Effect of dexamethasone and ramosetron on the prevention of postoperative nausea and vomiting in low-risk patients: a randomized, double-blind, placebo-controlled, multicenter trial.

BACKGROUND: Several studies have investigated the effect of antiemetics on postoperative nausea and vomiting (PONV) in high-risk groups. However, few studies have investigated the effect of antiemetics in patients at low risk of developing PONV. METHODS: In this prospective, randomized, double-blinded trial, 177 patients undergoing surgery under general anesthesia were randomly allocated to three groups. Patients allocated to group C (control group) received 2 mL of intravenous 0.9% saline, those allocated to group R (ramosetron group) received 0.3 mg of intravenous ramosetron, and those allocated to group DR (ramosetron plus dexamethasone group) received 5 mg of intravenous dexamethasone and 0.3 mg of intravenous ramosetron. RESULTS: Finally, 174 patients completed the study, and the types of surgeries were orthopedic (n = 80), rhinologic (n = 47), urologic (n = 29), and others (n = 18). The incidence of PONV up to 48 h postoperatively was significantly lower in group DR than in group C. The incidence of PONV up to 0-1 h postoperatively was significantly lower in groups R and DR than in group C. The usage pattern of rescue antiemetics was consistent with the incidence of PONV. The percentage of patients requiring rescue analgesics 0-1 h postoperatively was significantly lower in groups R and DR than in group C. CONCLUSIONS: The combination of dexamethasone and ramosetron demonstrated a superior effect in preventing PONV for 48 h after surgery under general anesthesia than saline in patients at low risk of developing PONV. Compared with saline injections, ramosetron injections yielded better outcomes for the incidence of PONV and the use of rescue antiemetics and rescue analgesics 0-1 h postoperatively. TRIAL REGISTRATION: Clinical trial registration number: criskorea@korea.kr, KCT0006749.

Outdoor Localization Using BLE RSSI and Accessible Pedestrian Signals for the Visually Impaired at Intersections.

One of the major challenges for blind and visually impaired (BVI) people is traveling safely to cross intersections on foot. Many countries are now generating audible signals at crossings for visually impaired people to help with this problem. However, these accessible pedestrian signals can result in confusion for visually impaired people as they do not know which signal must be interpreted for traveling multiple crosses in complex road architecture. To solve this problem, we propose an assistive system called CAS (Crossing Assistance System) which extends the principle of the BLE (Bluetooth Low Energy) RSSI (Received Signal Strength Indicator) signal for outdoor and indoor location tracking and overcomes the intrinsic limitation of outdoor noise to enable us to locate the user effectively. We installed the system on a real-world intersection and collected a set of data for demonstrating the feasibility of outdoor RSSI tracking in a series of two studies. In the first study, our goal was to show the feasibility of using outdoor RSSI on the localization of four zones. We used a k-nearest neighbors (kNN) method and showed it led to 99.8% accuracy. In the second study, we extended our work to a more complex setup with nine zones, evaluated both the kNN and an additional method, a Support Vector Machine (SVM) with various RSSI features for classification. We found that the SVM performed best using the RSSI average, standard deviation, median, interquartile range (IQR) of the RSSI over a 5 s window. The best method can localize people with 97.7% accuracy. We conclude this paper by discussing how our system can impact navigation for BVI users in outdoor and indoor setups and what are the implications of these findings on the design of both wearable and traffic assistive technology for blind pedestrian navigation.

Gait changes after using a temporomandibular joint exerciser in patients who underwent lower limb joint surgery.

[Purpose] The improvements in gait of the patients with lower limb disease who used a temporomandibular joint (TMJ) exerciser were verified. [Subjects and Methods] Eleven subjects were included. Their mean age was 53.2 years. The lower limb joint angles before and after using the TMJ exerciser were measured using a gait analyzer. Before the gait experiment, the TMJ exerciser setting process and one-leg stance balance test (OLST) were repeated until the balance maintenance time improved. [Results] Because of the OLST, the mean change in the body center point after the subjects used the exerciser improved from 5.76 mm to 4.20 mm. When the TMJ exerciser was used, the joint angle range of the subjects approached that of the normal individuals. [Conclusion] According to the gait experiments, the angles of the subjects' hips, knees, and ankle joints approached to those of the normal individuals after the subjects used the TMJ exerciser; however, the results did not completely match. The changes in the hip, knee, and ankle joint angles were statistically significant, which confirm the usefulness of the TMJ exerciser.

Development of a radial pulse tonometric (RPT) sensor with a temperature compensation mechanism.

Several RPT sensors have been developed to acquire objective and quantitative pulse waves. These sensors offer improved performance with respect to pressure calibration, size and sensor deployment, but not temperature. Since most pressure sensors are sensitive to temperature, various temperature compensation techniques have been developed, but these techniques are largely inapplicable to RPT sensors due to the size restrictions of the sensor, and incompatibility between the compensation techniques and the RPT sensor. Consequently, in this paper a new RPT sensor comprising six piezoresistive pressure sensors and one thermistor has been developed through finite element analysis and then a suitable temperature compensation technique has been proposed. This technique compensates for temperature variations by using the thermistor and simple compensation equations. As verification of the proposed compensation technique, pulse waves of all types were successfully compensated for temperature changes.

Changes in pain scores and walking distance after transforaminal epidural steroid injection in patients with lumbar foraminal spinal stenosis.

Transforaminal epidural steroid injections (TFESI) are widely used in patients with lumbar foraminal spinal stenosis. Previous studies have evaluated the effects of TFESI on lumbar foraminal spinal stenosis using only pain scores. However, no study has evaluated the effect of TFESI on pain scores and walking distance in patients with lumbar foraminal spinal stenosis. This study aimed to assess the effect of TFESI on pain scores and walking distance in patients with lumbar foraminal spinal stenosis stratified according to disease severity. This retrospective study reviewed the medical records of patients who received TFESI for lumbar foraminal spinal stenosis. A total of 128 patients were divided into the moderate and severe groups based on the extent of fat obliteration and the presence of nerve root compression. A significant decrease in the numeric rating scale (NRS) scores was observed in the moderate and severe groups compared with the corresponding baseline values 4 weeks after TFESI; however, the NRS pain scores were lower in the moderate group than those in the severe group. In addition, the proportion of patients who experienced pain reduction (≥50%) was higher in the moderate group than that in the severe group. The moderate and severe groups showed a significant increase in walking distance compared with the baseline values 4 weeks after the treatment. However, the walking distance values did not differ significantly between the moderate and severe groups. Furthermore, the degree of satisfaction was higher in the moderate group than that in the severe group. Lumbar TFESI may reduce pain scores and increase walking distance in patients with moderate or severe lumbar foraminal spinal stenosis. Patients with moderate foraminal stenosis had better pain relief outcomes than those with severe foraminal stenosis.

S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.

Our previous study presented evidence that the inflammation-related S100A9 gene is significantly upregulated in the brains of Alzheimer's disease (AD) animal models and human AD patients. In addition, experiments have shown that knockdown of S100A9 expression improves cognition function in AD model mice (Tg2576), and these animals exhibit reduced amyloid plaque burden. In this study, we established a new transgenic animal model of AD by crossbreeding the Tg2576 mouse with the S100A9 knockout (KO) mouse. We observed that S100A9KO/Tg2576 (KO/Tg) mice displayed an increased spatial reference memory in the Morris water maze task and Y-maze task as well as decreased amyloid beta peptide (Aß) neuropathology because of reduced levels of Aß, C-terminal fragments of amyloid precursor protein (APP-CT) and phosphorylated tau and increased expression of anti-inflammatory IL-10 and also decreased expression of inflammatory IL-6 and tumor neurosis factor (TNF)-α when compared with age-matched S100A9WT/Tg2576 (WT/Tg) mice. Overall, these results suggest that S100A9 is responsible for the neurodegeneration and cognitive deficits in Tg2576 mice. The mechanism of S100A9 is able to coincide with the inflammatory process. These findings indicate that knockout of S100A9 is a potential target for the pharmacological therapy of AD.

Swedish amyloid precursor protein mutation increases phosphorylation of eIF2alpha in vitro and in vivo.

Swedish double mutation (KM670/671NL) of amyloid precursor protein (Swe-APP), a prevailing cause of familial Alzheimer's disease (FAD), is known to increase in Abeta production both in vitro and in vivo, but its underlying molecular basis leading to Alzheimer's disease (AD) pathogenesis remains to be elucidated, especially for the early phase of disease. We have confirmed initially that the expression of Swe-APP mutant transgene reduced cell viability via ROS production but this effect was eliminated by an anti-oxidative agent, vitamin E. We also found that eukaryotic translation initiation factor-2alpha (eIF2alpha), which facilitates binding of initiator tRNA to ribosomes to set on protein synthesis, was phosphorylated in cultured cells expressing Swe-APP. This increase in phosphorylated eIF2alpha was also attenuated significantly by treatment with vitamin E. The finding that eIF2alpha became highly phosphorylated by increased production of Abeta was substantiated in brain tissues of both an AD animal model and AD patients. Although an increase in Abeta production would result in cell death eventually (in late-phase of the disease), the altered phosphorylation state of eIF2alpha evoked by Abeta may account for the decreased efficacy of mRNA translation and de novo protein synthesis required for synaptic plasticity, and may consequently be one of molecular causes for impairment of cognitive functions exhibited in the early phase of AD patients.

Mefenamic acid shows neuroprotective effects and improves cognitive impairment in in vitro and in vivo Alzheimer's disease models.

Nonsteroidal anti-inflammatory drugs (NSAIDs) exert anti-inflammatory, analgesic, and antipyretic activities and suppress prostaglandin synthesis by inhibiting cyclooxygenase, an enzyme that catalyzes the formation of prostaglandin precursors from arachidonic acid. Epidemiological observations indicate that the long-term treatment of patients suffering from rheumatoid arthritis with NSAIDs results in reduced risk and delayed onset of Alzheimer's disease. In this study, we investigated the therapeutic potential for Alzheimer's disease of mefenamic acid, a commonly used NSAID that is a cyclooxygenase-1 and 2 inhibitor with only moderate anti-inflammatory properties. We found that mefenamic acid attenuates the neurotoxicities induced by amyloid beta peptide (Abeta)(1-42) treatment and the expression of a Swedish double mutation (KM595/596NL) of amyloid precursor protein (Swe-APP) or the C-terminal fragments of APP (APP-CTs) in neuronal cells. We also show that mefenamic acid decreases the production of the free radical nitric oxide and reduces cytochrome c release from mitochondria induced by Abeta(1-42), Swe-APP, or APP-CTs in neuronal cells. In addition, mefenamic acid up-regulates expression of the antiapoptotic protein Bcl-X(L). Moreover, our study demonstrates for the first time that mefenamic acid improves learning and memory impairment in an Abeta(1-42)-infused Alzheimer's disease rat model. Taking these in vitro and in vivo results together, our study suggests that mefenamic acid could be used as a therapeutic agent in Alzheimer's disease.