scholarly journals Encephalomyocarditis (EMC) virus-induced testicular lesion in BALB/c mice

1994 ◽  
Vol 28 (4) ◽  
pp. 330-334 ◽  
Author(s):  
M. Shigesato ◽  
K. Hirasawa ◽  
M. Takeda ◽  
K. Doi

Characteristics of encephalomyocarditis (EMC) virus-induced testicular lesions were investigated in 4- and 8-week-old BALB/c male mice after intraperitoneal (i.p.) and intratesticular (left) (i.t.) inoculation of the D variant of EMC virus (EMC-D). Apart from variation in severity and incidence, the histopathological nature of the resultant testicular lesion was similar in all infected mice, and was characterized by degeneration and necrosis of germinal cells and spermatogonia with inflammatory infiltration. Almost all the inoculated left testes of the i.t. group developed marked lesions. In general, the virus titre in the testis and incidence of testicular lesions were higher in 4-week-old mice than in 8-week-old mice. In addition, testicular lesions developed earlier and with a higher incidence in the PBS-inoculated right testis of the i.t. group than in either testis of the i.p. group of the same age.

2021 ◽  
Vol 22 (22) ◽  
pp. 12557
Author(s):  
Sang R. Lee ◽  
Su Hee Jeong ◽  
Jun H. Heo ◽  
Seong Lae Jo ◽  
Je-Won Ko ◽  
...  

Hepatocellular carcinoma (HCC) is a male-oriented malignancy; its progression is affected by sex hormones. 17α-ethinylestradiol (EE2) is a synthetic estrogen widely used as an oral contraceptive; however, it is unknown whether EE2 regulates sex hormone action in HCC. We investigated whether EE2 influences HCC risk in male androgenic environments, using mice expressing human sex hormone-binding globulin (SHBG). Two-week-old male mice were injected with diethyl-nitrosamine (DEN, 25 mg/kg) and fed an EE2 diet for 10 weeks from 30 weeks of age. Development and characteristics of liver cancer were evaluated in 40-week-old mice via molecular and histological analyses. Although EE2 did not increase HCC progression in wild-type mice, SHBG mice exhibited remarkably higher HCC risk when fed EE2. The livers of EE2-treated SHBG mice exhibited substantially increased pro-inflammatory necrosis with high plasma levels of ALT and HMGB1, and intrahepatic injury and fibers. Additionally, increased androgen response and androgen-mediated proliferation in the livers of EE2-treated SHBG mice and EE2-exposed hepatocytes under SHBG conditions were observed. As a competitor of SHBG-androgen binding, EE2 could bind with SHBG and increase the bioavailability of androgen. Our results revealed that EE2 is a novel risk factor in androgen-dominant men, predisposing them to HCC risk.


1980 ◽  
Vol 152 (4) ◽  
pp. 878-892 ◽  
Author(s):  
J W Yoon ◽  
P R McClintock ◽  
T Onodera ◽  
A L Notkins

Plaque purification of the M variant of encephalomyocarditis (EMC) virus resulted in the isolation of two stable variants: one diabetogenic and designated D and the other nondiabetogenic and designated B. When the D variant was inoculated into SJL/J male mice, hypoinsulinemia and hyperglycemia developed in > 90% of the animals. In contrast, none of the mice inoculated with the B variant developed diabetes. Histologic examination of pancreata from mice infected with the D variant revealed insulitis and necrosis of beta cells, whereas islets from mice infected with the B variant showed little, if any, change. When islets were assayed for infectious virus, approximately 10 times more virus was recovered from animals inoculated with the D as compared with the B variant. Moreover, approximately 60% of islet cells from mice infected with the D variant contained viral antigens when stained with fluorescein-labeled anti-EMC virus antibody, whereas < 5% of islet cells from animals infected with the B variant contained viral antigens. Co-infection experiments showed that the induction of diabetes by the D variant was inhibited by the B variant. When the B and D variants were mixed together at B:D ratios of 1, 9, and 99, diabetes developed in 60, 11, and 0% of the mice, respectively. Tissue-culture experiments revealed that the B variant induced considerably more interferon than the D variant, and studies in animals showed that interferon appeared earlier and in greater amounts in the circulation of mice infected with the B as compared with the D variant. These studies suggest that the induction of interferon by the B variant is, at least in part, responsible for the inhibition of diabetes by the D variant.


1984 ◽  
Vol 46 (5) ◽  
pp. 697-704 ◽  
Author(s):  
Masahiro HIRANO ◽  
Keizo MAITA ◽  
Yasuhiko SHIRASU
Keyword(s):  

1990 ◽  
Vol 39 (1) ◽  
pp. 113-116 ◽  
Author(s):  
Kazuhiro SHICHINOHE ◽  
Masumi SHIMIZU ◽  
Masamichi ISHIZAKI ◽  
Mitsuo ASAKAWA
Keyword(s):  

2020 ◽  
Author(s):  
Jerzy Kotlinowski ◽  
Tomasz Hutsch ◽  
Izabela Czyzynska-Cichon ◽  
Marta Wadowska ◽  
Natalia Pydyn ◽  
...  

AbstractBackground & AimsPrimary biliary cholangitis (PBC) is an autoimmune disease characterized by progressive destruction of the intrahepatic bile ducts. The immunopathology of PBC involves excessive inflammation; therefore, negative regulators of inflammatory response, such as Monocyte Chemoattractant Protein-1-Induced Protein-1 (MCPIP1, alias Regnase1) may play important roles in the development of PBC. The aim of this work was to verify whether Mcpip1 expression protects against development of PBC.MethodsGenetic deletion of Zc3h12a was used to characterize the role of Mcpip1 in the pathogenesis of PBC. 6-52-week-old Mcpip1fl/fl and Mcpip1AlbKO mice were used for immunohistochemical, biochemical and molecular tests.ResultsWe found that Mcpip1 deficiency in the liver recapitulates most of the features of human PBC, in contrast to mice with Mcpip1 deficiency in myeloid cells (Mcpip1LysMKO mice), which present with robust myeloid cell-driven systemic inflammation. In Mcpip1AlbKO livers, intrahepatic bile ducts displayed proliferative changes with inflammatory infiltration, bile duct destruction, and fibrosis leading to cholestasis. In plasma, increased concentrations of IgG, IgM, and AMA autoantibodies (anti-PDC-E2) were detected. Interestingly, the phenotype of Mcpip1AlbKO mice was robust in 6-week-old and 52-week-old mice, but milder in 12-24-week-old mice, suggesting early prenatal origin of the phenotype and age-dependent progression of the disease. Hepatic transcriptome analysis of 6-week-old and 24-week-old Mcpip1AlbKO mice showed 812 and 8 differentially expressed genes (DEGs), respectively, compared with age-matched control mice, and revealed a distinct set of genes compared to those previously associated with development of PBC.ConclusionsThe phenotype of Mcpip1AlbKO mice recapitulates most of the features of human PBC, and demonstrates early prenatal origin and age-dependent progression of PBC. Therefore, Mcpip1AlbKO mice provide a unique model for the study of PBC.Lay summaryDeletion of hepatic Mcpip1 in Mcpip1AlbKO mice leads to development of PBC that recapitulates phenotype of human patients. These animals, show early prenatal origin and age-dependent progression of the disease. Thus, Mcpip1AlbKO mice provide a unique model for studying PBC.


2019 ◽  
Author(s):  
Gabriel Galea ◽  
Peter J Delisser ◽  
Lee Meakin ◽  
Lance E Lanyon ◽  
Joanna S Price ◽  
...  

AbstractThe primary aim of bone anabolic therapies is to strategically increase bone mass in skeletal regions likely to experience high strains. This is naturally achieved by mechanical loading of the young healthy skeleton. However, these bone anabolic responses fail with age. Here, we applied site specificity analysis to map regional differences in bone anabolic responses to axial loading of the tibia (tri-weekly, for two weeks) between young (19-week-old) and aged (19-month-old), male and female mice. Loading increased bone mass specifically in the proximal tibia in both sexes and ages. Young female mice gained more cortical bone than young males in specific regions of the tibia. However, these site-specific sex difference were lost with age such that bone gain following loading was not significantly different between old males and females. Having previously demonstrated that prior and concurrent disuse enhances bone gain following loading in old females, we established whether this “rescue” is sex-specific. Old male mice were subjected to sciatic neurectomy or sham surgery, and tri-weekly loading was initiated four days after surgery. Disuse augmented cortical bone gain in response to loading in old male mice, but only in the regions of the tibia which were load-responsive in the young. Increased understanding of how locally-activated load-responsive processes lead to site-specific bone formation, and how the age-related diminution of these processes can be site-specifically enhanced by disuse, may lead to the next generation of strategic bone anabolic therapies.HighlightsSex differences in cortical tissue area of young and old mice are not site-specificThe loading response in young, but not old, mice is sex- and site-specificThe cortical loading response is site-specifically enhanced by disuse in old mice of both sexesThe trabecular loading response can be rescued by disuse in old male, but not female, mice


10.12737/9072 ◽  
2015 ◽  
Vol 22 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Садовникова ◽  
I. Sadovnikova ◽  
Зудов ◽  
Andrey Zudov

The research of effective methods of treatment of broncho-obstructive diseases is one of the most important questions of the pediatric pulmonology. General clinical manifestations are characterized by attacks of breathlessness, prolonged exhalation, unproductive cough, whistling and noisy breathing sometimes with a help of auxiliary muscles. Often this disease leads to bronchial asthma, obstructive bronchitis, and malformations of the lung and bronchus. In the pathogenesis of bronchial obstruction whilst respiratory infections the main factors are inflammatory infiltration of the bronchial mucosa, its swelling, hypersecretion of viscous mucus and bronchospasm due to hyperactivity of the bronchi of the inflammatory nature. To diagnose this disease it is important to establish the presence or absence of the effectiveness of the protective mechanisms of the body at different hierarchic levels. To protect the respiratory tract from exposure to adverse environmental factors in the process of ontogenesis pro-tective mechanisms formed. The first stage of purification of the bronchial system is mucociliary clearance carried out by the cells of the ciliated epithelial cells and glands that produce bronchial secret. If the cause of the disease is established, the etiotropic and pathogenetic treatment of the underlying disease should be carried out. Of special interest in pediatric pulmonology is the experience of the combined drug Kashnol. It simultaneously affects almost all parts of the pathogenesis of acute and chronic broncho-pulmonary diseases.


PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109942 ◽  
Author(s):  
Sabry Mohamed Attia ◽  
Sheikh Fayaz Ahmad ◽  
Radwa Mohamed Okash ◽  
Saleh Abdulrahman Bakheet

1975 ◽  
Vol 37 (1) ◽  
pp. 112-114 ◽  
Author(s):  
Walter B. Essman ◽  
Fred Kimmelstiel ◽  
Barry Sporer

25-day-old male mice showed a greater incidence of body weight loss and a late peak of plasma corticosterone elevation when exposed to tobacco smoke for 5 successive days, as compared with mice exposed to filtered smoke (gas phase) or air. 50-day-old mice had a greater incidence and magnitude of body weight loss and a late plasma corticosterone peak after 5 days of air exposure, but not with gas phase or nicotine + gas phase. Diencephalic serotonin, while higher among 25-day-old mice, did not differ as a function of the stress of confinement during exposure to the ventillatory stimulus or as a function of the different stimuli. The results suggest that weight loss and the time following stimulation at which plasma corticosterone is maximally elevated may serve as indices of stress and are consistent even when the stressor-susceptibility is age-related.


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