Neural network modeling and control of type 1 diabetes mellitus

2004 ◽  
Vol 27 (2) ◽  
pp. 75-79 ◽  
Author(s):  
A. Karim El-Jabali
Keyword(s):  
Neural Network ◽  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Network Modeling ◽  
Neural Network Modeling ◽  
Modeling And Control ◽  
And Control

scholarly journals Endothelial dysfunction in children and adolescents with type 1 diabetes mellitus and its role in the development of diabetic peripheral polyneuropathy

2009 ◽  
Vol 12 (1) ◽  
pp. 29-32 ◽  
Author(s):  
A A Afonin ◽  
M V Komkova ◽  
G A Galkina ◽  
N V Morozova
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Endothelial Dysfunction ◽  
Type 1 Diabetes Mellitus ◽  
Children And Adolescents ◽  
Griess Reagent ◽  
Disability Score ◽  
Peripheral Polyneuropathy ◽  
And Control

Aim. To measure endothelial factors (nitric oxide (NOx) metabolites, endothelin-1 (ET-1), and basic fibroblast growth factor (bFGF)) in children and adolescentswith diabetes mellitus (DM) during development of diabetic peripheral polyneuropathy (DPNP). Materials and methods. A total of 130 children and adolescents with diabetes mellitus were examined. Duration of DM varied from 3 months to 14 years. Thecontrol group comprised 20 children and adolescents without DM or neurologic pathology. Subjective manifestations of DPNP were assessed based on thedata of a standardized Neuropathy Symptom Score (NSS) questionnaire. Neuropathy Disability Score (NDS) questionnaire was used to monitor objectivechanges of DPNP. NOx metabolites were detected with Griess reagent (Aldrich Chemical Co, USA). Serum ET-1 and bFGF were measured using solid-phaseimmunoenzyme assay (DRG, USA) and CYTIMMINE (USA) kits respectively. Results. All children and adolescents with DM1 had lower NOx and bFGF levels than controls. ET-1 level in DM patients was 3.5 times that in controls. DMpatients with DPNP had more pronounced endothelial dysfunction than DM patients without DPNP and control subjects. Patients with hyperproduction ofNOx had DM for more than 10 years and their total NDS score was significantly higher than in two other groups. Conclusion. Endothelial dysfunction in children and adolescents with type 1 diabetes mellitus progresses with the development of DPNP. Depletion of endothelialfunctional reserve is responsible for the unfavourable course of DPNP.

scholarly journals Physiological Models and Control for Type 1 Diabetes Mellitus: A Brief Review

2018 ◽  
Vol 51 (1) ◽  
pp. 289-294 ◽  
Author(s):  
Anirudh Nath ◽  
Shivanagouda Biradar ◽  
Archana Balan ◽  
Rajeeb Dey ◽  
Radhakant Padhi
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Physiological Models ◽  
And Control

scholarly journals Role of Soluble Epoxide Hydrolase in Exacerbation of Stroke by Streptozotocin-Induced Type 1 Diabetes Mellitus

2013 ◽  
Vol 33 (10) ◽  
pp. 1650-1656 ◽  
Author(s):  
Sari A Jouihan ◽  
Kristen L Zuloaga ◽  
Wenri Zhang ◽  
Robert E Shangraw ◽  
Stephanie M Krasnow ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 1 Diabetes ◽  
Type 1 Diabetes Mellitus ◽  
Epoxide Hydrolase ◽  
Soluble Epoxide Hydrolase ◽  
Artery Occlusion ◽  
Cerebral Injury ◽  
The Difference ◽  
And Control

Hyperglycemia worsens stroke, yet rigorous glycemic control does not improve neurologic outcome. An alternative is to target downstream molecular mediator(s) triggered by hyperglycemia but independent of prevailing glycemia. Soluble epoxide hydrolase (sEH) is a potential mediator of injury via its metabolism of neuroprotective epoxyeicosatrienoic acids (EETs). We tested whether hyperglycemia exacerbates cerebral injury by upregulating sEH and decreasing brain EET levels. Type 1 diabetes mellitus was modeled by streptozotocin (STZ;50 mg/kg per day intraperitoneally, 5 days) in male mice. At 4 weeks, STZ-treated and control mice underwent 45-minute middle cerebral artery occlusion (MCAO) with or without sEH blockade by trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB;1 mg/kg intraperitoneally daily for 6 days before MCAO). The STZ-treated mice had increased sEH mRNA expression in cerebral vessels and decreased EET concentrations in brain. There was no difference in cortical perfusion between groups. The STZ-treated mice sustained larger brain infarct than controls. Pretreatment with t-AUCB eliminated the difference in infarct size and EETs concentration between STZ-treated mice and controls, without altering glycemia. We conclude that type 1 diabetes mellitus upregulates sEH mRNA and decreases concentrations of neuroprotective EETs within the brain, leading to worse stroke outcome. The data indicate that sEH antagonism may be beneficial in the setting of hyperglycemic stroke.

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