An Improvement of Load Flow Solution for Power System Networks using Evolutionary-Swarm Intelligence Optimizers

Load flow report which reveals the existing state of the power system network under steady operating conditions, subject to certain constraints is being bedeviled by issues of accuracy and convergence. In this research, five AI-based load flow solutions classified under evolutionary-swarm intelligence optimizers are deployed for power flow studies in the 330kV, 34-bus, 38-branch section of the Nigerian transmission grid. The evolutionary-swarm optimizers used in this research consist of one evolutionary algorithm and four swarm intelligence algorithms namely; biogeography-based optimization (BBO), particle swarm optimization (PSO), spider monkey optimization (SMO), artificial bee colony optimization (ABCO) and ant colony optimization (ACO). BBO as a sole evolutionary algorithm is being configured alongside four swarm intelligence optimizers for an optimal power flow solution with the aim of performance evaluation through physical and statistical means. Assessment report upon application of these standalone algorithms on the 330kV Nigerian grid under two (accuracy and convergence) metrics produced PSO and ACO as the best-performed algorithms. Three test cases (scenarios) were adopted based on the number of iterations (100, 500, and 1000) for proper assessment of the algorithms and the results produced were validated using mean average percentage error (MAPE) with values of voltage profile created by each solution algorithm in line with the IEEE voltage regulatory standards. All algorithms proved to be good load flow solvers with distinct levels of precision and speed. While PSO and SMO produced the best and worst results for accuracy with MAPE values of 3.11% and 36.62%, ACO and PSO produced the best and worst results for convergence (computational speed) after 65 and 530 average number of iterations. Since accuracy supersedes speed from scientific considerations, PSO is the overall winner and should be cascaded with ACO for an automated hybrid swarm intelligence load flow model in future studies. Future research should consider hybridizing ACO and PSO for a more computationally efficient solution model

Low-cost Car Battery Security Alert System

This is a technical article that showcases a low-cost car battery security alert system that utilizes a multi-vibrator circuit into a dual-tone multi-frequency (DTMF) output (loud beep sound) alarm to monitor and safeguard the car battery from local theft. The entire circuitry is a simple one and low-cost in production. The incessant cases in which car batteries are stolen especially in developing countries is on the high side. And the cost of replacing car batteries is on the increase daily. Therefore, one needs to secure her car battery from street theft. Using both mechanical fastening and electronic security-based systems one could sleep with two eyes closed. The device serves as an electronic watchdog on the car battery in the car while it is parked outside the owner’s residence or elsewhere. The security system is provided with an internal rechargeable battery energizing the alarm circuitry, having a single-pole double-throw (SPDT) relay, and connected cables, with an output sound capable of alerting the neighbourhood. Whenever the car battery is disconnecting from the terminal heads or the loop cable is broken the connected alarm will be triggered and this will call the attention of the neighbourhood and the owner thereby deterring the intruder. The entire system was simulated using Circuit Wizard software with good results. The system was fabricated using discrete semiconductor devices that are relatively simple and available for operation and maintenance, packaged, and tested. The circuit voltage is 11.52 volts and draws a current of 3.79A resulting in a wattage of 44 watts. The device is affordable

Exercise and Health: Can Biotechnology Confer Similar Benefits?

Education and public policies are largely failing to encourage people to exercise. Could our knowledge of exercise biology lead to pharmaceutical treaments that could confer the same benefits as exercise

Deficiency of the Mitochondrial Electron Transport Chain in Muscle Does Not Cause Insulin Resistance

It has been proposed that muscle insulin resistance in type 2 diabetes is due to a selective decrease in the components of the mitochondrial electron transport chain and results from accumulation of toxic products of incomplete fat oxidation. The purpose of the present study was to test this hypothesis.Rats were made severely iron deficient, by means of an iron-deficient diet. Iron deficiency results in decreases of the iron containing mitochondrial respiratory chain proteins without affecting the enzymes of the fatty acid oxidation pathway. Insulin resistance was induced by feeding iron-deficient and control rats a high fat diet. Skeletal muscle insulin resistance was evaluated by measuring glucose transport activity in soleus muscle strips. Mitochondrial proteins were measured by Western blot. Iron deficiency resulted in a decrease in expression of iron containing proteins of the mitochondrial respiratory chain in muscle. Citrate synthase, a non-iron containing citrate cycle enzyme, and long chain acyl-CoA dehydrogenase (LCAD), used as a marker for the fatty acid oxidation pathway, were unaffected by the iron deficiency. Oleate oxidation by muscle homogenates was increased by high fat feeding and decreased by iron deficiency despite high fat feeding. The high fat diet caused severe insulin resistance of muscle glucose transport. Iron deficiency completely protected against the high fat diet-induced muscle insulin resistance.The results of the study argue against the hypothesis that a deficiency of the electron transport chain (ETC), and imbalance between the ETC and β-oxidation pathways, causes muscle insulin resistance

AMP-Activated Protein Kinase Plays an Important Evolutionary Conserved Role in the Regulation of Glucose Metabolism in Fish Skeletal Muscle Cells

AMPK, a master metabolic switch, mediates the observed increase of glucose uptake in locomotory muscle of mammals during exercise. AMPK is activated by changes in the intracellular AMP∶ATP ratio when ATP consumption is stimulated by contractile activity but also by AICAR and metformin, compounds that increase glucose transport in mammalian muscle cells. However, the possible role of AMPK in the regulation of glucose metabolism in skeletal muscle has not been investigated in other vertebrates, including fish. In this study, we investigated the effects of AMPK activators on glucose uptake, AMPK activity, cell surface levels of trout GLUT4 and expression of GLUT1 and GLUT4 as well as the expression of enzymes regulating glucose disposal and PGC1α in trout myotubes derived from a primary muscle cell culture. We show that AICAR and metformin significantly stimulated glucose uptake (1.6 and 1.3 fold, respectively) and that Compound C completely abrogated the stimulatory effects of the AMPK activators on glucose uptake. The combination of insulin and AMPK activators did not result in additive nor synergistic effects on glucose uptake. Moreover, exposure of trout myotubes to AICAR and metformin resulted in an increase in AMPK activity (3.8 and 3 fold, respectively). We also provide evidence suggesting that stimulation of glucose uptake by AMPK activators in trout myotubes may take place, at least in part, by increasing the cell surface and mRNA levels of trout GLUT4. Finally, AICAR increased the mRNA levels of genes involved in glucose disposal (hexokinase, 6-phosphofructokinase, pyruvate kinase and citrate synthase) and mitochondrial biogenesis (PGC-1α) and did not affect glycogen content or glycogen synthase mRNA levels in trout myotubes. Therefore, we provide evidence, for the first time in non-mammalian vertebrates, suggesting a potentially important role of AMPK in stimulating glucose uptake and utilization in the skeletal muscle of fish

Leptin Administration Favors Muscle Mass Accretion by Decreasing FoxO3a and Increasing PGC-1α in ob/ob Mice

Absence of leptin has been associated with reduced skeletal muscle mass in leptin-deficient ob/ob mice. The aim of our study was to examine the effect of leptin on the catabolic and anabolic pathways regulating muscle mass. Gastrocnemius, extensor digitorum longus and soleus muscle mass as well as fiber size were significantly lower in ob/ob mice compared to wild type littermates, being significantly increased by leptin administration (P<0.001). This effect was associated with an inactivation of the muscle atrophy-related transcription factor forkhead box class O3 (FoxO3a) (P<0.05), and with a decrease in the protein expression levels of the E3 ubiquitin-ligases muscle atrophy F-box (MAFbx) (P<0.05) and muscle RING finger 1 (MuRF1) (P<0.05). Moreover, leptin increased (P<0.01) protein expression levels of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), a regulator of muscle fiber type, and decreased (P<0.05) myostatin protein, a negative regulator of muscle growth. Leptin administration also activated (P<0.01) the regulators of cell cycle progression proliferating cell nuclear antigen (PCNA) and cyclin D1, and increased (P<0.01) myofibrillar protein troponin T. The present study provides evidence that leptin treatment may increase muscle mass of ob/ob mice by inhibiting myofibrillar protein degradation as well as enhancing muscle cell proliferation

The impact of sugar-sweetened beverage intake on rat cardiac function

Aims: Although there is evidence linking sugar-sweetened beverage (SSB) intake with the development of cardio-metabolic diseases, the underlying mechanisms remain unclear. The current study therefore evaluated the effects of SSB consumption by establishing a unique in-house in vivo experimental model. Main methods: Male Wistar rats were divided into two groups: a) one consuming a popular local SSB (SSB- Jive), and b) a control group (Control-water) for a period of three and six months (n = 6 per group), respectively. Rats were gavaged on a daily basis with an experimental dosage amounting to half a glass per day (in human terms) (SSB vs. water). Cardiac function was assessed at baseline (echocardiography) and following ex vivo ischemia-reperfusion of the isolated perfused working rat heart. Oral glucose tolerance tests and mitochondrial respiratory analyses were also performed. In addition, the role of non-oxidative glucose pathways (NOGPs), i.e. the polyol pathway, hexosamine biosynthetic pathway (HBP) and PKC were assessed. Key findings: These data show that SSB intake: a) resulted in increased weight gain, but did not elicit major effects in terms of insulin resistance and cardiac function after three and six months, respectively; b) triggered myocardial NOGP activation after three months with a reversion after six months; and c) resulted in some impairment in mitochondrial respiratory capacity in response to fatty acid substrate supply after six months. Significance: SSB intake did not result in cardiac dysfunction or insulin resistance. However, early changes at the molecular level may increase risk in the longer term