Neurotoxic Effects of Root Filling Materials on Rat Phrenic Nerve in vitro

1982 ◽  
Vol 61 (8) ◽  
pp. 1020-1023 ◽  
Author(s):  
P. Brodin ◽  
A. Røed ◽  
H. Aars ◽  
D. ørstavik
Toxics ◽  
2020 ◽  
Vol 8 (3) ◽  
pp. 51
Author(s):  
Jorge Humberto Limón-Pacheco ◽  
Natalie Jiménez-Barrios ◽  
Alejandro Déciga-Alcaraz ◽  
Adriana Martínez-Cuazitl ◽  
Mónica Maribel Mata-Miranda ◽  
...  

Some studies have shown that silicon dioxide nanoparticles (SiO2-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO2-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic effects of SiO2-NP (0–100 µg/mL) on rat astrocyte-rich cultures or neuron-rich cultures using scanning electron microscopy, Attenuated Total Reflection-Fourier Transform Infrared spectroscopy (ATR-FTIR), FTIR microspectroscopy mapping (IQ mapping), and cell viability tests. SiO2-NPs were amorphous particles and aggregated in saline and culture media. Both astrocytes and neurons treated with SiO2-NPs showed alterations in cell morphology and changes in the IR spectral regions corresponding to nucleic acids, proteins, and lipids. The analysis by the second derivative revealed a significant decrease in the signal of the amide I (α-helix, parallel β-strand, and random coil) at the concentration of 10 µg/mL in astrocytes but not in neurons. IQ mapping confirmed changes in nucleic acids, proteins, and lipids in astrocytes; cell death was higher in astrocytes than in neurons (10–100 µg/mL). We conclude that astrocytes were more vulnerable than neurons to SiO2-NPs toxicity. Therefore, the evaluation of human exposure to SiO2-NPs and possible neurotoxic effects must be followed up.


1992 ◽  
Vol 6 (4) ◽  
pp. 285-293 ◽  
Author(s):  
A. Bruinink ◽  
P. Reiser ◽  
M. Müller ◽  
B.H. Gähwiler ◽  
G. Zbinden
Keyword(s):  

2014 ◽  
Vol 60 (5) ◽  
pp. 200-203
Author(s):  
Andreea Borş ◽  
Cristina Molnar-Varlam ◽  
Melinda Székely

Abstract Objective: The aim of this in vitro study was to evaluate the influence of erosive conditions on the wear resistance of aesthetic direct restorative materials. Methods: Six dental filling materials were tested: two composites (Filtek Z550 and X-tra fil), two compomers (Dyract Extra and Twinky Star) and two glass ionomers (Ketac Molar and Fuji II LC). Twenty disks (10mm×2mm) of each material were prepared (n=120) and kept in artificial saliva at 37˚C for 24 hours. Specimens were cycled in acidic soft drink (Coca-Cola) 5×/day, for 5’, over 30 days. Initial surface roughness ISR (Ra-μm) and final surface roughness FSR were measured using a profilometer. The wear rate was calculated as difference of final minus the initial roughness (ΔSR=FSR-ISR). For statistical analysis t-test and one-way ANOVA test were used by GraphPad Prism version 5.03 statistical software. The level of significance was set at p<0.05. Results: The erosive wear rates (mean±SD, μm) after exposure to acidic beverage were: 0.30±0.03 (Ketac Molar), 0.28±0.04 (Fuji II LC), 0.27±0.00 (Filtek Z550), 0.23±0.01 (X-tra fil), 0.20±0.00 (Twinky Star) and 0.14±0.01 Dyract Extra, respectively. There were significant differences between the tested materials (p<0.05). Conclusions: Dental filling materials had different behaviour under the same erosive condition, however all investigated aesthetic restorative materials showed surface degradation. These findings suggest that erosive wear resistance of tooth coloured restoratives could influence their longevity in intraoral acidic conditions. Acknowledgements: The study was supported by the Internal Research Grant no. 5/30.01.2013 of the University of Medicine and Pharmacy of Tirgu Mureş.


1982 ◽  
Vol 60 (7) ◽  
pp. 877-884 ◽  
Author(s):  
John T. Hamilton ◽  
Peggy A. Stone

Changing trends in the use of anxiolytic agents and recent reassessment of their neuropharmacological activity has prompted this evaluation of the peripheral neuromuscular activity of the benzodiazepine, flurazepam. In previous reports we have documented peripheral neuromuscular activity of chlordiazepoxide and diazepam on the rat phrenic nerve diaphragm preparation. The water soluble benzodiazepine, flurazepam, has been studied on the rat phrenic nerve diaphragm and frog rectus abdominis in vitro. On the former preparation flurazepam enhanced and then blocked the response to indirect electrical stimulation (0.2 Hz) and readily blocked posttetanic potentiation and prevented the preparation from sustaining a tetanic contracture (30 Hz). On the later preparation, flurazepam blocked in a noncompetitive manner the response of the frog muscle to applied cholinergic agonists. Studies on the rat preparation with the neuromuscular blocking drug succinylcholine have shown an unexpected protection against blockade in preparations pretreated with low concentrations of flurazepam. This was not observed when flurazepam was given prior to d-tubocurarinc. The application of adenosine to rat diaphragms during steady-state partial blockade caused by flurazepam or d-tubocurarine showed an inhibiting action of adenosine which was reversed by theophylline. Pretreatment of rat preparations with dipyridamole significantly enhanced the blocking action of standard concentrations of succinylcholine.These results, along with those in the literature, encourage a reassessment of the action of purines and benzodiazepines on skeletal muscle and encourage a consideration of a possible involvement of purinergic neuromodulation of transmission which is unmasked when the safety factor for transmission is altered by muscle relaxants. The possible clinical significance of protection against succinylcholine by benzodiazepines is noted.


1995 ◽  
Vol 21 (4) ◽  
pp. 226
Author(s):  
S. Weeks ◽  
J. Vancura ◽  
E. Jacobsen ◽  
J. Daniel ◽  
E. Begole
Keyword(s):  

1982 ◽  
Vol 53 (2) ◽  
pp. 440-447 ◽  
Author(s):  
S. G. Kelsen ◽  
M. L. Nochomovitz

Diaphragm fatigue was studied in innervated diaphragm strips from 63 Sprague-Dawley rats. The experiments examined 1) the effect on the rate of diaphragmatic fatigue of increases in the diaphragm's duty cycle, i.e., the ratio of the period of diaphragmatic contraction (Ti) to the duration of a cycle of contraction and rest (Ttot) and 2) the possibility that impaired neural transmission contributed to the fatigue process. Alterations in the duty cycle of the diaphragm were simulated by varying the pattern of electrical stimuli applied cyclically to the phrenic nerve. Fatigue was assessed from the rate of fall of isometric tension when the muscle was made to contract 90 times/min. The contribution of neural element fatigue was assessed by comparing the tension during phrenic nerve stimulation to the tension developed when the muscle was stimulated directly. Increasing the duty cycle (Ti/Ttot) from 25 to 50 to 75% increased the rate of diaphragmatic fatigue progressively. Holding Ti/Ttot constant at 75%, while varying Ti and Ttot, did not affect the rate of fatigue. Increases in duty cycle appear to increase the rate of fatigue by increasing the number of times the contractile process was activated. In fatigued muscle strips diaphragmatic tension was greater in directly stimulated muscle than in muscle strips activated via the phrenic nerve. The results indicate that 1) when the breathing action of the diaphragm is simulated in vitro, increases in duty cycle accelerate the fatigue process and 2) failure of transmission of phrenic impulses to diaphragmatic muscle cells contributes to the fall in tension during fatigue.


Chemosphere ◽  
2015 ◽  
Vol 120 ◽  
pp. 321-327 ◽  
Author(s):  
Adam Jonas ◽  
Stefan Scholz ◽  
Eva Fetter ◽  
Eliska Sychrova ◽  
Katerina Novakova ◽  
...  

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