Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of human diabetic neuropathy likely involves the interplay of hyperglycemia, ischemia, and oxidative stress. Mild-moderate ischemia-reperfusion to streptozotocin (STZ)-induced diabetes results in florid fiber degeneration in diabetic but not in normal nerves. Uncertainty exists as to the influence of duration of diabetes on this susceptibility. We therefore studied diabetic tibial and sciatic nerves using a rat ischemia-reperfusion (IR) model after 1 month and 4 months of diabetes utilizing electrophysiological, behavioral, and neuropathological methods. Electrophysiological abnormalities were present in 1-month diabetic rats (D) and persisted over 4 months. Behavioral scores were decreased markedly at 4 months (p<0.05). Endoneurial edema and ischemia fiber degeneration (IFD) were observed at both the 1-month (p<0.01 and p<0.001) and 4-month (p<0.001) durations in diabetic nerves, whereas only mild or no damage was observed in age-matched control nerves. These findings demonstrate that STZ-induced diabetes exacerbates the morphological and electrophysiological pathology in peripheral nerve to IR injury both in the early timepoint of 1 month and late timepoint of 4 months, although there was a gradation of injury, which is more severe at the later timepoint. Reperfusion exaggerated morphological pathology in 1-month STZ-induced diabetic peripheral nerve.
 ...
PMID:Ischemia-reperfusion injury of peripheral nerve in experimental diabetic neuropathy. 1554 99

The incidence of diabetes and its complication have rapidly increased. Decreased quality of life and increased mortality are the major problems of people with diabetes. These problems are mainly caused by chronic complications. The incidence of diabetic neuropathy, which is one of these chronic complications, approaches 50% in most diabetic patients. The intensive metabolic management alone cannot completely prevent the development and progression of diabetic complications. Therefore, blocking and management of pathogenic mechanism of complication are required. Pathogenesis of diabetic neuropathy has multifactorial causes. Diabetic neuropathy is thought to occur both from direct hyperglycemia-induced damage to the nerve parenchyma and from neuronal ischemia brought about indirectly by hyperglycemia-induced decreases in neurovascular flow. The effects of hyperglycemia get converted to neuronal dysfunction via at least three secondary biochemical pathways: the polyol pathway, non-enzymatic glycation of proteins, oxidative stress and protein kinase C, and the interactions between them. Because of these interactions, interference with one of these biochemical pathways could either worsen or attenuate the effects of the others. So, the use of therapeutic intervention of these pathways is inevitable and valid to prevent the progression of diabetic neuropathy. As yet, a satisfactory and fundamental, preventive, and therapeutic method is not available with us to prevent progression. So, we will introduce the earlier diagnostic methods of diabetic neuropathy and will discuss the advantages and limitations of each method.
 ...
PMID:Can diabetic neuropathy be prevented? 1556 81

Decreased blood flow is one of the earliest physiological changes observed after the onset of either clinical or experimental diabetes. The reduction in blood flow is believed to lead to nerve hypoxia, which in conjunction with other metabolic alterations and degenerative processes in different nerve compartments, results in the dysfunction known as diabetic neuropathy. The transcriptional regulator hypoxia-inducible factor-1 alpha (HIF-1alpha) accumulates rapidly under hypoxic conditions and modulates the expression of several target genes that protect tissues against ischemia and infarction. At present it is unclear whether diabetic nerve injury results from an abnormal response of HIF-1alpha and its protective target genes. In the present study we have analyzed the expression and activity of HIF-1alpha and its target genes in diabetic nerves as a first step to determine their possible contribution to the development or maintenance of diabetic neuropathy. We observed a transient increase in the expression of HIF-1alpha that peaked between 4 and 6 weeks and declined 8 weeks after induction of experimental diabetes in rats. The increase in HIF-1alpha in diabetic nerves coincided with a similarly transient increase in the expression of several HIF-1alpha target genes including vascular endothelial growth factor, lactate dehydrogenase and erythropoietin, which subsided 8-10 weeks after induction of diabetes. These results suggest that the transient activation of neurotrophic and angiogenic genes, as opposed to a more sustained effect in response to the chronic injury, may be responsible for the alterations in nerve function and regeneration that characterize the diabetic neuropathy.
 ...
PMID:Transient expression of hypoxia-inducible factor-1 alpha and target genes in peripheral nerves from diabetic rats. 1566 58

This article reviews theories linked to endogenous bioelectric currents and the role they may play in wound repair with further appraisal of in vitro and in vivo research related to the effects of clinically applicable electrical currents on protein synthesis, cell migration, and antibacterial outcomes. In addition, studies on the effects of electrical stimulation (ES) on skin grafts, donor sites, and musculocutaneous flaps in animals are evaluated, as well as assessments of numerous clinical reports that examined the effects of ES on angiogenesis, perfusion, PtcO2, and epithelialization. Finally, a plethora of clinical trials related to the responses of chronic lower extremity wounds to ES therapy are reviewed, with emphasis on wounds caused by venous insufficiency, diabetic neuropathy, and ischemia in patients with and without diabetes mellitus. A glossary that addresses ES terminology is also included.
 ...
PMID:Electrical stimulation for wound healing: a review of evidence from in vitro studies, animal experiments, and clinical trials. 1586 Apr 50

Toe amputations are becoming more prevalent in the diabetic population. To prevent toe amputations, those individuals with the highest risk must be identified prior to developing a precipitating event. There are obvious risk factors for toe amputations, such as digital deformity, diabetic neuropathy, and ischemia. Other, less obvious, systemic comorbidities may be linked to toe amputations. This study also shows that gender plays a significant role as a risk factor for toe amputation. A foot infection, foot abscess, osteomyelitis, diabetic retinopathy, and diabetic nephropathy were also significant risk factors for toe amputations. This suggests a significant relationship between these complications and comorbidities that put these individuals at a higher risk for toe amputations.
 ...
PMID:A case-control study of the risk factors for toe amputation in a diabetic population. 1586 23

Diabetic neuropathy is a debilitating disorder that occurs in nearly 50 percent of patients with diabetes. It is a late finding in type 1 diabetes but can be an early finding in type 2 diabetes. The primary types of diabetic neuropathy are sensorimotor and autonomic. Patients may present with only one type of diabetic neuropathy or may develop combinations of neuropathies (e.g., distal symmetric polyneuropathy and autonomic neuropathy). Distal symmetric polyneuropathy is the most common form of diabetic neuropathy. Diabetic neuropathy also can cause motor deficits, silent cardiac ischemia, orthostatic hypotension, vasomotor instability, hyperhidrosis, gastroparesis, bladder dysfunction, and sexual dysfunction. Strict glycemic control and good daily foot care are key to preventing complications of diabetic neuropathy.
 ...
PMID:Evaluation and prevention of diabetic neuropathy. 1595 41

Diabetic nerve exhibits morphological vulnerability to ischemia and reperfusion, in contrast to its physiological resistance to ischemic conduction failure (RICF). To examine the sequence of ischemic conduction failure after reperfusion in diabetic nerve, we measured sciatic-tibial nerve conduction before and during 30-180 min of ischemia and after reperfusion for up to 1 week in streptozocin (STZ)-induced diabetic rats. RICF in diabetic rats was confirmed during ischemia. After reperfusion, control nerves showed an immediate recovery in amplitude of compound muscle action potential (CMAP) following ischemia for 120 min or less, and delayed recovery after 150 min of ischemia. In contrast, recovery in diabetic nerves was delayed even after 1 h of ischemia. Ischemia for 75 min in diabetic nerve resulted in either delayed or no recovery of the CMAP upon reperfusion. Following ischemia for 90 or 120 min, axonal degeneration was observed in diabetic nerve. Thus, severe ischemia for 60 or 75 min causes prolonged ischemic conduction failure in diabetic nerve, compared with 150 min in control nerve. In conclusion, diabetic nerve shows delayed recovery of ischemic conduction failure after brief ischemia, compared to controls, suggesting that patients with diabetic neuropathy have a worse prognosis when faced with nerve ischemia.
 ...
PMID:Prolonged ischemic conduction failure after reperfusion in diabetic nerve. 1632 Mar 11

Mild ischemia-reperfusion (IR) injury to diabetic peripheral nerve is known to cause severe ischemic fiber degeneration. Little information is available on its effects on Schwann cell (SC). In this study, we evaluated oxidative stress and apoptosis of SC following mild IR, using immunohistochemistry in streptozotocin (STZ)- induced diabetic rats. Twenty-six rats were divided into four groups according to the duration of diabetes: 1- month STZ-induced diabetic group (n=7) and age-matched control group (n=7); 4-month STZ-induced diabetic group (n=6) and age-matched control group (n=6). Using our established IR model of 3 h of ischemia followed by 7 days of reperfusion, sciatic and tibial nerves were harvested and labeled with 8-hydroxydeoxyguanosine (8-OHdG; oxidative stress marker), caspase-3 (apoptotic executor), and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) activity (apoptotic indicator). Marked positive staining with 8-OHdG, caspase-3, and TUNEL were found in diabetic ischemic nerves (right side) following IR in both 1-month and 4-month groups. Only mild positive staining or no staining was seen in the nonischemic side (left side) of diabetic and age-matched control groups. Co-labeling with S-100 confirmed that the cells labeled with 8-OHdG, caspase3, and TUNEL were SC. SC was susceptible to oxidative injury and apoptosis in experimental diabetic neuropathy when subjected to mild IR injury.
 ...
PMID:Ischemia-reperfusion injury causes oxidative stress and apoptosis of Schwann cell in acute and chronic experimental diabetic neuropathy. 1635 15

Managing patients with peripheral arterial disease (PAD) requires an accurate assessment of the severity of the condition and the risk factors likely to predict disease progression. The spectrum of patient presentation ranges from asymptomatic to critical limb ischemia. Because about half of patients with PAD have coronary or cerebrovascular disease, the examination of presenting patients should be directed toward the entire cardiovascular system. The main diagnostic goal is to establish whether the symptoms are predominantly caused by PAD and to what degree the presenting problem is compounded by other comorbidities, such as diabetic neuropathy, arthritis, or venous disorders. The diagnostic process includes history taking, physical examination, noninvasive diagnostic testing, differential diagnosis, laboratory studies, and the use of the various imaging modalities, which in general are reserved for those PAD cases in which the clinician has already decided to intervene.
 ...
PMID:Diagnosis and risk assessment of lower extremity peripheral arterial disease. 1647 8

Foot problems are common in diabetic patients and are one of the most expensive chronic complications to treat. The authors sought to determine the prevalence and risk factors of the diabetic foot in a clinic population. In this cross-sectional study of 300 diabetic patients, the authors reviewed records, carried out an interview, and performed a meticulous foot examination with assessment of neuropathy (monofilaments and tuning fork) and ischemia (pulses). Foot lesions were classified according to Wagner grades. The prevalence of foot lesions was 13.0% (inpatients 25.6% and outpatients 11.1%). Diabetic neuropathy assessed using monofilaments was found in 81 patients (27.3%) (monofilaments). The prevalence of ischemia was 21.3% and deformity was 17.3%, whereas 37 patients (12.3%) had a previous history of foot lesions. Foot examination was done in 14.3% of patients, and 47% had a risky nail-trimming habit, whereas 22% wore ill-fitting shoes. The prevalence of diabetic foot lesions is high, and known risk factors are significantly present, especially poor foot care.
 ...
PMID:A study of the prevalence and risk factors of foot problems in a population of diabetic patients in cameroon. 1669 10


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>