Improving the voltage quality of Abu Hummus network in Egypt

In this paper the performance of the electrical network of Egypt is studied by considering a small part on the network (Abu Hummus city). The transmission network of Abu Hummus city was created for 66 kV, 11 kV, and 0.4 kV in the digital simulation and electrical network calculation (DIgSILENT power factory software) to study the voltage profiles. The load flow operational analysis was performed to obtain the voltage magnitudes at every bus bar. The voltage magnitudes in 11 kV and 0.4 kV networks were 10% to 15% less than the nominal value due to overloading off the transmission lines and the voltage magnitudes in 66 kV was within permissible limits. By using automatic tap-changing transformer or Static VAR System, the main idea of this paper is to obtain the voltage profiles at every bus bar to improve the voltage quality of the networks, so as to achieve better voltage profiles on the low voltage side without much effect on high voltage side under various operating conditions

WFQ ENHANCEMENT USING INTELLIGENT DISTRIBUTED QUEUE BASED ANFIS FOR PACKET SWITCHING NETWORK

The proliferation of the Internet and its applications has led to a potential increase in users' requests for more services at economical prices and Quality of service. The diversity of Internet traffic requires some prioritization and prioritization because some visits deserve great attention while reducing delays and packet losses compared to others. Current swap scheduling mechanisms are characterized by three main characteristics: fairness, complexity, and protection. Therefore, the question remains how we can provide equity and protection with less complex implementation. In this paper present proposed scheduling mechanism to enhance the performance of computer network. Proposed method is utilize an adaptive neural fuzzy inference system in make schedule decision and adapted to handle with varying behaviors of network. It is programmed in object oriented programming C++ with OMNET++ environment. The proposed method ANFIS solving the problem of complexity run time for WFQ algorithm. It uses ANFIS to calculate the virtual finish time for packets instead of mathematically way in the ordinary WFQ. The main contributions of this paper are minimizing the delay, reduce the packet loss in routers service queue and increasing throughput. In order to enhance the performance of computer network

Statistical optimization of alginate immobilization process of candida stauntonica strain MY1 for bioethanol production

In this study a new yeast strain was isolated from Egyptian sugarcane molasses for its high capability of bioethanol fermentation,under anaerobic conditions.It was identified on the basis of its 18S rDNA to be Candida stauntonica MY1 (Accession No.KM657091). The central composite face centered design CCFD matrix and response surface methodology were applied in designing and optimizing the process of calcium-alginate immobilization of MY1 yeast cells to maximize its bioethanol productivity from glucose and evaluate the influence and interactive effect of three critical immobilization parameters; bead size (diameter,mm),initial inoculum size (g/L) and alginate concentration (g/L) on the bioethanol yield. Three quadratic model equations have been predicted ending out how statistically significant the effects of these variables (factors) and their interactions are in practice. The validity of the predicted models was confirmed. The optimum conditions for cell immobilization were found to be 2.5mm, 2.5 g/L and 5.5g/L,respectively. That produced 4.4 g/L bioethanol,with actual yield of 41.9% i.e. YP/S0.42g ethanol/g glucose, which was about 2.3 fold higher than that produced with free cells batch fermentation operated under the same conditions;48 h, pH5.5, 30oC and 100rpm. The immobilized cells showed good stability, with long storage time 21d and can be used for four successive batches with maximum bioethanol productivity

In Vivo Investigation of the Ameliorating Effect of Copper Albumin Complex on chondroitin sulfate in Monosodium iodoacetate -Induced Knee Osteoarthritis

Osteoarthritis (OA) is a condition that manifests as cartilage deterioration and subchondral bone sclerosis in the joint tissues. The weight-bearing joint is most severely impacted by OA. According to some research, consuming foods high in copper albumin complex (cu-albumin complex) can help with OA-related joint degeneration and pain relief. The current study's objective to determine how oral administration of the cu-albumin complex as an anti-inflammatory medication affected the development of rat knee osteoarthritis (KOA). Fifty adult albino rats were divided into three groups: negative control untreated (n= 10, no KOA induction); positive untreated control (n= 20, KOA induction); and treated group (n= 20, KOA induction with administration of cu-albumin complex). According to the severity of the clinical symptoms, treated and untreated arthritic groups were equally divided into mild and severe groups (n=10). Monosodium iodoacetate (MIA) was used as intra-articular injection for osteoarthritis induction. Rats were euthanized after a month of the beginning of the experiment, and the joints were examined histopathologically and immunohistochemically. It was indicated that the treatment was effective in reducing KOA severity and in improvement of chondroitin sulfate of the affected cartilages. In conclusion, the structure of the chondroitin sulphate in the knee joint cartilages of KOA-affected rats was modified by the cu-albumin complex

Identification of Molecular Pathologies Sufficient to Cause Neuropathic Excitability in Primary Somatosensory Afferents Using Dynamical Systems Theory

Pain caused by nerve injury (i.e. neuropathic pain) is associated with development of neuronal hyperexcitability at several points along the pain pathway. Within primary afferents, numerous injury-induced changes have been identified but it remains unclear which molecular changes are necessary and sufficient to explain cellular hyperexcitability. To investigate this, we built computational models that reproduce the switch from a normal spiking pattern characterized by a single spike at the onset of depolarization to a neuropathic one characterized by repetitive spiking throughout depolarization. Parameter changes that were sufficient to switch the spiking pattern also enabled membrane potential oscillations and bursting, suggesting that all three pathological changes are mechanistically linked. Dynamical analysis confirmed this prediction by showing that excitability changes co-develop when the nonlinear mechanism responsible for spike initiation switches from a quasi-separatrix-crossing to a subcritical Hopf bifurcation. This switch stems from biophysical changes that bias competition between oppositely directed fast- and slow-activating conductances operating at subthreshold potentials. Competition between activation and inactivation of a single conductance can be similarly biased with equivalent consequences for excitability. “Bias” can arise from a multitude of molecular changes occurring alone or in combination; in the latter case, changes can add or offset one another. Thus, our results identify pathological change in the nonlinear interaction between processes affecting spike initiation as the critical determinant of how simple injury-induced changes at the molecular level manifest complex excitability changes at the cellular level. We demonstrate that multiple distinct molecular changes are sufficient to produce neuropathic changes in excitability; however, given that nerve injury elicits numerous molecular changes that may be individually sufficient to alter spike initiation, our results argue that no single molecular change is necessary to produce neuropathic excitability. This deeper understanding of degenerate causal relationships has important implications for how we understand and treat neuropathic pain

Association Rate Constants of Ras-Effector Interactions Are Evolutionarily Conserved

Evolutionary conservation of protein interaction properties has been shown to be a valuable indication for functional importance. Here we use homology interface modeling of 10 Ras-effector complexes by selecting ortholog proteins from 12 organisms representing the major eukaryotic branches, except plants. We find that with increasing divergence time the sequence similarity decreases with respect to the human protein, but the affinities and association rate constants are conserved as predicted by the protein design algorithm, FoldX. In parallel we have done computer simulations on a minimal network based on Ras-effector interactions, and our results indicate that in the absence of negative feedback, changes in kinetics that result in similar binding constants have strong consequences on network behavior. This, together with the previous results, suggests an important biological role, not only for equilibrium binding constants but also for kinetics in signaling processes involving Ras-effector interactions. Our findings are important to take into consideration in system biology approaches and simulations of biological networks

Metastasis to the breast from an adenocarcinoma of the lung with extensive micropapillary component: a case report and review of the literature

Breast metastasis from extra-mammary malignancy is rare. Based on the literature an incidence of 0.4-1.3% is reported. The primary malignancies most commonly metastasizing to the breast are leukemia-lymphoma, and malignant melanoma. We present a case of metastasis to the breast from a pulmonary adenocarcinoma, with extensive micropapillary component, diagnosed concomitantly with the primary tumor. A 73-year-old female presented with dyspnea and dry cough of 4 weeks duration and a massive pleural effusion was found on a chest radiograph. Additionally, on physical examination a poorly defined mass was noted in the upper outer quadrant of the left breast. The patient underwent bronchoscopy, excisional breast biopsy and medical thoracoscopy. By cytology, histology and immunohistochemistry primary lung adenocarcinoma with metastasis to the breast and parietal pleura was diagnosed. Both the primary and metastatic anatomic sites demonstrated histologically extensive micropapillary component, which is recently recognized as an important prognostic factor. The patient received chemotherapy but passed away within 7 months. Accurate differentiation of metastatic from primary carcinoma is of crucial importance because the treatment and prognosis differ significantly

The RhoA GEF Syx Is a Target of Rnd3 and Regulated via a Raf1-Like Ubiquitin-Related Domain

Background: Rnd3 (RhoE) protein belongs to the unique branch of Rho family GTPases that has low intrinsic GTPase activity and consequently remains constitutively active [1,2]. The current consensus is that Rnd1 and Rnd3 function as important antagonists of RhoA signaling primarily by activating the ubiquitous p190 RhoGAP [3], but not by inhibiting the ROCK family kinases. Methodology/Principal Findings: Rnd3 is abundant in mouse embryonic stem (mES) cells and in an unbiased two-step affinity purification screen we identified a new Rnd3 target, termed synectin-binding RhoA exchange factor (Syx), by mass spectrometry. The Syx interaction with Rnd3 does not occur through the Syx DH domain but utilizes a region similar to the classic Raf1 Ras-binding domain (RBD), and most closely related to those in RGS12 and RGS14. We show that Syx behaves as a genuine effector of Rnd3 (and perhaps Rnd1), with binding characteristics similar to p190-RhoGAP. Morpholinooligonucleotide knockdown of Syx in zebrafish at the one cell stage resulted in embryos with shortened anterior-posterior body axis: this phenotype was effectively rescued by introducing mouse Syx1b mRNA. A Rnd3-binding defective mutant of Syx1b mutated in the RBD (E164A/R165D) was more potent in rescuing the embryonic defects than wild-type Syx1b, showing that Rnd3 negatively regulates Syx activity in vivo. Conclusions/Significance: This study uncovers a well defined Rnd3 effector Syx which is widely expressed and directl

Intrathecal lidocaine pretreatment attenuates immediate neuropathic pain by modulating Nav1.3 expression and decreasing spinal microglial activation

<p>Abstract</p> <p>Background</p> <p>Intrathecal lidocaine reverses tactile allodynia after nerve injury, but whether neuropathic pain is attenuated by intrathecal lidocaine pretreatment is uncertain.</p> <p>Methods</p> <p>Sixty six adult male Sprague-Dawley rats were divided into three treatment groups: (1) sham (Group S), which underwent removal of the L₆transverse process; (2) ligated (Group L), which underwent left L₅spinal nerve ligation (SNL); and (3) pretreated (Group P), which underwent L₅SNL and was pretreated with intrathecal 2% lidocaine (50 μl). Neuropathic pain was assessed based on behavioral responses to thermal and mechanical stimuli. Expression of sodium channels (Nav_1.3and Nav_1.8) in injured dorsal root ganglia and microglial proliferation/activation in the spinal cord were measured on post-operative days 3 (POD₃) and 7 (POD₇).</p> <p>Results</p> <p>Group L presented abnormal behavioral responses indicative of mechanical allodynia and thermal hyperalgesia, exhibited up-regulation of Nav_1.3and down-regulation of Nav_1.8, and showed increased microglial activation. Compared with ligation only, pretreatment with intrathecal lidocaine before nerve injury (Group P), as measured on POD₃, palliated both mechanical allodynia (<it>p </it>< 0.01) and thermal hyperalgesia (<it>p </it>< 0.001), attenuated Nav_1.3up-regulation (<it>p </it>= 0.003), and mitigated spinal microglial activation (<it>p </it>= 0.026) by inhibiting phosphorylation (activation) of p38 MAP kinase (<it>p </it>= 0.034). p38 activation was also suppressed on POD₇(<it>p </it>= 0.002).</p> <p>Conclusions</p> <p>Intrathecal lidocaine prior to SNL blunts the response to noxious stimuli by attenuating Nav_1.3up-regulation and suppressing activation of spinal microglia. Although its effects are limited to 3 days, intrathecal lidocaine pretreatment can alleviate acute SNL-induced neuropathic pain.</p