Growth inhibition of two solid tumors in mice, caused by polyamine depletion, is not attended by alterations in cell-cycle phase distribution

We studied the effect of polyamine depletion on growth and cell cycle characteristics of subcutaneously grown Lewis lung carcinoma (LLC) and fibrosarcoma (FIO 26) in mice. Polyamine depletion was achieved by inhibition of ornithine decarboxylase using 2-(difluoromethyl)ornithine, limitation of exogenous polyamines by administration of a polyamine-poor diet and decontamination of the gastrointestinal tract, and inhibition of endogenous polyamine reutilization by N,N'-bis-(2,3-butadienyl)putrescine (MDL 72527). Determination of S-phase cells was performed in tumor-cell suspensions by flow cytometry and in tumor tissue sections by microscopy, following in vivo labelling with 5-bromo-2'-deoxyuridine (BUdR). DNA synthesis rate was estimated from the incorporation of in vivo-injected [3H]-thymidine (3H-TdR). Both solid tumors almost completely stopped growing after access to polyamines was blocked. Growth inhibition was, however, not attended by changes in cell-cycle-phase distribution. Paradoxically, we measured increased in vivo 3H-TdR incorporation rates and unaltered BUdR-linked staining intensity in treated tumors. Injection of putrescine into treated LLC-bearing mice resulted in an increase in intracellular putrescine and spermidine concentrations, a slight increase in the number of S-phase cells and a marked drop in DNA synthesis rate within the following 9 hr.     

Chest radiography in acute traumatic rupture of the thoracic aorta

Of 123 patients who had suffered blunt trauma to the chest traumatic aortic rupture was eventually confirmed in 61 and absent in 62 patients. The chest radiographs of these patients were examined for 15 signs reported in the literature as being associated with traumatic aortic rupture. Although many individual signs were significantly more frequent in the aortic rupture group they were not useful in differentiating between patients with and those without rupture of the aorta. By using discriminant analysis combining 2 or 3 signs, patients were classified as having aortic rupture or not. The best discrimination between the two groups was obtained using the combined signs of a widened paratracheal stripe, an opacified pulmonary window, a widened right paraspinal interface and a displaced nasogastric tube.     

Analysis of Fluid in Cysts Accompanying Various Primary and Metastatic Brain Tumours: Proteins, Lactate and pH

Summary There is a growing interest in cystic lesions of the brain. By examining the cyst content of brain tumours more insight into the pathogenesis of cyst formation has been found. In this study, 39 samples of cyst fluid of 34 patients with a cyst accompanying a brain tumour were collected and studied biochemically regarding their protein content, lactate and pH. In this study we investigated the relation between the grade of malignancy and the lactate-concentration and the discrepancy between the high levels of lactate in cysts and their alkaline environment. The results of the measurements of the concentrations of albumin, immunoglobulins (IgG, IgA, IgM) and α₂-macroglobulin in cysts compared to those in sera suggest that cyst formation associated with tumour is based upon a disruption of the blood-brain barrier with exudation of plasma proteins into the brain parenchyma resulting in accumulation of fluid (oedema) and eventually in formation of a cyst. There appears to be a positive relation between the grade of malignancy and the concentration of lactate in the cysts with a significant 2-fold increase in lactate concentration in malignant tumour cysts compared to the more benign tumour cysts (p<0.001) probably on account of aerobic glycolysis with production of lactate by the tumour. The measured pH values in the cysts were above normal, resulting in a discrepancy of the high levels of lactate in the cyst with the alkaline environment and this suggests efflux of H⁺-ions by a Na/H exchange mechanism to compensate for the change of pH.     

Deletion-type allele of the angiotensin-converting enzyme gene is associated with progressive ventricular dilation after anterior myocardial infarction

Objectives. This study sought to determine whether patients who are homozygous for the deletion (D)-type allele of the angiotensin-converting enzyme gene display augmented ventricular dilation after myocardial infarction.

Background. Recent evidence suggests that the deletion-type allele of the angiotensin-converting enzyme gene (DD genotype) is associated with an increased prevalence of myocardial infarction and myocardial hypertrophy. However, it is unknown whether the DD genotype is associated with adverse cardiac remodeling. To address this question we determined the genotype in patients enrolled in the Captopril and Thrombolysis Study (CATS), a prospective trial in which patients received either captopril or placebo during and after thrombolysis for a first anterior myocardial infarction.

Methods. Cardiac volume was determined by echocardiography immediately after thrombolysis and at 1-year follow-up. The genotype for the angiotensin-converting enzyme was determined in 96 patients. Norepinephrine levels were assessed during and immediately after thrombolysis.

Results. Immediately after thrombolysis, cardiac volume did not differ between genotype groups. However, at 1-year follow-up, both end-systolic and end-diastolic left ventricular volumes were significantly greater in the DD-genotype group. Norepinephrine increased to higher levels in the DD-genotype group that received placebo therapy. Captopril treatment effectively blunted both the norepinephrine increase and cardiac dilation in the DD-genotype group.

Conclusions. This exploratory study suggests that homozygosity for the angiotensin-converting enzyme deletion-type allele is associated with augmented neurohumoral activation as well as augmented cardiac dilation after an acute anterior myocardial infarction, an effect that may be susceptible to angiotensin-converting enzyme inhibition.     

Cerebrovascular Complications of L-Asparaginase Therapy in Children with Leukemia: Aphasia and Other Neuropsychological Deficits

Children with acute lymphoblastic leukemia (ALL), treated with L-asparaginase are at risk for cerebral thrombosis or hemorrhage because of coagulation protein deficiencies. The results and the importance of serial neuropsychological examinations after such complications in three children with ALL are presented. All patients showed marked aphasia and other cognitive deficits. Recovery was complete in two of three children.     

A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion.

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.     

Measurements on glassy-carbon electrodes in saline

Results of measurements on glassy carbon used as physiological measuring electrodes and as stimulating electrodes are presented. The frequency dependence of the electrode impedance is shown to be comparable with that of metallic electrodes. Because of its inertness to body tissue, the glassy carbon electrode appears to have favourable properties for long-term implantation. When used with short current pulses, the glassy-carbon stimulating electrode shows a dominant ohmic polarisation similar to that of a silver anode; this holds for both the glassy-carbon anode and the cathode.