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)

Statistically identified information on the relationships between the sites of lesions in intracerebral hemorrhage (ICH), risk factors such as a smoking or drinking habit, anamnesis, and biochemical data through blood tests will extend assistance to neuromedical clinicians on their daily clinical duties. It will provide them with a useful guide to determine the method of treatment. Also, it will be a basic research material for their clinical studies on diagnosis, progress, or prognosis in ICH. In order to obtain such statistics with the help of the computer, we need to have a computationally effective image database system. As is generally known, medical image data especially requires a great amount of storage; high-speed processing techniques are therefore also needed to deal with such data effectively. In addition, it is desired that we have outputs from the analysis edited with well-visualized effect, using 3D computer graphics, etc. These are why most existing image processing systems have been designed to work on comparatively large-scale computers. So far as we know, it is hard to find a practical and inexpensive personal computer-based application system for visualized statistical analysis of lesional images in ICH. We have developed a desk top computer-based program for statistical analysis of lesional image data of ICH. With this system, we can organize a medical image database that consists of the personal data of patients with ICH (sex, age, occupation, diagnosis, symptoms, part of physical disorder, etc.), risk factors, anamnesis (cerebral apoplexy, hypertension, hypotension, corpulence, diabetes, hyperlipidemia, atrial fibrillation, valvular endocarditis, etc.), biochemical data of blood, and lesional image data from CT or MRI. This system consists of the following components: 1) database management, 2) information retrieval (IR), 3) lesional image processing, 4) statistical analysis, and 5) prognostic prediction. The images are drawn manually on prescribed data sheets by tracing CT or MRI films and are read through the image scanner; then the compressed data of the digitized images is recorded in the database. Each recorded image data consists of the following two components: the frame image that corresponds to the contour of tissues of interest on the corresponding sliced section, and the actual image that corresponds to the lesion itself. In our system, these two images are separately stored and managed so that we can effectively perform subsequent image analysis. Other variables in the database (risk factors, anamnesis, etc.) are mainly used as search keys for making the aggregate of image data by the IR subsystem. In any aggregate, its elements, namely image data, have common medical background descriptions with the search keys. These aggregates can be used as input for the lesional image processing subsystem. With this subsystem, we can obtain the accumulated distribution of frequencies within a specified range of any sliced section, display planar color maps and profiles associated with the distribution, reconstruct it in 3D form, perform transformations of 3D images (zooming, enhancement, rotation, etc.), and test the significant difference of frequencies between any two different sites. We have been making practical use of this system to find the neurological relationship between the symptom (dysarthria, and paralysis of upper/lower limbs) and the site of lesion with cerebral infarction in pons. This study is quite important since the distributions of pyramidal tract related to the above symptom in pons are not well-known compared to those in cerebral cortex, internal capsule, or cerebral peduncle. With our system, we have obtained several findings expected to be helpful for this study. However, since this study is still in the initial phases, we will only present the outcome as a working example of our system. Our system was originally developed for analyzing lesional images with ICH. However, it could
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PMID:A desk top computer program for visualized statistical analysis of lesional images in intracerebral hemorrhage. 859 83

A 63-year-old woman with NIDDM poorly controlled by insulin therapy was admitted to our hospital because of fever and severe lumbago. Laboratory data revealed diabetic ketosis and a hypercoagulable state with infection. Bone and gallium scintigrams revealed an abnormal accumulation of the isotopes at L4-L5, where magnetic resonance imaging showed inflammatory changes. The patient was then diagnosed as having pyogenic vertebral osteomyelitis. Antibiotic chemotherapy and the administration of gebexate mesilate improved the inflammation and hypercoagulable state. When diabetic patients suffer from severe lumbago with sustained fever, and show segmental knock pain along the spine, pyogenic vertebral osteomyelitis should be considered. Bone and gallium scintigrams, and MRI are of clinical value for the early diagnosis of the disease.
Diabetes Res Clin Pract 1995 Sep
PMID:A case of non-insulin-dependent diabetes mellitus with vertebral osteomyelitits: usefulness of imaging diagnosis. 859 15

We investigated the relationship between asymptomatic multiple lacunae (ASML) and related risk factors by using brain MRI in 209 patients including 152 NIDDM patients. Patients with ASML (97 cases) were significantly older (68 +/- 9 vs. 63 +/- 10) and hypertension was more frequent (57/97 vs. 33/112) than in patients without ASML. In addition, by multivariate analysis, ASML showed significant association with aging and hypertension, but not with NIDDM. In the NIDDM patients, diabetics with ASML were significantly older, and showed a higher association with hypertension and triopathy than those without ASML, although the results were the same for the middle-aged (< 65 years old) diabetics. From multivariate analysis, the lesions in the penetrating branch area were highly associated with hypertension (F = 8.46) and nephropathy (F = 4.75), while those in the subcortex and white matter were associated with aging (F = 6.02) and retinopathy (F = 5.15). In the middle-aged diabetics, the former was associated with hypertension (F = 10.72) and retinopathy (F = 13.32), whereas the latter was associated with retinopathy (F = 20.76). In the elderly diabetics, no significant association was found in either lesions. These results suggest that control of hypertension and prevention of microangiopathy by keeping good control of blood glucose, is essential to prevent asymptomatic lacunae in NIDDM patients.
Diabetes Res Clin Pract 1996 Mar
PMID:Asymptomatic multiple lacunae in diabetics and non-diabetics detected by brain magnetic resonance imaging. 879 5

Clinical data, MR-scans, time-dose fractionation schemes and neuropathologic findings of two cases of delayed radiation myelopathy (DRM), are presented. Both patients, a 72-year-old diabetic woman with cervical lymphnode metastasis from a squamous cell carcinoma and a 46-year-old woman with tonsillar carcinoma, developed paraparesis followed by quadriplegia, at 7 and at 10 months following radiation. The spinal cord received 46 and 49 Gy. (Fraction dose 2.25 Gy and 2.0 Gy, 4 times/week). Serial MR-scans showed spinal cord enlargement and focally increased signal intensity (T1-gd). The second patient survived and stabilized following therapy with coumarins. The first patient died 13 months after radiotherapy. At autopsy necrosis, local calcium deposits, lipid macrophages and swollen astrocytes were observed in the white matter. There was slight hyalinosis of the intramedullary vessel walls. We conclude that serial MRI may be helpful to distinguish DRM from other causes of spinal cord injury. DRM may occur at a total dose less than 50 Gy. Additional risk factors (diabetes, hypertension), and fraction doses above 2 Gy contribute to the development of DRM.
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PMID:Delayed radiation myelopathy: serial MR-imaging and pathology. 883 1

The risk of hypoglycaemia and the resulting impairment in brain function are major factors preventing those with diabetes achieving normoglycaemia. The need to define these risks more precisely has prompted an increasing research effort to identify which aspects of cerebral function are particularly vulnerable and at which glucose level. Much of the evidence is inconsistent, reflecting not only the wide range of methods for measuring cognitive function and inducing hypoglycaemia, but also the inherent variability of the response. Nevertheless, the data suggest that those mental activities which are relatively undemanding are often unaffected at all levels of experimental hypoglycaemia while the performance of more complex tasks deteriorates at glucose concentrations of around 3 mmol l-1. The relative imprecision of cognitive testing is reflected in the debate which surrounds the pathogenesis of hypoglycaemia unawareness. There is some evidence that the glycaemic threshold for autonomic activation and symptoms can vary while the threshold for cognitive impairment is fixed. This has led to the hypothesis that hypoglycaemia unawareness arises when the autonomic response develops at a blood glucose below that for impaired cognition, thus preventing patients from recognizing or responding to their usual symptoms. However, contradictory data suggest that the threshold for cognitive impairment can alter in line with the autonomic response, a conclusion which falls to fit either the above hypothesis or the clinical description of hypoglycaemia unawareness. These differences may be methodological or relate to the relative imprecision of measurements of cognitive function. Resolution of these discrepancies may have to await the development of advanced technology such as high resolution MRI or PET scanning. In the meantime, progress could be made if all groups agreed on a limited range of cognitive function tests and used them in a standardized manner.
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PMID:The measurement of cognitive function during acute hypoglycaemia: experimental limitations and their effect on the study of hypoglycaemia unawareness. 884 93

Primary CNS malignancies are responsible for approximately 12,000 deaths annually in the United States. There has been little change in the outcome for adults with malignant brain tumors over the past few decades, despite improvements in surgical techniques and advances in radiation therapy. These tumors are uniformly fatal one to two years after diagnosis. The morbidity and mortality of this disease arise from the effects of a locally invasive, non-metastasizing lesion. The patients may suffer from seizures, paralysis, incoordination, aphasia, confusion, memory loss, sensory deficits or visual loss, depending on the regions of the brain affected. In addition, they usually require large doses of corticosteroids early and late in their illness, and may experience disabling side effects of this treatment, such as edema, proximal myopathy, diabetes, fungal infections or deep vein thrombosis. Few patients in the older age group are able to work after the diagnosis. Most of the patients are incapable of self-care for several months before death. The localized transfer of new genes into cancer cells potentially permits the expression of proteins with specific biologic functions that may provide a means to alter the biology of tumor growth through a variety of mechanisms including increasing tumor immunogenicity, inducing the local expression of toxic agents, and sensitization of tumors to chemotherapeutic agents. Gene therapy with the transfer of the drug susceptibility gene Herpes virus thymidine kinase (HSV-TK) has shown promise in a number of animal models, including CNS tumors. This study will evaluate the use of adenovirus-mediated transfer of the HSV-TK gene into primary human brain tumors followed by systemic treatment with ganciclovir. The goals of this phase I study are to evaluate the overall safety and efficacy of this treatment and to gain insight into the parameters that may limit the general applicability of this approach. In this phase I study, patients with recurrent gliomas will receive stereotactic-guided injections of the virus into the brain tumor, followed by intravenous ganciclovir for 14 days. Patients eligible to undergo a palliative debulking procedure will receive the same treatment followed by resection on day 7. At the time of resection a second dose of virus will be administered intra-operatively into the residual, unresectable portion of the tumor, and intravenous ganciclovir will be continued for additional 14 days. Tissue removed at the time of resection will be analyzed for evidence of adenovirus infection, thymidine kinase expression and signs of inflammation. The size and metabolic activity of all tumors will be followed by volumetric MRI scans and Position Emission Tomography Scans, respectively. Patients will be enrolled in groups of three, with each group receiving successively larger doses of adenovirus. This study will quantify the toxicity of this therapy, and provide evidence as to the duration of transgene expression and virus induced inflammation.
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PMID:Treatment of advanced CNS malignancies with the recombinant adenovirus H5.010RSVTK: a phase I trial. 884 6

To investigate the influence of diabetes mellitus on higher cognitive functions electrophysiologically, we studied auditory P300 event-related potentials (P300) in 40 NIDDM patients, taking into account wave I-V latencies (I-V) in auditory brainstem evoked potentials, clinical parameters and head MRI findings. Compared with 20 controls, diabetics had significantly longer P300 and I-V latencies. P300 latencies in diabetics correlated with neither I-V, HbA1, blood glucose levels, nor disease duration. Of the 13 diabetics investigated neuroradiologically, four had lacunar infarcts with prolonged electrophysiological values. The remaining nine had normal MRI scans, but their physiological parameters were still significantly longer than those of controls. These findings suggest that NIDDM can independently alter higher cognitive and the central auditory pathway functions. Our data also suggest that these alterations occur regardless of the recent metabolic derangement and disease duration. Cerebrovascular ischemia, if present, also appears to contribute in part to cognitive alterations.
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PMID:Changes in auditory P300 event-related potentials and brainstem evoked potentials in diabetes mellitus. 884 38

A case of acromegaly associated with variegated spinal disorders was reported. The spinal disorders were multiple cervical disc herniations, spinal epidural cavernous angioma, multiple ossification of the spinal ligament and lumbar canal stenosis. A 51-year-old woman with acromegaly, complaining of disturbances of delicate hand movement and gate, consulted our department. Her past history included diabetes mellitus, hypertension and progressing enlargement of her extremities. Serum growth hormone level was 65.7 ng/ml and somatomedin-c level was 746 ng/ml. Brain MRI showed a pituitary tumor extending to the right cavernous sinus. Cervical MRI revealed disc herniations at C5/6 and C6/7. Thoracic MRI revealed osteoporosis, ossification of the posterior longitudinal ligament and multiple ossification of yellow ligament. Lumbar MRI disclosed ossification of yellow ligament and canal stenosis. Anterior fusion of C5-C7 and an intracapsular removal of the pituitary tumor were performed. Its pathology was that of eosinophilic adenoma. After 3 months, she suffered from paraparesis. On repeating MRI examination with Gd-DTPA, a spinal epidural mass was found at T4. Under laminectomy of Th3-5 and Th8-11, the epidural mass and ossified yellow ligament were removed. The epidural mass was cavernous angioma. She was able to walk without any assistance. An association of spinal canal stenosis with acromegaly is well known. But the association of disc herniation and with the ossification of spinal ligaments is rather rare in the literature. Spinal epidural cavernous angioma is very rare. We discussed the etiological aspects and the management of spinal disorders with acromegaly.
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PMID:[A case of acromegaly associated with variegated spinal disorders]. 891 52

Abdominal obesity, particularly excess intraperitoneal fat, is considered to play a major role in causing insulin resistance and NIDDM. To determine if NIDDM patients accumulate excess intraperitoneal fat, and whether this contributes significantly to their insulin resistance, 31 men with mild NIDDM with a wide range of adiposity were compared with 39 nondiabetic, control subjects for insulin sensitivity (measured using euglycemic-hyperinsulinemic clamp technique with [3-3H]glucose turnover) and total and regional adiposity (assessed by hydrodensitometry and by measuring subcutaneous abdominal, intraperitoneal, and retroperitoneal fat masses using magnetic resonance imaging [MRI], and truncal and peripheral skinfold thicknesses using calipers). MRI analysis revealed that intraperitoneal fat was not increased in NIDDM patients compared with control subjects; in both groups it averaged 11% of total body fat. NIDDM patients, however, had increased truncal-to-peripheral skinfolds thickness ratios. In NIDDM patients, as in control subjects, amounts of truncal subcutaneous fat showed a stronger correlation with glucose disposal rate than intraperitoneal or retroperitoneal fat; however, NIDDM patients were more insulin resistant at every level of total or regional adiposity. Further, no particular influence of excess intraperitoneal fat on hepatic insulin sensitivity was noted. We conclude that NIDDM patients do not have excess intraperitoneal fat, but that their fat distribution favors more truncal and less peripheral subcutaneous fat. Moreover, for each level of total and regional adiposity, NIDDM patients have a heightened state of insulin resistance.
Diabetes 1996 Dec
PMID:Relationship of generalized and regional adiposity to insulin sensitivity in men with NIDDM. 892 52

Chlorpropamide (CPM) has been reported to produce impaired water excretion due to the enhancement of renal vasopressin (ADH) action and/or due to centrally enhanced ADH release, but it is still unknown whether CPM gives rise to ADH release with a subsequent hyponatremia in diabetes mellitus (DM), which, in turn, causes an impairment of the central nervous system. In 3 patients with DM, who developed hyponatremia during the treatment with CPM, an acute water load (WL) was carried out in the presence and absence of the drug, and plasma ADH was determined with plasma and urine osmolalities. Moreover, in 2 cases, MRI scans of the brain were taken. In all the patients, acute WL tests failed to suppress completely ADH release in response to changes in plasma osmolality in the presence of CPM, which, in turn, resulted in the impaired water excretion. In the absence of CPM, an acute WL normally suppressed plasma ADH leading to the diuresis. MRI scans illustrated the presence of central pontine myelinolysis. It is likely that CPM might stimulate ADH release in DM with a subsequent hyponatremia and brain damages.
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PMID:Chlorpropamide-induced ADH release, hyponatremia and central pontine myelinolysis in diabetes mellitus. 892 90


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