Background: Planning for neurology training necessitated a reflection on the experience of graduates. We explored practice characteristics, and training experience of recent graduates. Methods: Graduates from 2010-2014 completed a survey. Results: Response rate was 37% of 211. 56% were female. 91% were adult neurologists. 65% practiced in an outpatient setting. 63% worked in academics. 85% completed subspecialty training (median 1 year). 36% work 3 days a week or less. 82% took general call (median 1 night weekly). Role preparation was considered very good or excellent for most; however poor or fair ratings were 17% in advocacy and 8% in leadership. Training feedback was at least “good” for 87%. Burnout a few times a week or more was noted by 5% (6% during residency, particularly PGY1 and 5). 64% felt overly burdened by paperwork. Although most felt training was adequate, it was poor or fair at preparing for practice management (85%) and personal balance (55%). Most conditions were under-observed in training environment. Many noted a need for more independent practice development and community neurology. Conclusions: Although our training was found to be very good, some identified needs included advocacy training, and more training in general neurology in the longitudinal outpatient/community settings.
Observations were made in eight cases of complete heart block; and the findings in five cases, admitted previously to Bellevue Hospital, were used as material. Over 300 electrocardiographic tracings of one minute duration were analyzed. Epinephrine was selected as a stimulant for the sympathetic end apparatus in the heart. Subcutaneous doses of 1 to 2 mg. increased the ventricular rate considerably. This increase persisted from 15 minutes to several hours. The auricular rate and the blood pressure showed no, or moderate, increase. Change in the auricular rate did not go parallel, as a rule, with the change in the ventricular rate. The experimental findings suggest that the ventricles have direct and rich sympathetic nerve supply. Atropine sulfate was administered in doses of 5.0 mg. and 3.5 mg. respectively. The results of these observations indicate that the influence of the vagus on the sinus node is the same in complete heart block as in normal individuals. The effect of atropine on the auricular rate lasted over three hours. The maximal increase was reached as early as 10 minutes and as late as 50 minutes after the injection. The ventricular rate was slightly but distinctly increased, indicating that the vagus exerts a slight inhibitory influence on the ventricles in complete block. If a certain amount of epinephrine, which increased the ventricular but not the auricular rate, was given after the vagus had been paralyzed; there was an increase in the rates of both the auricules and the ventricles. Following and probably during exercise there was a marked increase in the auricular rate. The ventricles showed but slight increase as late as 15 to 25 minutes after exercise.
The effects of systemic treatment with the AT1 receptor antagonist telmisartan on central effects of angiotensin II (Ang II), namely, increase in blood pressure, vasopressin release into the circulation, and drinking response, were investigated in conscious, normotensive rats. The central responses to i.c.v. Ang II (30 ng/kg) were measured at 0.5, 2, 4, and 24 h following acute i.v. or acute and chronic oral telmisartan application. At a dose of 10 mg/kg i.v., the drinking response to i.c.v. Ang II was completely blocked over 4 h, while the pressor response and the release of vasopressin in response to i.c.v. Ang II were blocked by 60 to 80%. The inhibition of the centrally mediated pressor and drinking response to Ang II was sustained over 24 h. The lower doses of telmisartan (0.3 and 1 mg/kg) significantly inhibited the Ang II-induced actions over 4 h. A consistent 24-h inhibition of the central responses to i.c.v. Ang II was obtained after acute and chronic oral treatment with 30 mg/kg telmisartan. Oral treatment with 1 and 3 mg/kg telmisartan produced a slight but inconsistent inhibition of the central actions of Ang II. Telmisartan concentrations measured in the cerebrospinal fluid following 8 days of consecutive daily oral treatment (1-30 mg/kg) ranged from 0.87 +/- 0.27 ng/ml (1 mg/kg/day) to 46.5 +/- 11.6 ng/ml (30 mg/kg/day). Our results demonstrate that, following peripheral administration, the AT1 receptor antagonist telmisartan can penetrate the blood-brain barrier in a dose- and time-dependent manner to inhibit centrally mediated effects of Ang II.
This study was undertaken to shed further light on the mechanism of circulatory failure caused by heart disease and on the circulatory changes that follow administration of large therapeutic doses of digitalis, and rest. Weiss and Ellis observed the effect of digitalis on the volume and velocity of blood flow and other aspects of the circulation after repeated control observations in patients with rheumatic heart disease and with compensated circulation at rest. In this study such repeated control observations on the aspects of the circulation measured, because of the clinical condition of the patients and of the methods used, were not feasible. A definite separation of the changes due to digitalis effect and rest between determinations, therefore, cannot be made, but the arrangement of the observations was similar to those used in the treatment of cardiac patients. To ascertain a possible correlation between the pulmonary circulation and ventilatory function, in some of the cases measurements of different components of the lung volume were also performed simultaneously with the circulatory observations. The following aspects of the circulation were studied simultaneously before and after digitalis: (1) electrocardiogram; (2) the degree of orthopnea; (3) arterial blood pressure; (4) venous pressure with the method of Moritz and Tabora; (5) cardiac minute volume output with the method of Moore, Kinsman, Hamilton, and Spurling; (6) the peripheral and pulmonary velocity of the blood flow according to the method of Weiss and Robb; (7) blood volume according to the method of Keith, Rowntree and Geraghty; (8) lung volume with the method of Van Slyke and Binger; (9) oxygen and carbon dioxide content of the blood samples obtained from the femoral artery and vein.
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