No description available.

Abstract: Background: At present, device closure of interatrial communication has become a well established technique in order to adequately treat severe left-to-right shunt associated with ASDs. During the traditional procedure, fluoroscopy with the waist of a compliant balloon is used to determine the appropriate size of the closure device and defect sizing. Choice of adequate closure device using transthoracic echocardiography (TTE) has been hitherto unreported. Methods & Materials: Between December 2002 and October 2004, 40 patients (15 males, 25 females, mean age; 11.7 ¡Ó 7.8 years ) with secundum ASDs underwent transcatheter closure at our institution. In group 1, 30 patients had the procedure by balloon sizing and TTE sizing. In 10 patients (group 2), TTE sizing was used as the sole too l for selecting device size and the device size was chosen to be based on the Amplatzer septal occluder ( ASO ) size and TTE size ratio in group 1. The procedure was performed under continuous transoesophageal echocardiographic monitor with general anesthesia. Results: The correlation was found between TTE and stretched balloon sizing diameter SBD ( y= 1.2645x-1.4465; R²=0.9861 ), and between TTE size and ASO size ( y = 1.3412x-1.2864; R²=0.9929 ) in group 1. In group 2, statistical correlation between TTE and ASO ( y=1.3419x-0.1172; R²=0.9934 ) was also found. Good linear regression between TTE size and ASO chosen size was noted in group 1 and group 2 (R²=0.99).In group 2, successful device implantation was accomplished in all patients whose device size was chosen to be based on the ASO and TTE ratio in group 1. Conclusions: TTE sizing is a safe and ideal method to measure interatrial defect and choose the occluding device respectively. With our experience, the sizing based on the TTE is generally easier than measurement from the balloon sizing.

Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2016-09-12T13:42:31Z No. of bitstreams: 1 Manuela dos Santos Caldas Alterações Iniciais...2016.pdf: 7635538 bytes, checksum: 6a93fba431df86f82cdcef4c267b57b0 (MD5) / Approved for entry into archive by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2016-09-12T13:54:54Z (GMT) No. of bitstreams: 1 Manuela dos Santos Caldas Alterações Iniciais...2016.pdf: 7635538 bytes, checksum: 6a93fba431df86f82cdcef4c267b57b0 (MD5) / Made available in DSpace on 2016-09-12T13:54:54Z (GMT). No. of bitstreams: 1 Manuela dos Santos Caldas Alterações Iniciais...2016.pdf: 7635538 bytes, checksum: 6a93fba431df86f82cdcef4c267b57b0 (MD5) Previous issue date: 2014-02-07 / Fundação Oswaldo Cruz. Instituto Gonçalo Moniz. Salvador, BA, Brasil / O espaço-porta é o local de origem da fibrose em muitas doenças crônicas hepáticas. Essa área do fígado participa da drenagem linfática hepática e abriga diversos elementos celulares potencialmente fibrogênicos. Estudos sobre a fibrose hepática relacionados à infecção experimental de ratos pelo helminto Capillaria hepatica têm demonstrado que a fibrose começa em áreas portais com a distribuição de septos que sulcam o parênquima hepático se desenvolvendo em áreas próximas ao espaço de Disse. Entretanto, apesar de esta fibrose ocorrer de forma paralela aos sinusóides, estudos têm revelado que não apenas as células estreladas hepáticas participam da fibrose septal, mas também outros tipos celulares residentes nos espaços-porta. Diante destes aspectos, o presente estudo desenvolveu-se com o intuito de investigar a contribuição das células potencialmente fibrogênicas dos espaços-porta, nas fases iniciais da infecção, onde a fibrose se concentra. Para isso, foram utilizados fragmentos de fígado, em blocos parafinados, disponíveis nos arquivos do Laboratório de Patologia Experimental (CPqGM/Fiocruz) provenientes de ratos infectados com 800 ovos de Capillaria hepatica e foi possível observar que ocorreu a proliferação de colangiócitos e a concentração de miofibroblastos em áreas portais, além da ativação de células estreladas hepáticas, sendo todos os resultados vistos por meio da coloração de rotina HE, Picro-sírius vermelho e imunohistoquímica para α-actina de músculo liso, CD31 e GFAP. / Portal space is the local of origin for fibrosis in many chronic liver diseases. This area is involved with lymph drainage and contains several cell types, potentially fibrogenic. Experimental studies related to hepatic fibrosis during Capillaria hepatica infection in rats have suggested that the septal fibrosis indeed takes origin from portal spaces, with the distribution of the septs in the parenchymal region in proximity areas of Disse space. However, despite this fibrosis occurs in parallel to sinusoids, studies have revealed that not only the hepatic stellate cells participate in septal fibrosis, but also other resident cell types in the portal spaces. In face these aspects, the goal of present study was investigate the contribution of the cells potentially fibrogenic in the portal space, in the early phases of the infection. For this, blocks in paraffin available of the liver of rats infected with 800 eggs of Capillaria hepatica archived in the Laboratory of Experimental Pathology (Research Center Gonçalo Moniz, Fiocruz - BA), were utilized and it was observed that proliferation of colangiocytes and concentration of myofibroblasts occurred portal areas, in addition to the activation of hepatic stellate cells. All results were analised by routine staining HE, Sirius red and immunohistochemistry for α-SMA, GFAP and CD31

BACKGROUND: Left ventricular outflow tract (LVOT) obstruction and paravalvular leak (PVL) are relatively uncommon, but are serious complications of prosthetic valve replacement. CASE PRESENTATION: We present a case that displays the unique therapeutic challenges of treating a patient who developed both LVOT obstruction and mitral PVL after undergoing surgical aortic and mitral valve replacement (MVR). We also describe the use of alcohol septal ablation and albumin-glutaraldehyde (BioGlue) for septal ablation to percutaneously treat the patient's LVOT obstruction, followed by use of an Amplatzer vascular plug for percutaneous closure of an antero-medial mitral PVL associated with severe regurgitation. CONCLUSION: Percutaneous interventional management of these entities may be considered as an initial therapeutic option, especially in high-risk patients with significant morbidity and mortality of repeat surgical operations.

published_or_final_version / Sports Science / Master / Master of Science in Sports Science

Objective: This retrospective longitudinal study attempts to determine the ontogenetic patterning of nasal septal deviation and if there is a relationship between a deviated septum and facial form growth and development. Methods: Nineteen females and twenty males were selected from the Iowa Facial Growth Study. Eighteen lateral cepalometric variables were analyzed and septal deviation was quantified using a percentage of deviation. A generalized Procrustes analysis was used to scale landmarks and generate principal components. Pearson correlation coefficients were used to analyze differences in shape. A Mann Whitney U-Test was used to analyze changes in septal deviation. Results: The first three principal components explained 56.23% of the variance. Only PC1 was significantly correlated with centroid size (r=0.82, P<0.0001). Mean percentage of septal deviation (0.620% ± 0.463%) was present at the youngest age group (3-4.9 years) and increased in each age group until adulthood, defined as over the age of 20 (0.991% ± 0.519). None of the first three principal components were found to be correlated to percentage of septal deviation. Conclusions: Nasal septal deviation has been found to increase in a longitudinal sample of subjects of northern European descent. Nasal septal deviation represents a disjunction in the growth of the nasal septum with the rest of the face. The amount and timing of nasal septal deviation that can cause nasal obstructions leading to vertical growth changes was not analyzed in this study and will require future study.

Congenital heart disease is the most common form of birth defect, affecting approximately 1% of liveborn babies. Secundum atrial septal defect (ASD) is the second most common form of congenital heart disease (CHD). Most cases have no known cause. Chromosomal, syndromal and teratogenic causes account for a minority of cases. The hypothesis that mutations in the ASD genes NKX2-5 and GATA4 may cause apparently sporadic ASD was tested by sequencing them in unrelated probands with ASD. In this study, 1/102 individuals with ASD had an NKX2-5 mutation, and 1/129 had a deletion of the GATA4 gene. The cardiac transcription factor TBX20 interacts with other ASD genes but had not previously been associated with human disease. Of 352 individuals with CHD, including 175 with ASD, 2 individuals, each with a family history of CHD, had pathogenic mutations in TBX20. Phenotypes included ASD, VSD, valvular abnormalities and dilated cardiomyopathy. These studies of NKX2-5, GATA4 and TBX20 indicate that dominant ASD genes account for a small minority of cases of ASD, and emphasize the considerable genetic heterogeneity in dominant ASD (also caused by mutations in MYH6 and ACTC). A new syndrome of dominant ASD and the Marcus Gunn jaw winking phenomenon is reported. Linkage to known loci was excluded, extending this heterogeneity, but a whole genome scan did not identify a candidate locus for this disorder. Previous studies of inbred laboratory mice showed an association between patent foramen ovale (PFO) and measures of atrial septal morphology, particularly septum primum length (???flap valve length??? or FVL). In humans, PFO is associated with cryptogenic stroke and migraine, and is regarded as being in a pathological contiuum with ASD. Twelve inbred strains, including 129T2/SvEms and QSi5, were studied, with generation of [129T2/SvEms x QSi5] F1, F2 and F14 mice. Studies of atrial morphology in 3017 mice confirmed the relationship between FVL and PFO but revealed considerable complexity. An F2 mapping study identified 7 significant and 6 suggestive quantitative trait loci (QTL), affecting FVL and two other traits, foramen ovale width (FOW) and crescent width (CRW). Binary analysis of PFO supported four of these.

名古屋大学博士学位論文 学位の種類 : 博士(医学)(論文) 学位授与年月日:平成4年10月19日 狩野良雄氏の博士論文として提出された

Thesis (M. Sc.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 68-75).

BACKGROUND: The ventricular septal defect (VSD), a hole between the ventricles of the heart, is the most common birth defect. Despite its commonality, little is known about related in utero functional deficits. Furthermore, although about 80% of clinical VSD resolve within a year, the long-term effects after their resolution are unknown due to lack of clinical follow-up. Chemical treatment was used to induce VSD in the rat and to investigate their functional consequences both in utero and postnatally. METHODS: Pregnant Sprague-Dawley rats were administered six 300mg/kg doses of dimethadione (DMO) by oral gavage every 12 hours beginning at 19h00 on gestational day (GD) 8 (Weston et al., 2011). DMO is the N-demethylated metabolite of the anticonvulsant trimethadione, a potent inducer of VSDs clinically and in laboratory animals. Fetal heart structure and function were examined with high-resolution ultrasound on GD 14, 15, 16, 17, and 21. A separate cohort of rats was dosed using the described paradigm, but offspring were allowed to reach parturition and mature naturally. Postnatal heart structure and function were assessed using telemetry (70 days postnatally), high-resolution ultrasound, and electrocardiography (ECG) (one year postnatally). RESULTS: Relative to controls, DMO-treated fetal rats had structural defects including VSD, an increased incidence of bradycardia (23 vs. 45%) and dysrhythmia (1.2 vs. 11%), and a reduction in cardiac output, stroke volume, and mean heart rate. Adult rats exposed to DMO in utero were more physically active, had elevated blood pressure, and had a higher incidence of dysrhythmia associated with ECG disturbances compared to controls. Both in utero and postnatal functional deficits occurred independent of septum patency. CONCLUSIONS: Gestational exposure to DMO disrupted cardiac function both in utero and postnatally, even in the absence of gross structural defects, indicating chemical exposures in utero may have permanent pathophysiological consequences on the heart. / Thesis (Master, Pharmacology & Toxicology) -- Queen's University, 2012-05-30 17:19:35.529