scholarly journals Pre-treatment with simvastatin prevents the induction of diet-induced atherosclerosis in a rabbit model

2016 ◽  
Vol 5 (6) ◽  
pp. 667-674 ◽  
Author(s):  
Nikolaos Oikonomidis ◽  
Nikolaos Kavantzas ◽  
Laskarina-Maria Korou ◽  
Panagiotis Konstantopoulos ◽  
Vasilios Pergialiotis ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Pre Treatment

scholarly journals Trypsin Pre‐Treatment Combined With Growth Factor Functionalized Self‐Assembling Peptide Hydrogel Improves Cartilage Repair in Rabbit Model

2019 ◽  
Vol 37 (11) ◽  
pp. 2307-2315 ◽  
Author(s):  
Gustavo Zanotto ◽  
Paul Liebesny ◽  
Myra Barrett ◽  
Hannah Zlotnick ◽  
Alan Grodzinsky ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cartilage Repair ◽  
Rabbit Model ◽  
Self Assembling ◽  
Pre Treatment ◽  
Peptide Hydrogel

EELS characterization of “Smut” layer films on steel surface prepared for chrome plating by anodic etching

1995 ◽  
Vol 53 ◽  
pp. 538-539
Author(s):  
E Y. Wang ◽  
J. T. Cherian ◽  
A. Madsen ◽  
R. M. Fisher
Keyword(s):  
Steel Surface ◽  
Surface Preparation ◽  
Treatment Method ◽  
Chrome Plating ◽  
Transmission Electron ◽  
Alloy Steels ◽  
Pre Treatment ◽  
Hard Chrome ◽  
Electron Energy Loss

Many steel parts are electro-plated with chromium to protect them against corrosion and to improve their wear-resistance. Good adhesion of the chrome plate to the steel surface, which is essential for long term durability of the part, is extremely dependent on surface preparation prior to plating. Recently, McDonnell Douglas developed a new pre-treatment method for chrome plating in which the steel is anodically etched in a sulfuric acid and hydrofluoric acid solution. On carbon steel surfaces, this anodic pre-treatment produces a dark, loosely adhering material that is commonly called the “smut” layer. On stainless steels and nickel alloys, the surface is only darkened by the anodic pre-treatment and little residue is produced. Anodic pre-treatment prior to hard chrome plating results in much better adherence to both carbon and alloy steels.We have characterized the anodic pre-treated steel surface and the resulting “smut” layer using various techniques including electron spectroscopy for chemical analysis (ESCA) on bulk samples and transmission electron microscopy (TEM) and electron energy-loss spectroscopy (EELS) on stripped films.

Evaluating the effect of a group pre-treatment chemotherapy psycho-education session for chemotherapy-naive gynecologic cancer patients and their caregivers

2021 ◽  
Vol 160 (1) ◽  
pp. 234-243
Author(s):  
Diana Samoil ◽  
Nazek Abdelmutti ◽  
Lisa Ould Gallagher ◽  
Nazlin Jivraj ◽  
Naa Kwarley Quartey ◽  
...  
Keyword(s):  
Cancer Patients ◽  
Gynecologic Cancer ◽  
Education Session ◽  
Pre Treatment

The Effect of Dietary Glutathione and Coenzyme Q10 on the Prevention and Treatment of Inflammatory Bowel Disease in Mice

2004 ◽  
Vol 74 (1) ◽  
pp. 74-85 ◽  
Author(s):  
Liu ◽  
Russell ◽  
Smith ◽  
Bronson ◽  
Milbury ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Dextran Sulfate ◽  
Coenzyme Q ◽  
Histological Evaluation ◽  
Therapeutic Effects ◽  
Prevention Study ◽  
Prevention And Treatment ◽  
Inflammatory Bowel ◽  
Pre Treatment

Because reactive oxygen species have been implicated as mediators of inflammatory bowel disease (IBD), we evaluated the potential preventive and therapeutic effects of two dietary antioxidants, glutathione (GSH) and coenzyme Q10 (CoQ10) on dextran sulfate sodium (DSS)-induced colitis in mice. Fifty female 8-wk old Swiss-Webster mice were randomly assigned to 4 groups for a pre-treatment 'prevention' study: (1) GSH (1% of diet); (2) CoQ10 (200 mg/kg/d); (3) DSS only (3% of drinking water); (4) control (no treatment). The mice in groups 1 and 2 were fed with GSH or CoQ10 for 21 wks, and the mice in groups 1, 2 and 3 were provided DSS from wk 7 for 4 cycles (1 cycle = 1 wk DSS followed by 2-wk water). Another 50 mice were randomly assigned to 4 groups for a 21-wk 'treatment' study where the mice in groups 1, 2, and 3 were administered DSS for 6 cycles (18 wks) to induce colitis. GSH and CoQ10 were added from wk 7 until the completion of the protocol. Loose stools and hemocult positivity were modestly but significantly reduced with GSH or CoQ10 at several periods during the intervention in both the prevention and treatment studies. In contrast, histological evaluation revealed increases in colonic dysplasia and ulceration with GSH or CoQ10. Thus, in this mouse model, GSH and CoQ10 appear to have a beneficial effect on acute signs of IBD, but may have an adverse impact on the chronic pathophysiology of the disease. Further studies using additional animal models are required to determine whether GSH or CoQ10 provide a favorable or unfavorable benefit:risk ratio in the prevention or treatment of IBD.

Cytoprotective Effect of Tocotrienol-Rich Fraction and α-Tocopherol Vitamin E Isoforms Against Glutamate-Induced Cell Death in Neuronal Cells

2014 ◽  
Vol 84 (3-4) ◽  
pp. 0140-0151 ◽  
Author(s):  
Thilaga Rati Selvaraju ◽  
Huzwah Khaza’ai ◽  
Sharmili Vidyadaran ◽  
Mohd Sokhini Abd Mutalib ◽  
Vasudevan Ramachandran ◽  
...  
Keyword(s):  
Vitamin E ◽  
Cell Viability ◽  
Neuronal Cells ◽  
Positive Control ◽  
Post Treatment ◽  
Mitochondrial Activity ◽  
Before And After ◽  
Pre Treatment ◽  
Tocotrienol Rich Fraction ◽  
Major Mediator

Glutamate is the major mediator of excitatory signals in the mammalian central nervous system. Extreme amounts of glutamate in the extracellular spaces can lead to numerous neurodegenerative diseases. We aimed to clarify the potential of the following vitamin E isomers, tocotrienol-rich fraction (TRF) and α-tocopherol (α-TCP), as potent neuroprotective agents against glutamate-induced injury in neuronal SK-N-SH cells. Cells were treated before and after glutamate injury (pre- and post-treatment, respectively) with 100 - 300 ng/ml TRF/α-TCP. Exposure to 120 mM glutamate significantly reduced cell viability to 76 % and 79 % in the pre- and post-treatment studies, respectively; however, pre- and post-treatment with TRF/α-TCP attenuated the cytotoxic effect of glutamate. Compared to the positive control (glutamate-injured cells not treated with TRF/α-TCP), pre-treatment with 100, 200, and 300 ng/ml TRF significantly improved cell viability following glutamate injury to 95.2 %, 95.0 %, and 95.6 %, respectively (p < 0.05).The isomers not only conferred neuroprotection by enhancing mitochondrial activity and depleting free radical production, but also increased cell viability and recovery upon glutamate insult. Our results suggest that vitamin E has potent antioxidant potential for protecting against glutamate injury and recovering glutamate-injured neuronal cells. Our findings also indicate that both TRF and α-TCP could play key roles as anti-apoptotic agents with neuroprotective properties.

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