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

The effect of diabetic control upon EEG has seldom been studied. In the present investigation, a significant positive correlation between EEG abnormalities and degree of diabetic control was found, but no definite increase was noted in relation to the duration of diabetes. Eighty per cent of our patients having more than 5 severe hypoglycemic attacks showed evidence of abnormal EEG, suggesting that hypoglycemic coma or convulsions are closely related to EEG abnormalities (minor hypoglycemic episodes had no effect on the EEG). With the sensitive technique of fluorescein angiography, we demonstrated a clear correlation between incipient retinal angiopathy and EEG abnormalities. The factors that most positively relate to pathologic electrocerebral (EEG) activity in diabetic children are frequent and severe hypoglycemic attacks, comas and/or convulsions, and vascular changes in the retina.
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PMID:EEG abnormalities in diabetic children: influence of hypoglycemia and vascular complications. 50 56

Groups of C57 Bl/6j mice (alcohol preferring) and DBA/2j mice (alcohol avoiding) were fasted for 24 hours and administered glucose. At 30, 120 and 300 minutes after glucose, the C57 Bl/6j mice had significantly higher levels of plasma glucose than the DBA/2j strain. These differences were observed in comparable groups given either forced access or no access to alcohol. In ad lib fed animals never exposed to alcohol, C57 Bl/6j mice had higher levels of plasma insulin than DBA/2j mice. Plasma levels of glucose and corticosterone were not significantly different in ad lib or fasted animals. The injection of insulin zinc protamine to DBA/2j mice produced 100% convulsions within one hour, but produced to convulsions in C57 Bl/6j mice for as long as 4 hours after administration. These data demonstrate that an insulin resistancy exists in C57 Bl/6j mice which is not dependent upon any prior alcohol experience. Evidence supporting a functional relationship between this diabetogenic disturbance and alcohol preference was obtained in C57 Bl/6j mice which were allowed to choose between water or a 10% alcohol solution (v/v). Insulin zinc protamine produced a selective dose-dependent reduction in alcohol intake. Additional support is received from the discovery that Chinese hamsters, a species genetically predisposed to diabetes, display an impressive preference for 10% alcohol.
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PMID:Endocrine factors contributing to the ethanol preferences of rodents. 57 51

Diabetes mellitus occurs in many animals species. However, only a few have been utilized in systematic studies designed to answer unsolved problems associated with the disorder in man such as molecular basis, pathogenesis of the vascular and neural lesions, and the roles of diet, exercise and obesity. Among the animal models available, rodents have been studied most thoroughly for a number of reasons: a) short generation time (sexually mature at about 3 mo of age, gestation time 21 days) and life-span is approximately 3 yr; b) hyperglycemia and/or obesity is known to be inherited in several species; c) environmental factors can be controlled easily in the laboratory because of small size; and d) economic considerations. The better-known rodent diabetes/obesity syndromes may be categorized as follows: 1) hyperglycemic with ketoacidosis, nonobese (Chinese hamster, South African hamster); 2) hyperglycemic with insulin hypersecretion, moderate obesity and may develop ketoacidosis (diabetic mouse (db/db), spiny mouse, sand rat); and 3) less pronounced hyperglycemia with hyperinsulinemia, insulin "resistance" and marked obesity (obese (ob/ob), yellow (Ay) and New Zealand obese (NZO) mice, and the Zucker "fatty" rat). The PBB/Ld mouse, described here in detail for the first time, is a new strain of mouse that also fits into the latter category. Members of this strain following maturity develop an obesity that is characterized by increasing cellularity of adipose tissue, increased serum immunoreactive insulin, reduced glucose tolerance, fatty liver, and hyperlipidemia. Therefore, this strain of mouse represents another model for study of adult onset obesity.
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PMID:Animal models of diabetes and obesity, including the PBB/Ld mouse. 77 Jan 97

Since Pincus and White's claim in 1933 that diabetes mellitus is an inherited disease, the precise mode of inheritance remains a matter of dispute. The reason for the controversy is that the geneticist is confronted with a number of impediments to genetic analysis. As pointed by Neel, "diabetes mellitus is in many respects a geneticists nightmare". The obstacles are : 1) a precise definition of diabetes is difficult to establish, 2) the frequency of the disease which is sex and age dependent is not well known, 3) the probability of genetic heterogeneity is great but whether early onset and late onset diabetes are different genetic diseases or the same one remains controversial, 4) the basic defect (s) is unknown, 5) environmental factors (e.g. nutritional status) influence the frequency of the disease. Despite these problems many studies have been devoted to the mode of inheritance of diabetes mellitus. Many authors favour an autosomal recessive mechanism. However, low penetrance (25 %) is necessary to support this mode of inheritance. Simple autosomal dominant mode of inheritance has also been suggested, but this pattern fits only few families. The majority of geneticists think, at the present time, that diabetes has a multifactorial mode of inhritance. The heritability which express the extent to which the phenotypes exhibited by parents are transmitted to their offspring is in the neighbourhood of 50%. Many arguments favour this mode of inheritance: 1) low penetrance is necessary to aistinct genetic diseases, and especially in chronic glaucoma, which also have a multifactorial mode of inheritance; in particular, one must note the association between glucose intolerance and ocular hypertension induced by dexamethasone, 3) the association between diabetes and antigen A of the ABO system and antigens HL-A8 and W 15 of the HL-A system.
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PMID:[Genetics of diabetes mellitus (author's transl)]. 78 46

Hypoglycemia was diagnosed in 118 patients admitted to the University Children's Hospital Basel over 13 years, altogether 137 times. A definition of infantile and childhood hypoglycemia is discussed. Hypoglycemia was accepted as the correct diagnosis in 72 cases (group I), where 2 or more blood sugar values or at least one blood sugar value and one glucose value in the cerebrospinal fluid were below the limit for the age-group. In 46 cases only one abnormal blood sugar value vas documented (group II). In 19 cases no value was found to be definitely below the normal range. 58 patients were newborns up to 10 days of age. 34 patients (43 hospital admissions) were children in the agegroup after the newborn period. 65% of the newborns in group I and 58% of them in group II showed clinical symptoms concomitant with hypoglycemia. Convulsions (62%) were the most frequent feature. In more of the 76 patients was hypoglycemia documented as an isolated symptom. 75% of newborns were premature and/or of low birth weight. 50% had hypoglycemia and 20% verified central nervous system disease. 4 patients (5%) died in the hospital for reasons other than hypoglycemia. 15% (11 patients) had definite neurological symptoms when discharged from hospital. 30 of the 72 surviving neonates could be reexamined at a mean age of 26,5 months. 18% (13 patients) showed evidence of neurological disorders. 4 patients were readmitted with hypoglycemia at a later age, 3 were diagnosed as idiopathic and one as a ketotic hypoglycemia. One child developed diabetes mellitus at the age of 8 years.
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PMID:[On the syndrome of childhood-hypoglycemia. I. Definition of hypoglycemia in different age-groups and problems of neonatal hypoglycemia (author's transl)]. 89 34

Hypoglycemia (h.) in the postneonatal period was predominantly observed in male infants and children. The incidence was 0,51/1000 hospitalizations. The majority of cases was found in the agegroup around 2 years. Concomitant diseases (mostly infections of the upper respiratory tract or gastrointestinal tract) were found in 30 out of 43 hospitalizations. Convulsions and coma were the most frequent symptoms which were found in 43%. In 30% some degree of somnolence was obvious. Hypoglycemia was not considered in the differential diagnosis in any case by the physician treating first. Only 7 out of 34 cases a complicated biochemical work up resulted in an etiological diagnosis: one leucininduced h.; one ketotic h,; one h. in dystrophy and bronchopneumonia with septicemia; one h. in meningococcic septicemia; one h. in adrenal insufficiency; one h. in isolated ACTH-deficiency; one ethyl-induced h.; one h. in polynesy of pancreas; one h. in insulinoma; one h. in diabetes mellitus under insulintherapy.
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PMID:[On the syndrome of childhood-hypoglycemia. II. Hypoglycemia in the postneonatal period (author's transl)]. 89 35

Water intoxication occurred in a 53-year-old woman with chronic simple schizophrenia and poorly controlled diabetes. For several years she had had a compulsive habit of drinking excessive amounts of water. Coma, fever, convulsions and other neurologic signs appeared suddenly, and she had severe hyponatremia. Her condition improved rapidly when the electrolyte abnormality was corrected.
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PMID:Self-induced water intoxication in a schizophrenic patient. 94 25

Twenty-six patients under 20 years of age having cerebrovascular disease were studied from 1968 to 1972. Common risk factors such as hypertension, diabetes mellitus, hyperlipidemia and heart disease were not present. Angiographical study showed a variety of abnormalities. No consistent defect was present. There was a high incidence of pyrexia and convulsions in the early stages of stroke and it appears possible that some form of arteritis might have been important in the production of the cerebral infarction.
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PMID:Stoke in the young: a four-year study, 1968 to 1972. 115 68

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

In this paper we review methods of cluster analysis in the context of classifying patients on the basis of clinical and/or laboratory type observations. Both hierarchical and non-hierarchical methods of clustering are considered, although the emphasis is on the latter type, with particular attention devoted to the mixture likelihood-based approach. For the purposes of dividing a given data set into g clusters, this approach fits a mixture model of g components, using the method of maximum likelihood. It thus provides a sound statistical basis for clustering. The important but difficult question of how many clusters are there in the data can be addressed within the framework of standard statistical theory, although theoretical and computational difficulties still remain. Two case studies, involving the cluster analysis of some haemophilia and diabetes data respectively, are reported to demonstrate the mixture likelihood-based approach to clustering.
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PMID:Cluster analysis and related techniques in medical research. 134 50


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