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)

We adapted the electrophoretic method of bone alkaline phosphatase (ALP) determination using neuraminidase from Vibrio cholerae to separate bone and liver ALP on cellulose acetate membrane. Treatment of separator plus serum (1:8, neuraminidase 111 U/l in final) for 10 min at room temperature (25 +/- 1 degree C) and subsequent electrophoresis made it possible to quantify bone ALP activity simply and rapidly. The precision of the data was at the level of CV of 1.6% (within-day) and 4.7% (day-to-day), with recovery rates of 97-103%. The normal range of bone ALP activity depended on age and sex. Seventy-eight diabetes mellitus (DM) patients, excluding those with renal failure, were divided into two groups of those with and without osteopenia with matching of age (+/- 3 years) and sex. Bone ALP (P < 0.001) and total ALP (P < 0.05) activities and urine calcium/creatinine ratio (P < 0.05) were significantly higher in DM with osteopenia than in DM without osteopenia. Therefore, bone formation and absorption may be accelerated in DM with osteopenia in comparison with DM without osteopenia.
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PMID:Cellulose acetate electrophoretic determination of bone alkaline phosphatase activity in healthy subjects and diabetic patients with and without osteopenia. 142 53

One to ten years after laser coagulation for diabetic retinopathy, 229 type I diabetics (mean age 44.3 years) and 157 type II diabetics (mean age 65 years) were re-studied for morbidity and mortality (progression of late damage, duration of survival, cause of death). The duration of diabetes at the first laser coagulation averaged 23.1 years for type I diabetics (15.9 years for type II). Average period from the first laser coagulation to the re-examination was 6.5 years for type I, 5.1 for type II diabetics. Of those patients still alive 6.7% had gone blind (type II: 7.3%). 2.1% and 4.6%, respectively, were receiving dialysis treatment, while renal transplantation had been performed in 3.1 and 1.8%, respectively. Stroke was the most frequent macrovascular complications (8.4 and 16.5%), followed by leg amputation (3.6 and 14.7%) and myocardial infarction (3.7 and 18.3%). 83 patients had died: 35 (15.3%) type I and 48 (30.6%) type II diabetics. Causes of death were septicaemia 14.3% (0%), uraemia 11.4% (8.3%), myocardial infarction 14.3% (33.3%), heart failure 8.6% (29.2%) and stroke 5.7% (6.3%). 10.7% (24.2%) had died within the first 5 years after laser coagulation. Despite a lower incidence of blindness in patients with diabetic retinopathy, the vascular disease progresses in other vascular regions so that a large proportion of diabetics will develop renal failure or die early from macrovascular complications.
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PMID:[Morbidity and mortality in type 1 and type 2 diabetes mellitus after the diagnosis of diabetic retinopathy]. 142 83

Four patients with postoperative mediastinitis who were treated by omentopexy at the Fukuoka University Hospital between 1989 and 1990. Three of the 4 patients healed successfully, another one died of multiple organ failure 83 days after surgery. All patients were received coronary artery bypass surgery harvesting a left internal thoracic artery for ischemic heart disease. Three patients had diabetes mellitus, one patient had renal failure preoperatively. Recognition of mediastinitis was made by sternal wound purulent discharge and sternal dehiscence. Culture of the discharge fluid yielded methicillin-resistant Staphylococcus aureus in three, and Enterococcus cloacae in one. Irrigation with popidone-iodine or blonopol were ineffective. Thus, the wound was treated with debridement and omentopexy with an omental pedicle flap, respectively. Postoperative course after omentopexy were excellent, had no complications. We conclude that the omentopexy is useful in the treatment of postoperative refractory anterior mediastinitis.
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PMID:[Treatment of postoperative mediastinitis using an omental pedicle flap]. 143 54

The hypothesis presented here is that cancer is not a phenomenon where the normal functions of the human body break down (like diabetes mellitus or renal failure) but rather a well planned and well coordinated physiological response (similar to the inflammatory response). 'Cancer initiating genes' are presumed neoplastic DNA sequences involved in sensing genome deterioration, consequently enhancing preservation. This genetic trait, different from the concept of oncogenes, actively triggers the neoplastic transformation once genome deterioration is sensed. This self destructive, altruistic phenomenon, obviously devastating to the organism, is nevertheless shown to be a possible mechanism of natural selection. The survival advantage of cancer initiation is discussed using both the concepts of group selection and gene selection. Natural selection, the driving force of evolution, is believed to operate solely on the basis of phenotype differences among individuals. In this paper cancer is hypothesized to be a mechanism that directly scrutinizes the gene contents of the individual, therefore representing natural selection based on genotype differences.
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PMID:Could cancer be a physiological phenomenon rather than a pathological misfortune? 766 35

A case of acute chylous diffuse peritonitis with recurrences was treated by peritoneal drainage. During the first hospital stay this drainage resulted in cure. After 17 months another recurrence treated in the same way led to death with increasing renal failure, diabetes, cardiorespiratory failure.
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PMID:[Recurrent acute chylous peritonitis]. 144 49

Up to now, little is known about the self-perpetuating mechanism leading to terminal renal failure in chronic renal disease. The common pathological feature of progressive renal insufficiency is focal and segmental glomerulosclerosis. The experimental counterpart of this process is represented for instance by the models of streptozotocin diabetes, Adriamycin nephropathy and Goldblatt hypertension. In fact, the main initiating hallmark of glomerulosclerosis is an accumulation of glomerular proteins, whose balance is apparently influenced by the activity of glomerular proteinases. In isolated glomeruli of kidneys from the experimental animals, the total proteinase activity was assayed with the unspecific but sensitive azocasein assay. In fact, the activity was significantly reduced in all experimental models at acid and neutral pH when relating enzyme activity to the glomerular protein and DNA content. We believe, that our data of reduced glomerular proteinase activity in the animal models of glomerulosclerosis represent perhaps a new additional common pathogenetic mechanism. The glomerular protein accumulation could be a result of a synergistical interaction between hemodynamic factors and biochemical ones; the latter, we suggest to be a decrease of glomerular proteinase activity.
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PMID:Effect of disease on glomerular proteinases. 145 96

Artificial cells contain biologically active materials. Artificial cells containing adsorbents have been a routine form of treatment in hemoperfusion for patients. This includes acute poisoning, high blood aluminum and iron, and supplement to dialysis in kidney failure. Artificial cells are being tested for use as red blood cell substitutes. Artificial cells encapsulated cell culture are being tested in animals for the treatment of diabetes and liver failure. A novel 2 step method has prevented xenograft rejection. Artificial cells containing enzymes are being studied for treatment in hereditary enzyme deficiency diseases and other diseases. Recent demonstration of extensive enterorecirculation of amino acids in the intestine has allowed its oral administration to deplete specific amino acids. Artificial cells containing complex enzyme system convert wastes like urea and ammonia into essential amino acids. Artificial cell is being used for the production of monoclonal antibodies, interferons and other biotechnological products. It is also being investigated for drug delivery, and for use in other applications in biotechnology, chemical engineering and medicine.
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PMID:Artificial cells in immobilization biotechnology. 145 87

The goal of this review was to assess the magnitude of coronary artery disease (CAD) mortality and its determinants in insulin-dependent diabetes mellitus (IDDM) patients with persistent proteinuria. By reanalyzing data from two previously published studies of patients with nephropathy, it was found that these patients had extremely high CAD mortality rates in comparison with IDDM patients without proteinuria, but only after the age of 35 yr. In addition, the risk of CAD death was associated with high serum cholesterol levels but was unrelated to systemic blood pressure, smoking habits, and obesity. Further studies of the determinants of CAD in patients with IDDM and proteinuria are urgently needed. Except for efforts to lower serum cholesterol, it is not known whether any other measure can be undertaken to reduce the extremely high mortality due to CAD that afflicts IDDM patients with persistent proteinuria, in particular those patients whose renal failure might have been "successfully" postponed by antihypertensive therapy.
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PMID:Coronary artery disease is the major determinant of excess mortality in patients with insulin-dependent diabetes mellitus and persistent proteinuria. 145 52

A cohort retrospective study was used to analyze the effect of comorbidity on survival of end-stage renal disease (ESRD) patients undergoing dialysis. The authors analyzed the survival of 255 patients (144 men, 111 women; median age 54 years; range 8-81 years) followed at the District Hemodialysis Unit in Foggia, Italy, over a 15 year period (median follow-up 30 months; range 1-190 months). Two subscales assessing the overall severity of the identified coexistent diseases and overall physical impairment, and a composite four level index of coexistent diseases (ICED) were assembled using information recorded at the time of admission. The Cox proportional hazard model was applied to evaluate the association of various patient characteristics with the probability of death. Mortality risk was associated with patient age (RR = 3.4 for patients aged 42-61; RR = 4.8 for patients older than age 61 compared with patients younger than age 42), initial condition leading to renal failure (RR = 3.1 for diabetes compared with primary renal disease) and ICED (RR = 3.0 for patients with uncontrolled coexistent disease or severe impairment compared with patients with no coexistent disease and no or mild impairment). Gender and type of dialysis were not associated with mortality risk. It was concluded that, as is the case with other chronic conditions, co-morbidity is a powerful independent prognostic factor in determining the mortality of ESRD patients.
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PMID:Effect of coexistent diseases on survival of patients undergoing dialysis. 145 68

Until now, little is known about the self-perpetuating mechanism leading to terminal renal failure in chronic renal disease. The common pathological feature of progressive renal insufficiency is focal and segmental glomerulosclerosis. The experimental counterpart of this process is represented by models of streptozotocin diabetes, Adriamycin nephropathy and Goldblatt hypertension. The main initiating hallmark of glomerulosclerosis is an accumulation of glomerular proteins, whose balance is apparently influenced by the activity of glomerular proteinases. In isolated glomeruli of kidneys from experimental animals, total proteinase activity was assayed with an unspecific but sensitive azocasein assay. The activity was significantly reduced in all experimental models at acid and neutral pH when relating enzyme activity to the glomerular protein and DNA content. The demonstration of reduced glomerular proteinase activity in the animal models of glomerulosclerosis could represent a new additional common pathogenetic mechanism. Glomerular protein accumulation could be a result of a synergistic interaction between hemodynamic and biochemical factors; we suggest the latter to be a decrease in glomerular proteinase activity.
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PMID:Effect of renal disease on glomerular proteinases. 146 87


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