scholarly journals Effect of Transcriptional Regulatory Factor FoxO3a on Central Nervous System Oxygen Toxicity

2020 ◽  
Vol 11 ◽  
Author(s):  
Yanan Zhang ◽  
Benming You ◽  
Yuliang Chen ◽  
Junlin Yang ◽  
Chengwei Xie ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Nuclear Translocation ◽  
Oxygen Toxicity ◽  
Knock Out ◽  
Toxic Reaction ◽  
Transcriptional Regulatory ◽  
Highly Sensitive ◽  
Short Time ◽  
Excessive Oxygen

Central nervous system (CNS) oxygen toxicity (CNS-OT) is a toxic reaction that appears after the inhalation of gas at an excessive oxygen partial pressure during underwater operation or hyperbaric oxygen (HBO) treatment. The mechanism of CNS-OT has not been clearly characterized. Though it has been attributed to the excessive oxidative stress induced by HBO, evidences against this hypothesis have been reported. Here we find that Forkhead box protein O3 (FoxO3a) is important for CNS-OT protection. FoxO3a knock-out (KO) mice had a shorter latency to develop convulsions and greater number of seizures within a certain period of time. The acute lung injury (ALI) induced by CNS-OT was also more severe in FoxO3a KO mice. Further analysis reveals a significant decrease in the activity of catalase (CAT), an antioxidant enzyme and a significant increase in the content of malondialdehyde (MDA), an oxidative product, in brain tissues of FoxO3a KO mice. Short-time HBO exposure could increase FoxO3a expression level and trigger its nuclear translocation. The level of nuclear localized FoxO3a peaked at 8 h after exposure. Our results demonstrate that the activity of FoxO3a is highly sensitive to HBO exposure and FoxO3a plays important roles in protecting CNS-OT. Further mechanic analysis reveals that FoxO3a protects CNS-OT via activating antioxidative signaling pathway.

Fluorescence Detection of Hydrazine Hydrate Using Carbon Nanodots Synthesized from Mandarin Rind

2019 ◽  
Vol 891 ◽  
pp. 71-77
Author(s):  
Phitsini Suvarnaphaet ◽  
Wattapong Pinyo ◽  
Suejit Pechprasarn ◽  
Naphat Albutt
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Respiratory Tract ◽  
Hydrazine Hydrate ◽  
Fluorescence Detection ◽  
Carbon Nanodots ◽  
Toxic Chemical ◽  
Highly Sensitive ◽  
Pharmaceutical Industries ◽  
Highly Sensitive Detection

Hydrazine hydrate is a highly toxic chemical widely used in agricultural and pharmaceutical industries. Exposure to hydrazine can induce an irritation of respiratory tract, blindness, damage of the DNA and central nervous system. In this paper, we will show the hydrazine hydrate (N2H4) detection using fluorescence carbon nanodots synthesized from mandarin rind, the so-called R-CNDs. Highly sensitive detection can be seen by naked eyes in a fluorescence red-shifting and by analyzing absorption spectra in case of micromolar concentrations of hydrazine hydrate solution.

A Newly Developed Mouse Monoclonal SOX10 Antibody Is a Highly Sensitive and Specific Marker for Malignant Melanoma, Including Spindle Cell and Desmoplastic Melanomas

2014 ◽  
Vol 139 (4) ◽  
pp. 530-536 ◽  
Author(s):  
David Tacha ◽  
Weimin Qi ◽  
Seong Ra ◽  
Ryan Bremer ◽  
Charlie Yu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Malignant Melanoma ◽  
Peripheral Nerve ◽  
Immunohistochemical Staining ◽  
Spindle Cell ◽  
Breast Carcinomas ◽  
Peripheral Nerve Sheath Tumors ◽  
Highly Sensitive ◽  
Wide Range

Context Recent immunohistochemical studies have demonstrated Sry-related HMG-Box gene 10 (SOX10) expression in malignant melanomas, malignant peripheral nerve sheath tumors, a subset of breast carcinomas, and gliomas. SOX10 has shown important clinical utility in its ability to detect desmoplastic and spindle cell melanomas. To date, most publications have employed a research use–only goat polyclonal SOX10 antibody for immunohistochemical staining. Objective To describe the development of a new mouse monoclonal SOX10 antibody (BC34) and evaluate its immunohistochemical staining profile in a wide range of normal and neoplastic tissues, with an emphasis on melanoma. Design SOX10 antibody was optimized for staining using a polymer detection system and visualization with diaminobenzidine. Results In normal tissues, SOX10 was expressed in skin melanocytes and eccrine cells, breast myoepithelial and lobular epithelial cells, salivary gland myoepithelial cells, peripheral nerve Schwann cells, and central nervous system glial cells. SOX10 was expressed in 238 of 257 melanomas (92.6%), including 50 of 51 of both spindle cell and desmoplastic melanomas (98%). SOX10 was expressed in 100% of nevi (20 of 20) and schwannomas (28 of 28). In other neoplasms, SOX10 was expressed in 18 of 109 invasive ductal breast carcinomas (16.5%). All other carcinomas were negative for SOX10. SOX10 was identified in 25 of 52 central nervous system neoplasms, primarily in astrocytomas (22 of 41; 53.7%), and in 4 of 99 various sarcomas examined (4.0%). Conclusions The newly developed mouse monoclonal SOX10 antibody BC34 is highly sensitive and specific for malignant melanoma, including desmoplastic and spindle cell variants, and appears highly suitable for clinical use.

Abstract 14: Central Nervous System Deletion of the Bbs1 Gene Causes Obesity and Hypertension in Mice

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Deng-Fu Guo ◽  
Donald A Morgan ◽  
Charles C Searby ◽  
Darryl Y Nishmura ◽  
Val C Sheffield ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Arterial Pressure ◽  
Energy Homeostasis ◽  
Autosomal Recessive Disorder ◽  
Conditional Knockout ◽  
Peripheral Tissues ◽  
Knock Out ◽  
Obesity Phenotype

Bardet-Biedl syndrome (BBS) is a pleiotropic autosomal recessive disorder with several features including obesity and hypertension. Systemic knock-out mouse models lacking expression of Bbs2, Bbs4 and Bbs6 genes, and Bbs1 M390R knock-in recapitulated many of the BBS phenotypes including obesity. However, the role and contribution of different tissues to the various phenotypes associated with BBS including obesity and hypertension remains unclear. To address this, we generated a new conditional knockout mouse where exon 3 of the Bbs1 gene is floxed. Cre-mediated recombination causes a frame shift resulting in a premature stop. We assessed whether deletion of the Bbs1 gene in the central nervous system (CNS) affects body weight and arterial pressure. Breeding Bbs1 flox with nestin Cre mice created mice deficient in Bbs1 gene only in the CNS as indicated by the loss of Bbs1 gene expression (by RT-PCR) in the hypothalamus, hippocampus, cortex and brainstem, but not in peripheral tissues such as adipose tissue, liver, kidney and skeletal muscle. Importantly, Bbs1 flox /nestin Cre mice display an obesity phenotype as indicated by the increased (P<0.05) body weight (40±1 g vs. 31±1 g in controls) and fat mass measured by MRI (23±2 g vs. 9±1 g in controls) in 25 weeks old mice. We found that the obesity phenotype in Bbs1 flox /nestin Cre mice is due to both an increase (P<0.05) in food intake (4.0±0.2 g vs. 3.1±0.3 g in controls) and reduction in energy expenditure as indicated by the decreased (P<0.05) O 2 consumption (2.8±0.3 mL/100g/min vs. 3.2±0.2 mL/100g/min in controls) and heat production (8.3±0.8 kcal/kg/h vs. 9.4±0.7 kcal/kg/h in controls). These results indicate that hyperphagia and low metabolic rate explain the development of obesity in Bbs1 flox /nestin Cre mice. Finally, we assessed by radiotelemetry the consequence on arterial pressure of ablating the Bbs1 gene throughout the CNS. Interestingly, CNS deletion of the Bbs1 gene recapitulates the hypertension phenotype of BBS as indicated by the elevated mean arterial pressure in Bbs1 flox /nestin Cre (123±3 mmHg) relative to littermate controls (112±4 mmHg, P=0.02). These findings demonstrate that Bbs genes in the CNS are critical for energy homeostasis and arterial pressure regulation.

Prediction of central nervous system oxygen toxicity in rats

1994 ◽  
Vol 77 (4) ◽  
pp. 1903-1906 ◽  
Author(s):  
R. Arieli ◽  
G. Hershko
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Exposure Time ◽  
Electrical Discharge ◽  
Oxygen Toxicity ◽  
Threshold Value ◽  
Power Equation ◽  
The Mean

Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

Ventilatory afterdischarge and central respiratory drive interactions in the awake goat

1994 ◽  
Vol 76 (1) ◽  
pp. 416-423 ◽  
Author(s):  
M. J. Engwall ◽  
C. A. Smith ◽  
J. A. Dempsey ◽  
G. E. Bisgard
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Time Constant ◽  
Minute Ventilation ◽  
Respiratory Drive ◽  
Arterial Pco2 ◽  
Expiratory Muscle ◽  
Series Of Experiments ◽  
Short Time ◽  
Animal Preparation

We have previously established the existence of ventilatory afterdischarge (VAD) in the awake goat by means of an isolated perfused carotid body (CB) technique. In the present series of experiments we used this animal preparation to examine the effects of systemic (central nervous system) hypoxia, mild hypercapnia, and hypocapnia on the manifestation of VAD in ventilatory variables and respiratory muscle electromyogram activity after hypoxic stimulation of the isolated CB. With systemic isocapnic normoxia, inspired minute ventilation remains above control for 30–40 s (time constant = 16.8 s) after termination of CB hypoxia; however, with systemic hypocapnia, VAD is short (time constant = 5.5 s) and hypoventilation is common after removal of CB stimulation. During mild systemic hypercapnia, VAD is prolonged (time constant = 39.9 s). However, systemic (central nervous system) hypoxia did not decrease VAD (time constant = 17.0 s). These results indicate that the manifestation of VAD is more sensitive to the level of arterial PCO2 and central chemoreceptor activity than it is to the state of central oxygenation. Inspiratory and expiratory muscle electromyogram activities qualitatively tracked ventilation during CB stimulation and during the VAD period in all conditions.

scholarly journals Effect of Luteolin and Apigenin on the Production of Il-31 and Il-33 in Lipopolysaccharides-Activated Microglia Cells and Their Mechanism of Action

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 811 ◽  
Author(s):  
Denis Nchang Che ◽  
Byoung Ok Cho ◽  
Ji-su Kim ◽  
Jae Young Shin ◽  
Hyun Ju Kang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Nuclear Translocation ◽  
Mapk Pathway ◽  
Microglial Cells ◽  
Stat3 Signaling ◽  
Protein Expressions ◽  
The Central Nervous System

Microglia cells are resident cells of the central nervous system (CNS) charged with modulating inflammation in the CNS. Overstimulation of microglia cells continuously releases inflammatory mediators that contribute to neurodegenerative diseases. Apigenin and Luteolin are flavonoids with reported anti-inflammatory activities. However, their effects on IL-31 and IL-33 production in microglial cells are unknown. Here, we investigated the effects of apigenin and luteolin on the production of IL-31 and IL-33 by microglia cells. SIM-A9 microglial cells were pre-treated with apigenin or luteolin and stimulated with lipopolysaccharides to evaluate the production of IL-31 and IL-33. The study revealed that apigenin and luteolin inhibited the production of IL-31 and IL-33 at the gene and protein expressions and the secretion levels. Using potent inhibitors of MAPK, NF-κB, and STAT3 signaling pathways, we demonstrated that apigenin and luteolin’s suppression of ERK and JNK contributed to the inhibition of IL-31 and IL-33 in the MAPK pathway. Luteolin’s suppression of NF-κB and STAT3 also contributed to the inhibition of IL-31 and IL-33. Further analysis revealed that both compounds prevented nuclear translocation of activated NF-κB and STAT3, an act that subsequently prevented their DNA binding activities. Collectively, the study suggested that apigenin and luteolin’s regulation of signaling pathways contributed to the inhibition of IL-31 and IL-33, thus suggesting its importance for the improvement of neurodegenerative diseases involving these two cytokines.

Effect of Interaction between Adenosine and Nitric Oxide on Central Nervous System Oxygen Toxicity

2019 ◽  
Vol 36 (1) ◽  
pp. 193-203 ◽  
Author(s):  
Cheng-wei Xie ◽  
Zhong-zhuang Wang ◽  
Ya-nan Zhang ◽  
Yu-liang Chen ◽  
Run-ping Li ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity

scholarly journals Female rats are more susceptible to central nervous system oxygen toxicity than male rats

2014 ◽  
Vol 2 (4) ◽  
pp. e00282 ◽  
Author(s):  
Heather E. Held ◽  
Raffaele Pilla ◽  
Geoffrey E. Ciarlone ◽  
Carol S. Landon ◽  
Jay B. Dean
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity ◽  
Female Rats ◽  
Male Rats

The effect of vigabatrin on central nervous system oxygen toxicity in rats

1991 ◽  
Vol 202 (2) ◽  
pp. 171-175 ◽  
Author(s):  
Tzahala Tzuk-Shina ◽  
Noemi Bitterman ◽  
Dan Harel
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Oxygen Toxicity
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