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

Sixty-two overweight gastric cancer patients were compared with 201 normal-weight patients to clarify the influences of excessive weight on the surgical treatment of gastric cancer. The frequencies of hypertension and diabetes mellitus were significantly higher in the overweight group (P < 0.01), but no pathologic differences in the resected tumor were found between the two groups. The operative times were longer (P < 0.01) and the number of lymph nodes extirpated and examined was smaller (P < 0.01) in the overweight group. The incidence of postoperative complications was not higher in the overweight group. The postoperative survival rate of patients with nodal metastasis was statistically lower in the overweight group (P < 0.05). Regarding the causes of death in patients with nodal metastasis, 61.1% of overweight patients and 43.8% of normal-weight patients died of recurrence of gastric cancer. In conclusion, surgical treatment of overweight patients with gastric cancer was found to be technically more difficult and the prognosis of such patients with nodal metastasis may thus be worse than that of their normal-weight counterparts.
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PMID:The influence of excess body weight on the surgical treatment of patients with gastric cancer. 864 17

Three men and one woman (mean age 52 years) were admitted to hospital for septicemia (2 cases), sudden partial loss of visual acuity (1 case) and suspected conjunctivitis (1 case). Three of the patients showed risk factors (diabetes, alcohol intoxication, immunosuppression). Panophthalmitis (affecting all tunics of the eye) was apparent from the initial examination in all 4 cases (2 bilateral and 2 unilateral). Ocular involvement was associated with endocarditis and meningitis (pneumococcus) in 1 case, with nocardiosis (pulmonary, cerebral and nodal) in 1 case, and with septicemia with bacterial arthritis (Escherichia coli, streptococcus A) in 2 cases. Hemocultures were positive in 3/4 cases. The micro-organism was also detected in the joint (n = 2), urine (n = 1) and cerebrospinal fluid (n = 1), during pulmonary transparietal puncture (n = 1) and in intraocular biopsy tissue (n = 1). All patients received appropriate antibiotic therapy intravenously and intraocularly. The infection was cured in all cases, but with severe functional sequelae: blindness in 2 cases, and unilateral enucleation in the other 2 cases.
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PMID:[Hematogenic bacterial endophthalmitis. A rare infection with very poor functional prognosis]. 879 96

Chronic nerve conduction showing in experimental diabetic neuropathy has been associated with decreased nodal Na+ permeability and an ultrastructurally identifiable loss of axo-glial junctions, which comprise the paranodal voltage channel barrier separating nodal Na+ channels from paranodal K+ channels. In human and experimental diabetic neuropathy these structural changes of the paranodal apparatus correlate closely with the nerve conduction defect. The present immunocytochemical study of the alpha-subunit of the Na+ channel examined whether the breach of the voltage channel barrier may account for a shift in the distribution of Na+ channels explaining decreased nodal Na+ permeability. Biobreeding Wistar (BB/W) rats diabetic for 4-8 months showed a progressive redistribution of nodal Na+ channels across the paranodal barrier into the paranodal and internodal domains which was associated with chronic nerve conduction slowing. The present data suggest that structural damage to the paranodal barrier system in diabetic nerve facilitates the lateral displacement of Na+ channels from the nodal axolemma thereby diminishing their nodal density and the nodal Na+ permeability associated with the chronic nerve conduction defect in experimental diabetes. These abnormalities were prevented by the treatment with an aldose reductase inhibitor, belonging to a class of drugs that, in neuropathic patients, improves nerve-conduction velocity and repairs axo-glial dysjunction of the paranodal apparatus.
J Diabetes Complications
PMID:Nodal Na(+)-channel displacement is associated with nerve-conduction slowing in the chronically diabetic BB/W rat: prevention by aldose reductase inhibition. 883 18

Nerve myo-inositol depletion, which has been implicated in the pathogenesis of acute experimental diabetic neuropathy, can be reproduced in normal rats by feeding diets enriched in L-fucose, a competitive inhibitor of sodium-dependent myo-inositol transport. Previously, we reported that L-fucose feeding for 6 weeks reproduces the effect of experimental diabetes on nerve Na+-K+-ATPase activity and conduction velocity, which can be prevented by simultaneous dietary myo-inositol supplementation. To further validate this model of myo-inositol depletion, we examined the effects of long-term (24-week) L-fucose feeding and dietary myo-inositol supplementation on nerve Na+-K+-ATPase, nerve conduction velocity, and myelinated nerve fiber pathology. After 24 weeks of L-fucose enriched (10 or 20%) diets, nerve myo-inositol levels and Na+-K+-ATPase activity decreased significantly (P < 0.05) and were associated with a 25-30% reduction in nerve conduction velocity, all of which were completely prevented by 1% dietary myo-inositol. Twenty percent L-fucose diet resulted in significant axonal atrophy, paranodal swelling (P < 0.001), and paranodal demyelination (P < 0.005), without increasing Wallerian degeneration or nerve fiber loss, a pattern qualitatively similar to that seen in early murine diabetic neuropathy. Dietary myo-inositol supplementation prevented these structural changes and increased nodal remyelination, supporting a role of myo-inositol depletion in the genesis of early diabetic neuropathy. The L-fucose model system may therefore serve as an experimental tool to elucidate the pathophysiological role of isolated myo-inositol depletion and its consequences in the multifactorial pathogenesis of diabetic neuropathy.
Diabetes 1997 Feb
PMID:Supplemental myo-inositol prevents L-fucose-induced diabetic neuropathy. 900 Jul 8

Although the detailed pathogenesis of diabetic polyneuropathy is not known, several mechanisms appear to be involved and may occur sequentially. Hence, the early and much researched activation of the polyol-pathway appears to secondarily affect nonenzymatic glycation, perturbation of vasoactive substances, the immune system and neurotrophism. These metabolic abnormalities may be differentially expressed in the neuropathy occurring in insulin dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM) diabetes. This notion is supported by differences in the structural abnormalities of the neuropathies in the two types of diabetes. Distinct and characteristic nodal changes occur in IDDM but not in NIDDM neuropathy, which also shows a milder axonal atrophy. On the other hand, nerve fiber loss which characterizes diabetic neuropathy tends to be focal in the older NIDDM patients, suggesting a more prominent vascular genesis. A further characteristic feature of diabetic neuropathy is blunted fiber regeneration, which probably is consequent to impairments of the necessary immune response and local synthesis of neurotrophic factors. Nerve biopsies from diabetic patients, although not necessary for diagnosis, provide valuable tissue for biochemical and molecular analysis of underlying mechanisms, the detailed elucidation of which will facilitate the design of targeted therapies.
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PMID:Neuropathology of diabetic neuropathy and its correlations with neurophysiology. 935 80

Aging and hypertension are associated with a progressive decline in renal blood flow and renal function. As a result, physicians planning therapeutic strategies to control blood pressure need to consider these changes and how they relate to potassium homeostasis, particularly in elderly patients. Commonly used antihypertensive drugs such as beta-blockers, angiotensin converting enzyme inhibitors and potassium-sparing diuretics need to be used with increasing caution in patients with declining renal function. This is especially important in patients with diabetes who may also have type IV renal tubular acidosis, and in patients given concomitant therapy with non-steroidal anti-inflammatory drugs. Other therapies such as calcium channel blockers, particularly those that gate atrioventricular nodal conduction, also need to be used with care in people with significant renal insufficiency and hyperkalemia, as this clinical scenario may result in a greater risk of complete heart block.
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PMID:Non-diuretic-based antihypertensive therapy and potassium homeostasis in elderly patients. 943 77

Breakdown of protective tissue barrier systems characterizes the chronic diabetic complications affecting the retina, and peripheral and central nerve tracts. The progressive damages to the blood-retina-, blood-nerve-, and paranodal ion channel barriers have pathophysiological consequences for the relentless progression of these complications. The continuing damage to the paranodal ion channel barrier in the spontaneously diabetic BB/W rat is associated with an increasingly irreversible nerve conduction defect, due to impaired nodal Na+ currents associated with displacement of nodal Na+ channels across the damaged paranodal barrier. The structural substrate for the mechanical barrier of the paranode is provided by electron-dense junctional complexes made up by a moiety of neural cell adhesive-(N-CAM), neural-glial adhesive (Ng-CAM), substrate adhesive molecules (SAMs) and polysialic acid (PSA). To further explore the mechanism underlying the protective barrier defect in diabetic neuropathy we examined the expression and immunolocalization of these molecules in peripheral nerve. In 6-month diabetic BB/W rats, direct and indirect ELISAs revealed significantly up-regulated N-CAM (P < 0.05), tenascin (Ng-CAM), (P < 0.001) and N-cadherin (A-CAM) (P < 0.03). On the other hand, SAMs showed little change, except for PSA which showed a significantly (P < 0.03) decreased concentration in the diabetic nerve. Immunocytochemical identification of these molecules revealed no visually detectable differences between diabetic and control rats. In conclusion, these data suggest that imbalances between highly interactive molecules responsible for the adhesiveness between terminal Schwann cell loops and the paranodal axolemma may underlie the critical paranodal barrier defect in diabetic neuropathy.
Diabetes Res Clin Pract 1998 Jun
PMID:Imbalances in N-CAM, SAM and polysialic acid may underlie the paranodal ion channel barrier defect in diabetic neuropathy. 971 18

We report on a 62 year old female patient treated with paroxetine, a selective serotonin reuptake inhibitor, because of an anxiety neurosis undergoing a vaginal hysterectomy in general anesthesia. Apart from a dietary treated diabetes mellitus there were no other diseases. There were no complications during the operation. At the end of the anesthesia an A-V nodal tachycardia appeared which spontaneously changed to a sinus rhythm ten hours after the end of the operation. No clinical or laboratory findings indicated a cardiac ischemia and an additional Holter ECG-Recording showed no further cardiac arrhythmias. No other complications occurred afterwards and the patient was discharged after two weeks. This case report demonstrates clearly that despite a reduced rate of cardiovascular complications compared to other types of antidepressants selective serotonin reuptake inhibitors can lead to perioperative cardiac arrhythmias.
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PMID:[A patient with nodal tachycardia after general anesthesia during medication with a selective serotonin reuptake inhibitor]. 1132 55

We examined the organization of the molecular components of the nodal region in spontaneously diabetic BB-Wistar rats. Frozen sections and teased fibers from the sciatic nerves were immunostained for nodal (voltage-gated Na(+) channels, ankyrin(G), and ezrin), paranodal (contactin, Caspr, and neurofascin 155 kDa), and juxtaparanodal (Caspr2, the Shaker-type K(+) channels Kv1.1 and Kv1.2, and their associated subunit Kvbeta2) proteins. All of these proteins were properly localized in myelinated fibers from rats that had been diabetic for 15-44 days, compared to age-matched, nondiabetic animals. These results demonstrate that the axonal membrane is not reorganized, so nodal reorganization is not likely to be the cause of nerve conduction slowing in this animal model of acute diabetes.
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PMID:Molecular organization of the nodal region is not altered in spontaneously diabetic BB-Wistar rats. 1174 56

Principal conclusions of the Second European Workshop in Aviation Cardiology are summarized. European standards for routine medical scrutiny of cardiovascular health are presented and the evolution of the standards is reviewed. Both single and multiple crew operations are considered. The papers summarized examine three major subject areas: prediction of vascular risk, coronary artery disease, arrhythmias and conduction disorders. The review of predicting vascular risk examines variation of cardiovascular risk with age, sex, and coronary risk factors; attributable and absolute risk, benefits of treatment and options for treatment of hypertension, the impact of intervention for lipid abnormalities, non-insulin-dependent diabetes mellitus and cardiovascular risk, and the aging pilot. The review of coronary artery disease includes coronary artery ectasia, abnormal exercise electrocardiographic responses in the presence of a normal coronary circulation, prognostic importance of patency of the infarct related artery, coronary artery angioplasty and stenting, acceptable revascularization of the myocardium, and myocardial perfusion imaging in certification. The review of arrhythmias and conduction disorders examines atrial fibrillation and flutter, atrioventricular nodal re-entry, sinoatrial disease, vasovagal syncope, risks and benefits of anticoagulation, cardiac rehabilitation, outcome of the impaired left ventricle, and mitral valve repair.
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PMID:Introduction and summary of principal conclusions of the Second European Workshop in Aviation Cardiology. 1154 88


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