电网设备线夹开裂原因

某电力公司变电站用铝合金设备线夹在运行过程发生批次开裂事故,通过宏观观察、断口分析、化学成分分析、力学性能测试、冷冻模拟试验等方法,对设备线夹的开裂原因和开裂机理进行了分析。结果表明:设备线夹焊缝存在焊接缺陷,导致焊缝强度下降;设备线夹接线管底部存在积水空间,寒冷天气下积水结冰,体积膨胀,使焊缝承受设计工况外的负载而过载开裂,造成了线夹开裂。     

Spinal Excitatory Dynorphinergic Interneurons Contribute to Burn Injury-Induced Nociception Mediated by Phosphorylated Histone 3 at Serine 10 in Rodents

The phosphorylation of serine 10 in histone 3 (p-S10H3) has recently been demonstrated to participate in spinal nociceptive processing. However, superficial dorsal horn (SDH) neurons involved in p-S10H3-mediated nociception have not been fully characterized. In the present work, we combined immunohistochemistry, in situ hybridization with the retrograde labeling of projection neurons to reveal the subset of dorsal horn neurons presenting an elevated level of p-S10H3 in response to noxious heat (60 °C), causing burn injury. Projection neurons only represented a small percentage (5%) of p-S10H3-positive cells, while the greater part of them belonged to excitatory SDH interneurons. The combined immunolabeling of p-S10H3 with markers of already established interneuronal classes of the SDH revealed that the largest subset of neurons with burn injury-induced p-S10H3 expression was dynorphin immunopositive in mice. Furthermore, the majority of p-S10H3-expressing dynorphinergic neurons proved to be excitatory, as they lacked Pax-2 and showed Lmx1b-immunopositivity. Thus, we showed that neurochemically heterogeneous SDH neurons exhibit the upregulation of p-S10H3 shortly after noxious heat-induced burn injury and consequential tissue damage, and that a dedicated subset of excitatory dynorphinergic neurons is likely a key player in the development of central sensitization via the p-S10H3 mediated pathway.     

Idiosyncratic Drug-Induced Liver Injury: Mechanistic and Clinical Challenges

Idiosyncratic drug-induced liver injury (IDILI) remains a significant problem for patients and drug development. The idiosyncratic nature of IDILI makes mechanistic studies difficult, and little is known of its pathogenesis for certain. Circumstantial evidence suggests that most, but not all, IDILI is caused by reactive metabolites of drugs that are bioactivated by cytochromes P450 and other enzymes in the liver. Additionally, there is overwhelming evidence that most IDILI is mediated by the adaptive immune system; one example being the association of IDILI caused by specific drugs with specific human leukocyte antigen (HLA) haplotypes, and this may in part explain the idiosyncratic nature of these reactions. The T cell receptor repertoire likely also contributes to the idiosyncratic nature. Although most of the liver injury is likely mediated by the adaptive immune system, specifically cytotoxic CD8+ T cells, adaptive immune activation first requires an innate immune response to activate antigen presenting cells and produce cytokines required for T cell proliferation. This innate response is likely caused by either a reactive metabolite or some form of cell stress that is clinically silent but not idiosyncratic. If this is true it would make it possible to study the early steps in the immune response that in some patients can lead to IDILI. Other hypotheses have been proposed, such as mitochondrial injury, inhibition of the bile salt export pump, unfolded protein response, and oxidative stress although, in most cases, it is likely that they are also involved in the initiation of an immune response rather than representing a completely separate mechanism. Using the clinical manifestations of liver injury from a number of examples of IDILI-associated drugs, this review aims to summarize and illustrate these mechanistic hypotheses.     

Effect of resiliency and age on musculoskeletal injuries and lost workdays in emergency medical service personnel

Emergency medical service (EMS) personnel are highly skilled health care professionals who often provide lifesaving clinical care to patients. Paradoxically, they may be repeatedly exposed to a unique set of occupational hazards that could endanger their own health. This cross-sectional study sought to examine the relation between resiliency and musculoskeletal injuries (MSIs) and between resiliency and lost workdays due to MSIs, and explore whether age modifies these associations. Multivariable Poisson main effects regression models showed that resiliency had a protective effect against MSIs, but not lost workdays. In the unadjusted regression model to evaluate the relation between resiliency and age, results suggested that no differences in distributions existed between younger and older EMS personnel and resiliency. However, given the same unit increase in resiliency, findings from multivariable Poisson interaction regression models indicated that older workers had a higher prevalence of MSIs and lost workdays than younger workers. Results from main effects models may reflect diverging routes on a pathophysiological pathway, in which resiliency acts as a prognostic factor for MSIs but not lost workdays. Findings might also indicate the association between resiliency, and MSIs and lost workdays varies by age.Relevance to industryThe largest growth of labor in the US is expected to occur in the oldest segments of the population. While older workers may offer more experience and show similar resiliency to younger workers, they might be more vulnerable to individual risk factors and occupational exposures. If management wants to retain older workers as assets, they should design the work environment to match the capabilities of all workers.     

Mitochondrial Bioenergetic,Photobiomodulation and Trigeminal Branches Nerve Damage,What’s the Connection? A Review

Background: Injury of the trigeminal nerve in oral and maxillofacial surgery can occur. Schwann cell mitochondria are regulators in the development, maintenance and regeneration of peripheral nerve axons. Evidence shows that after the nerve injury, mitochondrial bioenergetic dysfunction occurs and is associated with pain, neuropathy and nerve regeneration deficit. A challenge for research is to individuate new therapies able to normalise mitochondrial and energetic metabolism to aid nerve recovery after damage. Photobiomodulation therapy can be an interesting candidate, because it is a technique involving cell manipulation through the photonic energy of a non-ionising light source (visible and NIR light), which produces a nonthermal therapeutic effect on the stressed tissue. Methods: The review was based on the following questions: (1) Can photo-biomodulation by red and NIR light affect mitochondrial bioenergetics? (2) Can photobiomodulation support damage to the trigeminal nerve branches? (preclinical and clinical studies), and, if yes, (3) What is the best photobiomodulatory therapy for the recovery of the trigeminal nerve branches? The papers were searched using the PubMed, Scopus and Cochrane databases. This review followed the ARRIVE-2.0, PRISMA and Cochrane RoB-2 guidelines. Results and conclusions: The reliability of photobiomodulatory event strongly bases on biological and physical-chemical evidence. Its principal player is the mitochondrion, whether its cytochromes are directly involved as a photoacceptor or indirectly through a vibrational and energetic variation of bound water: water as the photoacceptor. The 808-nm and 100 J/cm² (0.07 W; 2.5 W/cm²; pulsed 50 Hz; 27 J per point; 80 s) on rats and 800-nm and 0.2 W/cm² (0.2 W; 12 J/cm²; 12 J per point; 60 s, CW) on humans resulted as trustworthy therapies, which could be supported by extensive studies.     

Botulinum Toxin: From Poison to Possible Treatment for Spasticity in Spinal Cord Injury

Botulism has been known for about three centuries, and since its discovery, botulinum toxin has been considered one of the most powerful toxins. However, throughout the 20th century, several medical applications have been discovered, among which the treatment of spasticity stands out. Botulinum toxin is the only pharmacological treatment recommended for spasticity of strokes and cerebral palsy. Although its use as an adjuvant treatment against spasticity in spinal cord injuries is not even approved, botulinum toxin is being used against such injuries. This article describes the advances that have been made throughout history leading to the therapeutic use of botulinum toxin and, in particular, its application to the treatment of spasticity in spinal cord injury.     

Study of key parameters in modeling liquid hydrogen release and dispersion in open environment

Hydrogen storage in liquid state is considered key feature to its efficient volumetric density for transportation applications. However, there are several hazards associated with handling liquid hydrogen, e.g. fire, explosion, asphyxiation in indoor accidents, and frostbites due to exposure in extremely low temperatures. Predictive capabilities of liquid hydrogen dispersion are essential for developing emergency response plans and facilitate the understanding of the physical problem. In the present study, the Computational Fluid Dynamics (CFD) methodology is employed to simulate the dispersion of liquid hydrogen based on experiment conducted by the Health Safety Laboratory (HSL), in order to investigate several factors that greatly influence dispersion modeling. The flashed vapour fraction at the pipe exit is estimated assuming isenthalpic expansion combined with the NIST equation of state. Modeling the condensation of ambient humidity and air components (nitrogen and oxygen) and imposing transient wind profile are the main issues addressed by the present study. The Homogeneous Equilibrium Model (HEM model) is compared against the Non-Homogeneous Equilibrium Model (NHEM model) to account for slip effects of the non-vapour phase. To estimate the slip velocity in the NHEM model a methodology (momentum slip model) is employed, which solves along with the conservation equations for the mixture the momentum conservation equation of the non-vapour phase. Comparison of the momentum slip model with the algebraic slip model shows that the latter overestimates the slip velocity for large particles and thus its use needs special attention. Overall satisfactory agreement was found with the experimental data when all the above parameters were modelled.     

Failed Neuroprotection of Combined Inhibition of L-Type and ASIC1a Calcium Channels with Nimodipine and Amiloride

Effective pharmacological neuroprotection is one of the most desired aims in modern medicine. We postulated that a combination of two clinically used drugs—nimodipine (L-Type voltage-gated calcium channel blocker) and amiloride (acid-sensing ion channel inhibitor)—might act synergistically in an experimental model of ischaemia, targeting the intracellular rise in calcium as a pathway in neuronal cell death. We used organotypic hippocampal slices of mice pups and a well-established regimen of oxygen-glucose deprivation (OGD) to assess a possible neuroprotective effect. Neither nimodipine (at 10 or 20 µM) alone or in combination with amiloride (at 100 µM) showed any amelioration. Dissolved at 2.0 Vol.% dimethyl-sulfoxide (DMSO), the combination of both components even increased cell damage (p = 0.0001), an effect not observed with amiloride alone. We conclude that neither amiloride nor nimodipine do offer neuroprotection in an in vitro ischaemia model. On a technical note, the use of DMSO should be carefully evaluated in neuroprotective experiments, since it possibly alters cell damage.     

Biodegradable Spheres Protect Traumatically Injured Spinal Cord by Alleviating the Glutamate‐Induced Excitotoxicity

New treatment strategies for spinal cord injury with good therapeutic efficacy are actively pursued. Here, acetalated dextran (AcDX), a biodegradable polymer obtained by modifying vicinal diols of dextran, is demonstrated to protect the traumatically injured spinal cord. To facilitate its administration, AcDX is formulated into microspheres (≈7.2 µm in diameter) by the droplet microfluidic technique. Intrathecally injected AcDX microspheres effectively reduce the traumatic lesion volume and inflammatory response in the injured spinal cord, protect the spinal cord neurons from apoptosis, and ultimately, recover the locomotor function of injured rats. The neuroprotective feature of AcDX microspheres is achieved by sequestering glutamate and calcium ions in cerebrospinal fluid. The scavenging of glutamate and calcium ion reduces the influx of calcium ions into neurons and inhibits the formation of reactive oxygen species. Consequently, AcDX microspheres attenuate the expression of proapoptotic proteins, Calpain, and Bax, and enhance the expression of antiapoptotic protein Bcl‐2. Overall, AcDX microspheres protect traumatically injured spinal cord by alleviating the glutamate‐induced excitotoxicity. This study opens an exciting perspective toward the application of neuroprotective AcDX for the treatment of severe neurological diseases.