ArticleOpen life sciences2022
A case report of
Article in Open life sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed, 1 citations in OpenAlex.
No citing paper in PubMed yet.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complex forms of diabetes are the ultimate common pathway involving multiple genetic variations and multiple environmental factors. Type 2 diabetes (T2DM) is classified as complex diabetes. Varying degrees of insulin deficiency and tissue insulin resistance are two key links to T2DM. The islet β cell dysfunction plays a crucial role in the pathogenesis of T2DM. The decompensation of the islet β cell to insulin resistance is a common mechanism leading to the pathogenesis of T2DM. Available data show that genetic factors mainly affect cell function. At present, a number of susceptibility genes related to T2DM have been reported at home and abroad. In this study, the diabetes-related genes in the case of early-onset diabetes with a significant family history were examined, and our results showed the presence of the intron mutations of catalase (
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.