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Biomedical subjects

J B Harris

Publications and source records attributed to J B Harris.

159 records · Page 9Linked to original sources
PubMed1969

Adenosine-3',5'-monophosphate: intracellular mediator for methyl xanthine stimulation of gastric secretion.

We postulated that methyl xanthines stimulate hydrochloric acid production in the isolated frog gastric mucosa by inhibiting the phosphodiesterase that destroys adenosine-3',5'-monophosphate (cyclic AMP). In support of this theory, several criteria were satisfied. Exogenously supplied cyclic AMP stimulated hydrogen and chloride transport in the spontaneously secreting mucosa and in the non-acid secreting mucosa in a similar fashion as did the methyl xanthines. Methyl xanthines increased the mucosal content of cyclic AMP, and the increase preceded the secretory response; thereafter, the magnitude of these two quantities paralleled each other. A correspondence was found between the concentration of methyl xanthines that affected acid secretion and the concentration of methyl xanthines that affected the tissue content of cyclic AMP. Theophylline was more effective than caffeine in increasing cyclic AMP content, which is in accord with the previously reported differences in their effect on acid secretion and phosphodiesterase activity.

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Morphology and physiology of skeletal muscle in aging rodents.

Aging in the rodent is accompanied by a progressive loss of skeletal muscle fibers. The muscle twitch also becomes slower, probably as a result of fiber-type conversion from "fast-twitch" to "slow-twitch." The loss of muscle fibers precedes signs of obvious weakness and appears to involve the loss of entire functioning motor units. In the mouse, this loss of motor units correlated with a loss of axons from the innervating nerve trunks.

Adenosine Triphosphatases↗
PubMedDate not supplied

Snake venoms in science and clinical medicine. 3. Neuropharmacological aspects of the activity of snake venoms.

Neuromuscular weakness is a common feature of snake bite. The toxins responsible for weakness either block neuromuscular transmission or they are myotoxic and damage skeletal muscle. In this article the major classes of toxins responsible for causing neuromuscular weakness are described. It is shown how a detailed knowledge of the biochemical and pharmacological properties of the toxins is essential if the clinical problems associated with bites by many species are to be properly understood. It is also shown that such an understanding allows apparent discrepancies between 'laboratory' and 'clinical' findings to be resolved.

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PubMedDate not supplied

A cerebellar abnormality in the mouse with motor end-plate disease.

The murine mutant with motor end-plate disease (med) exhibits a progressive weakness which is due to a functional denervation of skeletal muscle. It is inherited as an autosomal recessive trait and has two alleles. One of these is the jolting (medjo) mouse which also suffers from a disturbance of locomotion. Although the jolting animal was originally thought to suffer from a disorder of neuromuscular transmission, the organization of the peripheral nervous system is indistinguishable from normal and neuromuscular transmission is unimpaired. It is now clear that abnormalities in the cerebellum are responsible for the gait problems of the jolting mouse, and a preliminary morphological and neurophysiological examination of the mouse with motor end-plate disease has shown that it also has cerebellar abnormalities. Axonal spheroids may be seen on cerebellar Purkinje cell axons in the med mouse, and the character of extra-cellular recordings obtained from the Purkinje cells is abnormal.

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PubMedDate not supplied

Some biochemical responses of rat skeletal muscle to a single subcutaneous injection of a toxin (notexin) isolated from the venom of the Australian tiger snake Notechis scutatus scutatus.

1. Some biochemical responses of mammalian skeletal muscle to a single subcutaneous injection of a purified toxin from the venom of the Australian tiger snake, Notechis scutatus scutatus, have been investigated to determine the role of changes in peptide hydrolase enzymes in the muscle wasting caused by notexin administration. 2. Within 6 h of injection, serum creatine kinase activity was increased by five- to ten-fold, and remained elevated for at least 24 h. 3. There was an initial inflammatory response in the muscle adjacent to the site of injection; by 12 h after injection, muscle wet weight increased by 60%. 4. After the initial increase, wet weight fell to about 50% of normal at 7 days. Normal wet weight was achieved by 20 days after the injection. Over the period 1-20 days after the injection of the toxin, the changes in wet weight were mirrored by changes in non-collagen protein content. 5. The activities of cathepsin B and acid proteinase were increased following the injection of the toxin. By 2 days after injection, there was a ten-fold increase in the activity of cathepsin B, and a seven-fold increase in the activity of acid proteinase. The activity of both enzymes become normal by 20 days. 6. Experiments utilizing a variety of cytotoxic drugs suggested that the acid proteinase and cathespin B are primarily located within invading phagocytic cells. 7. The results are discussed with reference to the previously described pathology of toxin-damaged skeletal muscle.

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PubMedDate not supplied

Further observations on the pathological responses of rat skeletal muscle to toxins isolated from the venom of the Australian tiger snake, Notechis scutatus scutatus.

1. Some aspects of the response of mammalian skeletal muscle following the injection of purified toxins from the venom of the Australian tiger snake, Notechis scutatus scutatus, are described. 2. The toxins used were notexin, notechis II-5, notechis II-1 and a modified form of notexin (PBP-notexin). They were injected into the dorso-lateral aspect of one himd limb so that the soleus muscle would be exposed to the toxins. 3. Within 1 h after the injection of notexin, the soleus muscles were oedematous and by 3--6 h, polymorphonuclear leucocytes had entered the interstitial spaces. The invasion of necrotic muscle fibers was extensive by this time. Muscle spindles appeared relatively unaffected by the toxin. 4. The muscle regenerated via myoblasts at 2--3 days to myotubes at 3--5 days, immature muscle fibers at 7--14 days and fully differentiated muscle fibers by 21--28 days. Even after 6 months, however, the nuclei of many muscle fibres remained in a central position. 5. A second component of Australian tiger snake venom was also found to be myotoxic. It was slightly less potent than notexin, but caused qualitatively similar damage to that caused by notexin. It was identified as notechis II-5. A third fraction, notechis II-1, was found to be inactive. 6. Notexin could be neutralized by incubation with tiger snake antivenene; the simultaneous injection of antivenene with notexin did not afford complete protection against muscle damage.

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