Sensitivity of FL cells to polio- and adenoviruses

Summary Poliovirus plaque counts on the FL strain of human amnion cells were almost double the counts on rhesus monkey kidney for the same virus preparation, repeatedly assayed over more than six months. FL cells gave more consistent results in virus assay than monkey kidney cells. Plaque counts obtained with FL cells were 2 1/2 to 5 times higher than those obtained with HeLa, Chang's conjunctiva and Detroit-6 cells.Using the chick embryo-adapted MEF-1 strain of poliovirus, FL cells and primary human amnion cells reacted similarly in respect to plaque count and morphology, while no distinct plaques were seen on monkey kidney or HeLa monolayers under comparable conditions. For infectivity assays of adenovirus suspensions based on cytopathogenic effect, FL cells were found suitable, although no plaque formation was obtained.Aided by American Cancer Society Grant E-82 and a grant from the National Foundation.     

Platelets and anticoagulant capacity in patients with inflammatory bowel disease

Patients with inflammatory bowel disease (IBD) are susceptible to thromboembolic complications. Several mechanisms can be responsible, including abnormal regulation of coagulation activity, disturbances of fibrinolysis, inflammatory reactions and thrombocytosis. The aim of this study was to assess hemostatic alterations in these parameters during exacerbation of disease. We studied disease activity in 99 IBD patients receiving anti-inflammatory therapy, in relation to: procoagulant markers, i.e. prothrombin fragment F1 + 2 (F1 + 2), D-dimer and platelet count, anticoagulant markers, i.e. protein C, protein S and antithrombin, and a mediator of inflammation (IL-6). Coagulation activity and platelet count were increased during active disease in IBD patients compared with those in a state of remission. The IL-6 concentrations were positively correlated with disease activity and thrombocytosis in patients with ulcerative colitis, but no association with the anticoagulant capacity could be demonstrated except for a decrease in protein C during high disease activity.     

Evidence that peaks in EMG averages can sometimes be caused by inhibition of motoneurons

1. It has been reported that an excitatory response occurs before strong inhibition in masticatory muscles. We tested the hypothesis that this small monopolar wave in the EMG, called by us the early exteroceptive component (EEC), is in fact the first response to inhibition. 2. A mapping of the electrical activity of the masseter muscle was performed using a 3 x 4 matrix of surface electrodes with reference to the back of the neck. Subjects sat with the jaw closing muscles relaxed or contracting at approximately 75% of the maximum voluntary level. The chin was tapped to evoke a jaw jerk reflex and the EEC was elicited by electrical stimulation to the palate. 3. In addition, bipolar EMGs and jaw position were recorded at minimal bite forces and at contraction levels of 5, 10, 15, or 20 N. 4. Data were computer average, with and without rectification, for 32 stimuli. 5. The EEC [latency 12.1 +/- 1.0 (SD)ms] was found to have the same polarity, shape, and duration as the repolarizing wave of the stretch reflex. 6. After electrical stimulation, an increase of bite force was never observed during or immediately after the EEC. Instead, bite force began to decrease 5-7 ms after the onset of the EEC. 7. The amplitude of the EECs never exceeded the level of the peaks in the preceding background EMG, even when the left and right palatal electrodes were stimulated simultaneously at high intensity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolism of exercising skeletal muscle during beta 1-selective adrenoceptor blockade

Concentrations of glycogen, glucose, glucose-6-phosphate and lactate in the lateral vastus muscle were measured in seven subjects before and after dynamic muscle exercise at a work load of 75% of each subject's maximal working capacity, and with and without intravenous administration of the beta 1-selective beta-adrenoceptor blocking agent, atenolol. Pulmonary oxygen uptake was measured during exercise. Heart rate and arterial blood pressure were measured throughout the study. Arterial concentrations of glucose, lactate and free fatty acids were measured at rest and during exercise. The muscle concentration of glycogen and the extent of glycogen depletion with exercise were not influenced by the beta 1-adrenoceptor blocker. Similarly, there was no change in the muscle concentrations of glucose, glucose-6-phosphate and lactate. Heart rate decreased at rest and during exercise. Arterial blood pressure was not influenced by beta-blockade. Pulmonary oxygen uptake decreased by 6.5%. The exercise induced rise in arterial blood concentration of free fatty acids was abolished by beta 1-selective beta-blockade. It is concluded that the decrease in lactate release from exercising muscles during beta 1-adrenoceptor blockade seen in other studies cannot be explained by an impaired breakdown of muscle glycogen. It may be inferred, however, that a reduced availability of free fatty acids in the exercising muscles during beta 1-selective (and non-selective) beta-blockade may enhance the combustion of pyruvic acid and thereby decrease the production of lactate.     

A microiontophoretic study of the action of kainic acid and putative neurotransmitters in the rat mesencephalic trigeminal nucleus

The ‘excitotoxic’ hypothesis proposes that neurotoxic amino acids exert their effect through neuronal excitation (Olney, Ho &;Rhee, 1971).Colonnier, Steriade &;Landry (1979) have found that trigeminal mesencephalic neurons in the cat are resistant to the neurotoxic effect of kainic acid. In the present study it was found that the same neurons in the rat also resist the cytotoxic action of this amino acid. In addition, kainic acid, applied iontophoretically onto these neurons failed to alter their firing frequency. The resistance of these neurons to both neurotoxic and excitatory actions of kainic acid is consistent with the ‘excitotoxic’ hypothesis.Other putative neurotransmitters were applied by microiontophoresis on these neurons and none were found to alter their rate of discharge. Procaine however applied with relatively low ejecting currents consistently reduced their firing rates. The failure of the putative neurotransmitters tested to influence the rate of discharge of the trigeminal mesencephalic neurons suggests that the chemical synapses present on these neurons in the rat (Hinrichsen &;Larramendi, 1970) utilize another neurotransmitter from those tested. Alternatively the synapses might have a role other than the direct regulation of the firing frequency of these primary afferent neurons.     

Correlation of the chemical structure of 4-nitroquinolines inactivating human cytomegalovirus and established in vivo carcinogenicity tests

Inactivation of the infectivity of human cytomegalovirus (CMV) and herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) has been observed following exposure to 4-nitroquinoline 1-oxide (NQO) or its metabolite, 4-hydroxyaminoquinoline 1-oxide (HAQO). The present study of the specificity of the chemical structure of 4-nitroquinolines demonstrated that both the 4-nitro and 1-oxide groups were required for inactivation of virus infectivity. Reduction of the 4-nitro group to a 4-hydroxyamino group enhanced activity, while further reduction to an amino group resulted in loss of activity against virus infectivity. The capacity to inactivate virus was also lost by substitution of the pyridine ring for the quinoline nucleus of NQO. The relationship between the chemical structure and the ability to inactivate viruses studied here correlates well with earlier in vivo carcinogenicity studies of the same group of chemicals.