A Quantitative LC‐MS/MS Method for the Determination of Tissue Brincidofovir and Cidofovir Diphosphate in a MuPyV Infected Mouse Model

2021 ◽  
Author(s):  
Bryan B. Guzman ◽  
Amanda P. Schauer ◽  
John A. Dunn ◽  
Mackenzie L. Cottrell ◽  
Craig Sykes
Keyword(s):  
Mouse Model ◽  
Infected Mouse

scholarly journals Mice carrying an analogous heterozygous dynamin 2 K562E mutation that causes neuropathy in humans develop predominant characteristics of a primary myopathy

2020 ◽  
Vol 29 (8) ◽  
pp. 1253-1273
Author(s):  
Jorge A Pereira ◽  
Joanne Gerber ◽  
Monica Ghidinelli ◽  
Daniel Gerber ◽  
Luigi Tortola ◽  
...  
Keyword(s):  
Mouse Model ◽  
Treatment Strategies ◽  
Underlying Disease ◽  
Potential Treatment ◽  
Type B ◽  
Disease Mechanism ◽  
Demyelinating Neuropathy ◽  
Charcot Marie Tooth ◽  
Dynamin 2

Abstract Some mutations affecting dynamin 2 (DNM2) can cause dominantly inherited Charcot–Marie–Tooth (CMT) neuropathy. Here, we describe the analysis of mice carrying the DNM2 K562E mutation which has been associated with dominant-intermediate CMT type B (CMTDIB). Contrary to our expectations, heterozygous DNM2 K562E mutant mice did not develop definitive signs of an axonal or demyelinating neuropathy. Rather, we found a primary myopathy-like phenotype in these mice. A likely interpretation of these results is that the lack of a neuropathy in this mouse model has allowed the unmasking of a primary myopathy due to the DNM2 K562E mutation which might be overshadowed by the neuropathy in humans. Consequently, we hypothesize that a primary myopathy may also contribute to the disease mechanism in some CMTDIB patients. We propose that these findings should be considered in the evaluation of patients, the determination of the underlying disease processes and the development of tailored potential treatment strategies.

scholarly journals Detection of α-defensin in eosinophils in helminth-infected mouse model

2018 ◽  
Vol 80 (12) ◽  
pp. 1887-1894 ◽  
Author(s):  
Afia KHATUN ◽  
Masashi SAKURAI ◽  
Kazuki OKADA ◽  
Yusuke SAKAI ◽  
Masahiro MORIMOTO
Keyword(s):  
Mouse Model ◽  
Infected Mouse

Advances in the 5q− syndrome

Blood ◽  
2010 ◽  
Vol 116 (26) ◽  
pp. 5803-5811 ◽  
Author(s):  
Jacqueline Boultwood ◽  
Andrea Pellagatti ◽  
Andrew N. J. McKenzie ◽  
James S. Wainscoat
Keyword(s):  
Mouse Model ◽  
Large Scale ◽  
Ribosomal Gene ◽  
Functional Screening ◽  
Erythroid Progenitor ◽  
P53 Activation ◽  
Modeling Data ◽  
Mouse Modeling ◽  
Microrna Genes

AbstractThe 5q− syndrome is the most distinct of all the myelodysplastic syndromes with a clear genotype/phenotype relationship. The significant progress made during recent years has been based on the determination of the commonly deleted region and the demonstration of haploinsufficiency for the ribosomal gene RPS14. The functional screening of all the genes in the commonly deleted region determined that RPS14 haploinsufficiency is the probable cause of the erythroid defect in the 5q− syndrome. A mouse model of the human 5q− syndrome has now been created by chromosomal engineering involving a large-scale deletion of the Cd74-Nid67 interval (containing RPS14). A variety of lines of evidence support the model of ribosomal deficiency causing p53 activation and defective erythropoiesis, including most notably the crossing of the “5q− mice” with p53-deficient mice, thereby ameliorating the erythroid progenitor defect. Emerging evidence supports the notion that the p53 activation observed in the mouse model may also apply to the human 5q− syndrome. Other mouse modeling data suggest that haploinsufficiency of the microRNA genes miR-145 and miR-146a may contribute to the thrombocytosis seen in the 5q− syndrome. Lenalidomide has become an established therapy for the 5q− syndrome, although its precise mode of action remains uncertain.

scholarly journals Anti-trypanosomal effect of Malva sylvestris (Malvaceae) extract on a Trypanosoma brucei brucei-infected mouse model of sleeping sickness

2017 ◽  
Vol 16 (10) ◽  
pp. 2373-2378
Author(s):  
Yan-Bing Ding ◽  
Jun Chen ◽  
Li-Xia Huang ◽  
Ye-Li Gong ◽  
Fa-Hu Yuan ◽  
...  
Keyword(s):  
Mouse Model ◽  
Trypanosoma Brucei ◽  
Infected Mouse ◽  
Negative Control Group ◽  
Negative Control ◽  
Sleeping Sickness ◽  
Control Group ◽  
Trypanosoma Brucei Brucei ◽  
Parasite Count ◽  
Malva Sylvestris

Purpose: To evaluate the antitrypanosomal activity of Malva sylvestris (MS) extract in a Trypanosoma brucei brucei-infected  mouse model of sleeping sickness.Methods: Sleeping sickness was induced by the intraperitoneal injection of Trypanosoma brucei brucei infected blood in mice.  Confirmation of parasitaemia was performed by estimating the parasite count in the plasma on the 12th day after inoculation. All the mice were divided into five groups: control group that received neither infection nor treatment; negative control that was  infected with the parasite but did not receive treatment; MS-treated group that receive MS extract (250 and 500 mg/kg, ip) and standard (STD) group that received levamisole (7.5 mg/kg, ip) for 7 days after the development of parasitaemia. A further parasite count was performed in the blood and cerebrospinal fluid (CSF) after the treatment period. Humoral antibody response,  delayed hypersensitivity reaction, and mobilization of leucocytes were determined after the treatment period in SRBC-sensitized mice.Results: The results indicate that treatment with MS significantly decreased body weight and parasite count in the blood and CSF of mice with Trypanosoma brucei brucei-induced sleeping sickness compared with that in the negative control group. There was a significant increase in paw swelling and decrease in secondary antibody in the MS-treated group compared with that in the  negative control group. However, treatment with MS extract also enhanced the mobilization of the total leucocyte count compared with that in the negative control group.Conclusion: The results demonstrate the anti-trypanosomal activity of Malva sylvestris extract via immunomodulation in a  Trypanosoma brucei brucei-infected mouse model of sleeping sickness.Keywords: Malva sylvestris, Trypanosoma brucei brucei, Sleeping sickness, Immunomodulatory activity, Delayed hypersensitivity reaction

Discovery and genetic characterization of intestinal metaplasia in the Helicobacter felis-infected mouse model of gastric cancer

2018 ◽  
Vol 51 (2) ◽  
pp. 219-222
Author(s):  
Jiangrong Chen ◽  
Chunchao Zhu ◽  
Chaojie Wang ◽  
Xiaodan Zhang ◽  
Jian Ni ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Mouse Model ◽  
Intestinal Metaplasia ◽  
Infected Mouse ◽  
Genetic Characterization ◽  
Helicobacter Felis

RSV-infected mouse model for evaluation of health risk of brominated flame retardants

2007 ◽  
Vol 172 ◽  
pp. S110-S111
Author(s):  
Wataru Watanabe ◽  
Tomomi Shimizu ◽  
Akane Hino ◽  
Masahiko Kurokawa
Keyword(s):  
Mouse Model ◽  
Health Risk ◽  
Infected Mouse ◽  
Flame Retardants ◽  
Brominated Flame Retardants
Sign in / Sign up

Export Citation Format

Share Document