Studying of operation balance in single-phase induction motors is an issue of interest due to the need for reducing the power consumption and increasing the motors’ life. The paper focuses on improving the motor performance by balancing the stator phase operation for the most common-used connection diagrams of single-phase capacitor-run induction motors (SPCRIMs) and three-phase induction motors (TPIMs) operating from single-phase supply (SPS). Therefore, a mathematical model is used to balance the motor operation by varying the frequency supply voltage. Characteristics of balancing parameters are investigated, various methods of motor balancing are presented and comparisons were done among these balancing methods.
Senescence or programmed cell death is a process that interacts with many biochemical and physiological changes in living organism and is generally induced by aging. Many environmental stresses that accelerate the production of activated oxygen can also induce senescence artificially. One of the important aspects of senescence is possibly degradation of macromolecules such as DNA. It is believed that the random amplification of polymorphic DNA (RAPD) technique is a good method to compare the DNA quality of juvenile and senescence samples in which oxidative stress is induced. In this study, juvenile, senescence and plant paraquat treated leaves from tomato, tobacco and rose, as well as juvenile and senescence human tissues were processed for DNA extraction followed by RAPD technique. We discovered that plant and human genomes are influenced by senescence and environmental stresses underwent genome diversity. Using some molecular markers proved that senescence and oxidative treated samples show different DNA pattern compare to the juvenile-un- treated samples. We also concluded that RAPD technique can be used as a useful tool in genomics study to provide researchers reliable information of DNA quality and can effectively help to resolve the environment condition.
Aging is the leading risk factor for neurodegenerative diseases and oxidative stress involved in the pathophysiology of these diseases. These changes increase during menopausal condition in females when the level of estradiol is decreased. The aim of the present study was to determine the effect of tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 - 35) on 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. Aging brain functions were assayed by measuring the activities of antioxidant enzymes—superoxide dismutase (SOD) and monoamine oxidase (MAO) with neuropeptides. An in-vitro incubation of Aβ (25 - 35) in E2 treated brain synaptosomes showed toxic effects on all the parameters. However, NKB and NKB combined with Aβ (25 35) showed stimulating effects in E2 treated rat brain synaptosomes. In the present study, an increase in activity of SOD and decrease in the level of MAO, in the presence of NKB and combined NKB and Aβ in E2 treated brain synaptosomes of aging rats. This study elucidates that treatment of NKB and Aβ with E2 incombination exerts more protective influence than their individual application, against excitotoxicity in age related changes.
The brain experiences structural, molecular and functional alterations during aging. In aging brain tissue, the oxidative stress increases due to decreased activity of antioxidant enzymes and increased oxidative stress leading to neurodegeneration associated with excitotoxicity. In the present study, we observed the effect of tachykinin neuropeptide Neurokinin B (NKB) and amyloid beta fragment Aβ (25 - 35) on the activity of Acetylcholine esterase (AChE) and Lipid peroxidation (LPO) in brains of 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. An in-vitro incubation of E2 treated brain synaptosomes with Aβ (25 - 35) showed toxic effects on all the parameters. The treatment of NKB and combined NKB and Aβ (25 - 35) increased the AChE enzyme activity and decreased the level of LPO in E2 treated aging rats. The treatment of NKB and combined NKB and Aβ (25 - 35) in a concentration dependent manner reversed the effects of aging and Aβ (25 - 35) on AChE and LPO. The present finding suggests that E2 along with NKB reverse aging and Aβ (25 - 35) induced toxicity as well as AChE and LPO levels. The results of the current study showed a possible beneficial role of NKB with E2 inthe age related neurological diseases.