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Background: The upright posture imposes a significant challenge to blood pressure regulation that is compensated through baroreflex-mediated increases in heart rate and vascular resistance. Orthostatic cardiac responses are easily inferred from heart rate, but vascular resistance responses are harder to elucidate. One approach is to determine vascular resistance as arterial pressure/blood flow, where blood flow is inferred from ultrasound-based measurements of brachial blood velocity. This relies on the as yet unvalidated assumption that brachial artery diameter does not change during orthostatic stress, and so velocity is proportional to flow. It is also unknown whether the orthostatic vascular resistance response is related to initial blood vessel diameter. Methods: We determined beat-to-beat heart rate (ECG), blood pressure (Portapres) and vascular resistance (Doppler ultrasound) during a combined orthostatic stress test (head-upright tilting and lower body negative pressure) continued until presyncope. Participants were 16 men (aged 38.4±2.3 years) who lived permanently at high altitude (4450m). Results: The supine brachial diameter ranged from 2.9–5.6mm. Brachial diameter did not change during orthostatic stress (supine: 4.19±0.2mm; tilt: 4.20±0.2mm; -20mmHg lower body negative pressure: 4.19±0.2mm, p = 0.811). There was no significant correlation between supine brachial artery diameter and the maximum vascular resistance response (r = 0.323; p = 0.29). Forearm vascular resistance responses evaluated using brachial arterial flow and velocity were strongly correlated (r = 0.989, p<0.00001) and demonstrated high equivalency with minimal bias (-6.34±24.4%). Discussion: During severe orthostatic stress the diameter of the brachial artery remains constant, supporting use of brachial velocity for accurate continuous non-invasive orthostatic vascular resistance responses. The magnitude of the orthostatic forearm vascular resistance response was unrelated to the baseline brachial arterial diameter, suggesting that upstream vessel size does not matter in the ability to mount a vasoconstrictor response to orthostasis. [ABSTRACT FROM AUTHOR]

Many world-renowned scientists and artists had autism spectrum disorder (ASD). We suggest that the French mathematician and physicist Blaise Pascal (1623-1662) also had ASD. As a boy, he demonstrated his mastery of language, mathematics and science. He showed single-mindedness and obsessive interests in the pursuit of science in his younger years and later he pursued with religion with the same determination. Pascal neglected social interactions; he was cold and aloof and had an obsessive revulsion to any expression of emotional attachment. As shown by his funerary mask and the autopsy report Pascal had craniosynostosis (primary nonsyndromic oxycephaly) with atrophy of the right half of the face. Congenital facial asymmetry due to craniosynostosis has a genetic basis. This suggests that Pascal's facial deformity may betray his propensity to suffer from genetically determined diseases including ASD. Despite the intrinsic limitations of a diagnosis based only on biographical information, we surmise that Pascal had the three key symptoms (obsessive interests, difficulty in social relationship and problems in communicating) that characterize ASD individuals. [ABSTRACT FROM AUTHOR]

On October 17, 1849, Poland's greatest composer, Frédéric Chopin (1810-1849) died aged 39. His cause of death remains unknown. An investigation of the documental sources was performed to reconstruct the medical history of the artist. Since his earliest years, his life had been dominated by poor health. Recurrent episodes of cough, fever, headaches, lymphadenopathy- a series of symptoms that may be attributed to viral respiratory infections- manifested in his teens. Later in life, he had chest pain, hemoptysis, hematemesis, neuralgia, and arthralgia. Exhaustion and breathlessness characterized all his adult life. Coughing, choking, and edema of the legs and ankles manifested four months before his death. Several hypotheses ranging from cystic fibrosis to alpha-1 anti-trypsin deficiency and pulmonary tuberculosis have been proposed to explain Chopin's lifelong illness. We suggest that Chopin had dilated cardiomyopathy with consequent heart failure and cirrhosis that caused his death. [ABSTRACT FROM AUTHOR]

A1AT deficiency- a genetically inherited autosomal codominant disease with more than 120 identified alleles- was first identified by Laurell and Eriksson in 1963. The most common hereditary disorder in adults, A1AT causes an increased risk of developing pulmonary emphysema and liver disease. In A1AT patients, lung disease generally presents at a younger age than “usual” chronic obstructive pulmonary disease (COPD) and it may be misdiagnosed as asthma. Because A1AT deficiency patients can show the same clinical features as non-deficient COPD (including increased evidence of bronchiectasis, frequent exacerbations, impaired health status and a degree of reversibility of airflow obstruction), the World Health Organization recommend to test every patient with a diagnosis of COPD or adult-onset asthma for A1AT deficiency. Despite these recommendations, the epidemiology of A1AT deficiency remains uncertain. Although recently discovered A1AT deficiency has affected human populations since antiquity. By using scientific data and recently studied skeletons and historical cases, we show that it is now possible to reconstruct the natural history of pathological processes, whether due to genetic, infectious or environmental factors. We believe that the evolution of disease in patients and research to elucidate the relationship between social science and environmental are pertinent contemporaneous subjects. [ABSTRACT FROM AUTHOR]

Aim Interval hypoxic training was proposed as a technique for adapting hypoxia of various origins. Its effects on the hypoxic ventilatory response and on cardiovascular autonomic control are unknown.Methods and Results We recorded ventilation, end-tidal oxygen (PETO2) and carbon dioxide partial pressures, RR interval and blood pressure during progressive isocapnic hypoxia, before and after 14 days of: (a) interval hypoxic training (three to four periods of 7min progressive hypoxia in 1h, each day) in 12 healthy men (training group); (b) breathing into a spirometer by six age-matched male controls. The hypoxic ventilatory response was estimated by the hyperbolic relationship between PETO2and ventilation (shape factor A). Spectral analysis was used to characterize low- (mainly sympathetic) and high-frequency (vagal) cardiovascular fluctuations. Shape factor A was increased in the interval hypoxic training group from 268±59 to 984±196 l.mmHg−1(P<0·003), but not in the control group (from 525±180 to 808±245 l.mmHg−1,P =ns). Before interval hypoxic training, progressive hypoxia decreased, to a similar extent in both groups, mean RR, RR variability and high-frequency power. After interval hypoxic training, RR still decreased significantly, but the decrease in RR variability and high-frequency power was no longer significant in the training group. No significant changes were observed in blood pressure fluctuations. No changes were observed in the control group.Conclusions Two weeks of interval hypoxic training increased the hypoxic ventilatory response, in association with reduced vagal withdrawal during progressive hypoxia. [ABSTRACT FROM PUBLISHER]

White rami communicantes were studied quantitatively in patients with chronic alcoholism or diabetes mellitus. The fascicular area of interganglionic segments of the paravertebral sympathetic chain showed less variation than that previously reported for controls. Fibre densities were higher in the patients than in controls of similar age and the percentage of small fibres in alcoholics and diabetics is larger than in controls. Only 17% of fibres were larger than 5 μm in diameter in the patients, whereas, in controls, 33% of fibres were larger than 5 μm in diameter. No correlation between internodal lengths and fibre diameter was found in the patients who showed uniformly short internodes averaging only about half of internodal distances found in control subjects. The uniformly short internodes are attributed to complete degeneration followed by partial regeneration and are compatible with either Wallerian degeneration or a `dying back' phenomenon. The short internodal lengths should be reflected in slowed conduction velocities in white rami communicantes and could account for abnormalities in baroreflex activity, sweating, and in visceral dysfunction commonly seen in patients with chronic alcoholism or diabetes. [ABSTRACT FROM AUTHOR]