Multiple Threshold Spatially Uniform ReliefF for the Genetic Analysis of Complex Human Diseases

Author(s):  
Delaney Granizo-Mackenzie ◽  
Jason H. Moore
2018 ◽  
Vol 50 (3) ◽  
pp. 390-400 ◽  
Author(s):  
Masahiro Kanai ◽  
Masato Akiyama ◽  
Atsushi Takahashi ◽  
Nana Matoba ◽  
Yukihide Momozawa ◽  
...  

2008 ◽  
Vol 124 (1) ◽  
pp. 19-29 ◽  
Author(s):  
Kristine A. Pattin ◽  
Jason H. Moore

1999 ◽  
Vol 19 (6) ◽  
pp. 4153-4158 ◽  
Author(s):  
Haim Cohen ◽  
Dorothy D. Sears ◽  
Drora Zenvirth ◽  
Philip Hieter ◽  
Giora Simchen

ABSTRACT Expansion of trinucleotide repeat tracts has been shown to be associated with numerous human diseases. The mechanism and timing of the expansion events are poorly understood, however. We show that CTG repeats, associated with the human DMPK gene and implanted in two homologous yeast artificial chromosomes (YACs), are very unstable. The instability is 6 to 10 times more pronounced in meiosis than during mitotic division. The influence of meiosis on instability is 4.4 times greater when the second YAC with a repeat tract is not present. Most of the changes we observed in trinucleotide repeat tracts are large contractions of 21 to 50 repeats. The orientation of the insert with the repeats has no effect on the frequency and distribution of the contractions. In our experiments, expansions were found almost exclusively during gametogenesis. Genetic analysis of segregating markers among meiotic progeny excluded unequal crossover as the mechanism for instability. These unique patterns have novel implications for possible mechanisms of repeat instability.


Genes ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 96
Author(s):  
David Q.-H. Wang

Any changes in gene expression or protein functions can cause abnormal anatomical, physiological, biochemical, and behavioral modifications in human beings, which can lead to disease [...]


Author(s):  
A. Kawaoi

Numbers of immunological approach have been made to the amyloidosis through the variety of predisposing human diseases and the experimentally induced animals by the greater number of agents. The results suggest an important role of impaired immunity involving both humoral and cell-mediated aspects.Recently the author has succeeded in producing amyloidosis in the rabbits and mice by the injections of immune complex of heat denatured DNA.The aim of this report is to demonstrate the details of the ultrastructure of the amyloidosis induced by heterologous insoluble immune complex. Eleven of twelve mice, dd strain, subcutaneously injected twice a week with Freund's complete adjuvant and four of seven animals intraperitonially injected developed systemic amyloidosis two months later from the initial injections. The spleens were electron microscopically observed.


Sign in / Sign up

Export Citation Format

Share Document