Rapid Recovery of Visual Acuity after Lumboperitoneal Shunt Operation in Malignant Idiopathic Intracranial Hypertension

Background. Idiopathic intracranial hypertension can cause rapid deterioration of visual acuity in some severe cases, and these cases are usually thought to have “malignant” form of this disease. Case. In this paper, we report on a 16-year-old girl who is a typical example for malignant idiopathic intracranial hypertension with a rapid recovery of visual acuity after lumboperitoneal shunt operation. Observations and Conclusions. Malignant form of idiopathic intracranial hypertension must be kept in mind in selected patients to avoid irreversible visual loss

Three dimensional design optimization using analytical and numerical jacobians

A design optimization method based on three dimensional Euler equations is developed. A finite volume method is implemented to discretize the Euler equations. Newton's method is used to solve the discretized form of Euler equations. Newton's method requires the calculation of the Jacobian matrix which is the derivative of the residual vector with respect to the flux vector. Different upwind methods are used in the calculation of flux vectors. Numerical and analytical methods are utilized in the evaluation of Jacobian matrices. The efficiency and accuracy of the analytical and numerical Jacobian evaluations are compared. In order to improve the accuracy of numerical method, detailed error analyses are performed. The optimum finite difference perturbation magnitude that minimizes the error is searched. The computation time of numerical Jacobian evaluation is reduced by calculating the flux vectors with perturbed flow variables only in related cells. The performances of different sparse matrix solvers are also compared. The effects of errors in numerical Jacobians on the accuracy of sensitivities is analyzed. Results show that the finitedifference perturbation magnitude and computer precision are the most important parameters that affect the accuracy of numerical Jacobians. Approximately the same optimum perturbation magnitude enables the most accurate numerical flux Jacobian and sensitivity calculations. © 2011 by the American Institute of Aeronautics and Astronautics, Inc. All rights reserved

Interrelated In Vitro Mechanisms of Sibutramine-Induced Cardiotoxicity.

Consumption of illicit pharmaceutical products containing sibutramine has been reported to cause cardiovascular toxicity problems. This study aimed to demonstrate the toxicity profile of sibutramine, and thereby provide important implications for the development of more effective strategies in both clinical approaches and drug design studies. Action potentials (APs) were determined from freshly isolated ventricular cardiomyocytes with whole-cell configuration of current clamp as online. The maximum amplitude of APs (MAPs), the resting membrane potential (RMP), and AP duration from the repolarization phases were calculated from original records. The voltage-dependent K-channel currents (I) were recorded in the presence of external Cd and both inward and outward parts of the current were calculated, while their expression levels were determined with qPCR. The levels of intracellular free Ca and H (pH) as well as reactive oxygen species (ROS) were measured using either a ratiometric micro-spectrofluorometer or confocal microscope. The mechanical activity of isolated hearts was observed with Langendorff-perfusion system. Acute sibutramine applications (10-10 M) induced significant alterations in both MAPs and RMP as well as the repolarization phases of APs and I in a concentration-dependent manner. Sibutramine (10 μM) induced Ca-release from the sarcoplasmic reticulum under either electrical or caffeine stimulation, whereas it depressed left ventricular developed pressure with a marked decrease in the end-diastolic pressure. pH inhibition by sibutramine supports the observed negative alterations in contractility. Changes in mRNA levels of different I subunits are consistent with the acute inhibition of the repolarizing I, affecting AP parameters, and provoke the cardiotoxicity

A SGLT2 inhibitor dapagliflozin suppresses prolonged ventricular-repolarization through augmentation of mitochondrial function in insulin-resistant metabolic syndrome rats

Abstract Background Metabolic syndrome (MetS) is a prevalent risk factor for cardiac dysfunction. Although SGLT2-inhibitors have important cardioprotective effects in hyperglycemia, their underlying mechanisms are complex and not completely understood. Therefore, we examined mechanisms of a SGLT2-inhibitor dapagliflozin (DAPA)-related cardioprotection in overweight insulin-resistant MetS-rats comparison with insulin (INSU), behind its glucose-lowering effect. Methods A 28-week high-carbohydrate diet-induced MetS-rats received DAPA (5 mg/kg), INSU (0.15 mg/kg) or vehicle for 2 weeks. To validate MetS-induction, we monitored all animals weekly by measuring body weight, blood glucose and HOMO-IR index, electrocardiograms, heart rate, systolic and diastolic pressures. Results DAPA-treatment of MetS-rats significantly augmented the increased blood pressure, prolonged Q–R interval, and low heart rate with depressed left ventricular function and relaxation of the aorta. Prolonged-action potentials were preserved with DAPA-treatment, more prominently than INSU-treatment, at most, through the augmentation in depressed voltage-gated K+-channel currents. DAPA, more prominently than INSU-treatment, preserved the depolarized mitochondrial membrane potential, and altered mitochondrial protein levels such as Mfn-1, Mfn-2, and Fis-1 as well as provided significant augmentation in cytosolic Ca2+-homeostasis. Furthermore, DAPA also induced significant augmentation in voltage-gated Na+-currents and intracellular pH, and the cellular levels of increased oxidative stress, protein-thiol oxidation and ADP/ATP ratio in cardiomyocytes from MetS rats. Moreover, DAPA-treatment normalized the increases in the mRNA level of SGLT2 in MetS-rat heart. Conclusions Overall, our data provided a new insight into DAPA-associated cardioprotection in MetS rats, including suppression of prolonged ventricular-repolarization through augmentation of mitochondrial function and oxidative stress followed by improvement of fusion–fission proteins, out of its glucose-lowering effect

Treatment delays and in-hospital outcomes in acute myocardial infarction during the COVID-19 pandemic: A nationwide study

© 2020 by Turkish Society of Cardiology.Objective: Delayed admission of myocardial infarction (MI) patients is an important prognostic factor. In the present nationwide registry (TURKMI-2), we evaluated the treatment delays and outcomes of patients with acute MI during the Covid-19 pandemic and compaired with a recent pre-pandemic registry (TURKMI-1). Methods: The pandemic and pre-pandemic studies were conducted prospectively as 15-day snapshot registries in the same 48 centers. The inclusion criteria for both registries were aged ≥18 years and a final diagnosis of acute MI (AMI) with positive troponin levels. The only difference between the 2 registries was that the pre-pandemic (TURKMI-1) registry (n=1872) included only patients presenting within the first 48 hours after symptom-onset. TURKMI-2 enrolled all consecutive patients (n=1113) presenting with AMI during the pandemic period. Results: A comparison of the patients with acute MI presenting within the 48-hour of symptom-onset in the pre-pandemic and pandemic registries revealed an overall 47.1% decrease in acute MI admissions during the pandemic. Median time from symptom-onset to hospital-arrival increased from 150 min to 185 min in patients with ST elevation MI (STEMI) and 295 min to 419 min in patients presenting with non-STEMI (NSTEMI) (p-values <0.001). Door-to-balloon time was similar in the two periods (37 vs. 40 min, p=0.448). In the pandemic period, percutaneous coronary intervention (PCI) decreased, especially in the NSTEMI group (60.3% vs. 47.4% in NSTEMI, p<0.001; 94.8% vs. 91.1% in STEMI, p=0.013) but the decrease was not significant in STEMI patients admitted within 12 hours of symptom-onset (94.9% vs. 92.1%; p=0.075). In-hospital major adverse cardiac events (MACE) were significantly increased during the pandemic period [4.8% vs. 8.9%; p<0.001; age- and sex-adjusted Odds ratio (95% CI) 1.96 (1.20-3.22) for NSTEMI, p=0.007; and 2.08 (1.38-3.13) for STEMI, p<0.001]. Conclusion: The present comparison of 2 nationwide registries showed a significant delay in treatment of patients presenting with acute MI during the COVID-19 pandemic. Although PCI was performed in a timely fashion, an increase in treatment delay might be responsible for the increased risk of MACE. Public education and establishing COVID-free hospitals are necessary to overcome patients' fear of using healthcare services and mitigate the potential complications of AMI during the pandemic