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

Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8

Two voltage gated sodium channel α-subunits, Na(v)1.7 and Na(v)1.8, are expressed at high levels in nociceptor terminals and have been implicated in the development of inflammatory pain. Mis-expression of voltage-gated sodium channels by damaged sensory neurons has also been implicated in the development of neuropathic pain, but the role of Na(v)1.7 and Na(v)1.8 is uncertain. Here we show that deleting Na(v)1.7 has no effect on the development of neuropathic pain. Double knockouts of both Na(v)1.7 and Na(v)1.8 also develop normal levels of neuropathic pain, despite a lack of inflammatory pain symptoms and altered mechanical and thermal acute pain thresholds. These studies demonstrate that, in contrast to the highly significant role for Na(v)1.7 in determining inflammatory pain thresholds, the development of neuropathic pain does not require the presence of either Na(v)1.7 or Na(v)1.8 alone or in combination

Sodium channels and mammalian sensory mechanotransduction

BACKGROUND: Members of the degenerin/epithelial (DEG/ENaC) sodium channel family are mechanosensors in C elegans, and Nav1.7 and Nav1.8 voltage-gated sodium channel knockout mice have major deficits in mechanosensation. β and γENaC sodium channel subunits are present with acid sensing ion channels (ASICs) in mammalian sensory neurons of the dorsal root ganglia (DRG). The extent to which epithelial or voltage-gated sodium channels are involved in transduction of mechanical stimuli is unclear. RESULTS: Here we show that deleting β and γENaC sodium channels in sensory neurons does not result in mechanosensory behavioural deficits. We had shown previously that Nav1.7/Nav1.8 double knockout mice have major deficits in behavioural responses to noxious mechanical pressure. However, all classes of mechanically activated currents in DRG neurons are unaffected by deletion of the two sodium channels. In contrast, the ability of Nav1.7/Nav1.8 knockout DRG neurons to generate action potentials is compromised with 50% of the small diameter sensory neurons unable to respond to electrical stimulation in vitro. CONCLUSION: Behavioural deficits in Nav1.7/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents. DEG/ENaC sodium channels are not mechanosensors in mouse sensory neurons

Nerve injury induces robust allodynia and ectopic discharges in Na(v)1.3 null mutant mice

Changes in sodium channel activity and neuronal hyperexcitability contribute to neuropathic pain, a major clinical problem. There is strong evidence that the re-expression of the embryonic voltage-gated sodium channel subunit Na(v)1.3 underlies neuronal hyperexcitability and neuropathic pain. Here we show that acute and inflammatory pain behaviour is unchanged in global Na(v)1.3 mutant mice. Surprisingly, neuropathic pain also developed normally in the Na(v)1.3 mutant mouse. To rule out any genetic compensation mechanisms that may have masked the phenotype, we investigated neuropathic pain in two conditional Na(v)1.3 mutant mouse lines. We used Na(v)1.8-Cre mice to delete Nav1.3 in nociceptors at E14 and NFH-Cre mice to delete Na(v)1.3 throughout the nervous system postnatally. Again normal levels of neuropathic pain developed after nerve injury in both lines. Furthermore, ectopic discharges from damaged nerves were unaffected by the absence of Na(v)1.3 in global knock-out mice. Our data demonstrate that Na(v)1.3 is neither necessary nor sufficient for the development of nerve-injury related pain

Nociceptor-expressed ephrin-B2 regulates inflammatory and neuropathic pain

Background: EphB receptors and their ephrin-B ligands play an important role in nervous system development, as well as synapse formation and plasticity in the adult brain. Recent studies show that intrathecal treatment with EphB-receptor activator ephrinB2-Fc induced thermal hyperalgesia and mechanical allodynia in rat, indicating that ephrin-B2 in small dorsal root ganglia (DRG) neurons and EphB receptors in the spinal cord modulate pain processing. To examine the role of ephrin-B2 in peripheral pain pathways, we deleted ephrin-B2 in Nav1.8+ nociceptive sensory neurons with the Cre-loxP system. Sensory neuron numbers and terminals were examined using neuronal makers. Pain behavior in acute, inflammatory and neuropathic pain models was assessed in the ephrin-B2 conditional knockout (CKO) mice. We also investigated the c-Fos expression and NMDA receptor NR2B phosphorylation in ephrin-B2 CKO mice and littermate controls.Results: The ephrin-B2 CKO mice were healthy with no sensory neuron loss. However, pain-related behavior was substantially altered. Although acute pain behavior and motor co-ordination were normal, inflammatory pain was attenuated in ephrin-B2 mutant mice. Complete Freund's adjuvant (CFA)-induced mechanical hyperalgesia was halved. Formalin-induced pain behavior was attenuated in the second phase, and this correlated with diminished tyrosine phosphorylation of N-methyl-D-aspartic acid (NMDA) receptor subunit NR2B in the dorsal horn. Thermal hyperalgesia and mechanical allodynia were significantly reduced in the Seltzer model of neuropathic pain.Conclusions: Presynaptic ephrin-B2 expression thus plays an important role in regulating inflammatory pain through the regulation of synaptic plasticity in the dorsal horn and is also involved in the pathogenesis of some types of neuropathic pain

EVALUATION OF THE IMMUNE RESPONSE TO POLIO VACCINE IN MALNOURISHED CHILDREN IN SANA'A CITY

Objective: This study was made to evaluate the immune response to polio virus vaccine among PEM children by measuring the level of circulating Immunoglobulin G (IgG) antibodies against polio virus (IgG-PV) after immunization with the primary series of POV, and determining the coverage rate of universal childhood vaccine for polio virus. A cross-sectional laboratory study was conducted in Department of Medical Microbiology and Clinical Immunology, Faculty of Medicine and Health Sciences, and Al-Sabeen University Hospital, Sana’a University. Methods: A total of 279 PEM children were selected and investigated for universal childhood vaccination coverage rate for polio vaccine. Blood samples were collected from all, then tested for levels of IgG-PV by ELISA method. For assessment IgG-PV levels more than 10 units/ml were considered protected against polio virus infection. Results: The coverage rate of polio virus vaccine for first year vaccine was 96.8%; and 91.1% of vaccinated PEM children responded to the vaccine with mean level of 46.2 U/ml. A statistically significant difference was observed with respect to sero-protective IgG-PV between males and females (85.7% and 94.1% respectively, p=0.002); and older children (>37 months) (97.7%). Conclusion: We conclude that a small proportion of malnourished vaccinated children with a normal immune status were not serologically immune to polio virus infection, and remain to be reconsidered for either revaccination or booster doses due to lack of or inadequate response. PEM group gave slightly reduced response to OPV hence there is need to give this group IPV (injectable polio vaccine) along with OPV and different micro-nutrition deficiencies like Zinc and iron. Peer Review History: Received 29 March 2018;   Revised 20 April; Accepted 7 May, Available online 15 May 2018 UJPR follows the most transparent and toughest ‘Advanced OPEN peer review’ system. The identity of the authors and, reviewers will be known to each other. This transparent process will help to eradicate any possible malicious/purposeful interference by any person (publishing staff, reviewer, editor, author, etc) during peer review. As a result of this unique system, all reviewers will get their due recognition and respect, once their names are published in the papers. We expect that, by publishing peer review reports with published papers, will be helpful to many authors for drafting their article according to the specifications. Auhors will remove any error of their article and they will improve their article(s) according to the previous reports displayed with published article(s). The main purpose of it is ‘to improve the quality of a candidate manuscript’. Our reviewers check the ‘strength and weakness of a manuscript honestly’. There will increase in the perfection, and transparency. Received file:        Reviewer's Comments: Average Peer review marks at initial stage: 4.5/10 Average Peer review marks at publication stage: 8.0/10 Reviewer(s) detail: Dr. O.J Owolabi, University of Benin, Nigeria, [email protected] Dr. Sameh Abdelmoneem Mohammed Ali, Faculty of Pharmacy, Beni-Suef University, Egypt, [email protected] Similar Articles: COCCIDIAN INTESTINAL PARASITES AMONG CHILDREN IN AL-TORBAH CITY IN YEMEN: IN COUNTRY WITH HIGH INCIDENCE OF MALNUTRITION PREVALENCE AND POTENTIAL RISK FACTORS OF HEPATITIS B VIRUS IN A SAMPLE OF CHILDREN IN TWO SELECTED AREAS IN YEME

Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons

Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions

The effect of surface treatment and thermal aging on the bonding of clear aligner attachments to provisional resin-based material: shear bond strength analysis

ObjectivesThe aim of this study is to evaluate the effect of different surface treatments on the shear bond strength (SBS) of clear aligner attachments bonded to Bis-acryl provisional crowns.Methods120 cylindrical bisacrylic composite material (ProTemp type) specimens were prepared and divided into six groups (n = 20) based on surface treatment, control: (no treatment); super coarse grit diamond bur, carbide bur, alumina-blasting, non-thermal plasma treatment, and Er:YAG laser treatment. The features of treated surfaces were examined using scanning electron microscopy (SEM). A flowable composite resin (Transbond XT; 3M Unitek) was bonded to the specimens forming the attachment. Half of specimens were subjected to thermal cycling (5,000 cycles). SBS was measured before and after thermal cycling. Each specimen was loaded at the attachment/resin interface at a speed of 0.5 mm/min until failure. The nature of the failure was analyzed using the composite remnants index (CRI). Two-way ANOVA and Tukey HSD were used for data analysis α =  0.5. For CRI scores analysis, Kruskal-Wallis test and Dunn's multiple comparison were used as post-hoc test.ResultsSEM analysis showed that all surface treatments altered surface properties and increase surface bonding area. The specimens treated with plasma, Er:YAG laser, and alumina-blasting had higher SBS values before and after thermal cycling. In comparison to control plasma, Er:YAG laser, and alumina-blasting showed a significant increase in SBS (P < 0.001) while carbide and diamond bur groups showed no significant differences (P > 0.05). Thermal cycling significantly decreased the SBS of control, carbide bur, diamond bur, and Er:YAG laser while no significant effect of alumina-blasting and plasma group. Er:YAG laser and plasma groups significantly exhibited more dominance for scores 2 and score 3 and the absence of score 0.ConclusionAlumina-blasting, Er:YAG laser, or non-thermal plasma surface treatments increased the shear bond strength between clear aligner attachments and resin-based restorations

Absence of Whisker-Related Pattern Formation in Mice with NMDA Receptors Lacking Coincidence Detection Properties and Calcium Signaling

Precise refinement of synaptic connectivity is the result of activity-dependent mechanisms in which coincidence-dependent calcium signaling by NMDA receptors (NMDARs) under control of the voltage-dependent Mg2+ block might play a special role. In the developing rodent trigeminal system, the pattern of synaptic connections between whisker-specific inputs and their target cells in the brainstem is refined to form functionally and morphologically distinct units (barrelettes). To test the role of NMDA receptor signaling in this process, we introduced the N598R mutation into the native NR1 gene. This leads to the expression of functional NMDARs that are Mg2+ insensitive and Ca2+impermeable. Newborn mice expressing exclusively NR1 N598R-containing NMDARs do not show any whisker-related patterning in the brainstem, whereas the topographic projection of trigeminal afferents and gross brain morphology appear normal. Furthermore, the NR1 N598R mutation does not affect expression levels of NMDAR subunits and other important neurotransmitter receptors. Our results show that coincidence detection by, and/or Ca2+ permeability of, NMDARs is necessary for the development of somatotopic maps in the brainstem and suggest that highly specific signaling underlies synaptic refinement