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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1932, Horton, Magath and Brown reported two cases of a "new form of arteritis affecting the temporal vessels ... which probably represents a new clinical syndrome". In reality, several publications, devoted to the same pathology already preceded this article. The most ancient is that of an ophthalmologist from Baghdad, Ali Ibn Isa (940 to 1010). In his memories, translated and published in english in 1936, the author states that "he undertook excision and cauterisation of arteries to treat patients who were suffering from heat and inflammation of their temporal muscles and which sometimes ended in loss of vision ...". In 1890, J. Hutchinson, an English surgeon, reported a case "... of inflammed and swollen temporal arteries ...". This article was only brought to light in 1946. In 1930, M. Schmidt, published a probable case of temporal arteritis, subsequently reported in 1947. In 1934 and 1936, Horton published new cases of temporal arteritis and defined the clinical characteristics of the disease and its histology. In 1938, Jennings made a particular contribution in reporting the first case of blindness. From this time on, cases of temporal arteritis became increasingly common in the literature. The first French case was described by J. Paviot et al. in 1934, but remained largely unrecognized until 1942. In 1936, J. Chavany was the first to describe the pillow sign, but more particularly in 1948, he prescribed the first treatment with steroids, with spectacular results. It was only in 1950 that R.M. Shick et al. published the effects of steroid therapy in temporal arteritis.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mal Vasc 1989
PMID:[The history of Horton's disease or ... 10 centuries of a fascinating adventure]. 269 72

The purpose of study was to investigate the role of angiotensin II in idiopathic primary aldosteronism (IPA) and to evaluate the interest of angiotensin converting enzyme inhibitors (ACEI) in its management. The study concerned 10 hypertensive patients, mean 49 +/- 11 years with idiopathic primary aldosteronism due to bilateral adrenal hyperplasia: plasma renin activity (PRA) less than 1.5 ng/ml/h and plasma aldosterone (PA) greater than 25 ng/100 ml. Adrenal venography and adrenal vein aldosterone levels demonstrated bilateral hyperplasia. PRA and PA were evaluated in recumbent position, then after 4 hours in upright posture. The next day, a "captopril screening test" was performed with PA assays before and three hours after a single oral administration of captopril (1 mg/kg). Upright PRA and PA were slightly increased and acute administration of captopril reduced significantly PA levels in all patients. Blood pressure (BP was unmodified under captopril. These hormonal results demonstrated that adrenal glomerulosa remained sensitive to low concentrations of angiotensin II, and underlined the potential interest of ACEI in the management of IPA. Brown R. demonstrated already an increase of adrenal sensitivity to angiotensin II infusions, and isolated an aldosterone-stimulating factor (ASF). Plasma aldosterone levels were related to increased ASF concentrations but there was no link between PRA and ASF. Carey R. suggested that ASF acts through an increase of the sensitivity of aldosterone production to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Influence of angiotensin on the secretion of aldosterone in idiopathic hyperaldosteronism]. 311

Genetically hypertensive rats of the Lyon strain (LH) associate high blood pressure (BP), exaggerated salt-sensitivity, and a metabolic syndrome made of overweight together with increased plasma lipids and insulin/glucose ratio. A genetic mapping study in a large population of F2 rats derived from a cross between hypertensive (LH) and normotensive rats (LN) showed the existence, on chromosome 17, of two clusters of Quantitative Traits Loci (QTLs). The first one was associated to morphological parameters whereas the second influenced blood pressure and plasma lipids level. In order to determine the functional importance of this QTLs, we generated a consomic strain LH-17BN in which the LH chromosome 17 has been fully substituted by a normotensive Brown Norway (BN) one. These LH-17BN, as well as LH and BN male rats of the parental strain were phenotyped. This included radio telemetric measurement of BP during normal and elevated salt intake (1% and then 2% in the drinking water) as well as the determination of morphological, metabolic (triglycerides, cholesterol) and renal (creatinine clearance, proteinuria) parameters. LH-17BN, compared to LH rats, exhibited significant decreases in body weight and blood pressure. Renal functions are improved (decreased of proteinuria). Finally, plasma triglycerides were reduced and reach the level observed in BN rats. In conclusion, the present work demonstrates that, in our model, chromosome 17 contains genes which influence morphology, blood pressure, renal function, and lipid metabolism. Interestingly, chromosome 17 almost completely explains the spontaneous hypertriglyceridemia observed in Lyon Hypertensive rats.
Arch Mal Coeur Vaiss 2007 Aug
PMID:[Importance of chromosome 17 in genetically hypertensive rats of the Lyon strain (LH): study of a consomic strain]. 1792 82

Mal de debarquement (MdD), the "sickness of disembarkment," occurs when habituation to background rhythmic movement becomes resistant to readaption to stable conditions and results in a phantom perception of self motion typically described as rocking, bobbing, or swaying. Although several studies have shown that brief periods of MdD are common in healthy individuals, this otherwise natural phenomenon can become persistent in some individuals and lead to severe balance problems. Increased recognition of MdD in a persistent pathological form occurred after the publication of a case series of six patients by Brown and Baloh in 1987. Over 20 years later, although more is known about the clinical syndrome of persistent MdD, little is known about what leads to this persistence. This review addresses the clinical features of MdD, the associated symptoms in the persistent form, theories on pathogenesis, experience with treatment, and future directions for research.
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PMID:Mal de debarquement. 1983 63

Newcastle disease virus (NDV) is a highly contagious avian pathogen that poses a tremendous threat to poultry producers in endemic zones due to its epidemic potential. To investigate host genetic resistance to NDV while under the effects of heat stress, a genome-wide association study (GWAS) was performed on Hy-Line Brown layer chickens that were challenged with NDV while under high ambient temperature to identify regions associated with host viral titer, circulating anti-NDV antibody titer, and body weight change. A single nucleotide polymorphism (SNP) on chromosome 1 was associated with viral titer at two days post-infection (dpi), while 30 SNPs spanning a quantitative trait loci (QTL) on chromosome 24 were associated with viral titer at 6 dpi. Immune related genes, such as CAMK1d and CCDC3 on chromosome 1, associated with viral titer at 2 dpi, and TIRAP, ETS1, and KIRREL3, associated with viral titer at 6 dpi, were located in two QTL regions for viral titer that were identified in this study. This study identified genomic regions and candidate genes that are associated with response to NDV during heat stress in Hy-Line Brown layer chickens. Regions identified for viral titer on chromosome 1 and 24, at 2 and 6 dpi, respectively, included several genes that have key roles in regulating the immune response.
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PMID:Genetics and Genomic Regions Affecting Response to Newcastle Disease Virus Infection under Heat Stress in Layer Chickens. 3066 51

Newcastle disease (ND) is a global threat to domestic poultry, especially in rural areas of Africa and Asia, where the loss of entire backyard local chicken flocks often threatens household food security and income. To investigate the genetics of Ghanaian local chicken ecotypes to Newcastle disease virus (NDV), in this study, three popular Ghanaian chicken ecotypes (regional populations) were challenged with a lentogenic NDV strain at 28 days of age. This study was conducted in parallel with a similar study that used three popular Tanzanian local chicken ecotypes and after two companion studies in the United States, using Hy-line Brown commercial laying birds. In addition to growth rate, NDV response traits were measured following infection, including anti-NDV antibody levels [pre-infection and 10 days post-infection (dpi)], and viral load (2 and 6 dpi). Genetic parameters were estimated, and two genome-wide association study analysis methods were used on data from 1,440 Ghanaian chickens that were genotyped on a chicken 600K Single Nucleotide Polymorphism (SNP) chip. Both Ghana and Tanzania NDV challenge studies revealed moderate to high (0.18 - 0.55) estimates of heritability for all traits, except viral clearance where the heritability estimate was not different from zero for the Tanzanian ecotypes. For the Ghana study, 12 quantitative trait loci (QTL) for growth and/or response to NDV from single-SNP analyses and 20 genomic regions that explained more than 1% of genetic variance using the Bayes B method were identified. Seven of these windows were also identified as having at least one significant SNP in the single SNP analyses for growth rate, anti-NDV antibody levels, and viral load at 2 and 6 dpi. An important gene for growth during stress, CHORDC1 associated with post-infection growth rate was identified as a positional candidate gene, as well as other immune related genes, including VAV2, IL12B, DUSP1, and IL17B. The QTL identified in the Ghana study did not overlap with those identified in the Tanzania study. However, both studies revealed QTL with genes vital for growth and immune response during NDV challenge. The Tanzania parallel study revealed an overlapping QTL on chromosome 24 for viral load at 6 dpi with the US NDV study in which birds were challenged with NDV under heat stress. This QTL region includes genes related to immune response, including TIRAP, ETS1, and KIRREL3. The moderate to high estimates of heritability and the identified QTL suggest that host response to NDV of local African chicken ecotypes can be improved through selective breeding to enhance increased NDV resistance and vaccine efficacy.
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PMID:Genetic Basis of Response of Ghanaian Local Chickens to Infection With a Lentogenic Newcastle Disease Virus. 3284 79