•Diode arc-back fault occurs whenever a diode is short-circuited inside one rectifier bridge.•Diode arc-back fault generally gives a short circuit curent dynamic peak which is higher than a ...three-phase short circuit current peak.•Diode arc-back fault can cause mechanical damage to multi-winding transformers used for adjustable speed drive applications.•Diode arc-back fault phenomenon is treated in IEEE Std. 551, while it is instead completely disregarded by IEC Std. 60,909–0.
In polypropylene petrochemical plants power adjustable speed drives (ASDs) are normally used to drive extruder or pump machines required by this type of industrial process. Each one of these ASDs is fed by a dedicated converter transformer which supplies a diode-front-end rectifier in the input converter part of the ASD. In case one diode of the input rectifier is faulted and becomes short-circuited, the converter transformer can be subjected to a dynamic short circuit stress being higher than that due to a fault occurring just at transformer terminals: this phenomenon is called diode arc-back fault in technical literature. Simulations are carried out by means of EMTP-ATP software in order to show the effect of diode arc-back fault on the dynamic peak short circuit currents to which transformer windings are exposed
In vivo Engineering of Organs: The Bone Bioreactor Stevens, Molly M.; Marini, Robert P.; Schaefer, Dirk ...
Proceedings of the National Academy of Sciences - PNAS,
08/2005, Letnik:
102, Številka:
32
Journal Article
Recenzirano
Odprti dostop
Treatment of large defects requires the harvest of fresh living bone from the iliac crest. Harvest of this limited supply of bone is accompanied by extreme pain and morbidity. This has prompted the ...exploration of other alternatives to generate new bone using traditional principles of tissue engineering, wherein harvested cells are combined with porous scaffolds and stimulated with exogenous mitogens and morphogens in vitro and/or in vivo. We now show that large volumes of bone can be engineered in a predictable manner, without the need for cell transplantation and growth factor administration. The crux of the approach lies in the deliberate creation and manipulation of an artificial space (bioreactor) between the tibia and the periosteum, a mesenchymal layer rich in pluripotent cells, in such a way that the body's healing mechanism is leveraged in the engineering of neotissue. Using the "in vivo bioreactor" in New Zealand White rabbits, we have engineered bone that is biomechanically identical to native bone. The neo-bone formation followed predominantly an intramembraneous path, with woven bone matrix subsequently maturing into fully mineralized compact bone exhibiting all of the histological markers and mechanical properties of native bone. We harvested the bone after 6 weeks and transplanted it into contralateral tibial defects, resulting in complete integration after 6 weeks with no apparent morbidity at the donor site. Furthermore, in a proof-of-principle study, we have shown that by inhibiting angiogenesis and promoting a more hypoxic environment within the "in vivo bioreactor space," cartilage formation can be exclusively promoted.
Our study has shown that plasma levels of ghrelin, a stomach-derived peptide, are significantly reduced in sepsis, and that ghrelin administration improves organ blood flow via a nuclear factor ...(NF)-kappaB-dependent pathway. However, it remains unknown whether ghrelin has any protective effects on severe sepsis-induced acute lung injury (ALI) and, if so, whether inhibition of NF-kappaB plays any role in it.
To test the hypothesis that ghrelin reduces severe sepsis-induced ALI and mortality through inhibition of NF-kappaB.
Sepsis was induced in rats by cecal ligation and puncture (CLP). Five hours after CLP, a bolus intravenous injection of 2 nmol of ghrelin was followed by continuous infusion of 12 nmol of ghrelin via a minipump for 15 hours. Samples were harvested 20 hours post-CLP (i.e., severe sepsis). Pulmonary levels of ghrelin and proinflammatory cytokines were measured by ELISA. NF-kappaB p65 and IkappaBalpha expression and NF-kappaB activity were measured by Western blot analysis and ELISA, respectively. Pulmonary blood flow was measured with radioactive microspheres. In additional animals, the necrotic cecum was excised 20 hours post-CLP and 10-day survival was recorded.
Pulmonary levels of ghrelin decreased significantly 20 hours post-CLP. Ghrelin administration restored pulmonary levels of ghrelin, reduced lung injury, increased pulmonary blood flow, down-regulated proinflammatory cytokines, inhibited NF-kappaB activation, and improved survival in sepsis. Administration of a specific ghrelin receptor antagonist worsened the survival rate after CLP and cecal excision.
Ghrelin can be developed as a novel treatment for severe sepsis-induced ALI. The protective effect of ghrelin is mediated through inhibition of NF-kappaB.
Introduction
Trauma during pregnancy is the leading non-obstetrical cause of maternal death and a significant public health burden. This study reviews the most common causes of trauma during ...pregnancy, morbidity, and mortality, and the impact upon perinatal outcomes associated with trauma, providing a management approach to pregnant trauma patients.
Materials and methods
A systematic review of the current literature from January 2006 to July 2016 was performed.
Results
Fifty-one articles were identified, including a total of 95,949 patients. Motor vehicle crash was the most frequent cause of blunt trauma, followed by falls, assault both domestic and interpersonal violence, and penetrating injuries (gunshot and stab wounds).
Conclusions
Trauma in pregnant women is associated with high rates of adverse maternal and neonatal outcomes. Knowledge of the mechanism of injury is important to identify the potential injuries and the complexity of the management of these patients. As in all traumatic events, prevention is of paramount importance.
•A large synchronous motor with a very low inrush current could have a critical direct-on-line starting: critical starting means that the starting time is higher than the time the rotor can withstand ...in blocked condition.•It is necessary to assess the actual motor rotation to be sure that the motor is being self-ventilating during its acceleration and can survive the critical starting.•The historical solution of using an under-impedance relay (ANSI code 21) for starting supervision can give some troubles for the correct and safe protection of the starting of the motor due to inherent measuring errors of instrument transformers.•For the aim of starting supervision, the use of a supervision switch relay (ANSI code 14) based on rotor speed measurement is more reliable and safe than using the solution of under-impedance relay (ANSI code 21).•The under-impedance relay (ANSI code 21) can be useful instead for detecting a blocked rotor condition occurring only after each starting while the motor is already running (equivalent to ANSI function 51R – rotor jam during running).
Some petrochemical plants (low density polyethylene type) always require the use of big synchronous motors to feed large power compressors (typically from 10 to 30 MW).
In certain supply network conditions, it could happen that the motor undergoes a critical starting which takes several tens of seconds to be completed. “Critical” means that the starting time is higher than the time the rotor can withstand in blocked condition: therefore, it is necessary to assess the actual motor rotation to be sure that the motor is being self-ventilating during its acceleration and can survive the critical starting.
By means of numerical simulations, it is demonstrated that the solution of using an under-impedance relay (ANSI code 21) for starting supervision, as is proposed in technical literature since many years, gives some troubles for the correct and safe protection of the starting of the motor, with respect to the most common solution of adopting a supervision switch relay (ANSI code 14) based on rotor speed measurement.
To assess the value and efficacy of real-time shear-wave elastography (SWE) of normal testicular parenchyma and various common testicular diseases in clinical practice.
SWE was undertaken in 338 ...patients (mean age: 43.2±17.2 years, range 17–78 years) comprising normal testicles (n = 358), testicular microlithiasis (n = 40), and various testicular diseases (n = 208) and the stiffness was recorded. The final diagnosis was correlated with the clinical context, long-term follow-up, or histopathology. Statistical evaluation was performed to provide a stiffness threshold for pathological diagnosis.
The mean size of testicular lesions was 2.6±1.5 cm (range: 10–42 mm). The mean Young's modulus value for normal testis was recorded at 4.55±2.54 kPa. Whatever the stage of microlithiasis, a higher statistically significant stiffness value was recorded. For acute orchitis, the mean stiffness value was slightly higher, but not statistically significantly. The testicular tumoural processes presented a median stiffness value of 21.02 kPa with a cut-off of 16.1 kPa. Fibrosis presented the highest median stiffness value of 30.03 kPa with a cut-off of 26.3 kPa. By analysing the distribution of the different pathological groups, the difference was statistically significant between fibrosis and tumoural processes (p = 0.001).
SWE is a feasible technique in the exploration of the testicular parenchyma. SWE values can be used to differentiate testicular fibrosis from a tumoural process with confidence.
•Real-time SWE is a feasible technique in the exploration of testicular parenchyma.•SWE is not a time consuming process without impact on the workflow.•The stiffness value can be used to distinguish fibrosis from a tumoral process.•The reference for normal value is dependent of the type of elastography software.
Gut ischemia/reperfusion (I/R) injury is a serious condition in intensive care patients. Activation of immune cells adjacent to the huge endothelial cell surface area of the intestinal ...microvasculature produces initially local and then systemic inflammatory responses. Stimulation of the vagus nerve can rapidly attenuate systemic inflammatory responses through inhibiting the activation of macrophages and endothelial cells. Ghrelin, a novel orexigenic hormone, is produced predominately in the gastrointestinal system. Ghrelin receptors are expressed at a high density in the dorsal vagal complex of the brain stem. In this study, we investigated the regulation of the cholinergic anti-inflammatory pathway by the novel gastrointestinal hormone, ghrelin, after gut I/R.
Gut ischemia was induced by placing a microvascular clip across the superior mesenteric artery for 90 min in male adult rats. Our results showed that ghrelin levels were significantly reduced after gut I/R and that ghrelin administration inhibited pro-inflammatory cytokine release, reduced neutrophil infiltration, ameliorated intestinal barrier dysfunction, attenuated organ injury, and improved survival after gut I/R. Administration of a specific ghrelin receptor antagonist worsened gut I/R-induced organ injury and mortality. To determine whether ghrelin's beneficial effects after gut I/R require the intact vagus nerve, vagotomy was performed in sham and gut I/R animals immediately prior to the induction of gut ischemia. Our result showed that vagotomy completely eliminated ghrelin's beneficial effect after gut I/R. To further confirm that ghrelin's beneficial effects after gut I/R are mediated through the central nervous system, intracerebroventricular administration of ghrelin was performed at the beginning of reperfusion after 90-min gut ischemia. Our result showed that intracerebroventricular injection of ghrelin also protected the rats from gut I/R injury.
These findings suggest that ghrelin attenuates excessive inflammation and reduces organ injury after gut I/R through activation of the cholinergic anti-inflammatory pathway.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Accurate multiplicities of prompt fission neutrons emitted in neutron-induced fission on a large energy range are essential for fundamental and applied nuclear physics. Measuring them to high ...precision for radioactive fissioning nuclides remains, however, an experimental challenge. In this work, the average prompt-neutron multiplicity emitted in the 239Pu(n,f) reaction was extracted as a function of the incident-neutron energy, over the range 1-700 MeV, with a novel technique, which allowed to minimize and correct for the main sources of bias and thus achieve unprecedented precision.
At low energies, our data validate for the first time the ENDF/B-VIII.0 nuclear data evaluation with an independent measurement and reduce the evaluated uncertainty by up to 60%. This work opens up the possibility of precisely measuring prompt fission neutron multiplicities on highly radioactive nuclei relevant for an essential component of energy production world-wide.
Milk fat globule epidermal growth factor 8 (MFG-E8) is a potent opsonin for the clearance of apoptotic cells and is produced by mononuclear cells of immune competent organs including the spleen and ...lungs. It attenuates chronic and acute inflammation such as autoimmune glomerulonephritis and bacterial sepsis by enhancing apoptotic cell clearance. Ischemia-reperfusion (I/R) injury of the gut results in severe inflammation, apoptosis, and remote organ damage, including acute lung injury (ALI).
To determine whether MFG-E8 attenuates intestinal and pulmonary inflammation after gut I/R.
Wild-type (WT) and MFG-E8(-/-) mice underwent superior mesenteric artery occlusion for 90 minutes, followed by reperfusion for 4 hours. A group of WT mice was treated with 0.4 microg/20 g recombinant murine MFG-E8 (rmMFG-E8) at the beginning of reperfusion. Four hours after reperfusion, MFG-E8, cytokines, myeloperoxidase activity, apoptosis, and histopathology were assessed. A 24-hour survival study was conducted in rmMFG-E8- and vehicle-treated WT mice.
Mesenteric I/R caused severe widespread injury and inflammation of the small intestines and remote organs, including the lungs. MFG-E8 levels decreased in the spleen and lungs by 50 to 60%, suggesting impaired apoptotic cell clearance. Treatment with rmMFG-E8 significantly suppressed inflammation (TNF-alpha, IL-6, IL-1beta, and myeloperoxidase) and injury of the lungs, liver, and kidneys. MFG-E8-deficient mice suffered from greatly increased inflammation and potentiated ALI, whereas treatment with rmMFG-E8 significantly improved the survival in WT mice.
MFG-E8 attenuates inflammation and ALI after gut I/R and may represent a novel therapeutic agent.
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