scholarly journals Methane alleviates sepsis-induced injury by inhibiting pyroptosis and apoptosis: in vivo and in vitro experiments

Aging ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 1226-1239 ◽  
Author(s):  
Zeyu Li ◽  
Yifan Jia ◽  
Yang Feng ◽  
Ruixia Cui ◽  
Runchen Miao ◽  
...  
Keyword(s):  
In Vitro Experiments

scholarly journals Development of a gel dedicated to gel immersion endoscopy

2021 ◽  
Vol 09 (06) ◽  
pp. E918-E924
Author(s):  
Tomonori Yano ◽  
Atsushi Ohata ◽  
Yuji Hiraki ◽  
Makoto Tanaka ◽  
Satoshi Shinozaki ◽  
...  
Keyword(s):  
Electrical Conductivity ◽  
Porcine Model ◽  
Ex Vivo ◽  
In Vitro Experiments ◽  
Efficacy And Safety ◽  
Coagulative Necrosis ◽  
Novel Technique ◽  
In Vivo Experiments

Abstract Backgrounds and study aims Gel immersion endoscopy is a novel technique to secure the visual field during endoscopy. The aim of this study was to develop a dedicated gel for this technique. Methods To identify appropriate viscoelasticity and electrical conductivity, various gels were examined. Based on these results, the dedicated gel “OPF-203” was developed. Efficacy and safety of OPF-203 were evaluated in a porcine model. Results  In vitro experiments showed that a viscosity of 230 to 1900 mPa·s, loss tangent (tanδ) ≤ 0.6, and hardness of 240 to 540 N/cm2 were suitable. Ex vivo experiments showed electrical conductivity ≤ 220 μS/cm is appropriate. In vivo experiments using gastrointestinal bleeding showed that OPF-203 provided clear visualization compared to water. After electrocoagulation of gastric mucosa in OPF-203, severe coagulative necrosis was not observed in the muscularis but limited to the mucosa. Conclusions OPF-203 is useful for gel immersion endoscopy.

scholarly journals Study on Establishing Reference Safe Concentrations of MRI Contrast Agents for Optimized Images: Paramagnetic Gd-DTPA-BMEA and Superparamagnetic Ferucarbotran

2021 ◽  
Vol 11 (3) ◽  
pp. 1165
Author(s):  
Wen-Tien Hsiao ◽  
Yi-Hong Chou ◽  
Jhong-Wei Tu ◽  
Ai-Yih Wang ◽  
Lu-Han Lai
Keyword(s):  
Contrast Agent ◽  
Contrast Agents ◽  
Mri Contrast Agents ◽  
Mri Contrast Agent ◽  
In Vitro Experiments ◽  
Mri Contrast ◽  
In Vivo Experiments ◽  
Contrast Agent Injection

The purpose of this study is to establish the minimal injection doses of magnetic resonance imaging (MRI) contrast agents that can achieve optimized images while improving the safety of injectable MRI drugs. Gadolinium-diethylenetriamine penta-acetic acid (Gd-DTPA) and ferucarbotran, commonly used in clinical practice, were selected and evaluated with in vitro and in vivo experiments. MRI was acquired using T1-weighted (T1W) and T2-weighted (T2W) sequences, and the results were quantitatively analyzed. For in vitro experiments, results showed that T1W and T2W images were optimal when Gd-DTPA-bisamide (2-oxoethyl) (Gd-DTPA-BMEA) and ferucarbotran were diluted to a volume percentage of 0.6% and 0.05%; all comparisons were significant differences in grayscale statistics using one-way analysis of variance (ANOVA). For in vivo experiments, the contrast agent with optimal concentration percentages determined from in vitro experiments were injected into mice with an injection volume of 100 μL, and the images of brain, heart, liver, and mesentery before and after injection were compared. The statistical results showed that the p values of both T1W and T2W were less than 0.001, which were statistically significant. Under safety considerations for MRI contrast agent injection, optimized MRI images could still be obtained after reducing the injection concentration, which can provide a reference for the safety concentrations of MRI contrast agent injection in the future.

Anticancer effect of arsenic trioxide on cholangiocarcinoma: in vitro experiments and in vivo xenograft mouse model

2013 ◽  
Vol 14 (2) ◽  
pp. 215-224 ◽  
Author(s):  
Eun-Young Kim ◽  
Sang Soo Lee ◽  
Ji Hoon Shin ◽  
Soo Hyun Kim ◽  
Dong-Ho Shin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Arsenic Trioxide ◽  
In Vitro Experiments ◽  
Anticancer Effect ◽  
Xenograft Mouse Model

scholarly journals Reversible neutralization by congo red of the anthracidal power of serum

1937 ◽  
Vol 37 (3) ◽  
pp. 471-473 ◽  
Author(s):  
J. Gordon ◽  
N. Wood
Keyword(s):  
Guinea Pig ◽  
Congo Red ◽  
Inhibitory Action ◽  
Protein Solutions ◽  
Haemolytic Activity ◽  
In Vitro Experiments ◽  
Serum Complement ◽  
Destructive Effect

In earlier papers (Gordon, 1930) it was shown that congo red has an inactivating effect on serum complement, both haemolytic and bactericidal, and that this effect can be reversed by treating the serum and congo red mixture with charcoal, the charcoal removing the congo red and leaving the complement active again. A similar reversal of inactivation is obtained by using instead of the charcoal, heated serum (55° C. for 30 min.) or protein solutions. Later (Gordon, 1931), it was shown that congo red had an inactivating effect on the haemolysins of Streptococcus haemolyticus and B. welchii. The reversibility of this effect was not so easy to demonstrate as with complement. Charcoal had a destructive effect on the haemolysins and so could not be used. It was found, however, that when the concentration of congo red was just sufficient to neutralize the streptococcal haemolysin, the addition of cuprammonium artificial silk adsorbed the congo red and liberated the haemolysin. In the case of B. welchii this method of reversal was not suitable, as the artificial silk had a destructive effect on the haemolysin. Instead, reversibility was demonstrated by adding ox serum to the mixture of congo red and haemolysin. This brought about a redistribution of the congo red between the ox serum and the haemolysin and if the amount of congo red used had been only just sufficient to neutralize the haemolysin of B. welchii, then the haemolytic activity could again be demonstrated. Gordon and Robson (1933) showed that congo red interfered with the anaphylactic reaction tested both in vivo and in vitro, the guinea-pig uterus being used in the in vitro experiments, in which the inhibitory action of the dye was shown to be reversible. It was suggested that the congo red interfered with the entrance of antigen into the cell.

scholarly journals Interaction of integrins alpha 3 beta 1 and alpha 2 beta 1: potential role in keratinocyte intercellular adhesion.

1993 ◽  
Vol 120 (2) ◽  
pp. 523-535 ◽  
Author(s):  
B E Symington ◽  
Y Takada ◽  
W G Carter
Keyword(s):  
Potential Role ◽  
Intercellular Adhesion ◽  
Epidermal Cells ◽  
Intercellular Contact ◽  
In Vitro Experiments ◽  
Selective Binding ◽  
Contact Sites ◽  
Do So

The colocalization of integrins alpha 2 beta 1 and alpha 3 beta 1 at intercellular contact sites of keratinocytes in culture and in epidermis suggests that these integrins may mediate intercellular adhesion (ICA). P1B5, an anti-alpha 3 beta 1 mAb previously reported to inhibit keratinocyte adhesion to epiligrin, was also found to induce ICA. Evidence that P1B5-induced ICA was mediated by alpha 2 beta 1 and alpha 3 beta 1 was obtained using both ICA assays and assays with purified, mAb-immobilized integrins. Selective binding of alpha 2 beta 1-coated beads to epidermal cells or plate-bound alpha 3 beta 1 was observed. This binding was inhibited by mAbs to integrin alpha 3, alpha 2, or beta 1 subunits and could be stimulated by P1B5. We also demonstrate a selective and inhibitable interaction between affinity-purified integrins alpha 2 beta 1 and alpha 3 beta 1. Finally, we show that expression of alpha 2 beta 1 by CHO fibroblasts results in the acquisition of collagen and alpha 3 beta 1 binding. Binding to both of these ligands is inhibited by P1H5, an anti-alpha 2 beta 1 specific mAb. Results of these in vitro experiments suggest that integrins alpha 2 beta 1 and alpha 3 beta 1 can interact and may do so to mediate ICA in vivo. Thus, alpha 3 beta 1 mediates keratinocyte adhesion to epiligrin and plays a second role in ICA via alpha 2 beta 1.

scholarly journals Cilengitide Inhibits Neovascularization in a Rabbit Abdominal Aortic Plaque Model by Impairing the VEGF Signaling

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Fawang Zhu ◽  
Shuai Yuan ◽  
Jing Li ◽  
Yun Mou ◽  
Zhiqiang Hu ◽  
...  
Keyword(s):  
Umbilical Vein ◽  
Tube Formation ◽  
Control Group ◽  
In Vitro Experiments ◽  
Aortic Plaque ◽  
Abdominal Aortic ◽  
Aortic Plaques ◽  
Different Doses

Background. Cilengitide is a selective αvβ3 and αvβ5 integrin inhibitor. We sought to investigate the effect of cilengitide on the neovascularization of abdominal aortic plaques in rabbits and explore its underlying antiangiogenic mechanism on human umbilical vein endothelial cells (HUVECs). Materials and Methods. For the in vivo experiment, the abdominal aortic plaque model of rabbits was established and injected with different doses of cilengitide or saline for 14 consecutive days. Conventional ultrasound (CUS) and contrast-enhanced ultrasound (CEUS) were applied to measure the vascular structure and blood flow parameters. CD31 immunofluorescence staining was performed for examining neovascularization. Relative expressions of vascular endothelial growth factor (VEGF) and integrin of the plaque were determined. For in vitro experiments, HUVECs were tested for proliferation, migration, apoptosis, and tube formation in the presence of different doses of cilengitide. Relative expressions of VEGF, integrin, and Ras/ERK/AKT signaling pathways were determined for the exploration of underlying mechanism. Results. CEUS showed modestly increased size and eccentricity index (EI) of plaques in the control group. Different degrees of reduced size and EI of plaques were observed in two cilengitide treatment groups. The expressions of VEGF and integrin in the plaque were inhibited after 14 days of cilengitide treatment. The neovascularization and apoptosis of the abdominal aorta were also significantly alleviated by cilengitide treatment. For in vitro experiments, cilengitide treatment was found to inhibit the proliferation, migration, and tube formation of HUVECs. However, cilengitide did not induce the apoptosis of HUVECs. A higher dose of cilengitide inhibited the mRNA expression of VEGF-A, β3, and β5, but not αV. Lastly, cilengitide treatment significantly inhibited the Ras/ERK/AKT pathway in the HUVECs. Conclusions. This study showed that cilengitide effectively inhibited the growth of plaque size by inhibiting the angiogenesis of the abdominal aortic plaques and blocking the VEGF-mediated angiogenic effect on HUVECs.

Effect of α-melanocyte-stimulating hormone on tyrosinase activity in hair follicular and epidermal melanocytes of the mouse

1988 ◽  
Vol 119 (3) ◽  
pp. 517-522 ◽  
Author(s):  
P. Seechurn ◽  
S. A. Burchill ◽  
A. J. Thody
Keyword(s):  
Tyrosinase Activity ◽  
In Vitro Experiments ◽  
Dorsal Skin ◽  
Wild Type ◽  
Melanocyte Stimulating Hormone ◽  
Tyrosinase Expression ◽  
In Vivo Administration ◽  
Agouti Gene

ABSTRACT In this study, the effect of α-MSH on tyrosinase activity was compared in epidermal and hair follicular melanocytes of mice. It had no effect on epidermal tyrosinase activity in dorsal skin from neonatal non-agouti black mice (C57BL/6J) in both in-vivo and in-vitro experiments. Theophylline and 8-bromocyclic (c)AMP were similarly without effect in in-vitro experiments. In-vivo administration of α-MSH and theophylline for 7 days was also without effect on epidermal tyrosinase activity in ear skin of adult non-agouti mice, and the same was true for α-MSH in wild-type agouti mice. Activation of the epidermal melanocytes in the non-agouti and wild-type agouti mice with ultraviolet radiation also failed to bring about a response to α-MSH and to theophylline in the case of the former. No tyrosinase activity was detected in the epidermis of viable yellow mice (C3H-HeAvy), but, as shown previously, tyrosinase activity was present in the hair follicle when the hair was actively growing and was increased in those mice given either α-MSH or theophylline. α-MSH and theophylline had no such effects on hair follicular tyrosinase activity in the non-agouti mice. The present results suggest that α-MSH- and cAMP-dependent mechanisms have little or no importance in the regulation of tyrosinase expression in mouse epidermal melanocytes. α-MSH may, however, regulate tyrosinase expression in hair follicular melanocytes, but even in these melanocytes its action may be restricted to mice that express the agouti gene. J. Endocr. (1988) 119, 517–522

scholarly journals STAT3 inhibitor mitigates cerebral amyloid angiopathy and parenchymal amyloid plaques while improving cognitive functions and brain networks

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jogender Mehla ◽  
Itender Singh ◽  
Deepti Diwan ◽  
James W. Nelson ◽  
Molly Lawrence ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Brain ◽  
Cognitive Functions ◽  
Specific Inhibitor ◽  
Amyloid Angiopathy ◽  
In Vitro Experiments ◽  
Aβ Peptides ◽  
Cerebral Amyloid

AbstractPrevious reports indicate a potential role for signal transducer and activator of transcription 3 (STAT3) in amyloid-β (Aβ) processing and neuritic plaque pathogenesis. In the present study, the impact of STAT3 inhibition on cognition, cerebrovascular function, amyloid pathology, oxidative stress, and neuroinflammation was studied using in vitro and in vivo models of Alzheimer’s disease (AD)-related pathology. For in vitro experiments, human brain vascular smooth muscle cells (HBVSMC) and human brain microvascular endothelial cells (HBMEC) were used, and these cultured cells were exposed to Aβ peptides followed by measurement of activated forms of STAT3 expression and reactive oxygen species (ROS) generation. Further, 6 months old 5XFAD/APOE4 (5XE4) mice and age-matched negative littermates were used for in vivo experiments. These mice were treated with STAT3 specific inhibitor, LLL-12 for 2 months followed by neurobehavioral and histopathological assessment. In vitro experiments showed exposure of cerebrovascular cells to Aβ peptides upregulated activated forms of STAT3 and produced STAT3-mediated vascular oxidative stress. 5XE4 mice treated with the STAT3-specific inhibitor (LLL-12) improved cognitive functions and functional connectivity and augmented cerebral blood flow. These functional improvements were associated with a reduction in neuritic plaques, cerebral amyloid angiopathy (CAA), oxidative stress, and neuroinflammation. Reduction in amyloid precursor protein (APP) processing and attenuation of oxidative modification of lipoprotein receptor related protein-1 (LRP-1) were identified as potential underlying mechanisms. These results demonstrate the broad impact of STAT3 on cognitive functions, parenchymal and vascular amyloid pathology and highlight the therapeutic potential of STAT3 specific inhibition for treatment of AD and CAA.

Studies on Chitin Synthesis in the Desert Locust

1962 ◽  
Vol 39 (1) ◽  
pp. 129-140 ◽  
Author(s):  
D. J. CANDY ◽  
B. A. KILBY
Keyword(s):  
Schistocerca Gregaria ◽  
In Vivo Studies ◽  
Desert Locust ◽  
Uridine Diphosphate ◽  
In Vitro Experiments ◽  
Chitin Synthesis ◽  
Acetyl Coenzyme A ◽  
Phosphohexose Isomerase

1. In vivo studies on 5th instar and adult locusts revealed that chitin formation in thorax, abdomen, hind leg and wing was greatest during the first few days after moulting. 2. Wing extracts were used for in vitro experiments, and evidence was obtained for the presence of the following enzymes: hexokinase, phosphohexose isomerase, glutamine transaminase, phosphoglucosamine transacetylase, acetyl coenzyme-A synthetase, phosphoacetylglucosamine mutase and uridine diphosphate N-acetylglucosamine pyrophosphorylase. 3. The results are discussed, and a tentative scheme is presented for the biosynthesis of chitin in the wing of Schistocerca gregaria.

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