Academic literature on the topic 'Brain – Congestion'

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Journal articles on the topic "Brain – Congestion"

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Ibitayo, A. O., O. B. Afolabi, A. J. Akinyemi, T. I. Ojiezeh, K. O. Adekoya, and O. O. Ojewunmi. "RAPD Profiling, DNA Fragmentation, and Histomorphometric Examination in Brains of Wistar Rats Exposed to Indoor 2.5 Ghz Wi-Fi Devices Radiation." BioMed Research International 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/8653286.

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The advent of Wi-Fi connected high technology devices in executing day-to-day activities is fast evolving especially in developing countries of the world and hence the need to assess its safety among others. The present study was conducted to investigate the injurious effect of radiofrequency emissions from installed Wi-Fi devices in brains of young male rats. Animals were divided into four equal groups; group 1 served as control while groups 2, 3, and 4 were exposed to 2.5 Ghz at intervals of 30, 45, and 60 consecutive days with free access to food and water ad libitum. Alterations in harvested brain tissues were confirmed by histopathological analyses which showed vascular congestion and DNA damage in the brain was assayed using agarose gel electrophoresis. Histomorphometry analyses of their brain tissues showed perivascular congestion and tissue damage as well.
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Mailhot, T., A. Denault, S. Cossette, et al. "POST-CARDIAC SURGERY DELIRIUM: VENOUS CONGESTION REACHING THE BRAIN?" Canadian Journal of Cardiology 33, no. 10 (2017): S93. http://dx.doi.org/10.1016/j.cjca.2017.07.184.

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Takahashi, S., I. Sakuma, T. Otani, et al. "Carotid-Cavernous Fistula Associated with an Intracranial Lesion Caused by Cortical Venous Reflux." Interventional Neuroradiology 12, no. 1_suppl (2006): 167–73. http://dx.doi.org/10.1177/15910199060120s129.

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Digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) findings in 20 patients with carotid-cavernous fistula (CCF; 3 direct CCFs and 17 indirect CCFs) were retrospectively reviewed to evaluate venous drainage patterns that may cause intracerebral haemorrhage or venous congestion of the brain parenchyma. We evaluated the relationship between cortical venous reflux and abnormal signal intensity of the brain parenchyma on MRI. Cortical venous reflux was identified on DSA in 12 of 20 patients (60.0%) into the superficial middle cerebral vein (SMCV; n=4), the uncal vein (n=2), the petrosal vein (n=2), the lateral mesencephalic vein (LMCV; n=1), the anterior pontomesencephalic vein (APMV; n=1), both the APMV and the petrosal vein (n=1) and both the uncal vein and the SMCV (n=1). Features of venous congestion, such as tortuous and engorged veins, focal staining and delayed appearance of the veins, were demonstrated along the region of cortical venous reflux in the venous phase of internal carotid or vertebral arteriography in six of 20 patients (30.0%). These findings were not observed in the eight CCF patients who did not demonstrate cortical venous reflux. MRI revealed abnormal signal intensity of the brain parenchyma along the region with cortical venous reflux in four of 20 indirect CCF patients (20%). Of these four patients, one presented with putaminal haemorrhage, while the other three presented with hyperintensity of the pons, the middle cerebellar peduncle or both on T2-weighted images, reflecting venous congestion. The venous drainage routes were obliterated except for cortical venous reflux in these four patients and the patients without abnormal signal intensity on MRI had other patent venous outlets in addition to cortical venous reflux. CCF is commonly associated with cortical venous reflux. The obliteration or stenosis of venous drainage routes causes a converging venous outflow that develops into cortical venous reflux and results in venous congestion of the brain parenchyma or intracerebral haemorrhage. Hyperintensity of brain parenchyma along the region of cortical venous reflux on T2-weighted images reflects venous congestion and is the crucial finding that indicates concentration of venous drainage into cortical venous reflux.
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Takahashi, S., I. Sakuma, T. Otani, et al. "Carotid-Cavernous Fistula Associated with an Intracranial Lesion Caused by Cortical Venous Reflux." Rivista di Neuroradiologia 8, no. 6 (1995): 167–73. http://dx.doi.org/10.1177/197140099500800629.

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Digital subtraction angiography (DSA) and magnetic resonance imaging (MRI) findings in 20 patients with carotid-cavernous fistula (CCF; 3 direct CCFs and 17 indirect CCFs) were retrospectively reviewed to evaluate venous drainage patterns that may cause intracerebral haemorrhage or venous congestion of the brain parenchyma. We evaluated the relationship between cortical venous reflux and abnormal signal intensity of the brain parenchyma on MRI. Cortical venous reflux was identified on DSA in 12 of 20 patients (60.0%) into the superficial middle cerebral vein (SMCV; n=4), the uncal vein (n=2), the petrosal vein (n=2), the lateral mesencephalic vein (LMCV; n=1), the anterior pontomesencephalic vein (APMV; n=1), both the APMV and the petrosal vein (n=1) and both the uncal vein and the SMCV (n=1). Features of venous congestion, such as tortuous and engorged veins, focal staining and delayed appearance of the veins, were demonstrated along the region of cortical venous reflux in the venous phase of internal carotid or vertebral arteriography in six of 20 patients (30.0%). These findings were not observed in the eight CCF patients who did not demonstrate cortical venous reflux. MRI revealed abnormal signal intensity of the brain parenchyma along the region with cortical venous reflux in four of 20 indirect CCF patients (20%). Of these four patients, one presented with putaminal haemorrhage, while the other three presented with hyperintensity of the pons, the middle cerebellar peduncle or both on T2-weighted images, reflecting venous congestion. The venous drainage routes were obliterated except for cortical venous reflux in these four patients and the patients without abnormal signal intensity on MRI had other patent venous outlets in addition to cortical venous reflux. CCF is commonly associated with cortical venous reflux. The obliteration or stenosis of venous drainage routes causes a converging venous outflow that develops into cortical venous reflux and results in venous congestion of the brain parenchyma or intracerebral haemorrhage. Hyperintensity of brain parenchyma along the region of cortical venous reflux on T2-weighted images reflects venous congestion and is the crucial finding that indicates concentration of venous drainage into cortical venous reflux.
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Gojkovic, Slaven, Ivan Krezic, Hrvoje Vranes, et al. "Robert’s Intragastric Alcohol-Induced Gastric Lesion Model as an Escalated General Peripheral and Central Syndrome, Counteracted by the Stable Gastric Pentadecapeptide BPC 157." Biomedicines 9, no. 10 (2021): 1300. http://dx.doi.org/10.3390/biomedicines9101300.

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We redefined Robert’s prototypical cytoprotection model, namely the intragastric administration of 96% alcohol in order to generate a general peripheral and central syndrome similar to that which occurs when major central or peripheral veins are occluded in animal models. With this redefinition, we used Robert’s model to examine the cytoprotective effects of the stable gastric pentadecapeptide BPC 157. The intragastric administration of alcohol induced gastric lesions, intracranial (superior sagittal sinus) hypertension, severe brain swelling and lesions, portal and vena caval hypertension, aortal hypotension, severe thrombosis, inferior vena cava and superior mesenteric vein congestion, azygos vein failure (as a failed collateral pathway), electrocardiogram disturbances, and heart, lung, liver and kidney lesions. The use of BPC 157 therapy (10 µg/kg or 10 ng/kg given intraperitoneally 1 min after alcohol) counteracted these deficits rapidly. Specifically, BPC 157 reversed brain swelling and superior mesenteric vein and inferior vena caval congestion, and helped the azygos vein to recover, which improved the collateral blood flow pathway. Microscopically, BPC 157 counteracted brain (i.e., intracerebral hemorrhage with degenerative changes of cerebral and cerebellar neurons), heart (acute subendocardial infarct), lung (parenchymal hemorrhage), liver (congestion), kidney (congestion) and gastrointestinal (epithelium loss, hemorrhagic gastritis) lesions. In addition, this may have taken place along with the activation of specific molecular pathways. In conclusion, these findings clarify and extend the theory of cytoprotection, offer an approach to its practical application, and establish BPC 157 as a prospective cytoprotective treatment.
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Danilovic, Milos, Jelena Isailovic, Ivan Aleksic, Jelena Dzambas, and Nadica Marinkovic. "Accidental colchicine poisoning with fatal outcome after ingestion of meadow saffron (Colchicum autumnale L.) - Report of autopsy case." Vojnosanitetski pregled 77, no. 10 (2020): 1104–8. http://dx.doi.org/10.2298/vsp180413034d.

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Introduction. Meadow saffron (Colchicum autumnale L.) is a perennial herbaceous plant belonging to the Lily family (Liliacea). It is similar to the edible wild garlic (Allium ursinum L.). Toxic substance in meadow saffron is alkaloid colchicine. Colchicine poisoning is a very dangerous condition which can lead to a fatal outcome. Case report. A 50-yearsold male was addmited to the hospital complaining of weakness, abdominal pain, nausea, vomiting and diarrhea without blood. The day before, the patient ate two plants thinking they were wild garlic and seven hours after ingestion he felt first symptoms. During the course of the hospital stay, he had gastroenterocolitis, acute renal faliure, hepatic lesions and cardiorespiratory insufficiency with a fatal outcome. Post-mortem examination revealed: brain oedema, lung oedema and congestion, heart weighing 700 g with ventricular hypertrophy, myocardial fibrosis, liver congestion and steatosis, spleen congestion, pancreatic fibrosis. Organs sections were taken for histopathological analysis. Body fluids and parts of organs were toxicologically analyzed. Histopathological findings were: brain oedema, diffuse perivascular and interstitial myocardial fibrosis, myocardial haemorrhage, lungs congestion and oedema, microvesicular and macrovesicular liver steatosis, centrilobular liver necrosis, lymphocytic inflammatory infiltrate in liver portions, red pulp congestion of the spleen, kidney congestion and interstitial bleeding, coagulation necrosis of the proximal tubules of the kidney. Toxicological analysis showed colchicine in the blood ? 0.011 mg/L, urine ? 0.051 mg/L, liver with gallbladder ? 0.007 mg/kg, kidney ? 0.008 mg/kg. Conclusion. Ingestion of meadow saffron can lead to poisoning with a fatal outcome due to the presence of the alkaloid colchicine. Colchicine intoxication should be suspected in patients with gastrointestinal symptoms after consuming wild plants.
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Takashima, Sachio, and Yukinori Ando. "Reflectance spectrophotometry, cerebral blood flow and congestion in young rabbit brain." Brain and Development 10, no. 1 (1988): 20–23. http://dx.doi.org/10.1016/s0387-7604(88)80040-8.

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STOIMENOV, G. M., G. V. GOUJGOULOVA, B. NIKOLOV, R. PETROVA, A. TENEVA, and I. DIMITROVA. "Histopathological findings in Dalmatian pelicans (Pelecanus crispus) naturally infected with avian influenza subtype A H5N1 in Bulgaria." Journal of the Hellenic Veterinary Medical Society 68, no. 3 (2018): 369. http://dx.doi.org/10.12681/jhvms.15493.

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The aim of this study is to estimate the histopathological changes in visceral organs of naturally infected with the avian influenza virus (AIV) subtype A H5N1 dalmatian pelicans in Bulgaria. The identified gross lesions are: haemorrhagic small intestine, sparse content in gizzard and proventriculus, well defined hyperemia of the tracheal mucosa associated with petechiae, as well as meningeal and brain congestion. The infected birds exhibited the following histopathological changes: edema of the tracheal mucosa with loss of mucosal glands, mild to moderate congestion with focal necrosis and multifocal non suppurative encephalitis and gliosis, mononuclear infiltration in the cecum, and diffuse mononuclear infiltration in the submucosa of the small intestine. The virus was detected by virus isolation (VI) and RT-PCR from tissue samples (lung, trachea, small intestine, brain, proventriculus, cloaca) from the infected birds.
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Barral, Marselha Marques, Maria Carmo Pereira Nunes, Marcia Melo Barbosa, Cid Sérgio Ferreira, Wilson Campos Tavares Júnior, and Manoel Otávio da Costa Rocha. "Echocardiographic parameters associated with pulmonary congestion in Chagas cardiomyopathy." Revista da Sociedade Brasileira de Medicina Tropical 43, no. 3 (2010): 244–48. http://dx.doi.org/10.1590/s0037-86822010000300006.

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INTRODUCTION: Discrepancy between the intensity of pulmonary congestion and the grade of cardiomegaly seems to be a common finding of Chagas cardiomyopathy, in spite of significant systolic dysfunction of the left ventricle. Its mechanism has not been established. The aim of this study was to investigate pulmonary congestion and to analyze if it correlated with Doppler echocardiographic parameters in patients with Chagas dilated cardiomyopathy. METHODS: Fifty-five patients with positive serology tests for Trypanosoma cruzi and Chagas dilated cardiomyopathy were studied. Chest x-rays, Doppler echocardiogram and plasmatic brain natriuretic peptide levels were obtained in all patients. The degree of pulmonary venous vessels changes on chest x-ray was graded using a pulmonary congestion score, and then compared to Doppler echocardiographic parameters. RESULTS: Mean age was 48.5 ± 11.2 years and 29% were women. The majority (95%) of patients were in NYHA functional class I and II. Mild pulmonary congestion by chest x-ray was found in 80% of the patients. In a multivariate analysis, left ventricular ejection fraction, right ventricular TEI index and the color M-mode velocity correlated with the degree of pulmonary congestion. CONCLUSIONS: Pulmonary venous changes on chest x-rays are frequent, but usually mild in patients with Chagas dilated cardiomyopathy. The degree of pulmonary congestion correlates with Doppler echocardiographic left and right ventricular dysfunction and with color M-mode velocity.
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Mišić, Bratislav, Olaf Sporns, and Anthony R. McIntosh. "Communication Efficiency and Congestion of Signal Traffic in Large-Scale Brain Networks." PLoS Computational Biology 10, no. 1 (2014): e1003427. http://dx.doi.org/10.1371/journal.pcbi.1003427.

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Dissertations / Theses on the topic "Brain – Congestion"

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Abboud, Sherine. "Susceptibility genes in ischemic stroke and intracranial atherosclerosis: clinical and autopsy studies." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210290.

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Stroke is the third leading cause of death and the most common cause of disability in the world. To relieve the heavy burden of stroke, we need to understand the mechanisms that will form the basis of improved prevention and treatment. Epidemiological studies have found evidence for a genetic influence on the common form of stroke. However the genetic of stroke is still in its infancy. Subclinical intracranial atherosclerosis is sometime a predisposing factor for ischemic stroke (IS). This study was carried out to elucidate genetic factors influencing the complex phenotype of IS and subclinical intracranial atherosclerosis.<p>In the Belgium Stroke Study (BSS), we collected 237 middle-aged (45-60 yrs) patients with small vessel occlusion (SVO) or large vessel atherosclerosis (LVA) IS, according to the Acute Stroke Treatment (TOAST) criteria, 326 ethnicity and gender matched subjects were used as controls. We tested variants in cholesterol-related candidate genes (sterol regulatory element binding protein, SREBP, SREBP-cleavage activating protein, SCAP, Apolipoprotein E, APOE, and Proprotein convertase subtilisin/kexin type 9, PCSKA) for association with IS. Significant gene-IS associations were further tested in a Finnish autopsy collection of 1004 cases with a quantitative assessment of atherosclerosis in the circle of Willis.<p>While we could not detect any significant association between polymorphisms in the SREBP and SCAP genes and IS, we found evidence for association at the APOE and PCSK9 loci. The APOE &949;4+ genotype was related to a more severe intracranial atherosclerosis score in men, and within the most common APOE &949;3/&949;3 genotype group a higher risk of IS was associated with the G-allele at the -219G/T promoter polymorphisms. At PCSK9, the minor allele (G) of the tagging E670G polymorphism appeared as a significant predictor of LVA (OR = 3.52, 95% CI 1.25-9.85; p = 0.017). Accordingly, in the Finnish autopsy series, G-allele carriers tended to have more severe allele copy number-dependent (p=0.095) atherosclerosis in the circle of Willis and in its branches. <p>Our findings in this unique combination of clinical and autopsy data suggest a multifaceted role of apoE on the risk of cerebrovascular diseases. The APOE &949;4+ genotype did not predict the risk of IS, but was associated with severity of subclinical intracranial atherosclerosis in men. In contrast, the promoter variants affecting apoE expression were significant predictors of IS, suggesting that quantitative rather than qualitative variation of apoE is related to IS independently of subclinical intracranial atherosclerosis. Furthermore, we demonstrated that PCSK9 associates with the risk of LVA stroke subtype, and suggest that the risk is related to the severity of the underlying intracranial atherosclerosis. <p>Atherogenesis is considered as an active, inflammatory process, interleukin (IL)-18 a proinflammatory cytokine, is thought to play a central role in the development of atherosclerosis and more specifically in plaque rupture. We genotyped four haplotype tagging polymorphisms at the IL18 gene in the BSS and the Finnish autopsy series. The minor alleles of the IL18 -607 and +127 polymorphisms, as well as the haplotype carrying both minor alleles, associated with IS after adjustment for all cardiovascular risk factors. No association was seen with the development of subclinical intracranial atherosclerosis. Our findings suggest that variation in the IL18 gene influences the acute atherosclerotic IS event, but not the previous development of subclinical intracranial atherosclerosis, suggesting a causal role of IL18 in the vulnerability of cerebral arterial atherosclerotic plaques to acute rupture and subsequent thrombosis. <p><p><br>Doctorat en Sciences médicales<br>info:eu-repo/semantics/nonPublished
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Sharma, Vibhu. "The clinical utility of daily B-type natriuretic peptide testing in patients admitted with acute exacerbations of congestive heart failure /." Access full-text from WCMC :, 2008. http://proquest.umi.com/pqdweb?did=1527840061&sid=12&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Neto, Felicio Savioli. "Efeitos de diferentes doses de um inibidor da ECA nas concentrações plasmáticas do peptídeo natriurético B, em idosos com insuficiência cardíaca." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-24102007-085514/.

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A Insuficiência cardíaca (IC), síndrome clínica que afeta predominantemente os idosos, caracteriza-se por graus variados de comprometimento hemodinâmico e contínua estimulação neuro-hormonal, com conseqüente redução da capacidade funcional e elevação nas concentrações plasmáticas do peptídeo natriurético B (PNB). Diversos ensaios clínicos demonstraram os benefícios dos inibidores da ECA na atividade neuro-hormonal e na capacidade funcional de pacientes com IC, com a magnitude desses efeitos proporcional à dose desses agentes. Entretanto, a sistemática exclusão dos idosos, observada na grande maioria desses estudos, tem questionado a validação e incorporação de tais resultados na população geriátrica. O objetivo deste estudo foi avaliar os efeitos de diferentes doses de quinapril, um inibidor da ECA com meia-vida biológica >24 horas, nas concentrações plasmáticas do PNB, nas distâncias percorridas no teste da caminhada de 6 minutos (TC-6 min) e na incidência de reações adversas, em idosos com IC sistólica. Métodos: Ensaio clínico, aberto, não randomizado e prospectivo. Foram avaliados, segundo os critérios de inclusão e exclusão, 30 pacientes (76,1 ± 5,3 anos; 15 homens e 15 mulheres) com IC classe funcional II-III (NYHA), com fração de ejeção ventricular esquerda < 40% (33,5 ± 4,5%), em uso de diuréticos (30), digoxina (24) e nitratos (13). As avaliações foram realizadas no momento da inclusão (condição basal) e a cada dois meses, com a adição de 10, 20, 30 e 40 mg de quinapril, e incluíam avaliações clínicas, exames bioquímicos, análises das concentrações plasmáticas do PNB e TC-6 min. Resultados: Completados oito meses de terapêutica com inibidor da ECA, as concentrações plasmáticas do PNB foram 67,4% menores em relação à condição basal: redução de 33,3% com a dose de 10 mg em relação à condição basal, 27,1% com 20 mg em relação à dose de 10 mg, 23,6% com 30 mg em relação à dose de 20 mg e 12,5% com 40 mg em relação à dose de 30 mg de quinapril, com p<0,005 em todas as comparações. Do mesmo modo, as distâncias percorridas no TC-6 min foram, em média, 64,9% maiores no final do estudo em relação à condição basal: aumento de 22,8% com a dose de 10 mg em relação à condição basal, 13,3% com 20 mg em relação à dose de 10 mg, 12,2% com 30 mg em relação à dose de 20 mg e 5,6% com 40 mg em relação à dose de 30 mg de quinapril, com p<0,005 em todas as comparações. Reações adversas graves, como hipotensão arterial associada a sintomas de baixo débito cerebral e/ou disfunção renal, não foram observadas, o que possibilitou o emprego da dose máxima de quinapril (40 mg/dia) em todos os pacientes, incluindo-se dois octogenários e dois nonagenários. Conclusão: Os resultados deste estudo demonstraram os benefícios da terapêutica com inibidores da ECA no perfil neuro-hormonal e na capacidade funcional de idosos com insuficiência cardíaca sistólica, bem como a relação positiva entre a dose e o efeito dos inibidores da ECA. Ademais, os sucessivos aumentos nas doses de quinapril não foram associados a reações adversas, possibilitando o emprego da dose máxima em todos os pacientes, incluindo-se dois octogenários e dois nonagenários.<br>Heart Failure (HF), a clinical syndrome that affects specially the elderly, is characterized by varied degrees of hemodinamic compromise and continuous neuro-hormonal stimulation, with consequent reduction of the functional capacity and elevation in the plasmatic concentrations of the natriuretic peptide B (BNP). Several clinical attempts showed the benefits of the ACE inhibitors in the neuro-hormonal activity and in the functional capacity of patients with HF, with the magnitude of those effects being proportional to the dose of the agents. However, the observed systematic exclusion of the elderly in the most of studies, has questioned the validation and the incorporation of such results in the geriatric population. The objective of this paper was the evaluation of the effects caused by different doses of quinapril, an ACE inhibitor with biological half-life> 24 hours, in the plasmatic concentrations of BPN, in the distances in the walk test of 6 minutes and in the incidence of adverse reactions in elderly with sistolic HF. Methods: prospective and not randomized study. 30 patients (76,1 ± 5,3 years; 15 men and 15 women with HF - class II-III (NYHA) - were evaluated, following the criteria of enclosure and exclusion, with ejection fraction of left ventricular <40% (33,5 ± 4,5%), in use of diuretics (30), digoxina (24) and nitrates (13). The evaluations were carried out in the moment of the enclosure (basic condition) and every other month, with the addition of 10 mg, 20 mg, 30 mg and 40 mg of quinapril. It was included clinical evaluations, biochemical exams, analyses of the BNP plasmatic concentrations and walk test of 6 minutes. Results: After eight months of treatment with the ACE inhibitor, the plasmatic concentrations of BNP were 67,4% smaller than the ones in the basic condition: reduction of 33,3% with the dose of 10 mg regarding the basic condition, 27,1% with 20 mg regarding the dose of 10 mg, 23,6% with 30 mg regarding the dose of 20 mg and 12,5% with 40 mg regarding the dose of 30 mg of quinapril, with p<0,005 in all the comparisons. In the same way, the distances in the walk test of 6 minutes were, on average, 64,9% bigger in the end of the study regarding the basic condition; there was the increase of 22,8% with the dose of 10 mg regarding the basic condition; 13,3% with 20 mg regarding the dose of 10 mg; 12,2% with 30 mg regarding the dose of 20 mg and 5,6% with 40 mg regarding the dose of 30 mg of quinapril, with p<0,005 in all the comparisons. Serious adverse reactions, as arterial hypotension associated to syncope and/or kidney dysfunction, were not observed, which made possible the use of the maximum dose of quinapril (40 mg/day) in all patients, including two octogenarians and two nonagenarians. Conclusion: The results of the study showed the benefits of the treatment with ACE inhibitors in the neuro-hormonal profile and in the functional capacity of elderly with sistolic heart failure, as well as the positive relation between the dose and the effect of the ACE inhibitors. Moreover, the successive increases in the doses of quinapril were not associated to adverse reactions, making possible the use of the maximum dose in all of the patients, including two octogenarians and two nonagenarians.
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Alehagen, Urban. "Heart failure in primary health care : special emphasis on natriuretic peptides in the elderly /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med819s.pdf.

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Ancheta, Irma B. "The relationship between B-type natriuretic peptide levels and hospital length of stay and quality of life in congestive heart failure patients." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001871.

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Books on the topic "Brain – Congestion"

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M, Tomita, ed. Cerebral hyperemia and ischemia, from the standpoint of cerebral blood volume: Proceedings of the statellite symposium, Brain Section, Fourth World Congress for Microcirculation, Osaka, Japan, 1-2 August 1987. Excerpta Medica, 1988.

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(Editor), T. Sawada, H. Naritomi (Editor), and W. D. Heiss (Editor), eds. Cerebral Circulation (International Congress). Elsevier, 1988.

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Baloh, Robert W. Ménière Recognizes That Vertigo Can Originate from the Inner Ear. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190600129.003.0002.

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Prosper Ménière was the first clinician to conclude that vertigo can result from diseases of the inner ear. The symptom of vertigo originally fell under the rubric of apoplectiform cerebral congestion, a disorder thought to result from overfilling of blood vessels in the brain. Ménière noted that patients with vertigo and hearing loss associated with damage to the inner ear often have a benign course, and aggressive treatments such as bleeding can be more dangerous than the underlying disease. The first hint that the semicircular canals may be related to balance rather than hearing was provided by a Frenchman, Marie Jean Pierre Flourens. He systematically cut each semicircular canal in the pigeon and noted that the animal’s head and body tended to move in the plane of the damaged canal. The gyrations of the animals described by Flourens made Ménière think that vertigo in humans might be a similar phenomenon.
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Book chapters on the topic "Brain – Congestion"

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Takeuchi, Satoru, Hiroshi Nawashiro, Kojiro Wada, et al. "Cerebrospinal Fluid Congestion in the Perioptic Space." In Brain Edema XV. Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1434-6_40.

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Li, Jie Jack. "Cholesterol." In Triumph of the Heart. Oxford University Press, 2009. http://dx.doi.org/10.1093/oso/9780195323573.003.0007.

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The story of statins starts with cholesterol because statins are a class of drugs that reduce low-density lipoprotein (LDL) cholesterol, the “bad” cholesterol. LDL cholesterol, in turn, is a major risk factor for coronary heart disease, the leading cause of death worldwide and projected to remain so through 2025. About 1.5 million Americans suffer heart attacks each year, and heart disease has emerged as the biggest cause of death in the United States, killing 911,000 people in 2003. Before the 1940s, the average lifespan in America was 47 years, and heart disease did not contribute to mortality to a large extent because people often died of infections. Currently, an average American lives to celebrate her 77th birthday. As a consequence, heart-related disease has risen to be the number one killer. Coronary heart disease manifests in many forms: angina, arrhythmia, atrial fibrillation, congestive heart failure, hypertension, atherosclerosis, myocardial infarction (heart attack), and sudden cardiac death. Atherosclerosis, or blockage in arteries, results when a buildup of cholesterol, inflammatory cells, and fibrous tissue called plaques forms on an artery wall. If these plaques rupture, they can block blood flow to critical organs such as the heart or brain and can lead to heart attack or stroke. Despite the many different forms of cardiovascular disease, the molecule cholesterol is a common denominator for most of them. Therefore, in order to understand coronary heart disease, we first need to take a look at the cholesterol molecule. According to Roman mythology, Janus is the guardian of portals and patron of beginnings and endings. Just like the two-faced Roman god, cholesterol is a double-edged sword for the human body. On the one hand, it is an essential building block for many crucial ingredients the body needs. On the other hand, it can be lethal when it forms plaques on the surface of the arteries and subsequently causes coronary heart disease. Make no mistake, cholesterol is vital to our existence. It is most abundant in our brains—23% of total body cholesterol resides there, making up 1/10th of the solid substance of the brain.
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Sinharay, Ricky. "Radiology." In Oxford Assess and Progress: Clinical Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198812968.003.0021.

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You have teased out the history, elicited the signs, and generated a list of differential diagnoses— now to confirm your suspicions, by selecting an appropriate radiological investigation. From the ubiquitous chest X-ray for diagnosing community- acquired pneumonia or congestive cardiac failure to an urgent computed tomography (CT) scan of the brain to confirm a suspected subarachnoid haemorrhage, radiological investiga­tions are an essential (if sometimes overused) resource for diagnosing disease. When working in the acute hospital setting, some knowledge and experience in interpreting X- rays and some types of CT imaging are important in order to ensure your patient is managed correctly and quickly. Going back to basic principles and using your hard- learnt anatomy will set you in good stead when looking at both X- rays and cross- sectional imaging. This chapter has been written to expose you to clinical situations where imaging is required to make a diagnosis or to make a decision on patient management. As well as this, I hope the questions in this chapter will help you think about what the correct modality of imaging to request would be to investigate pathology in the various body systems. For instance, an ultrasound of the liver may be more useful to assess liver cirrhosis than a CT scan (as well as preventing exposures to high- dose radiation). And again, in practice, if there is any doubt about the result of a radiological investigation, or indeed which type of investigation to request, your local radiologist would be more than happy to help.
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4

Li, Jie Jack. "Cardiovascular Drugs: From Nitroglycerin to Lipitor." In Laughing Gas, Viagra, and Lipitor. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195300994.003.0008.

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Cardiovascular diseases are the leading cause of death worldwide and are projected to remain in the lead through 2025. Heart-related diseases include angina, arrhythmia, atrial fibrillation, congestive heart failure, hypertension, atherosclerosis, myocardial infarction (heart attack), and sudden cardiac death. More than 300,000 Americans suffer sudden heart attacks each year. In addition, one of the more important recently identified drug-induced cardiac events, which has occasionally resulted in drugs being withdrawn, is drug-induced torsade des pointes. This is a rare, fatal arrhythmia that has been associated with some drugs that prolong the QT interval of the electrocardiogram (ECG). Hypertension is America’s number one chronic disease. Fifty million Americans, one in six, suffer from high blood pressure. Similarly, high blood pressure affects about one-sixth of the world’s population (1 billion people) worldwide—mostly in the developed world. If uncontrolled, it can lead to heart attack, heart failure, stroke, and other potentially fatal events. Great strides have been made during the past 50 years in conquering cardiovascular diseases. Cardiopulmonary resuscitation (CPR) was developed by a group of researchers at the Johns Hopkins University in 1961. The 1960s also saw the emergence of beta-blockers. Calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, and statins appeared in the 1980s and the 1990s. Angiotensin II receptor blockers (ARBs) also emerged in the 1990s. The heart, about the size of a person’s fist, beats about 2.8 billion times in a lifetime, pumping blood and oxygen through the body. Although its function was shrouded in mystery for centuries, mankind has come a long way in understanding how the heart works anatomically and physiologically, although we haven’t made much progress in understanding its “emotional” nature. Greek philosopher and anatomist Aristotle (384–322 B.C.) was the founder of biology. He was very interested in human and animal anatomy, especially the cardiovascular systems in higher animals. In his books he described, for the first time, the human blood system with an emphasis on the deeper-lying vessels. He incorrectly believed that the heart was the organ in which emotions were generated, whereas the function of the brain was to cool the blood. More than 500 years later, the German-born Roman physician Galen (130–200 A.D.) made two revolutionary discoveries about the cardiovascular system.
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Conference papers on the topic "Brain – Congestion"

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Xiaoqian, Li, He Jiancheng, Fu Deyu, Shen Lin, Hu Dongpei, and Cao Xuebin. "Correlative study on TCM syndromes of congestive heart failure, cardiac function and brain natriuretic peptide." In 2013 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2013. http://dx.doi.org/10.1109/bibm.2013.6732648.

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Tong, K., T. Colburn, and P. Brauer. "E-103 Short-term in-hospital outcomes of thrombolysis for acute ischemic stroke patients with non-primary brain tumors and congestive heart failure." In SNIS 16TH ANNUAL MEETING. BMJ Publishing Group Ltd., 2019. http://dx.doi.org/10.1136/neurintsurg-2019-snis.178.

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