Changes in fatty acid composition in wheat cultivars of contrasting hardiness.
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Biomedical subjects
Publications and source records attributed to C J Andrews.
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The effect of temperature on respiration of mitochondria and tissue segments from three wheat (Triticum aestivum L.) and one rye (Secale cereale L.) cultivar grown at 2 and 24 C has been examined. Discontinuities in Arrhenius plots of respiratory activity against temperature were observed for mitochondria and tissue segments from seedlings grown at both temperatures. The rates of respiration decreased abruptly below the transition temperatures, resulting in increased energy of activation values for respiration. Transition temperatures were observed from 6 to 10 C during tissue segment respiration, and from 10 to 14 C during respiration by isolated mitochondria. Respiratory control and efficiency of phosphorylation were not affected markedly by either reaction temperature or growth temperature of the seedlings. No correlation was observed between the cold hardiness of the cultivars and the temperature at which structural transitions occurred in the mitochondria. Dry matter content of the seedlings increased markedly during growth at 2 C, but no appreciable changes in the levels of mitochondrial protein were observed. The results support the view that changes other than fatty acid unsaturation are involved in the abrupt change in mitochondrial membrane properties at low temperature.
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Evaluation of various solvent systems for lipid extraction of wheat Triticum aestivum L. cv. Rideau seeds showed that boiling 2-propanol followed by the Bligh-Dyer procedure was the most efficient method, with respect to lipid yield and ability to inactivate lipolytic enzymes. Ten phospholipids were identified in dry seeds; the major components being phosphatidylcholine, lysophosphatidylcholine, N-acyl lysophosphatidyl-ethanolamine, N-acylphosphatidylethanolamine, and phosphatidylethanolamine. After growth for 1 week (2 C) or 31 hours (24 C), the proportions of phosphatidylethanolamine + lysophosphatidic acid and phosphatidic acid increased, lysophosphatidylcholine decreased, and the remaining phospholipids showed little change. At 5 weeks (2 C) or 72 hours (24 C), the seedlings showed 5-fold increases in the proportion of phosphatidic acid largely at the expense of phosphatidylcholine, small decreases in N-acyl lysophosphatidylethanolamine and N-acylphosphatidylethanolamine, and significant increases in lysophosphatidylcholine. The changes in phosphatidic acid and phosphatidylcholine are interpreted as being partially due to increasing phospholipase D activity during germination. In general, the phospholipid composition was similar in morphologically equivalent seedlings grown at 2 C or 24 C. The increased membrane content in seedlings grown at 2 C does not reflect any preferential synthesis of individual phospholipids.
The static and dynamic components of the tonic stretch reflex and shortening reactions have been studied in 10 patients with athetosis. EMG activity could be recorded only from the biceps muscle when the patient was at rest. The dynamic stretch reflex increased with the velocity of stretching in all muscles examined except the biceps. The biceps stretch reflex was found to be inhibited by increasing muscle length, whereas the stretch reflexes of triceps, hamstrings, and quadriceps muscles were facilitated by increasing muscle length. Reinforcement increased resting activity in the biceps and the dynamic shortening reaction of the triceps muscle. Both these effects were suppressed by the action of phenoxybenzamine. Although phenoxybenzamine was shown to reduce muscle tone in a double-blind controlled trial, no corresponding improvement was detected in involuntary movements or the patients' performance in a tracking test. The differences between the pattern of hypertonus in athetosis, Parkinson's disease, spasticity, and activated normal subjects are presented in discussion.
The static and dynamic components of the tonic stretch reflex and shortening reactions have been studied in biceps brachii, triceps, hamstrings, and quadriceps muscles of 19 patients with Parkinson's disease before and during L-dopa therapy. Clinical improvement during L-dopa administration correlated with a reduction in the dynamic component of the tonic stretch reflex in biceps, triceps, and quadriceps but not the hamstrings muscle, and with the static component of the tonic stretch reflex in biceps and triceps but not quadriceps and hamstrings muscles. The only shortening reaction consistently reduced during the L-dopa treatment period was the dynamic shortening reaction of the triceps muscle. The responses of the stretch reflexes to changes in muscle length were not altered by L-dopa therapy. In severely disabled patients the hamstrings and quadriceps stretch reflexes were maximal in a position of partial flexion of the knee joint and this response to muscle length was not altered in these patients despite a dramatic lessening of rigidity in some patients. Shortening reactions commonly remained in some patients after the stretch reflex of the antagonistic muscle was abolished by L-dopa therapy. The administration of phenoxybenzamine to patients being treated with L-dopa reduced the different components of rigidity more than L-dopa alone, and the responses were consistent with phenoxybenzamine suppressing predominantly the descending noradrenergic pathway.
The stretch reflexes and shortening reactions evoked in six normal subjects during reinforcement were compared with those recorded from patients with Parkinson's disease. Although the responses to stretch and shortening of triceps were similar in both groups, they differed in the biceps muscle. In Parkinson's disease increasing muscle stretch of biceps was associated with increasing reflex activity, whereas the reverse relationship occurred in the activated normal subjects. The biceps EMG during sinusoidal stretching comprised two peaks in the activated normal group, a phenomenon not seen in Parkinson's disease. It is postulated that this response in the activated normal group is due to activation or reinforcement engaging long-loop reflexes. It is concluded that the rigidity of Parkinson's disease is not simply an exaggeration of the stretch reflexes found in normal man but differs in that the effects of flexor reflex afferent nerve fibres are submerged by group Ia afferent activity, and that some long-loop reflex pathways are no longer operative in Parkinson's disease.
An electromyographic technique was used to record the tonic stretch reflex (TSR) responses to passive sinusoidal stretching of biceps brachii muscle in athetotic patients. The TSR transmission characteristics measured while the patient was in a relaxed state were compared with those measured while the patient was voluntarily active. The resting TSR and action TSR were found to differ markedly. Sensitivity, pattern, duration, and timing of the TSR responses were all changed during voluntary activity. The results suggest that the TSR in athetosis is functionally reorganized by supraspinal influences during voluntary activity. It is proposed that athetoid movements and action tremor may be a manifestation of abnormal action TSR caused by faulty supra-spinal control during activity.
The gait of normal subjects was examined electromyographically and the pattern was altered during preferential blockade of large nerve fibres to alternating activity in flexor and extensor muscles.The EMG activity was disrupted more in flexor than extensor muscles by preferential ischaemic blockade. Normal gait was associated with flexor contraction only when the foot was lifted and placed on the ground, whereas during ischaemic blockade flexor contraction continued during the interval between foot lifting and foot placement.The `freezing' or `blocking' gait in Parkinson's disease was found to be associated with coactivation of flexor and extensor muscles and this phenomenon occurred only in patients with features of flexion dystonia in the electromyographic recordings of their tonic stretch reflexes. Eight of nine patients with evidence of flexion dystonia showed a deterioration in their response to l-dopa therapy over a two year period, whereas four patients without flexion dystonia maintained their clinical improvement.
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1. The proximal ends of the distal portions of severed nerves coming from the small intestine were monitored for nerve impulses. When the mesenteric venous pressure was increased by mechanical obstruction of the portal vein there was a proportional increase in the frequency of afferent action potentials, the frequency falling immediately the venous pressure was reduced. The stimulus for the increased rate of nerve discharge appeared to be pressure within the mesenteric venous bed and not anoxia, for obstruction of the arterial supply to the gastrointestinal tract did not activate the same fibres.2. Obstruction of the portal vein led to an increased efferent nervous discharge to the intestines. The reflex increase persisted after bilateral vagotomy, after transection of the spinal cord at the level of C7 and after section of the hepatic nerves, but was abolished by section of the intestinal nerves.3. It is suggested that the spinal reflex is concerned with local distribution of blood and that the mesenteric venous ;volume' or ;stretch' receptors which initiate the reflex are similar to those described elsewhere in the body.
The tonic vibration reflex (TVR) has been studied in the quadriceps and triceps surae muscles of 34 spastic, 15 Parkinsonism, and 10 normal subjects. The TVR of spasticity develops rapidly, reaching a plateau level within 2-4 sec of the onset of vibration. The tonic contraction was often preceded by a phasic spike which appeared to be a vibration-induced equivalent of the tendon jerk. The initial phasic spike was usually followed by a silent period, and induced clonus in some patients. No correlation was found between the shape of the TVR and the site of the lesion in the central nervous system. The TVR of normal subjects and patients with Parkinsonism developed slowly, starting some seconds after the onset of vibration, and reaching a plateau level in 20-60 sec. A phasic spike was recorded occasionally in these subjects, but the subsequent tonic contraction followed the usual time course. Muscle stretch increased the quadriceps TVR of all subjects, including those with spasticity in whom the quadriceps stretch reflex decreased with increasing stretch. It is suggested that this difference between the tonic vibration reflex and the tonic stretch reflex arises from the selective activation of spindle primary endings by vibration, while both the primary and the secondary endings are responsive to muscle stretch. The TVR could be potentiated by reinforcement in some subjects. Potentiation outlasted the reinforcing manoeuvre, and was most apparent at short muscle lengths. As muscle stretch increased, thus producing a larger TVR, the degree of potentiation decreased. It is therefore suggested that the effects of reinforcement result at least partially from the activation of the fusimotor system. Since reinforcement potentiated the TVR of patients with spinal spasticity in whom a prominent clasp-knife phenomenon could be demonstrated, it is suggested that the effects of reinforcement are mediated by a descending pathway that traverses the anterior quadrant of the spinal cord.