Retrograde Thromboembolism from the Proximal Descending Thoracic Aorta Leading to Recurrent Acute Cerebrovascular Events

In the United States, approximately 800,000 individuals experience a stroke every year Nearly 25% of strokes are recurrent Cryptogenic strokes, or those with unknown causes after testing, make up a significant portion of ischemic strokes, as many as 32% Retrograde thromboembolic events originating from the proximal descending thoracic aorta should be considered as a potential etiology in cryptogenic strokes The appropriate management of embolic events from aortic atheroma needs further research Here, we present a case of a 55-year-old male who had recurrent cryptogenic strokes whose origin was discovered to stem from retrograde embolic phenomena from atheroma located within the proximal descending thoracic aort

Optimal Control of CSTR

Nonlinear Model PredictiveControl (MPC) of Continuous Stirred Tank Reactor (CSTR) has been demostrated in this work. Optimal state estimation has been done using Extended Kalman Filter (EKF). Second order mathematical model for CSTR has been developed and further used for dynamic simulations. It is found that optimal control of temperature inside the CSTR is achieved better with the help of MPC strategy compared to conventional control strategies. It is seen that setpoint tracking performance using this optimal control strategy is satisfactory achieved

Performance analysis of IMC based PID controller tuning on approximated process model

Classical Proportional Integral Derivative(PID) controller remains the most popular approach for industrial process control. Poor tuning of PID controller can lead to mechanical wear associated with excessive control activity, poor control performance and even poor quality products. In this paper, we design procedure for the internal model control(IMC) approach for tuning of conventional PID controller with proper tuning rules. Furthermore, with help of analytical rule of step test obtaining the effective first order time delay model of the process. A simulation example of continuous stirred tank reactor is used in which the IMC based PID tuning method implemented and the step response of the closed loop system is compared with classical tuning methods like Ziegler-Nichols and Cohen-Coon

Neuronal overexpression of cyclooxygenase-2 does not alter the neuroinflammatory response during brain innate immune activation

Neuroinflammation is a critical component in the progression of several neurological and neurodegenerative diseases and cyclooxygenases (COX)-1 and -2 are key regulators of innate immune responses. We recently demonstrated that COX-1 deletion attenuates, whereas COX-2 deletion enhances, the neuroinflammatory response, blood-brain barrier permeability and leukocyte recruitment during lipopolysaccharide (LPS)-induced innate immune activation. Here, we used transgenic mice, which overexpressed human COX-2 via neuron-specific Thy-1 promoter (TgCOX-2), causing elevated prostaglandins (PGs) levels. We tested whether neuronal COX-2 overexpression affects the glial response to a single intracerebroventricular injection of LPS, which produces a robust neuroinflammatory reaction. Relative to non-transgenic controls (NTg), 7 month-old TgCOX-2 did not show any basal neuroinflammation, as assessed by gene expression of markers of inflammation and oxidative stress, neuronal damage, as assessed by Fluoro-JadeB staining, or systemic inflammation, as assessed by plasma levels of IL-1beta and corticosterone. Twenty-four hours after LPS injection, all mice showed increased microglial activation, as indicated by Iba1 immunostaining, neuronal damage, mRNA expression of cytokines (TNF-alpha, IL-6), reactive oxygen expressing enzymes (iNOS and NADPH oxidase subunits), endogenous COX-2, cPLA(2) and mPGES-1, and hippocampal and cortical IL-1beta levels. However, the increases were similar in TgCOX-2 and NTg. In NTg, LPS increased brain PGE(2) to the levels observed in TgCOX-2. These results suggest that PGs derived from neuronal COX-2 do not play a role in the neuroinflammatory response to acute activation of brain innate immunity. This is likely due to the direct effect of LPS on glial rather than neuronal cells