Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The phases of wound healing--inflammatory, fibroblastic, and maturation--are continuous, though they overlap and do not always occur in an orderly fashion. Wound healing may be retarded by age, diabetes, smoking, immunosuppression, poor nutrition, cell hypoxia, dehydration, bacteria, and other factors. Bacteria and pus may be so great at the inflammatory phase that the wound remains at that phase. It is important that the nurse recognize when pus is a major factor in an unhealed wound and initiate local care to assist in cleaning the wound bed. It is also important to recognize a clean wound and to initiate appropriate local care that facilitates wound healing. New information about wound healing at the cellular level continues to become available. Epidermal growth factors, platelet-derived growth factors, and the growth hormone somatomedin are being studied, and new methods based on these studies may change local wound care measures. It is essential to understand the phases of wound healing to determine appropriate wound care measures for individual patients.
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PMID:Phases of wound healing. 182 67

Diabetes mellitus is a major risk factor for coronary heart disease, peripheral vascular disease, and cardiovascular disease. The prevalence of these complications is increased about two- to four-fold in people with diabetes in the United States, and they contribute substantially to morbidity, mortality, and healthcare costs. The pathogenesis of macrovascular disease in diabetes is multifactorial. Endothelial injury is an early event, followed by macrophage adherence and uptake of lipids to produce a fatty streak. Platelet adherence, aggregation, and release of thromboxane and platelet-derived growth factors may then occur. Quantitative and qualitative alterations of lipoproteins are seen, particularly in uncontrolled insulin-dependent and non-insulin-dependent diabetes. Hyperinsulinemia may be contributory, as may elevated plasma proinsulin levels. Glycation of plasma proteins and of components of the vascular wall occurs, and altered coagulation and/or fibrinolysis may lead to thrombosis. The process is accelerated by hypertension, smoking, and hypercholesterolemia. Gliclazide is an oral sulfonylurea agent that has been reported to have actions on platelet function and fibrinolysis in addition to its effects on glycemia. The evidence for this is reviewed, and recommendations for future studies are made.
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PMID:Pathophysiology of vascular disease in diabetes: effects of gliclazide. 187 5

Previous studies have suggested that topically applied platelet-derived wound healing factors (PDWHF) accelerate wound healing by stimulating angiogenesis, fibroblast proliferation, and collagen synthesis. To assess the ability of platelet factors to facilitate healing of chronic cutaneous ulcers we performed a randomized, prospective, double-blind, placebo-controlled study of topical PDWHF in 18 patients with 26 lower extremity wounds refractory to conventional therapy. Wounds were present for at least 8 weeks (mean, 5.5 +/- 4.3 months). They were extensively debrided initially and were measured and photographed at weekly intervals for 12 weeks. Eight patients with nine wounds were treated with placebo solution (controls), and 10 patients with 17 wounds were treated with PDWHF (treatment group). Seventy-eight percent of patients had diabetes mellitus, 72% had occlusive peripheral vascular disease, and 28% had venous disease; distribution of these disorders was equivalent in both groups. Ankle-brachial indexes, which were often spuriously elevated, averaged 0.93 +/- 0.54 in controls and 1.04 +/- 0.56 in patients treated with PDWHF (p greater than 0.5). Mean transcutaneous oxygen tension was 37.8 +/- 11.9 mmHg in controls and 37.1 +/- 9.1 mmHg in patients treated with PDWHF. Initial wound area was larger in controls than in the patients treated with PDWHF (28.9 +/- 45.2 cm2 vs 13.0 +/- 4.4 cm2), but this difference was not statistically significant (p = 0.19). Three (33%) wounds (in two patients) healed in controls, and four (24%) wounds (in three patients) healed in the PDWHF group (p greater than 0.5). The rate of healing in controls was 1.9 +/- 2.7 cm2/week.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective randomized trial of autologous platelet-derived wound healing factors for treatment of chronic nonhealing wounds: a preliminary report. 161 16

Epidermal and platelet-derived growth factors are potent mitogens for many types of cells, including smooth muscle cells. Epidermal growth factor in blood of humans is present both in platelets (as reflected in its serum level) and in plasma, the source(s) of which remains unknown. We assayed its level in 82 diabetic patients and 53 age-matched controls. In diabetes, epidermal growth factor level was increased in serum (191 +/- 43 vs 155 +/- 64 pmol/l, p = 0.0002) and plasma (53 +/- 9 vs 38 +/- 14 pmol/l, p less than 0.0001), without any difference between the patients with and without complications. Platelet-derived growth factor level was assayed only in serum of 19 patients with uncomplicated diabetes and found elevated (222 +/- 47) as compared with 13 controls (160 +/- 26 pmol/l), (p = 0.0002). Type of diabetes, its duration, mode of therapy, control, presence of retinopathy or albuminuria (in case of epidermal growth factor), as well as C-peptide age and sex did not correlate with epidermal or platelet-derived growth factor levels. Serum but not plasma epidermal and platelet-derived growth factor were negatively correlated with serum creatinine (correspondingly, r = -0.373, p = 0.0008 and r = -0.564, p = 0.0285). It is concluded that diabetes itself and not its complications cause increased levels of epidermal growth factor in plasma and serum and of platelet-derived growth factor in serum.
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PMID:Epidermal growth factor and platelet-derived growth factor in blood in diabetes mellitus. 223 81

We used homologous platelet-derived wound healing factors (HPDWHF) to achieve complete healing of recalcitrant ulcers of diverse cause. Twenty-three patients with 27 skin ulcers who had been receiving conventional wound care with no evidence of healing for an average period of 25 weeks (range, 12 to 156 weeks) were studied. The patients were first subjected to controlled wound care for 3 months, with saline solution and silver sulfadiazine dressings used in all cases. At the end of this period, persistent nonhealing ulcers were treated by topical use of HPDWHF and silver sulfadiazine. Ulcer parameters were recorded on the first day and every week during therapy until complete epithelization was achieved in either group. Each ulcer acted as its own control. In the controlled wound care group, only three ulcers in three patients achieved complete healing; the remaining 24 ulcers in 20 patients failed to achieve even 50% healing in the stipulated 3-month period. However, when subjected to HPDWHF applications, these ulcers healed completely, 100% healing occurring in 9.67 +/- 4.9 weeks (range, 3 to 19 weeks), which is highly significant (p less than 0.01). The healing response to HPDWHF applications was of uniform progression over the weeks. Only the basic cause of the ulcer determined the healing rates in this group. The shortest and the longest time to achieve 100% healing occurred in patients with diabetes (6.88 +/- 2.97 weeks) and in the venous stasis group (14.00 +/- 7.07 weeks). Age, sex, location of ulcer, ulcer duration, and ulcer measurements had no influence on the HPDWHF-stimulated healing rates. This is the earliest report of HPDWHF-stimulated repair in chronic nonhealing skin ulcers.
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PMID:Use of homologous platelet factors in achieving total healing of recalcitrant skin ulcers. 239 95

Certain arachidonic metabolites may play a pathogenic role in psoriasis. Platelets are rich sources of 12-hydroxy-eicosatetraenoic acid (12-HETE) and thromboxane A2, mediators of skin inflammation and platelet aggregation, respectively. We have studied untreated psoriatic patients without a history of diabetes mellitus and smoking. In psoriatics, platelet aggregation elicited by thrombin, ADP, and ristocetin was significantly enhanced as compared with healthy adult volunteers. Enhancement of platelet aggregation was detected in patients with both minimal and widespread disease. The formation of 12-hydroxy-5,8,10-heptadecatrienoic acid (HHT), a cyclooxygenase product, and 12-HETE, a 12-lipoxygenase product, was increased in psoriatics with widespread disease but not in those with minimal disease. Formation of 12-HETE was stimulated to a higher degree (125%) than HHT (98%) in psoriasis (P less than 0.05). Addition of platelet-derived 12-HETE to cultured human epidermal keratinocytes resulted in a stimulation of the DNA synthesis (68% at 10(-7) M). These data suggest that platelet activation occurs in psoriasis, and that release of inflammatory and mitogenic compounds by activated platelets may play a role in the pathophysiology of psoriasis. Whether enhanced platelet aggregation in psoriasis is associated with occlusive vascular disease needs further investigation.
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PMID:Increased aggregation and arachidonic acid transformation by psoriatic platelets: evidence that platelet-derived 12-hydroxy-eicosatetraenoic acid increases keratinocyte DNA synthesis in vitro. 243 57

The pathogenesis of macrovascular disease in diabetes mellitus is still incompletely understood. Within the various pathomechanisms abnormal growth of vascular cells is well established as an intrinsic part of the angiopathic process. In this regard, there are different groups of vascular growth factors that are of potential relevance for the development of macrovascular disease in diabetes : hormones, locally released growth factors of platelet and of arterial wall cell origin. The following hormones whose blood levels could increase under various conditions in diabetes have to be considered : growth hormone, insulin-like growth factor I and II and insulin. Human platelets contain at least eight growth peptides or proteins that all stimulate in vitro growth of arterial wall cells : platelet-derived-, epidermal-, fibroblast-, diabetic serum-, endothelial- and transforming growth factor, vascular endothelial cell proliferation factor and platelet-derived endothelial cell mitogen. In serum and plasma from type II diabetics only the diabetic serum growth factor has been shown to be increased. Platelets from type I and II diabetic patients contain increased growth stimulating activity. This increased growth activity returned to normal levels in both types of diabetes after strict metabolic control. Arterial endothelial and smooth muscle cells, fibroblasts and monocyte/macrophages of different species release at least in culture a variety of growth factors that could participate in an autocrine or paracrine manner in the growth regulation of the arterial wall. Diabetes may affect the release of these factors, but direct evidence to which degree this would contribute to the development of macrovascular disease is lacking.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vascular growth factors and the development of macrovascular disease in diabetes mellitus. 330 59

We investigated the association between low-density lipoprotein (LDL), triglycerides, and platelet activation in 18 patients with hypertension age 41-64 years and 18 with diabetes mellitus aged 43-70 years. Platelet P-selectin positivity and the microparticle level (indicators of activation) were both significantly higher in the diabetics than in healthy controls (P-selectin: 28.0% +/- 7.5% vs. 7.3% +/- 4.2%, P < 0.001; microparticles: 1900 +/- 966 vs. 526 +/- 158/10(4) platelets, P < 0.01). In contrast, there was no significant increase of either parameter in the patients with hypertension. Plasma microparticle levels were also significantly greater in the diabetics with high LDL levels than in those with low LDL levels (2375 +/- 949 vs. 1519 +/- 796/10(4) platelets, P < 0.05), and in those with high rather than low triglyceride levels (2188 +/- 845 vs. 1492 +/- 783/10(4) platelets, P < 0.05). However, platelet positivity for P-selectin was not significantly different between these two subgroups. Microparticle and P-selectin levels both showed no significant difference between the hypertensive patients with high and low LDL or triglyceride levels. These results suggest that platelet-derived microparticles may participate in the development or progression of atherosclerosis in patients with diabetes mellitus.
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PMID:Platelet-derived microparticles may influence the development of atherosclerosis in diabetes mellitus. 757 78

Endothelium-derived vasoactive factors are produced by the endothelium activated by effective stimulus, and with paracrine regulatory activity of the tone/proliferation of the vascular smooth muscle and platelet function. They are divided in two groups: endothelium-derived relaxing and contracting factors. Among the endothelium-derived relaxing factors, PG I2, EDRF (NO or other nitrous compound) and EDHF (still unidentified) have been considered Synthetized by the endothelium after stimulation by plasmatic, platelet-derived and endothelium-derived substances and mechanisms, towards the vascular smooth muscle (myorelaxing/cytostatic) and the platelets (antiaggregation). The endothelium-derived contracting factors include the EDCF1 (endothelins, 21 amino acids peptides), EDCF2 (O2-) and TxA2. Its production, induced by stimulus similar to those for relaxing factors, promotes constriction/mitogenesis of the vascular smooth muscle and platelet aggregation. Probably, endothelin-1 has indirect actions over hormonal mechanisms of cardiovascular and renal regulation. The vascular system establishes a tight regulation over the production of these endothelium-derived vasoactive factors. Its loss (usually due to alteration of endothelial responsiveness to stimulation) allows local or generalized modifications of the vascular tone. These can depend on hypertension, atherosclerosis, ischemia-reperfusion lesion, diabetes, inflammation and situations of farmacotoxicity (all developing vasoconstriction/vasospasm) or by septicemia (leading to vasodilation). This disregulation is also involved in the pathogenesis of hypertension, atherosclerosis and ischemia-reperfusion. The vascular tone regulation by endothelium also leads to systemic consequences. Essentially by decreasing cardiac, cerebral and renal blood flow it implies morphologic and functional modifications of these organs.
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PMID:[Vasoactive endothelial factors]. 833 93

Actin is a neuronal protein involved in axonal transport and nerve regeneration, both of which are known to be impaired in experimental diabetes. To determine if actin is subject to glycation, we rendered rats diabetic by injection of streptozotocin. Two or 6 weeks later brains were removed and a preparation of cytoskeletal proteins was analyzed by two-dimensional polyacrylamide gel electrophoresis. Brains from diabetic animals contained an extra polypeptide that migrated close to actin and reacted with monoclonal antibody C4 against actin. It was also found in a preparation of soluble synaptic proteins from diabetic rat brain, indicating that it was at least partly neuronal in origin. This polypeptide could be produced by incubation of cytoskeletal proteins from brains of nondiabetic rats with glucose-6-phosphate in vitro. The appearance of this glycated actin in diabetic animals was prevented by administration of insulin for a period of 6 weeks. We could not detect any effect of glycation in vitro on the ability of muscle G-actin to form F-actin filaments and its significance for the function of actin remains to be determined. The finding that glycation of platelet-derived actin from diabetic patients was significantly increased implies that the abnormality may also occur in clinical diabetes.
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PMID:Glycation of brain actin in experimental diabetes. 833 32


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