion. At the base of these baskets venules were formed. On the fetal side, arterioles branched centrally in the fetal rugae into a capillary network in a bulbous form, complementary to the opposite maternal depressions forming the baskets. At the base of the bulbous protrusions, the fetal venules arise. The blood vessel orientation in the materno-fetal interface of the placentae of collared peccaries suggests a blood flow pattern of the type countercurrent to crosscurrent. The same pattern has been reported in domestic swine demonstrating that, even after 38 million years, the Tayassuidae and Suidae families exhibit similar placental morphology, which is here characterized at the microvascular level.

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Hydrocephalus is associated with reduced blood flow in periventricular white matter. To investigate hypoxic and oxidative damage in the brains of rats with hydrocephalus, kaolin was injected into the cisterna magna of newborn 7- and 21-day-old Sprague-Dawley rats, and ventricle size was assessed by magnetic resonance imaging at 7, 21, and 42 days of age. In-situ evidence of hypoxia in periventricular capillaries and glial cells was shown by pimonidazole hydrochloride binding. Biochemical assay of thiobarbituric acid reaction and immunohistochemical detection of malondialdehyde and 4-hydroxy-2-nonenal indicated the presence of lipid peroxidation in white matter. Biochemical assay of nitrite indicated increased nitric oxide production. Nitrotyrosine immunohistochemistry showed nitrosylated proteins in white matter reactive microglia and astrocytes. Activities of the antioxidant enzymes catalase and glutathione peroxidase were not increased, and altered hypoxia-inducible factor 1 alpha was not detected by quantitative reverse transcription-polymerase chain reaction. Cerebral vascular endothelial growth factor expression determined by quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay was not changed, but vascular endothelial growth factor immunoreactivity was increased in reactive astrocytes of hydrocephalic white matter. To determine if nitric oxide synthase is involved in the pathogenesis, we induced hydrocephalus in 7-day-old wild-type and neuronal nitric oxide synthase-deficient mice. At 7 days, the wild-type and mutant mice exhibited equally severe ventriculomegaly and no behavioral differences, although increased glial fibrillary acidic protein was less in the mutant mice. We conclude that hypoxia, via peroxidation and nitrosylation, contributes to brain changes in young rodents with hydrocephalus and that compensatory mechanisms are negligible.