scholarly journals Lips and incisors position in normal class I occlusion

2020 ◽  
Vol 1 (1) ◽  
pp. 8-17
Author(s):  
Fadhil jasim ◽  
Neam AGHA
Keyword(s):  
Class I ◽  
2021 ◽  
Vol 118 (47) ◽  
pp. e2107543118
Author(s):  
Xiang Li ◽  
Jun Zhang ◽  
Jiyue Huang ◽  
Jing Xu ◽  
Zhiyu Chen ◽  
...  

During meiosis, crossovers (COs) are typically required to ensure faithful chromosomal segregation. Despite the requirement for at least one CO between each pair of chromosomes, closely spaced double COs are usually underrepresented due to a phenomenon called CO interference. Like Mus musculus and Saccharomyces cerevisiae, Arabidopsis thaliana has both interference-sensitive (Class I) and interference-insensitive (Class II) COs. However, the underlying mechanism controlling CO distribution remains largely elusive. Both AtMUS81 and AtFANCD2 promote the formation of Class II CO. Using both AtHEI10 and AtMLH1 immunostaining, two markers of Class I COs, we show that AtFANCD2 but not AtMUS81 is required for normal Class I CO distribution among chromosomes. Depleting AtFANCD2 leads to a CO distribution pattern that is intermediate between that of wild-type and a Poisson distribution. Moreover, in Atfancm, Atfigl1, and Atrmi1 mutants where increased Class II CO frequency has been reported previously, we observe Class I CO distribution patterns that are strikingly similar to Atfancd2. Surprisingly, we found that AtFANCD2 plays opposite roles in regulating CO frequency in Atfancm compared with either in Atfigl1 or Atrmi1. Together, these results reveal that although AtFANCD2, AtFANCM, AtFIGL1, and AtRMI1 regulate Class II CO frequency by distinct mechanisms, they have similar roles in controlling the distribution of Class I COs among chromosomes.


2008 ◽  
Vol 78 (3) ◽  
pp. 466-474 ◽  
Author(s):  
Omar Gabriel da Silva Filho ◽  
Flávio Mauro Ferrari Júnior ◽  
Terumi Okada Ozawa

Abstract Objective: To test the hypothesis that there is no difference in the dimensions of the upper and lower dental arches in Class II division 1 malocclusion with a mandibular deficiency compared to normal Class I occlusion dental arches. Materials and Methods: Photocopies of the dental arches of 48 patients exhibiting Class II division 1 malocclusion with mandibular deficiency and of 51 individuals with normal occlusion were compared. Mandibular deficiency was diagnosed clinically. All 99 individuals were in the permanent dentition. The ages of the subjects ranged from 11 years 4 months to 20 years (mean age = 12 years 5 months). Results: When compared to subjects with normal occlusion, the upper dental arches of the Class II division 1 patients presented reduced transverse dimensions and longer sagittal dimensions while the lower arches were less influenced. Conclusion: The hypothesis is rejected. Significant differences are present between the dimensions of the upper and lower dental arches in Class II division 1 malocclusion (with a mandibular deficiency and in the permanent dentition) compared to normal Class I occlusion dental arches.


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.


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