Brain-Computer Interfacing for Wheelchair Control by Detecting Voluntary Eye Blinks

The human brain is considered as one of the most powerful quantum computers and combining the human brain with technology can even outperform artificial intelligence. Using a Brain-Computer Interface (BCI) system, the brain signals can be analyzed and programmed for specific tasks. This research work employs BCI technology for a medical application that gives the unfortunate paralyzed individuals the capability to interact with their surroundings solely using voluntary eye blinks. This research contributes to the existing technology to be more feasible by introducing a modular design with three physically separated components: a headwear, a computer, and a wheelchair. As the signal-to-noise ratio (SNR) of the existing systems is too high to separate the eye blink artifacts from the regular EEG signal, a precise ThinkGear module is used which acquired the raw EEG signal through a single dry electrode. This chip offers an advanced filtering technology that has a high noise immunity along with an embedded Bluetooth module using which the acquired signal is transferred wirelessly to a computer. A MATLAB program captures voluntary eye blink artifacts from the brain waves and commands the movement of a miniature wheelchair via Bluetooth. To distinguish voluntary eye blinks from involuntary eye blinks, blink strength thresholds are determined. A Graphical User Interface (GUI) designed in MATLAB displays the EEG waves in real-time and enables the user to determine the movements of the wheelchair which is specially designed to take commands from the GUI.  The findings from the testing phase unveil the advantages of a modular design and the efficacy of using eye blink artifacts as the control element for brain-controlled wheelchairs. The work presented here gives a basic understanding of the functionality of a BCI system, and provides eye blink-controlled navigation of a wheelchair for patients suffering from severe paralysis

Diabetic cardiomyopathy is associated with defective myocellular copper regulation and both defects are rectified by divalent copper chelation

BACKGROUND: Heart disease is the leading cause of death in diabetic patients, and defective copper metabolism may play important roles in the pathogenesis of diabetic cardiomyopathy (DCM). The present study sought to determine how myocardial copper status and key copper-proteins might become impaired by diabetes, and how they respond to treatment with the Cu (II)-selective chelator triethylenetetramine (TETA) in DCM. METHODS: Experiments were performed in Wistar rats with streptozotocin (STZ)-induced diabetes with or without TETA treatment. Cardiac function was analyzed in isolated-perfused working hearts, and myocardial total copper content measured by particle-induced x-ray emission spectroscopy (PIXE) coupled with Rutherford backscattering spectrometry (RBS). Quantitative expression (mRNA and protein) and/or activity of key proteins that mediate LV-tissue-copper binding and transport, were analyzed by combined RT-qPCR, western blotting, immunofluorescence microscopy, and enzyme activity assays. Statistical analysis was performed using Student’s t-tests or ANOVA and p-values of < 0.05 have been considered significant. RESULTS: Left-ventricular (LV) copper levels and function were severely depressed in rats following 16-weeks’ diabetes, but both were unexpectedly normalized 8-weeks after treatment with TETA was instituted. Localized myocardial copper deficiency was accompanied by decreased expression and increased polymerization of the copper-responsive transition-metal-binding metallothionein proteins (MT1/MT2), consistent with impaired anti-oxidant defences and elevated susceptibility to pro-oxidant stress. Levels of the high-affinity copper transporter-1 (CTR1) were depressed in diabetes, consistent with impaired membrane copper uptake, and were not modified by TETA which, contrastingly, renormalized myocardial copper and increased levels and cell-membrane localization of the low-affinity copper transporter-2 (CTR2). Diabetes also lowered indexes of intracellular (IC) copper delivery via the copper chaperone for superoxide dismutase (CCS) to its target cuproenzyme, superoxide dismutase-1 (SOD1): this pathway was rectified by TETA treatment, which normalized SOD1 activity with consequent bolstering of anti-oxidant defenses. Furthermore, diabetes depressed levels of additional intracellular copper-transporting proteins, including antioxidant-protein-1 (ATOX1) and copper-transporting-ATPase-2 (ATP7B), whereas TETA elevated copper-transporting-ATPase-1 (ATP7A). CONCLUSIONS: Myocardial copper deficiency and defective cellular copper transport/trafficking are revealed as key molecular defects underlying LV impairment in diabetes, and TETA-mediated restoration of copper regulation provides a potential new class of therapeutic molecules for DCM

Study and Analysis of Drying Characteristics of Ginger using Solar Drier with Evacuated Tube Collectors

ABSTRACT In the present study, a solar drier is designed and fabricated with evacuated tube collectors and its performance is studied for drying ginger under the meteorological condition of Thanjavur district, Tamilnadu, India. Ginger is also dried separately by natural sun drying and is compared with the designed drier. Ginger is used in treating variety of ailments due to its high medicinal properties. The drier is employed with different air velocity flow rates (4 m/s, 4.25 m/s, 4.5 m/s, 4.75 m/s, 5 m/s). Drying of ginger in the designed drier reduces the average initial moisture content from 85.62% to a final moisture content of 0.92% in 6 hours. This is less than half the time taken by natural sun drying (13 hours). The efficiency of the drier varied from 31% -40.4% for different air flow rates. The results show that the rate of drying is more if the air flow is more. It is also found that the quality of the dried ginger in the designed solar drier is high as compared to the one dried in natural sun drying. From the performance, quality and quick rate of drying it is evident that solar drier with evacuated tube collector is more compatible than other driers

Polycystic ovary syndrome (PCOS) and kisspeptin – A Sri Lankan study

Context: Polycystic ovary syndrome (PCOS) is the commonest endocrine disorder affecting young women. Kisspeptins are a family of closely related peptides encoded by Kiss1 gene that controls the hypothalamic–pituitary–gonadal axis by binding to its receptor (GPR54) expressed in gonadotropin-releasing hormone (GnRH) neurons and releases GnRH. Since GnRH secretion is deregulated in PCOS, we hypothesized that dysregulated gonadotropin secretion in PCOS is reflected by kisspeptin levels. Aim: We aimed to measure serum kisspeptin levels of subjects with well-characterized PCOS versus controls and explore any correlation between kisspeptin and PCOS-related reproductive and metabolic disturbances. Materials and Methods: Consecutive women with PCOS manifesting from adolescence (n = 55) and adult controls (n = 110) were recruited. Pre-treatment baseline clinical, anthropometry, and biochemical parameters were measured in all. Serum kisspeptin and testosterone levels were determined by enzyme-linked immunosorbent assay method. Results: Serum kisspeptin and testosterone concentrations were significantly higher in women with PCOS (kisspeptin 4.873 nmol/L; testosterone 4.713 nmol/L) than controls (kisspeptin 4.127 nmol/L; testosterone 3.415 nmol/L; P < 0.05). Serum kisspeptin levels were positively associated with PCOS (odds ratio: 1.853; 95% confidence interval: 1.246–2.755; P = 0.002) in our studied population. Conclusion: Serum kisspeptin levels are higher in Sri Lankan women with PCOS manifesting from adolescence compared with controls regardless of body mass index. We propose serum kisspeptin concentration as a useful marker to recognize PCOS that manifests from adolescence

Target Mechanism-Based Whole-Cell Screening Identifies Bortezomib as an Inhibitor of Caseinolytic Protease in Mycobacteria

ABSTRACT A novel type of antibacterial screening method, a target mechanism-based whole-cell screening method, was developed to combine the advantages of target mechanism- and whole-cell-based approaches. A mycobacterial reporter strain with a synthetic phenotype for caseinolytic protease (ClpP1P2) activity was engineered, allowing the detection of inhibitors of this enzyme inside intact bacilli. A high-throughput screening method identified bortezomib, a human 26S proteasome drug, as a potent inhibitor of ClpP1P2 activity and bacterial growth. A battery of secondary assays was employed to demonstrate that bortezomib indeed exerts its antimicrobial activity via inhibition of ClpP1P2: Down- or upmodulation of the intracellular protease level resulted in hyper- or hyposensitivity of the bacteria, the drug showed specific potentiation of translation error-inducing aminoglycosides, ClpP1P2-specific substrate WhiB1 accumulated upon exposure, and growth inhibition potencies of bortezomib derivatives correlated with ClpP1P2 inhibition potencies. Furthermore, molecular modeling showed that the drug can bind to the catalytic sites of ClpP1P2. This work demonstrates the feasibility of target mechanism-based whole-cell screening, provides chemical validation of ClpP1P2 as a target, and identifies a drug in clinical use as a new lead compound for tuberculosis therapy

AIF suppresses chemical stress-induced apoptosis and maintains the transformed state of tumor cells

Apoptosis-inducing factor (AIF) exhibits reactive oxygen species (ROS)-generating NADH oxidase activity of unknown significance, which is dispensable for apoptosis. We knocked out the aif gene in two human colon carcinoma cell lines that displayed lower mitochondrial complex I oxidoreductase activity and produced less ROS, but showed increased sensitivity to peroxide- or drug-induced apoptosis. AIF knockout cells failed to form tumors in athymic mice or grow in soft agar. Only AIF with intact NADH oxidase activity restored complex I activity and anchorage-independent growth of aif knockout cells, and induced aif-transfected mouse NIH3T3 cells to form foci. AIF knockdown in different carcinoma cell types resulted in lower superoxide levels, enhanced apoptosis sensitivity and loss of tumorigenicity. Antioxidants sensitized AIF-expressing cells to apoptosis, but had no effect on tumorigenicity. In summary, AIF-mediated resistance to chemical stress involves ROS and probably also mitochondrial complex I. AIF maintains the transformed state of colon cancer cells through its NADH oxidase activity, by mechanisms that involve complex I function. On both counts, AIF represents a novel type of cancer drug target