Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In hypertensive disease and atherosclerosis without acute disorders of cerebral circulation it was established that in the cerebral vessel walls there was a high activity of alkaline phosphatase and adenosintriphosphtase. In the symmetrical areas of the subcortical nodes differences in the activity of these enzymes were insignificant and not valid. In vessel walls, located in the peripheral zone of the apoplectic hemorrhage and in the adjacent brain tissue the activity of alkaline phosphatase and adenosintriphosphatase drops. The existence of a high activity of enzymes in the vessel walls on the early stages of hemorrhages gives ground to the authors to claim that in the peripheral zone of an extensive hemorrhage a drop in the enzyme activity appears in the process of a development of a stroke.
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PMID:[Alkaline phosphatase and ATPase activity in the walls of the cerebral vessels in hypertension and arteriosclerosis with disorders of the cerebral circulation]. 14 93

A total of 35 cases of periarticular new bone formation (PNBF) was observed among 160 patients with coma following severe craniocerebral trauma. All cases were associated with blunt trauma and none with penetrating wounds. Only 6 of 500 cases of acute non-traumatic hemiplegia developed PNBR, and all 6 of them followed craniotomy, brain surgery and coma. New bone formation first appeared mainly between 50 and 120 days after craniocerebral injury with prolonged coma. Three-quarters of the patients with PNBF showed involvement of the shoulder joint, but this was not associated with previous subluxation. Metabolic studies were done in some patients; no disturbances were found in the metabolism of calcium, phosphorus or alkaline phosphatase. The pathologic process of PNBF seemed to stabilize some 6 to 8 months following trauma, and surgery after this period produced functional improvement in the 3 patients in whom it was tried. No satisfactory pathophysiological explanation has been found for the phenomenon of PNBR. Prolonged coma is common to all patients who suffered from PNBF and is probably an etiologic factor. The absence of PNBF in cases of cerebrovascular accident with subluxations of the gleno-humeral joint and intensive physiotherapy seems to contradict the suggestion of microtrauma as an etiological factor.
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PMID:Periarticular new bone formation in patients suffering from severe head injuries. 81 2

The present clinical aspects of Paget's osteodystrophy are reviewed. The nosological definition, localiztion, natural course and signs are described and the recent description of "rheumatoid manifestations" in Paget's disease by FRANCK et al. is mentioned. The same authors revealed a positive correlation between the grade of extenstion of Paget's disease in the whole skeleton and the concentration values for alkaline phosphatase and uric acid in the serum. Among the complications of Paget's disease the orthopedic, neurological, haemodynamic, oncologic, hematological and dermatological are reviewed X-ray of the involved skeleton, which in most cases is diagnostic, may be supported by isotope scanning with 18F or 87mSr and bone biopsy for establishment of diagnosis. Current drug therapy is confined to diphosphonate and calcitonin. The antibiotic mithramycin, which is cytotoxic, reduces bone turnover and may improve the course in Paget's disease. However, toxic side effects on kidney, liver and hemopoiesis do not allow its further therapeutic use in this disease. A case is described which demonstrates that a spontaneous or traumatic fracture in the area of osteodystrophy exhibits almost the same potential for conso lidation as normal bone tissue following both conservative and osteosynthetic treatment of the fracture. In a further instance corrective osteotomy with osteosynthesis (plate) because of serious varisation and antecurvature of the femur due to Paget's disease were performed sucessfully without assisting drug therapy. A third patient displayed extensive osteodystrophy of the whole pelvic skeleton, which was discovered by X-ray as rehabilitation following CVA failed to progress due to severe bilateral reduction of hip joint function. In view of the age and general status of the patient and the absence of pain, no medication or surgical therapy was performed in this case.
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PMID:[Paget's deforming osteodysttophy]. 115 90

Clinical and experimental heart irradiation can cause a variety of sequelae. A single dose of greater than or equal to 15 Gy leads to a reversible exudative pericarditis, occurring in dogs, rabbits or rats at around 100 days. Its time-course is very similar in all species investigated, but there are considerable species and strain differences in severity and incidence. After longer, dose-dependent latency times chronic congestive myocardial failure develops. At histological examination myocardial degeneration and necrosis is observed, which in some species is accompanied by a variable degree of interstitial fibrosis. In rabbits and rats, myocardial degeneration becomes apparent at around 70 days after 20 Gy and is preceded by a marked reduction in capillary density as well as ultrastructural endothelial cell degeneration. Simultaneously to structural capillary damage, a focal loss of the endothelial marker enzyme alkaline phosphatase was observed in rats in areas with subsequent myocardial degeneration. Cell kinetic studies in rabbits and rats revealed a radiation-induced wave of increased endothelial cell proliferation at 30-100 days postirradiation. In the rat it is exclusively seen in conjunction with alteration of endothelial cell marker enzymes. The temporal and spatial pattern of proliferative response exludes endothelial cell death in mitosis as the sole pathogenetic mechanism causing capillary loss and myocardial degeneration. Parallel to development of morphological damage, haemodynamic studies in various rats strains revealed a drop in cardiac output and left ventricular ejection fraction to about 64% of normal values after 20 Gy. In vivo, this slightly reduced cardiac function was then maintained in a steady state for many weeks, probably due to a compensatory up-regulation of cardiac beta-adrenergic receptors. In denervated working heart preparations in vitro, however, these compensatory mechanisms are not effective and stroke volume as well as cardiac contractility show a rapid and steady deterioration. In many respects radiation-induced heart disease conforms to radiobiological concepts of late-responding tissues, showing a chronic progressive time-course and a very pronounced fractionation effect. However, pathogenesis cannot be understood in terms of target cell depletion alone, and experimental evidence indicates the importance of alterations of regulatory mechanisms.
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PMID:Radiation-induced heart disease: review of experimental data on dose response and pathogenesis. 135 1

Twenty-six patients with various brain tumors or carcinomatous meningitis were examined for alkaline phosphatase (ALP) in the cerebrospinal fluid. ALP enzyme levels were compared with the respective levels in control groups of 75 patients with epilepsy, stroke, bacterial and viral meningitis and intervertebral disc prolapse. Extremely high ALP levels in CSF (9516 mu/l, 1425 mu/l, and 871 mu/l) were found in patients with pulmonary carcinomatous meningitis. Among all other patients with brain tumors, ALP levels in CSF were in the normal range. Examination of ALP in serum yielded normal results in all patients. In patients with pulmonary carcinomatous meningitis, the enzyme level in CSF was examined during various stages of radiotherapy and chemotherapy. Decreased ALP enzyme level was found during treatment followed by recurring rising levels a month after the treatment coinciding with clinical relapse. No correlation was found between the level of ALP enzyme and the biochemical and cellular content of the CSF during the various stages of treatment.
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PMID:Alkaline phosphatase level in CSF in various brain tumors and pulmonary carcinomatous meningitis. 221 14

A 6-year-old girl with cerebral palsy developed conscious disturbance and generalized convulsion after one-hour hot herb drug bath. Physical examination on admission revealed rectal temperature 41 degrees C, hot skin, respiration 46/min, regular heart beat 98/min, BP 130/60 mmHg, Glascow coma scale 4 (E2M1V1), soft and flat abdomen, no hepatosplenomegaly, no skin rash, no focal neurological sign, increased generalized muscle ton. Laboratory data showed CBC: WBC 20400 cumm (Neutrophils 31%, Lymphocytes 69%), Hb 11.6gm%, ESR 11 mm/hr, arterial blood gas: PH 7.077, PO2 43mmHg, PCO2 57.1mmHg, HCO3- 16 mEq/L, BE-11.5mEq/L, serum sodium 143 mEq./L, potassium 5.2 mEq/L, chloride 101 mEq/L, free calcium ion 3.8mg%, GOT 63IU/L, GPT 263 IU/L, amylase 193 IU/L, alkaline phosphatase 388 IU/L, LDH 1245 IU/L, CPK 677 IU/L, total bilirubin 0.8 mg/dl, direct type 0.1 mg/dl, BUN 18 mg/dl, Glucose 35 mg/dl. Urinalysis revealed proteinuria( ) trace hematuria and pyuria, but no cast. Lumbar puncture is within normal limits. Bacteriology including blood and CSF are normal. Multiple organ failure was noted at that time. Intensive cooling methods were performed including central and peripheral cooling. We used luminal and valium to control the seizure. Condition didn't improve. Afterwards cardiopulmonary arrest developed. Patient expired 8 hours after admission despite of resuscitation. Heat stroke in infancy and childhood is different from that in adulthood. The predisposing factors are high ambient temperature, dehydration, very young baby, sweat gland dysfunction, or ectodermal dysplasia. Definition of heat stroke includes 1) rectal temperature above 41 degrees C, 2) behavioral change, 3) warm skin, wet or dry.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Status epilepticus induced by prolonged immersion in hot herb bath: report of one case]. 263 19

Recent studies show that acute and chronic hyperglycemia cause a diffuse decrease in regional cerebral blood flow and that chronic hyperglycemia decreases the brain L-glucose space. Since these changes can be caused by a decreased density of perfused brain capillaries, we used 30 adult male Wistar rats to study the effect of acute and chronic hyperglycemia on 1) the brain intravascular space using radioiodinated albumin, 2) the anatomic density of brain capillaries using alkaline phosphatase histochemistry, and 3) the fraction of brain capillaries that are perfused using the fluorescein isothiocyanate-dextran method. Our results indicate that acute and chronic hyperglycemia do not affect the brain intravascular space nor the anatomic density of brain capillaries. Also, there were no differences in capillary recruitment among normoglycemic, acutely hyperglycemic, and chronically hyperglycemic rats. These results suggest that the shrinkage of the brain L-glucose space in chronic hyperglycemia is more likely due to changes in the blood-brain barrier permeability to L-glucose.
Stroke 1989 Aug
PMID:Brain perfusion in acute and chronic hyperglycemia in rats. 266 99

The Hypertension Detection and Follow-up Program was a randomised trial to compare all-cause mortality of patients receiving antihypertensive therapy in special clinics with those referred to the usual sources of care. All-cause mortality was significantly reduced overall, and in the mildest hypertensives, by stepped care. This specificity of the antihypertensive effect was shown by the proportionate lowering of stroke deaths, and the persistence of the mortality effect, when analysed by time-dependent co-variants, which took into account the amount of antihypertensive therapy the patients were receiving. Cardiovascular and coronary heart disease mortality were reduced in stepped care, as judged by death certificates. The benefits of stepped care were still present when analyses were confined to those with baseline ECG abnormalities. The 5-year incidence of angina pectoris and myocardial infarction, as judged by the Rose Questionnaire, was decreased in stepped care. Serum alkaline phosphatase fell in thiazide treated patients, suggesting a favourable influence on calcium balance. Eight-year analyses suggest that the favourable influence on mortality persisted after the end of the program for all except the eldest participants.
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PMID:Further analyses of the hypertension detection and follow-up program. 294 Dec 67

The effect of 6-month hypokinesia on the cardiac function and pathomorphological changes in 8 dogs was investigated. The heart size during systolic and diastolic contractions, stroke volume and contractile function were measured once a month, using an X-ray unit and a kymograph. After the hypokinetic exposure 6 dogs were sacrificed and their hearts were examined morphologically and histochemically. The recovery processes were investigated on 2 other dogs that were allowed to survive for 30 days after exposure. The 6-month hypokinesia led to a significant decrease in the heart size, stroke volume, cardiac index, and the contractile function. Post-mortem morphological examinations revealed atrophic changes in the myocardium. Electron-microscopy investigations demonstrated focal destructive changes in myofibers and in mitochondria: some of them were denser while others had a more transparent matrix and degraded crystae. Histochemical data (increased acid and alkaline phosphatase) also suggested atrophic and destructive changes in the myocardium. The above changes did not return to normal within 30 days of the recovery period.
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PMID:[Roentgenological and pathomorphological changes in the canine heart during 6-months hypokinesia]. 406 45

The metabolism of inositol phospholipids of the erythrocyte membrane was compared in normotensive Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone SHR (SHR-SP) rats. This was performed on isolated ghost membranes by measuring the incorporation of 32P from [ gamma-32P ] adenosine triphosphate (ATP) into the diphosphoinositides (DPI) and the triphosphoinositides (TPI) which were the only 32P-labeled phospholipids. 32P-labeling of TPI was altered in adult and 3-week-old SHR as well as in SHR-SP compared to WKY controls; the radioactivity associated with TPI in hypertensive rats was about 30% lower than that associated with TPI in age-matched normotensive controls. By contrast, the radioactivity associated with DPI was similar in both hypertensive and normotensive rats. Measurement of the phosphoinositide distribution in both SHR and WKY indicates that the change observed in 32P-TPI could not be accounted for by a reduced phosphatidylinositol content in SHR membrane. Measurement of the Mg2+-activated TPI-phosphomonoesterase and of the Ca2+-activated polyphosphoinositide phosphodiesterase activities did not show any significant difference between SHR and WKY. It thus appears that the altered phosphoinositide metabolism observed in hypertensive rats was a consequence of some alteration in the activity of kinases which are responsible for the conversion of phosphatidylinositol into DPI and TPI. These results also suggest that the defect in phosphoinositide metabolism observed in genetically hypertensive rats was not a consequence of the blood pressure elevation and could be related to the pathogenesis of hypertension.
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PMID:Altered turnover of polyphosphoinositides in the erythrocyte membrane of the spontaneously hypertensive rat. 630 31


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