Autonomous Self-exam Monitoring for Early Diabetes Detection

Author(s):  
Rohana Abdul Karim ◽  
Nur Alia Fatiha Azhar ◽  
Nurul Wahidah Arshad ◽  
Nor Farizan Zakaria ◽  
M. Zabri Abu Bakar
Keyword(s):  
Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 2374-PUB
Author(s):  
SPIROS FOURLANOS ◽  
NICHOLAS D. MINGOS ◽  
LOIS M. ROWAN ◽  
RAHUL BARMANRAY ◽  
MERVYN KYI

Author(s):  
Rebecca E. Weiss ◽  
Nevert Badreldin ◽  
Kathleen Drexler ◽  
Charlotte Niznik ◽  
Lynn M. Yee

Objective The study aimed to evaluate perinatal outcomes associated with introduction of and adherence to early diabetes screening guidelines. Study Design Retrospective cohort study of all women who received prenatal care at a single, high-volume tertiary care center before (“preguidelines”) and after (“postguidelines”) American College of Obstetrics and Gynecology guidelines for early pregnancy diabetes screening for women at high risk for diabetes. Women with known pregestational diabetes, late entry to prenatal care, a fetus with a known anomaly, or multiple gestation were excluded. Multivariable linear and logistic regression models were constructed to compare maternal and neonatal outcomes between women in the preguidelines cohort to those in the postguidelines cohort. Similarly, adherence to screening guidelines was assessed, and among all women who were eligible for early diabetes screening, multivariable linear, and logistic models were created to compare outcomes between those women who were screened early to those who were not. Results Of the 2,069 women eligible for analysis, 64.6% (n = 1,337) were in the postguideline cohort. Women in the postguideline cohort were older, less likely to have a history of smoking, and more likely to be non-Hispanic white. On multivariable analysis, women in the postguideline cohort had significantly less gestational weight gain (aβ = −2.3; 95% confidence interval [CI]: −3.4 to −1.1), but a higher odds of 5-minute Apgar's score of <7 (adjusted odds ratio: 2.51; 95% CI: 1.11–5.66). Of 461 women who met ACOG early diabetes screening criteria, 58.7% (n = 270) were screened appropriately. Adherence to screening was associated with parity, race, insurance, and BMI. On multivariable analysis, there were no significant differences in neonatal outcomes between women meeting early screening criteria who were screened early and those who were not. Conclusion Introduction of early diabetes screening guidelines was associated with a significant decrease in gestational weight gain, but did not improve neonatal outcomes. Key Points


2007 ◽  
Vol 293 (2) ◽  
pp. R707-R713 ◽  
Author(s):  
Sharyn M. Fitzgerald ◽  
Barbara K. Kemp-Harper ◽  
Helena C. Parkington ◽  
Geoffrey A. Head ◽  
Roger G. Evans

We determined whether nitric oxide (NO) counters the development of hypertension at the onset of diabetes in mice, whether this is dependent on endothelial NO synthase (eNOS), and whether non-NO endothelium-dependent vasodilator mechanisms are altered in diabetes in mice. Male mice were instrumented for chronic measurement of mean arterial pressure (MAP). In wild-type mice, MAP was greater after 5 wk of Nω-nitro-l-arginine methyl ester (l-NAME; 100 mg·kg−1·day−1 in drinking water; 97 ± 3 mmHg) than after vehicle treatment (88 ± 3 mmHg). MAP was also elevated in eNOS null mice (113 ± 4 mmHg). Seven days after streptozotocin treatment (200 mg/kg iv) MAP was further increased in l-NAME-treated mice (108 ± 5 mmHg) but not in vehicle-treated mice (88 ± 3 mmHg) nor eNOS null mice (104 ± 3 mmHg). In wild-type mice, maximal vasorelaxation of mesenteric arteries to acetylcholine was not altered by chronic l-NAME or induction of diabetes but was reduced by 42 ± 6% in l-NAME-treated diabetic mice. Furthermore, the relative roles of NO and endothelium-derived hyperpolarizing factor (EDHF) in acetylcholine-induced vasorelaxation were altered; the EDHF component was enhanced by l-NAME and blunted by diabetes. These data suggest that NO protects against the development of hypertension during early-stage diabetes in mice, even in the absence of eNOS. Furthermore, in mesenteric arteries, diabetes is associated with reduced EDHF function, with an apparent compensatory increase in NO function. Thus, prior inhibition of NOS results in endothelial dysfunction in early diabetes, since the diabetes-induced reduction in EDHF function cannot be compensated by increases in NO production.


2003 ◽  
Vol 16 (9) ◽  
pp. 761-766 ◽  
Author(s):  
R Hoeldtke
Keyword(s):  

Author(s):  
Pamela K. Carmines ◽  
Joseph P. Bast ◽  
Naohito Ishii

1965 ◽  
Vol 14 (2) ◽  
pp. 190
Author(s):  
Joan B. Walker ◽  
P E Brown
Keyword(s):  

2015 ◽  
Vol 22 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Hiroshi Nakamoto ◽  
Kazuhiko Nakayama ◽  
Noriaki Emoto ◽  
Fumihiko Kajiya

2019 ◽  
Author(s):  
Ashani R Lecamwasam ◽  
Mohammadreza Mohebbi ◽  
Elif I Ekinci ◽  
Karen M Dwyer ◽  
Richard Saffery

BACKGROUND The importance of identifying people with diabetes and progressive kidney dysfunction relates to the excess morbidity and mortality of this group. Rates of cardiovascular disease are much higher in people with both diabetes and kidney dysfunction than in those with only one of these conditions. By the time these people are identified in current clinical practice, proteinuria and renal dysfunction are already established, limiting the effectiveness of therapeutic interventions. The identification of an epigenetic or blood metabolite signature or gut microbiome profile may identify those with diabetes at risk of progressive chronic kidney disease, in turn providing targeted intervention to improve patient outcomes. OBJECTIVE This study aims to identify potential biomarkers in people with diabetes and chronic kidney disease (CKD) associated with progressive renal injury and to distinguish between stages of chronic kidney disease. Three sources of biomarkers will be explored, including DNA methylation profiles in blood lymphocytes, the metabolomic profile of blood-derived plasma and urine, and the gut microbiome. METHODS The cross-sectional study recruited 121 people with diabetes and varying stages (stages 1-5) of chronic kidney disease. Single-point data collection included blood, urine, and fecal samples in addition to clinical data such as anthropometric measurements and biochemical parameters. Additional information obtained from medical records included patient demographics, medical comorbidities, and medications. RESULTS Data collection commenced in January 2018 and was completed in June 2018. At the time of submission, 121 patients had been recruited, and 119 samples remained after quality control. There were 83 participants in the early diabetes-associated CKD group with a mean estimated glomerular filtration rate (eGFR) of 61.2 mL/min/1.73 m2 (early CKD group consisting of stage 1, 2, and 3a CKD), and 36 participants in the late diabetic CKD group with a mean eGFR of 23.9 mL/min/1.73 m2 (late CKD group, consisting of stage 3b, 4, and 5), <i>P</i><.001. We have successfully obtained DNA for methylation and microbiome analyses using the biospecimens collected via this protocol and are currently analyzing these results together with the metabolome of this cohort of individuals with diabetic CKD. CONCLUSIONS Recent advances have improved our understanding of the epigenome, metabolomics, and the influence of the gut microbiome on the incidence of diseases such as cancers, particularly those related to environmental exposures. However, there is a paucity of literature surrounding these influencers in renal disease. This study will provide insight into the fundamental understanding of the pathophysiology of CKD in individuals with diabetes, especially in novel areas such as epigenetics, metabolomics, and the kidney-gut axis. INTERNATIONAL REGISTERED REPORT DERR1-10.2196/16277


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