Design and Implementation of Wireless Point-Of-Care Health Monitoring Systems: Diagnosis For Sleep Disorders and Cardiovascular Diseases

Chronic sleep disorders are present in 40 million people in the United States. More than 25 million people remain undiagnosed and untreated, which accounts for over $22 billion in unnecessary healthcare costs. In addition, another major chronic disease is the heart diseases which cause 23.8% of the deaths in the United States. Thus, there is a need for a low cost, reliable, and ubiquitous patient monitoring system. A remote point-of-care system can satisfy this need by providing real time monitoring of the patient\u27s health condition at remote places. However, the currently available POC systems have some drawbacks; the fixed number of physiological channels and lack of real time monitoring. In this dissertation, several remote POC systems are reported to diagnose sleep disorders and cardiovascular diseases to overcome the drawbacks of the current systems. First, two types of remote POC systems were developed for sleep disorders. One was designed with ZigBee and Wi-Fi network, which provides increase/decrease the number of physiological channels flexibly by using ZigBee star network. It also supports the remote real-time monitoring by extending WPAN to WLAN with combination of two wireless communication topologies, ZigBee and Wi-Fi. The other system was designed with GSM/WCDMA network, which removes the restriction of testing places and provides remote real-time monitoring in the true sense of the word. Second, a fully wearable textile integrated real-time ECG acquisition system for football players was developed to prevent sudden cardiac death. To reduce power consumption, adaptive RF output power control was implemented based on RSSI and the power consumption was reduced up to 20%. Third, as an application of measuring physiological signals, a wireless brain machine interface by using the extracted features of EOG and EEG was implemented to control the movement of a robot. The acceleration/deceleration of the robot is controlled based on the attention level from EEG. The left/right motion of eyeballs of EOG is used to control the direction of the robot. The accuracy rate was about 95%. These kinds of health monitoring systems can reduce the exponentially increasing healthcare costs and cater the most important healthcare needs of the society

Acute Cerebral Infarction Following Intravenous Glycoprotein IIb/IIIa Inhibitor for Acute Myocardial Infarction

Stroke is a rare but serious complication of acute myocardial infarction (AMI). Currently, glycoprotein (GP) IIb/IIIa inhibitor is used in clinical practice for acute coronary syndromes and percutaneous coronary interventions (PCIs). The incidence of stroke in patients receiving GP IIb/IIIa inhibitor during PCIs is very low. We report the case of a 47-year-old man who presented with AMI and suffered an acute cerebral infarction after infusion of a GP IIb/IIIa inhibitor following primary PCI

Evaluation of the pathogenicity of GJB3 and GJB6 variants associated with nonsyndromic hearing loss

AbstractA number of genes responsible for hearing loss are related to ion recycling and homeostasis in the inner ear. Connexins (Cx26 encoded by GJB2, Cx31 encoded by GJB3 and Cx30 encoded by GJB6) are core components of gap junctions in the inner ear. Gap junctions are intercellular communication channels and important factors that are associated with hearing loss. To date, a molecular genetics study of GJB3 and GJB6 as a causative gene for hearing loss has not been performed in Korea. This study was therefore performed to elucidate the genetic characteristics of Korean patients with nonsyndromic sensorineural hearing loss and to determine the pathological mechanism of hearing loss by analyzing the intercellular communication function of Cx30 and Cx31 variants. Sequencing analysis of the GJB3 and GJB6 genes in our population revealed a total of nine variants, including four novel variants in the two genes. Three of the novel variants (Cx31-p.V27M, Cx31-p.V43M and Cx-30-p.I248V) and two previously reported variants (Cx31-p.V84I and Cx30-p.A40V) were selected for functional studies using a pathogenicity prediction program and assessed for whether the mutations were located in a conserved region of the protein. The results of biochemical and ionic coupling tests showed that both the Cx31-p.V27M and Cx31-p.V84I variants did not function normally when each was expressed as a heterozygote with the wild-type Cx31. This study demonstrated that two variants of Cx31 were pathogenic mutations with deleterious effect. This information will be valuable in understanding the pathogenic role of GJB3 and GJB6 mutations associated with hearing loss