scholarly journals Neural cell injury pathology due to high-rate mechanical loading

2021 ◽  
pp. 100034
Author(s):  
Jonathan B. Estrada ◽  
Harry C. Cramer ◽  
Mark T. Scimone ◽  
Selda Buyukozturk ◽  
Christian Franck
Keyword(s):  
Mechanical Loading ◽  
Cell Injury ◽  
Neural Cell ◽  
High Rate

Neurotoxicity of General Anaesthetics

2019 ◽  
pp. 93-110
Author(s):  
Margaret K. Menzel Ellis ◽  
Ansgar Brambrink
Keyword(s):  
Animal Models ◽  
Prospective Studies ◽  
Cell Injury ◽  
Large Body ◽  
Neural Cell ◽  
Developing Brain ◽  
Human Studies ◽  
Childhood Exposure

This chapter covers the neurotoxicity of general anaesthetics. It discusses how a large body of preclinical evidence shows an association of anaesthetic exposure with neural cell injury and death in the developing brain. Several putative mechanisms have been demonstrated in vitro and in in vivo animal models. Furthermore, these exposures have been associated with impaired behavioural and cognitive development in young animals. Several retrospective human studies of neurocognitive and behavioural disorders following childhood exposure to anaesthesia suggest a similar association, and prospective studies in humans are currently ongoing. The implication of this information on anaesthetic practise remains to be seen.

scholarly journals Tonicity-responsive enhancer-binding protein promotes hepatocellular carcinogenesis, recurrence and metastasis

Gut ◽  
2018 ◽  
Vol 68 (2) ◽  
pp. 347-358 ◽  
Author(s):  
Jun Ho Lee ◽  
Jae Hee Suh ◽  
Soo Youn Choi ◽  
Hyun Je Kang ◽  
Hwan Hee Lee ◽  
...  
Keyword(s):  
Cell Injury ◽  
Tumour Progression ◽  
Binding Protein ◽  
Tissue Microarrays ◽  
High Rate ◽  
Enhancer Binding Protein ◽  
Attractive Therapeutic Target ◽  
Cox 2 ◽  
Personalised Treatment

ObjectivesHepatocellular carcinoma (HCC) is a common cancer with high rate of recurrence and mortality. Diverse aetiological agents and wide heterogeneity in individual tumours impede effective and personalised treatment. Tonicity-responsive enhancer-binding protein (TonEBP) is a transcriptional cofactor for the expression of proinflammatory genes. Although inflammation is intimately associated with the pathogenesis of HCC, the role of TonEBP is unknown. We aimed to identify function of TonEBP in HCC.DesignTumours with surrounding hepatic tissues were obtained from 296 patients with HCC who received completion resection. TonEBP expression was analysed by quantitative reverse transcription–quantitative real-time PCR (RT-PCR) and immunohfistochemical analyses of tissue microarrays. Mice with TonEBP haplodeficiency, and hepatocyte-specific and myeloid-specific TonEBP deletion were used along with HCC and hepatocyte cell lines.ResultsTonEBP expression is higher in tumours than in adjacent non-tumour tissues in 92.6% of patients with HCC regardless of aetiology associated. The TonEBP expression in tumours and adjacent non-tumour tissues predicts recurrence, metastasis and death in multivariate analyses. TonEBP drives the expression of cyclo-oxygenase-2 (COX-2) by stimulating the promoter. In mouse models of HCC, three common sites of TonEBP action in response to diverse aetiological agents leading to tumourigenesis and tumour growth were found: cell injury and inflammation, induction by oxidative stress and stimulation of the COX-2 promoter.ConclusionsTonEBP is a key component of the common pathway in tumourigenesis and tumour progression of HCC in response to diverse aetiological insults. TonEBP is involved in multiple steps along the pathway, rendering it an attractive therapeutic target as well as a prognostic biomarker.

Effect of estrogen and its receptors on glutamate-induced neural cell injury

2011 ◽  
Vol 31 (7) ◽  
pp. 795-798
Author(s):  
Guang-yun ZHANG ◽  
Xiao HU ◽  
Lei LOU ◽  
Jian-yi WANG
Keyword(s):  
Cell Injury ◽  
Neural Cell

scholarly journals Spinal cord stimulation using differential target multiplexed programming modulates neural cell-specific transcriptomes in an animal model of neuropathic pain

2020 ◽  
Vol 16 ◽  
pp. 174480692096436
Author(s):  
David L Cedeño ◽  
William J Smith ◽  
Courtney A Kelley ◽  
Ricardo Vallejo
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Nerve Injury ◽  
Spinal Cord Stimulation ◽  
Neural Cell ◽  
High Rate ◽  
Spared Nerve Injury ◽  
Expression Levels ◽  
Injury Model ◽  
Low Rate

Spinal cord stimulation is a proven effective therapy for treating chronic neuropathic pain. Previous work in our laboratory demonstrated that spinal cord stimulation based on a differential target multiplexed programming approach provided significant relief of pain-like behavior in rodents subjected to the spared nerve injury model of neuropathic pain. The relief was significantly better than obtained using high rate and low rate programming. Furthermore, transcriptomics-based results implied that differential target multiplexed programming modulates neuronal–glial interactions that have been perturbed by the pain process. Although differential target multiplexed programming was developed to differentially target neurons and glial cells, our previous work did not address this. This work presents transcriptomes, specific to each of the main neural cell populations (neurons, microglia, astrocytes, and oligodendrocytes), obtained from spinal cord subjected to continuous spinal cord stimulation treatment with differential target multiplexed programming, high rate programming, or low rate programming compared with no spinal cord stimulation treatment, using the spared nerve injury model. To assess the effect of each spinal cord stimulation treatment on these cell-specific transcriptomes, gene expression levels were compared with that of healthy animals, naïve to injury and interventional procedures. Pearson correlations and cell population analysis indicate that differential target multiplexed programming yielded strong and significant correlations to expression levels found in the healthy animals across every evaluated cell-specific transcriptome. In contrast, high rate programming only yielded a strong correlation for the microglia-specific transcriptome, while low rate programming did not yield strong correlations with any cell types. This work provides evidence that differential target multiplexed programming distinctively targeted and modulated the expression of cell-specific genes in the direction of the healthy state thus supporting its previously established action on regulating neuronal–glial interaction processes in a pain model.

scholarly journals Neural cell injury pathology due to high-rate mechanical loading

2021 ◽  
Author(s):  
Jonathan B Estrada ◽  
Harry C Cramer ◽  
Mark T Scimone ◽  
Selda Buyukozturk ◽  
Christian Franck
Keyword(s):  
Brain Injuries ◽  
Cell Injury ◽  
High Rate ◽  
Neural Cells ◽  
Filamentous Actin ◽  
Lower Strain ◽  
Biochemical Activation ◽  
Primary Injury ◽  
Critical Injury

Successful detection and prevention of brain injuries relies on the quantitative identification of cellular injury thresholds associated with the underlying pathology. Here, by combining a recently developed inertial microcavitation rheology technique with a 3D in vitro neural tissue model, we quantify and resolve the structural pathology and critical injury strain thresholds of neural cells occurring at high loading rates such as encountered in blast exposures or cavitation-based medical procedures. We find that neuronal dendritic spines characterized by MAP2 displayed the lowest physical failure strain at 7.3%, whereas microtubules and filamentous actin were able to tolerate appreciably higher strains (14%) prior to injury. Interestingly, while these critical injury thresholds were similar to previous literature values reported for moderate and lower strain rates (<100 1/s), the pathology of primary injury reported here was distinctly different by being purely physical in nature as compared to biochemical activation during apoptosis or necrosis.

Change in the structural state of grain boundaries under high-rate mechanical loading

1999 ◽  
Vol 35 (6) ◽  
pp. 704-706
Author(s):  
S. G. Psakh'e ◽  
K. P. Zol'nikov ◽  
D. Yu. Saraev
Keyword(s):  
Grain Boundaries ◽  
Mechanical Loading ◽  
Structural State ◽  
High Rate

Amaryllidaceae alkaloids as agents with protective effects against oxidative neural cell injury

Life Sciences ◽  
2018 ◽  
Vol 203 ◽  
pp. 54-65 ◽  
Author(s):  
Natalie Cortes ◽  
Carol Castañeda ◽  
Edison H. Osorio ◽  
Gloria Patricia Cardona-Gomez ◽  
Edison Osorio
Keyword(s):  
Cell Injury ◽  
Neural Cell ◽  
Protective Effects ◽  
Amaryllidaceae Alkaloids

scholarly journals Neuroprotective Norsesquiterpenoids and Triterpenoids from Populus euphratica Resins

Molecules ◽  
2019 ◽  
Vol 24 (23) ◽  
pp. 4379 ◽  
Author(s):  
Yun-Yun Liu ◽  
Dan-Ling Huang ◽  
Yun Dong ◽  
Da-Peng Qin ◽  
Yong-Ming Yan ◽  
...  
Keyword(s):  
Computational Methods ◽  
Cell Injury ◽  
Populus Euphratica ◽  
Biological Evaluation ◽  
Neural Cell ◽  
Activity Relationship ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Structure Activity ◽  
New Compounds

Two new octanorlanostane-type triterpenes, euphraticanoids A and B (1 and 2), two new trinorsesquiterpenoids, euphraticanoids C and D (3 and 4), and eight known triterpenoids (5, 6, 8–13) along with one steroid (7) were isolated from Populus euphratica resins. The structures of these new compounds, including their absolute configurations, were characterized by spectrocsopic, chemical, and computational methods. Biological evaluation revealed that compounds 4, 7–9, 12, and 13 display neuroprotective activities in H2O2-induced HT-22 cells with 4, 8, and 9 occurring in a concentration-dependent manner and 7, 12, and 13 reaching the maximum effects at 20 μM. Meanwhile, the neuroprotective properties of all isolates were accessed using glutamate-induced SH-SY5Y cells and disclosed that compounds 3, 4, 8, and 9 could dose-dependently protect neural cell injury in a concentration range of 10–40 μM. Finally, a brief structure–activity relationship was briefly discussed.

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