268 research outputs found

    Effects of Yohimbine and Tolazoline on Isoproterenol and Angiotensin 2-Induced Water Intake in Rats

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    Subcutaneous administration of the alpha(sub 2)-adrenoreceptor antagonists, yohimbine and tolazoline, at doses up to 1000 micro-g/kg, had no effect on water intake of female rats. However, when these compounds were administered SC in combination with either the beta-adrenoreceptor agonist, isoproterenol (10 to 25 micro-g/kg, SC), or with angiotensin 2 (200 micro-g/kg, SC). water intake was enhanced. In contrast, intraventricular administration of either tolazoline (10 and 20 micro-g/kg) or yohimbine (300 micro-g/kg) failed to augment the dipsogenic response to angiotensin 2 (150 micro-g/kg, SC). Thus, the enhancing effect of these alpha(sub 2)-adrenoreceptor antagonists on isoproterenol- and angiotensin 2-induced water intakes appears to be manifested peripherally, rather than centrally. In view of the fact that clonidine, an alpha(sub 2)-adrenoreceptor agonist, has been shown to inhibit water intake induced by both isoproterenol and angiotensin 2, the results suggest that the alpha(sub 2)-adrenoreceptor may play a role in modulating water intake induced by these two dipsogenic agents

    Tackling the Dual Economic and Public Health Crises Caused by Covid-19 in Baltimore: Early Lessons from the Baltimore Health Corps Pilot

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    On March 12, 2020, the first case of Covid-19 was diagnosed in Baltimore City. Its infection rate increased rapidly through March and into April and May, proving to be 4 times higher among Latino residents and 1.5 times higher among Black residents than the city's White population. At the same time, the city's unemployment rate surged from 4.9 percent in March to a peak of 11.6 percent in April 2020. In June, The Rockefeller Foundation supported the Baltimore City government in launching the Baltimore Health Corps (BHC), a pilot program to recruit, train, and employ 275 new community health workers who were unemployed, furloughed, or underemployed, living in neighborhoods hardest hit by the health crisis and especially those residents unemployed as a result of Covid-19. BHC used equitable recruitment and hiring practices to employ contact tracers, care coordinators, and support staff, with a focus on good jobs, fair pay, training, skill-building, and support to improve career trajectories. This report, compiling data and interviews midway through the project, is a look at some of the early successes and the challenges ahead

    Clinical and pathophysiologic spectrum of acquired distal renal tubular acidosis

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    Clinical and pathophysiologic spectrum of acquired distal renal tubular acidosis. Urinary acidification was studied in nine patients with hyper-chloremic metabolic acidosis. The aim of this study was to investigate the mechanism(s) of impaired distal acidification by the systematic administration of sodium sulfate and neutral phosphate. No impairment of proximal acidification was apparent because all patients had a fractional bicarbonate excretion below 5% at plasma bicarbonate concentrations above 22 mEq/liter. All patients except two were unable to lower urine pH below 5.5 despite systemic metabolic acidosis. The two patients who lowered urine pH normally were hyperkalemic and had selective aldosterone deficiency. Six patients failed to lower the urine pH below 5.5 with sodium sulfate (6.04 ± 0.16) and were unable to achieve a normal urine minus blood (U-B) Pco2 gradient with neutral phosphate (2.8 ± 3.5mm Hg). Control subjects, the two patients with selective aldosterone deficiency, and the remaining patient lowered the urine pH below 5.5 and increased the U-B Pco2 gradient above 25mm Hg in response to sodium sulfate and neutral phosphate infusion, respectively. The abnormal response to these agents exhibited by six patients strongly suggests that the mechanism of impaired distal acidification was that of secretory failure of the proton pump. The normal response of the remaining three patients indicates that the proton pump was able to secrete hydrogen ions normally under maximal stimulation. This pattern is totally predictable in patients with isolated selective aldosterone deficiency who are also capable of lowering the urine pH normally in the presence of systemic metabolic acidosis. The distinctive acidification pattern of the remaining patient who was also hyperkalemic can be explained on the basis of a voltage-dependent type of distal renal tubular acidosis. This type may be disclosed by the findings of impairment of both hydrogen ion and potassium secretion.Aspects clinique et physiopathologique de l'acidose tubulaire distale acquise. L'acidification urinaire a été étudiée chez neuf malades ayant une acidose métabolique hyperchlorémique. Le but de ce travail était d'étudier le mécanisme de l'altération de l'acidification distale par l'administration de sulfate de sodium et de phosphate neutre. Il n'est pas apparu d'altération de l'acidication proximale puisque tous les malades avaient une excrétion fractionnelle de bicarbonate inférieure à 5% à des concentrations de bicarbonate plasmatique supérieures à 22 mEq/litre. Tous les malades sauf deux étaient incapables d'abaisser leur pH urinaire au dessous de 5,5 malgré l'acidose métabolique. Les deux malades qui abaissaient le pH de l'urine à des valeurs normales étaient hyperkaliémiques et avaient un déficit sélectif d'aldostérone. Six malades n'ont pu abaisser leur pH urinaire en dessous de 5,5 avec le sulfate de sodium (6,04 ± 0,16) et ont été incapables de réaliser un gradient de Pco2 normal urine-sang sous phosphate neutre (2,8 ± 3,5mm Hg). Les sujets contrôles, les deux malades ayant un déficit d'aldostérone et le dernier malade ont abaissé le pH de l'urine au dessous de 5,5 et augmenté le gradient de Pco2 à plus de 25mm Hg en réponse aux administrations de sulfate de sodium et de phosphate neutre, respectivement. La résponse anormale des six malades suggère fortement que le mécanisme de l'altération de l'acidification distale est un défaut de fonctionnement de la pompe à protons. La réponse normale des trois derniers malades indique que la pompe était capable de sécréter des ions hydrogène dans des conditions de stimulation maximales. Cette modalité est prévisible chez les malades qui ont un déficit sélectif et isolé d'aldostérone et qui sont aussi capables d'abaisser le pH de leur urine en présence d'une acidose métabolique systémique. La modalité d'acidification particulière du dernier malade qui était en même temps hyperkaliémique peut être expliquée par un mécanisme dépendant de la différence de potentiel. Cette situation peut être reconnue par la constatation d'un désordre portant à la fois sur la sécrétion de ions hydrogène et celle de potassium

    Group CBT for men with intellectual disabilities and/or autism who have harmful sexual behaviour

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    Objectives: Men with intellectual disabilities and/or autism sometimes engage in harmful sexual behaviour (HSB), but it may be harder for them to access treatment, than it is for non‐disabled men. The aim of this study was to evaluate the effect of attending an adapted CBT group, known as SOTSEC‐ID, on men with intellectual disabilities and/or autism who had HSB. Method: Ninety‐eight men from intellectual disability services, who had ID and/or autism and a history of HSB were recruited, and they received group CBT for a year (46 of these men have been previously reported). Harmful sexual behaviour, sexual knowledge, distorted cognitions and victim empathy were measured before and after treatment, and at 6 month follow‐up. Results: There were low levels of further harmful sexual behaviour: 12% of men engaged in further HSB during the 1‐year period of the group, and 8% engaged in further HSB in the 6‐month follow‐up period. There were also significant improvements in sexual knowledge, distorted cognitions and victim empathy following treatment, maintained at 6‐month follow‐up. Men with autism showed significantly more non‐contact HSB, were less likely to have been interviewed by police and had higher rates of further HSB, compared to men without autism. Conclusions: It is concluded that SOTSEC‐ID is a promising treatment for men with ID/autism and HSB. Nevertheless, the study had a number of limitations and lacked a control group, so there is now an urgent need for a proper controlled study

    Effect of Arteriovenous Anastomosis on Blood Pressure Reduction in Patients With Isolated Systolic Hypertension Compared With Combined Hypertension

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    Background: Options for interventional therapy to lower blood pressure (BP) in patients with treatment‐resistant hypertension include renal denervation and the creation of an arteriovenous anastomosis using the ROX coupler. It has been shown that BP response after renal denervation is greater in patients with combined hypertension (CH) than in patients with isolated systolic hypertension (ISH). We analyzed the effect of ROX coupler implantation in patients with CH as compared with ISH. Methods and Results: The randomized, controlled, prospective ROX Control Hypertension Study included patients with true treatment‐resistant hypertension (office systolic BP ≥140 mm Hg, average daytime ambulatory BP ≥135/85 mm Hg, and treatment with ≥3 antihypertensive drugs including a diuretic). In a post hoc analysis, we stratified patients with CH (n=31) and ISH (n=11). Baseline office systolic BP (177±18 mm Hg versus 169±17 mm Hg, P=0.163) and 24‐hour ambulatory systolic BP (159±16 mm Hg versus 154±11 mm Hg, P=0.463) did not differ between patients with CH and those with ISH. ROX coupler implementation resulted in a significant reduction in office systolic BP (CH: −29±21 mm Hg versus ISH: −22±31 mm Hg, P=0.445) and 24‐hour ambulatory systolic BP (CH: −14±20 mm Hg versus ISH: −13±15 mm Hg, P=0.672), without significant differences between the two groups. The responder rate (office systolic BP reduction ≥10 mm Hg) after 6 months was not different (CH: 81% versus ISH: 82%, P=0.932). Conclusions: Our data suggest that creation of an arteriovenous anastomosis using the ROX coupler system leads to a similar reduction of office and 24‐hour ambulatory systolic BP in patients with combined and isolated systolic hypertension. Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01642498
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