Feline Panleukopenia: II. The Relationship of Intestinal Mucosal Cell Proliferation Rates to Viral Infection and Development of Lesions

1977 ◽  
Vol 14 (2) ◽  
pp. 173-181 ◽  
Author(s):  
J. H. Carlson ◽  
F. W. Scott

Proliferation rates of small intestinal mucosal cells of noninfected germfree and specific pathogen-free kittens were compared to the incidence of infected cells and microscopic lesions in kittens experimentally infected with panleukopenia virus. Mucosal crypt length, cells per crypt, mitotic index and villous length were greater in specific pathogen-free kittens than in germfree kittens. Crypt cells per unit length and villous length per crypt length ratio were greater in germfree kittens. The cryptal cell proliferation rate of specific pathogen-free kittens was 2.24 times that of germfree kittens. Mucosal crypt length, cell per crypt and villous length were greater in the proximal jejunum than in the midjejunum of kittens within groups. Cell proliferation rates per crypt did not differ between areas of the intestine in kittens within groups. There were more virus-infected cells and lesions in specific pathogen-free kittens than in germfree kittens. The incidence of virus-infected cells and lesions was greater in the proximal jejunum and decreased along the small intestine.

Observations of temperatures and heat flux near major thrust zones indicate that in their deep levels shear stresses may exceed 50-100 MPa. Within strike-slip zones shear stresses in the lower lithosphere may also approach 50-100 MPa, though shear stresses in the upper crust of those regions are probably much lower. The relationship of tectonic style to surface elevation in the Andes and Tibet yields an estimate of about 5 x 10 12 N m -1 for the force per unit length required to deform the lithosphere of these regions. This force per unit length is equivalent to an average shear stress of about 25 MPa through a lithosphere 100 km thick. The width-to-length ratios of active belts are consistent with deformation determined by the creep of the lower lithosphere rather than by friction on faults. The patterns of rotation of crustal blocks in western North America suggest that these blocks passively follow the deformation of a continuous substrate. The observations of deformation and the estimates of stress derived from them, both suggest that the upper continental crust is weak, relative to the lower parts of the lithosphere the deformation of which it follows passively. If this is so, determinations of stress in the upper crust may have only limited relevance to the deformation of the lithosphere as a whole.


1969 ◽  
Vol 130 (1) ◽  
pp. 121-140 ◽  
Author(s):  
Frederik B. Bang ◽  
Marie A. Foard

Chickens 3 wk old, inoculated intranasally with a mesogenic (moderately virulent) strain of Newcastle disease virus, developed necrotic lesions of the mucous acini, predominantly of the middle turbinates. The infection subsequently spread to involve much of the rest of the mucosa, including mucous and ciliated epithelial cells, and other acini. The early phase of adsorption of a virulent strain of the virus to the middle turbinates of chicks 5–21 days of age was studied by giving a standard inoculum intranasally to unanesthetized animals. Variation in amounts adsorbed by individual chickens was large, but was minimized by making measurements on pools of turbinates from three chicks at intervals of 1, 3, and 5 hr after exposure of the excised turbinates to antibody, by washing, and by trypsinization. The virus released from the cells into the trypsin was designated as adherent virus, and the infectious virus in the cells after destruction of the cells by water grinding, as cell virus. Paralysis of ciliary action by cocaine increased the number of infected cells in the turbinates about 10-fold at all three time intervals. Pilocarpine injection before virus inoculation caused a large increase in the amount of infected cells 1 hr after virus administration, but was followed by a sharp drop in infected cells by 3 or 5 hr. Pilocarpine given after the virus decreased the number of infected cells and changed the relationship of infected cells to adherent virus. Exposure of chicks to sustained or severe cold caused a similar but less marked effect. The drop in infected cells was restored to control values if chicks were returned to brooder temperatures. The marked drop of infected cells produced by pilocarpine and cold in living chicks, and in cultures of chicken trachea (previous study), is consonant with the idea that virus has been adsorbed on mucus granules in the mucous cells of the turbinates and then has been reexcreted, as unincorporated virus, into the moving mucous sheet. A series of accessory data support this interpretation.


1979 ◽  
Vol 32 (3) ◽  
pp. 317 ◽  
Author(s):  
Patricia A Wilson ◽  
BF Short

The relationship of wool growth to cell proliferation in the follicle bulb and to the subsequent migration and growth of the fibre cortical cells was investigated in 10 Peppin Merino sheep. These sheep had been maintained on a low, medium or high level of nutrient intake to ensure a wide range in wool growth. The number and mitotic activity of the germinal cells in the follicle bulb were determined after administration of colchicine. Cortical cell size was measured following isolation of the fibre cells by acid-treatment of wool.


2020 ◽  
Vol 10 (7) ◽  
pp. 1052-1058
Author(s):  
Zhichao Li ◽  
Jin Wang ◽  
Jing Yang

Background: This study investigated whether miR-21 regulates the expression of STAT3 and affects FLS cells. Methods: MiR-21 and STAT3 mRNA level was assessed by qRT-PCR and STAT3 and p-STAT3 level was evaluated by Western blot. Spearman correlation was used to analyze the relationship between miR-21 and STAT3 mRNA expression in synovial tissue of RA patients. FLS cells were treated with IL-17A, and the cells without treatment was included as the control group. Under IL-17A treatment, FLS cells were divided into 2 groups: miR-NC group and miR-21 mimic group. MiR-21, STAT3, p-STAT3 expression were detected and compared. EdU staining was used to detect cell proliferation and flow cytometry was used to measure cell apoptosis. Results: There was a target relationship of miR-21 with STAT3 mRNA. IL-17A treatment significantly downregulated miR-21 in FLS cells, upregulated STAT3 and p-STAT3 and enhanced cell proliferation. Transfection of miR21 mimic significantly downregulated STAT3 and p-STAT3 in FLS cells, reduced cell proliferation and increased cell apoptosis. Conclusion: MiR-21 overexpression down-regulates STAT3, inhibits FLS cell proliferation and promotes apoptosis, indicating that it might be a therapeutic target for treating RA.


2010 ◽  
Vol 28 (6) ◽  
pp. 353-360 ◽  
Author(s):  
Yucel Erbilgin ◽  
Muge Sayitoglu ◽  
Ozden Hatirnaz ◽  
Omer Dogru ◽  
Arzu Akcay ◽  
...  

The NOTCH signaling pathway plays important role in the development of multicellular organisms, as it regulates cell proliferation, survival, and differentiation. In adults, it is essential for the T- or B-lymphocyte lineage commitment.NOTCH1and FBXW7 mutations both lead the activation of theNOTCH1pathway and are found in the majority of T-ALL patients. In this study, the mutation analysis ofNOTCH1andFBXW7genes was performed in 87 pediatric T-ALLs who were treated on the ALL-BFM protocols. In 19 patients (22%), activatingNOTCH1mutations were observed either in the heterodimerization domain or in the PEST domain and 7 cases (10%) demonstrated FBXW7 mutations (2 cases had bothNOTCH1andFBXW7mutations). We also analyzed the relationship of the mutation data between the clinical and biological data of the patients.NOTCH1andFBXW7,NOTCH1alone were found correlated with lower initial leucocyte counts which was independent from the sex and T- cell immunophenotype. However,NOTCH1andFBXW7mutations were not predictive of outcome in the overall cohort of pediatric T-ALLs.


2007 ◽  
Vol 81 (10) ◽  
pp. 4973-4980 ◽  
Author(s):  
Michael S. Bennett ◽  
Hwee L. Ng ◽  
Mirabelle Dagarag ◽  
Ayub Ali ◽  
Otto O. Yang

ABSTRACT Cytotoxic T lymphocytes (CTLs) are crucial for immune control of viral infections. “Functional avidity,” defined by the sensitizing dose of exogenously added epitope yielding half-maximal CTL triggering against uninfected target cells (SD50), has been utilized extensively as a measure of antiviral efficiency. However, CTLs recognize infected cells via endogenously produced epitopes, and the relationship of SD50 to antiviral activity has never been directly revealed. We elucidate this relationship by comparing CTL killing of cells infected with panels of epitope-variant viruses to the corresponding SD50 for the variant epitopes. This reveals a steeply sigmoid relationship between avidity and infected cell killing, with avidity thresholds (defined as the SD50 required for CTL to achieve 50% efficiency of infected cell killing [KE50]), below which infected cell killing rapidly drops to none and above which killing efficiency rapidly plateaus. Three CTL clones recognizing the same viral epitope show the same KE50 despite differential recognition of individual epitope variants, while CTLs recognizing another epitope show a 10-fold-higher KE50, demonstrating epitope dependence of KE50. Finally, the ability of CTLs to suppress viral replication depends on the same threshold KE50. Thus, defining KE50 values is required to interpret the significance of functional avidity measurements and predict CTL efficacy against virus-infected cells in pathogenesis and vaccine studies.


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