Multivariable-adjusted incident risk of complications according to healthy sleep score among 30 915 T2D participants.

The change in total daily insulin requirements (units) between pre-transplant and 6 months post-transplant.

Glucose-lowering medication expenditures per user by different payers among patients with diabetes.

We first collected the patients with diabetes, including the clinical data and blood. Then the high-throughput sequencing platform was used to detected gene mutation using blood samples. After screening the possible mutation sites, we collected blood from the patient's family members and performed Sanger sequencing for verification. And we analyzed their pathogenicity and conservation using bioinformatics software, and constructed a three-dimensional Wolfram protein structure. Finally, we analyzed the distribution of WFS1 mutations and associated clinical phenotypes by summarizing the genetic variations of the WFS1 gene recorded in the Human Gene Mutation Database. We got results as follows: (1) c.1523_ 1524 del/p Y508Cfs*34 is a frameshift mutation, c.766A>G/p. K256E and c.985T>A/p. F329I are missense mutations. (2) c.766A>G/p. K256E is a benign and novel mutation, while the rest are pathogenic mutations. (3) c.985T>A/p. F329I can cause MODY in a family. (4) Phenotype and clinical presentations diverse in patients with WFS1-associated disease. (5) The proportion of WFS1 mutations corresponding to different clinical phenotypes were highest in missense mutations, mainly distributed in exon 8. We concluded that c.766A>G/p.K256E is a new WFS1 mutation that has never been reported before, and that inactivating mutations and benign missense mutations lead to more severe WS phenotypes than pure pathogenic missense mutations. We also verified that c.985T>A/p. F329I as a MODY-related gene. Finally, by summarizing the genotype–phenotype relationship of WFS1, we concluded that the clinical manifestations of WFS1 mutation-related disease are diverse and require accurate differential diagnosis based on laboratory tests and genetic sequencing.

From 1990 to 2021, there has been a substantial increase in the global burden of vision impairment due to diabetic retinopathy among working-age individuals.

Severe cardiac autonomic dysfunction (SDNN<50 ms), and diabetic neurogenic bladder are independently associated with LVDD in individuals with T2DM.

This study examined the relationship between ET-1 and MACE in CAD patients with differing renal function and with or without diabetes undergoing PCI. CAD patients who have elevated ET-1 levels, renal insufficiency (eGFR ≤ 60 mL/min/1.73 m²) and DM faced the greatest risk for MACE.