Relevant bibliographies by topics / Diabetic angiopathies

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters

Academic literature on the topic 'Diabetic angiopathies'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2024

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Journal articles on the topic "Diabetic angiopathies"

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Zhuk, E. A. "The use of the HELPER device for determining infrared radiation of the skin in the diagnosis of diabetic angiopathies." Problems of Endocrinology 44, no. 2 (September 23, 2019): 10–12. http://dx.doi.org/10.14341/probl199844210-12.

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A HELPER device is offered for the early diagnosis and monitoring of patients with diabetic angiopathies. The device picks up the limb skin temperature gradient. The temperature gradient in the diabetics increases with the progress of diabetic angiopathies in comparison with normal subjects.
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Malkova, T. A. "Effect of hyperbaric oxygenation on liver function in diabetic patients." Kazan medical journal 66, no. 1 (February 15, 1985): 18–20. http://dx.doi.org/10.17816/kazmj60405.

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&NA;. "LY-333531 corrects diabetic angiopathies." Inpharma Weekly &NA;, no. 1038 (May 1996): 9. http://dx.doi.org/10.2165/00128413-199610380-00016.

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Bobyreva, L. E. "Free-radical oxidation, antioxidants, and diabetic angiopathies." Problems of Endocrinology 42, no. 6 (December 15, 1996): 14–20. http://dx.doi.org/10.14341/probl12052.

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The leading pathology in endocrinology is diabetes mellitus, which is characterized by a high incidence of disability and high mortality. According to the data of A. G. Mazovetsky, by 2000 compared with 1985, an increase in the number of patients with diabetes mellitus is expected to be 2.9 times. The frequency of vascular lesions in diabetes is 6891.3%. The results of D. Greene indicate that peripheral vascular damage in this group of patients is observed 30 times more often than in people of a similar age without diabetes mellitus. Free radical pathology. Recent studies of domestic and foreign authors indicate the important role of non-enzymatic free radical oxidation (FRO) of lipids in the pathogenesis of many chronic diseases of modern man. Before analyzing the role of free radical mechanisms in the pathogenesis of diabetes mellitus and diabetic angiopathies, it is necessary to briefly familiarize yourself with the general ideas about the nature of FRO lipids and their inhibition systems. Due to the spin properties of triplet oxygen, when it interacts with a pair of donor electrons, the probability of free radical formation is high. The one-electron form of reduced oxygen can be protonated НО2*(hydroperoxyl radical) and anionic О2- (superoxide radical).
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Petrik, G. G., and S. A. Pavlishchuk. "Metabolic and hemostatic characteristics of patients with type 2 diabetes mellitus differing in the severity of angiopathy." Problems of Endocrinology 56, no. 2 (April 15, 2010): 15–19. http://dx.doi.org/10.14341/probl201056215-19.

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The objective of the present study was to identify risk factors of developing vascular disorders in patients at different stages of type 2 diabetes mellitus (DM2) by comprehensive analysis of metabolic parameters, hemograms, thrombocytic and plasma hemostasis. The study involved 75 patients (22 men and 53 women of mean age 57,3±9,7 years) having angiopathies of different severity. The data obtained confirmed the presence of risk factors of vascular pathology in different phases of DM2. All the examined patients including those without angiopathies in the early period of diabetes showed triglyceridemia, cholesterolemia, enhanced platelet aggregation activity, and shortened activated partial thromboplastin time. Patients with diabetic nephropathy at the stage of microalbuminuria and with non-proliferative retinopathy were distinct from the remaining ones in that they had significantly higher blood alpha-2 globulin and fibrinogen levels. Diabetic patients with micro- and macrovascular problems were characterized by marked dysproteinemia and abnormal platelet disaggregation.
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Frolov, Denis V. "The Role of Physical Therapy in the Combined Treatment of Patients with Lower Extremities Diabetic Angiopathies." Bulletin of Rehabilitation Medicine 20, no. 2 (April 30, 2021): 80–87. http://dx.doi.org/10.38025/2078-1962-2021-20-2-80-87.

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One of the most disabling complications of diabetes mellitus is angiopathy of the lower extremities. Diabetic polyneuropathy and diabetic foot syndrome are closely associated with vascular complications of diabetes mellitus, which significantly aggravate the course of the disease and contribute to high mortality. Diabetic polyneuropathy and diabetic foot syndrome are closely associated with the diabetes mellitus vascular complications that significantly aggravate the course of the disease and contribute to high mortality. Despite the improvement in the results of pharmacotherapy of diabetes mellitus, the problem of treating its vascular complications is far from being solved. Traditionally, therapeutic physical training is used among the methods of non-drug treatment of diabetes mellitus and its complications. As a method of pathogenetic focus on many risk factors for the development of diabetes and its complications, physical therapy exercises contribute to the correction of the syndrome of hypodynamia, obesity, and muscle atrophy. At the same time, there is insufficient data on how exercise therapy affects the quality of life of patients, functional characteristics of walking and objective indicators of blood flow in the lower extremities. This review identifies the main approaches to the application, advantages and disadvantages of individual methods of therapeutic physical training in the correction of functional disorders in patients with lower extremities diabetic angiopathies. We can currently talk about the proven safety of the physical therapy use in patients with diabetic angiopathies. Meanwhile, the scientific data on the high efficiency of this method is still insufficient.
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Gonchar, М. G., Zh М. Vavrik, Ye I. Deltsova, and R. G. Zelenetsky. "Effect of hyperbaric oxygenation on microcirculation, oxygen budget, and acid base balance of patients with diabetic angiopathies of the lower limbs." Problems of Endocrinology 39, no. 2 (December 15, 1993): 11–13. http://dx.doi.org/10.14341/probl11943.

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These effects were studied in 52 patients with degrees III-IV diabetic angiopathies of the lower limbs. Microcirculation parameters were found changed in this patient population, this leading to disorders of the oxygen budget and development of metabolic acidosis. Development of destructive changes in the limb evidences failure of the compensatory adaptive mechanisms of microcirculation. Addition of hyperbaric oxygenation to multiple-modality treatment of patients with diabetic angiopathies was conducive to improvement of the blood rheology, of tissue saturation with oxygen, and to essential reduction of metabolic acidosis. The detected microcirculation disorders necessitate addition to the therapeutic complex of the drugs improving the biophysical characteristics of the blood.
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Anestiadi, V., Z. Anestiadi, and V. Anestiadis. "P35 EVALUATION OF DIABETIC ANGIOPATHIES BY DIGITAL THERMOGRAPHY." Atherosclerosis Supplements 11, no. 2 (June 2010): 24. http://dx.doi.org/10.1016/s1567-5688(10)70102-1.

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Bondar', I. A., and V. V. Klimontov. "Hyperhomocysteinemia: a risk factor for vascular complications of diabetes." Problems of Endocrinology 50, no. 2 (April 15, 2004): 24–29. http://dx.doi.org/10.14341/probl11390.

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Vascular complications are a leading cause of reduced quality and longer life of patients with diabetes mellitus (DM). The mechanisms of development of these complications are not fully disclosed. It is known that in not all cases the occurrence and progression of diabetic angiopathies can be explained by traditional risk factors, such as hyperglycemia, arterial hypertension, smoking or dyslipidemia. Therefore, the search for the missing links in the pathogenesis of angiopathy remains an extremely urgent task.
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Vartanian, Natalia L., Vitali I. Odin, Vladimir V. Zarubajev, Andrey A. Novik, Ella S. Pushkova, and Anna A. Sominina. "Islet cell antibodies and diabetic angiopathies in elderly diabetes type 2 patients." Diabetes Research and Clinical Practice 50 (September 2000): 131. http://dx.doi.org/10.1016/s0168-8227(00)81902-6.

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Dissertations / Theses on the topic "Diabetic angiopathies"

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Kalani, Majid. "Diabetic skin microangiopathy : studies on pathogenesis and treatment /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-680-4.

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Yngen, Marianne. "Platelet function in diabetes mellitus : relationships to hyperglycaemia, antidiabetic treatment and microangiopathy /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-062-1/.

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Rosenfeld, Ellie. "The care of the feet of people with type 2 diabetes in South Australian general practice /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09MPM/09mpmr813.pdf.

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Mak, Shiu-kwong Thomas, and 麥肇鑛. "Modeling diabetic cardiomyopathy using embryonic stem cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193562.

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Diabetic cardiomyopathy (DCM), a disorder of the heart muscle, is one of the major and most rampant culprits claiming thousands and thousands of lives around the globe every year by interfering with the blood circulation and causing the development of heart failure eventually. The progression of the disease is asymptomatic and having a long latent period, and it is characterized functionally by ventricular dilation, diastolic dysfunction, interstitial fibrosis and cardiomyocytes hypertrophy. It was suggested the pathogenesis of the disease and the related complications are related to the effects of hyperglycemia on cardiomyocytes. So understanding the physiology of both the normal and pathological conditions, and the underlying mechanisms involved are of paramount importance to derive therapies to cope with this disease. However, it is difficult, if not impossible, to study the physiology in vivo using a live sample or to build a cellular model with adult cardiomyocytes due to the insufficient number of the cells harvested. This is not until the emergence of Embryonic Stem Cells (ESCs) that a cellular model with clinical sufficient number of cardiomyocytes could be built for investigation and drug screening. With a view to mimicking the situation of the Diabetic cardiomyopathy of the Type II Diabetes mellitus (DM) patients, mouse ESCs are used to differentiate into cardiomyocytes using the traditional hanging drop method to produce Embryoid body (EB). The cardiomyocytes were then enriched and plated so that different testing conditions could be applied. The effect of high glucose (HG), Insulin and the combination of high glucose and insulin were then analyzed. This was to show the significance of hyperglycemia, hyperinsulinemia due to insulin resistance and the role of insulin in hyperglycemia on cardiomyocytes respectively. The results agreed with previous findings that high glucose and insulin alone do induce cells apoptosis while the combination of insulin and glucose did decrease the number of apoptosis and while the co-culture of insulin with High dosage of glucose has shown to reduce the effect of hypertrophy.
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Medicine
Master
Master of Medical Sciences
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Fang, Zhi You. "Mechanisms and therapeutic implications of diabetic heart disease /." [St. Lucia, Qld], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18240.pdf.

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Wong, Vincent Wing-Ming. "Hyperglycaemia and insulin therapy : their role in acute myocardial infarction." Thesis, The University of Sydney, 2005. https://hdl.handle.net/2123/28040.

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Diabetes mellitus represents a state of insulin insufficiency with elevated glucose levels. Previous studies have shown that patients with diabetes not only have an increased risk for cardiovascular disease, but they are also more likely to suffer adverse outcomes following acute myocardial infarction (AMI). Even in people without known diabetes, stress-induced hyperglycaemia at the time of AMI has been associated with poor outcomes. It is uncertain if hyperglycaemia causes direct myocardial injury following acute ischaemia and reperfusion, and if short term insulin therapy protects the ischaemic myocardium. A number of clinical trials, however, suggest that insulin therapy is beneficial. In this thesis, through a number of experimental studies, the effe􀀓ts of glucose and insulin on the myocardium were assessed. After studying these effects in animal models, the impact of an insulin-dextrose infusion regimen aimed at maintaining norrnoglycaemia during the peri-infarct period was also evaluated in a clinical trial. In the first part of the thesis, a retrospective review of patients admitted to Westmead Hospital with AMI over a 12-month period was conducted. Clinical, historical and biochemical parameters were correlated against adverse cardiac outcomes (mortality, cardiac failure, re-infarction etc). From multi-variate logistic regression analysis, admission glucose level was a consistent predictor of mortality and morbidity in all AMIpatients as well as in those who received reperfusion therapy for up to 6 months following index AMI admission. The study confirmed that hyperglycaemia remains a significant predictor of cardiac mortality and morbidity in the reperfusion era. To evaluate whether elevated glucose levels have a direct pathological role on the ischaemic myocardium, an adult rat cardiomyocyte culture model was adopted to assess the impact of glucose and insulin on cardiomyocyte viability. Rat cardiomyocytes from primary culture were incubated in media containing different levels of glucose as well as insulin under a normoxic environment. Exposure of cardiomyocytes to higher concentration of glucose (without insulin) resulted in significantly greater cytotoxicity, while cells incubated in media containing the highest insulin concentration (at normal glucose levels) had the lowest cytotoxicity. When the high glucose media was supplemented with insulin, the cytotoxic effect of high glucose was negated. To study the effects of glucose and insulin on the ischaemic myocardium, an isolated rabbit heart model of regional ischaemia and reperfusion was also developed. The hearts were perfused with buffers containing varying levels of glucose and insulin, and the infarct size for each heart was assessed. In the high-glucose protocol, the infarct size was significantly greater than that when hearts were exposed to normal glucose levels. On the other hand, insulin, when given just before reperfusion, reduced infarct size in a dose­dependent manner. Furthermore, insulin attenuated the extent of infarction in hearts that were exposed to high glucose levels. Therefore, from these 2 different animal models, elevated glucose levels were found to be harmful to the myocardium by increasingcardiomyocyte death (in the culture model) and inducing greater infarct size (in the ischaemic model). Conversely, insulin preserved cardiomyocyte viability and reduced infarct size following an ischaemic insult. The cellular mechanism for the action of insulin on the myocardium was beyond the scope of this thesis, and it is difficult to speculate whether insulin confers protection through insulin receptor or other pathways such as the insulin-like growth factor receptor. Extending these findings to clinical practice, a randomized controlled trial was conducted to evaluate the effects of maintaining normoglycaemia by an insulin infusion regimen at the time of AMI. Patients presenting with AMI who either had known diabetes or were hyperglycemic on admission were recruited into the Hyperglycemia: Intensive Insulin Infusion !n !nfarction (HI-5) Study. Subjects were randomized to receive either intensive therapy (insulin/dextrose infusion for 24 hours to keep glucose level 4 - lOmmol/1) or conventional therapy. Intensive insulin therapy did not confer survival advantage for patients following AMI up to 6 months following admission, but it resulted in a lower incidence of in-hospital cardiac failure. Insulin therapy also reduced the incidence of composite endpoints for subjects with antero-lateral AMI or those who received reperfusion therapy. Patients with pre-existing diabetes did not derive clinical benefit from insulin therapy, but as a group, they did not have greater adverse outcomes compared to those without diabetes. Unfortunately, due to the suboptimal patient recruitment as well as the better than expected overall survival for AMI patients, the power of the study was substantially reduced. Elevated inflammatory markers have been associated with worse outcomes in myocardial infarction. In the HI-5 Study, insulin therapy reduced free fatty acid (FFA) levels and attenuated the rise of C-reactive protein (CRP) levels. Day 2 CRP levels also correlated with the mean glucose levels of subjects during the first 24 hours of treatment. Suppression of FFA and the attenuation of the rise of CRP may have theoretical benefits for the preservation of ischaemic myocardium, but it has not translated into improved clinical outcomes in the HI-5 study. In summary, from experimental studies conducted in this thesis, elevated glucose levels were found to be detrimental to the myocardium during normoxia or following ischaemia, while insulin confers cardio-protection in both conditions. However, despite the reduction of FFA levels and markers of inflammation, clinical benefits were not clearly evident in the HI-5 study. The findings of other very recent clinical studies also did not support the use of insulin-based therapy following AMI, but it is possible that a higher dose of insulin maintaining tighter glycaemic control may still improve outcomes for patients following AMI. For the time being, in the absence of consistent clinical trial evidence, one cannot justify the routine use of intensive insulin-based treatment to control glucose levels during AMI. However, optimization of the management of coronary artery disease for patients with hyperglycaemia remains an important research priority of this era.
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Esche, Curtis A. "The effects of streptozotocin-induced diabetes on control of serum cholesterol levels in female strain A/ST mice." Virtual Press, 1991. http://liblink.bsu.edu/uhtbin/catkey/834628.

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Diabetics often have elevated levels of serum lipids and cholesterol and increased risk of cardiovascular disease. Streptozotocin-induced diabetes was used to determine whether elevated serum cholesterol levels in diabetics are due to loss of control of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, which catalyzes the committed step in cholesterol synthesis. Strain A/ST female mice were fed 10% corn oil diets, half with 2% cholesterol. Experimental groups were injected with 9.0 mg streptozotocin / 100g body weight. Diabetes was confirmed by weight loss, elevated blood sugars, and enlarged spleens. Reductase activity was assayed spectrophotometrically. Serum cholesterol levels were determined by gas liquid chromatography. Both diabetic and control mice fed cholesterol had elevated serum cholesterol levels and decreased reductase activities. These observations suggest that HMG CoA reductase is not the primary control point in the control of serum cholesterol levels in diabetic mice. The increase in serum cholesterol in the SI mice was not more than in the control group, suggesting that increased serum cholesterol is not a key factor in the control of coronary heart disease and related diseases in diabetics. The HMG CoA reductase activity was reduced in both SI and control mice fed 2% cholesterol, but not significantly, possibly due to a small sample size. Other substances that control serum cholesterol are all density classes of lipoproteins (high, intermediate, low, and very low) as well as the chylomicrons.
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Bassirat, Maryam. "Mechanisms underlying changes in microvascular blood flow in a diabetic rat model : relevance to tissue repair /." Connect to thesis, 2002. http://eprints.unimelb.edu.au/archive/00001363.

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Nyström, Thomas. "On endothelial function in type 2 diabetic patients with coronary artery disease /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-318-3/.

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Woodman, Richard John. "The independent effects of purified EPA and DHA supplementation on cardiovascular risk in treated-hypertensive type 2 diabetic individuals." University of Western Australia. School of Medicine and Pharmacology, 2003. http://theses.library.uwa.edu.au/adt-WU2003.0028.

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[Formulae and special characters can only be approximated here. Please see the pdf version of the Abtract for an accurate reproduction.] Type 2 diabetes at least doubles the risk of cardiovascular disease. This can partly be explained by the increased prevalence of risk factors such as hypertension, dyslipidaemia and obesity. However, the underlying abnormality of insulin resistance and the presence of more recently identified risk factors including endothelial dysfunction, increased inflammation, and increased oxidative stress might also contribute towards the heightened cardiovascular risk. Fish oil, which contains eicosapentaenoic acid (EPA, 20:5 n-3), has wide-ranging beneficial effects on these and other abnormalities, and has reduced cardiovascular mortality in secondary prevention studies. Animal and human studies have recently established that in addition to EPA, docosahexaenoic acid (DHA, 22:6 n-3) also has beneficial effects, and furthermore, may have less detrimental effects than EPA on glycaemic control which has worsened in some fish and fish oil studies involving Type 2 diabetic subjects. Study 1 : This intervention study aimed to determine the independent effects of EPA and DHA on cardiovascular risk factors and glycaemic control in individuals with Type 2 diabetes receiving treatment for hypertension. In a double-blind placebo-controlled trial of parallel design, 59 subjects in good to moderate glycaemic control (HbA1c < 9%) were recruited from media advertising and randomised to 4 g/day of EPA, DHA or olive oil (placebo) for 6 weeks. Thirty-nine men and 12 post-menopausal women aged 61.2±1.2 yrs completed the study. Relative to placebo, and with Bonferroni adjustments for multiple comparisons, serum triglycerides fell by 19% (p=0.022) and 15% (p=0.022) in the EPA and DHA groups respectively. There were no changes in serum total cholesterol, or LDL- and HDL-cholesterol, although HDL2-cholesterol increased 16% with EPA (p=0.026) and 12% with DHA (p=0.05). HDL3-cholesterol fell by 11% (p=0.026) with EPA supplementation and LDL particle size increased by 0.26±0.10 nm (p=0.02) with DHA. Urinary F2-isoprostanes, an in-vivo marker of oxidative stress was reduced by 19% following EPA (p=0.034) and by 20% following DHA. DHA but not EPA supplementation reduced collagen-stimulated platelet aggregation (16.9%, p=0.05) and thromboxane release (18.8%, p=0.03), but there were no significant changes in PAF-stimulated platelet aggregation. Fasting glucose rose by 1.40±0.29 mmol/l (p=0.002) following EPA and 0.98±0.29 mmol/l (p=0.002) following DHA. Neither EPA nor DHA had any significant effect on HbA1c, fasting serum insulin or C-peptide, insulin sensitivity, stimulated insulin secretion, 24-hr ambulatory blood pressure and heart rate, markers of inflammation, and fibrinolytic or vascular function. Study 2 : This study aimed to examine the influence and causes of increased inflammation on vascular function in subjects recruited for Study 1. Compared with healthy controls (n=17), the diabetic subjects (n=29) had impaired flow-mediated dilatation (FMD) (3.9±3.0% vs 5.5±2.4%, p=0.07) and glyceryl-trinitrate mediated dilatation (GTNMD) (11.4±4.8% vs 15.4±7.1%, p=0.04) of the brachial artery. They also had higher levels of the inflammatory markers C-reactive protein (2.7±2.6 mg/l vs 1.4±1.1 mg/l, p=0.03), fibrinogen (3.4±0.7 g/l vs 2.7±0.3 g/l, p<0.001) and tumor necrosis factor-alpha (20.9±13.4 pg/l vs 2.5±1.7 pg/l, p<0.001). In diabetic subjects, after adjustment for age and gender, leukocyte count was an independent predictor of FMD (p=0.02), accounting for 17% of total variance. Similarly, leukocyte count accounted for 23% (p<0.001) and IL-6 for 12% (p=0.03) of variance in GTNMD. Von Willebrand factor, a marker of endothelial cell activation was correlated with leukocyte count (r=0.38, p=0.04), FMD (r=-0.35, p=0.06) and GTNMD (r=-0.47, p=0.009), whilst P-selectin, a marker of platelet activation was correlated with fibrinogen (r=0.58, p=0.001). Conclusion : EPA and DHA have similar beneficial effects on triglycerides, HDL2 cholesterol and oxidative stress in individuals with Type 2 diabetes and hypertension. However, DHA also increases LDL particle size and reduces collagen-stimulated platelet aggregation and thromboxane release, thus offering more potential than EPA as an anti-thrombotic agent. The beneficial effects of both oils were potentially offset by deterioration in glycaemic control. Neither oil affected blood pressure or vascular function. Longer-term studies with major morbidity and mortality as the primary outcome measures are required to assess the overall benefits and risks of EPA and DHA. The cross-sectional observations from Study 2 are consistent with the hypothesis that impaired vascular function in individuals with Type 2 diabetes and hypertension is at least in part secondary to increased inflammation, with associated endothelial and platelet activation.
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Books on the topic "Diabetic angiopathies"

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Satellite Symposium on Endothelial Cell Function in Diabetic Microangiopathy: Problems in Methodology and Clinical Aspects (1988 Melbourne, Vic.). Endothelial cell function in diabetic microangiopathy: Problems in methodology and clinical aspects. Edited by Molinatti G. M and International Diabetes Federation Congress. Basel ; New York: Karger, 1990.

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Bosevski, Marijan. Diabeto-angiology. Hauppauge, N.Y: Nova Science Publishers, 2011.

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D, Kerstein Morris, ed. Diabetes and vascular disease. Philadelphia: Lippincott, 1990.

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E, Tooke John, ed. Diabetic angiopathy. London: Arnold, 1999.

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Weber, Bruno, Prof. Dr. med., ed. Early vascular complications in children with diabetes mellitus: Proceedings of an International Workshop on Diabetic Angiopathy in Children, Berlin, September 25-26, 1986. Basel: Karger, 1988.

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International Diabetes Conference on Vascular and Neurologic Complications of Diabetes Mellitus. (2nd 1985 Florence, Italy). Vascular and neurologic complications of diabetes mellitus. Edited by Belfiore Francesco, Molinatti G. M, and Williamson J. R. Basel ; New York: Karger, 1987.

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A, Gries F., ed. Haemostasis and diabetic angiopathy: Pathophysiology and therapeutic concepts : proceedings of the second Düsseldorf Conference. Stuttgart: Georg Thieme Verlag, 1993.

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Barnett, A. H. Diabetes and the heart. Edinburgh: Elsevier/Churchill Livingstone, 2005.

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Donnelly, Richard, and Edward S. Horton. Vascular complications of diabetes: Current issues in pathogenesis and treatment. Edited by Wiley online library. 2nd ed. Malden, Mass: Blackwell Pub., 2005.

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Neil, Ruderman, Williamson J. R, Brownlee Michael 1948-, and American Physiological Society (1887-), eds. Hyperglycemia, diabetes, and vascular disease. New York: Published for the American Physiological Society by Oxford University Press, 1992.

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Book chapters on the topic "Diabetic angiopathies"

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Krzywanek, H. J. "Klinik der diabetischen Angiopathie." In Diabetes und Angiopathie, 89–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_7.

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Holtz, J. "Mechanismen der Insulinresistenz." In Diabetes und Angiopathie, 1–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_1.

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Fiedler, H. "Bewertung verschiedener labordiagnostischer Methoden zur Therapieführung und Verlaufskontrolle des Diabetes mellitus." In Diabetes und Angiopathie, 121–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_10.

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Hepp, K. D. "Insulinresistenz und metabolisches Syndrom." In Diabetes und Angiopathie, 21–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_2.

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Nawroth, P. P., J. Lu, M. Abel, Y. Zhang, J. Riedesel, A. Bierhaus, B. Liliensiek, et al. "Endothelzellstimulation durch AGE — Ein In-vitro-Modell diabetischer Spätschäden." In Diabetes und Angiopathie, 33–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_3.

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Mann, J., H. Walter, K. Hilgers, and F. Luft. "Das Renin-Angiotensin-System bei Diabetes mellitus." In Diabetes und Angiopathie, 43–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_4.

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Lüddecke, H. J. "Zur Epidemiologie der diabetischen Angiopathie." In Diabetes und Angiopathie, 55–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_5.

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Tschöpe, D., P. Rösen, and B. Schwippert. "Aktivierte zelluläre Hämostase und diabetische Angiopathie." In Diabetes und Angiopathie, 73–87. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_6.

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Hamm, C. W. "Neue Aspekte zur Pathogenese und Diagnostik der instabilen Angina pectoris." In Diabetes und Angiopathie, 99–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_8.

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Hasslacher, C. "Klinische Relevanz der Mikroalbuminurie." In Diabetes und Angiopathie, 109–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-47621-1_9.

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