scholarly journals Aberrant expression of MYD88 via RNA‐controlling CNOT4 and EXOSC3 in colonic mucosa impacts generation of colonic cancer

2021 ◽  
Author(s):  
Masumi Tsuda ◽  
Misa Noguchi ◽  
Tsuyoshi Kurai ◽  
Yuji Ichihashi ◽  
Koki Ise ◽  
...  
1994 ◽  
Vol 15 (10) ◽  
pp. 2081-2085 ◽  
Author(s):  
Vikram Jit Singh Chhatwal ◽  
Sing Shang Ngoi ◽  
Steven T.F. Chan ◽  
Yee Wen Chia ◽  
Shabbir M. Moochhala

2001 ◽  
Vol 10 (5) ◽  
pp. 269-272 ◽  
Author(s):  
Max Nyström ◽  
Ulla Peterson Westin ◽  
Carina Linder ◽  
Kjell Ohlsson

Secretory leukocyte protease inhibitor (SLPI) is a wellknown protease inhibitor. Its function is thought to be protease/protease-inhibitor balance. Free proteolytic activity, mainly pancreatic elastase, anionic trypsin and granulocytic elastase, has been demonstrated in faecal extracts from patients with ulcerative colitis. We wanted to verify that SLPI is actually secreted from normal human colonic mucosa. Also, we wanted to ascertain whether studies of SLPI secretion based on punch biopsies were dependent on biopsy area or on biopsy circumference. Normal colonic mucosa was sampled during surgery for colonic cancer. A total of 36 samples from four patients were used. Mucosa preparation was carried out using a punch biopsy technique, and samples of 3, 4 and 6 mm diameter were used. All media contained SLPI at varying concentrations. When expressed in terms of the sample area, the secretion per millimetre-squared seemed to decrease with increasing area. When calculated as secretion per circumference, secretion seemed to be constant. In conclusion, SLPI was secreted from normal human colonic mucosa. The SLPI secretion seemed dependent on the circumference of the biopsy rather than on the area of the biopsy.


Author(s):  
T. A. Stewart ◽  
D. Liggitt ◽  
S. Pitts ◽  
L. Martin ◽  
M. Siegel ◽  
...  

Insulin-dependant (Type I) diabetes mellitus (IDDM) is a metabolic disorder resulting from the lack of endogenous insulin secretion. The disease is thought to result from the autoimmune mediated destruction of the insulin producing ß cells within the islets of Langerhans. The disease process is probably triggered by environmental agents, e.g. virus or chemical toxins on a background of genetic susceptibility associated with particular alleles within the major histocompatiblity complex (MHC). The relation between IDDM and the MHC locus has been reinforced by the demonstration of both class I and class II MHC proteins on the surface of ß cells from newly diagnosed patients as well as mounting evidence that IDDM has an autoimmune pathogenesis. In 1984, a series of observations were used to advance a hypothesis, in which it was suggested that aberrant expression of class II MHC molecules, perhaps induced by gamma-interferon (IFN γ) could present self antigens and initiate an autoimmune disease. We have tested some aspects of this model and demonstrated that expression of IFN γ by pancreatic ß cells can initiate an inflammatory destruction of both the islets and pancreas and does lead to IDDM.


1965 ◽  
Vol 48 (5) ◽  
pp. 593-601 ◽  
Author(s):  
Monira K. Rifaat ◽  
Oscar A. Iseri ◽  
Leonard S. Gottlieb

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