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Biomedical subjects

A W Clark

Publications and source records attributed to A W Clark.

At least 91 records · Page 5Linked to original sources
PubMed1977

Suppression by elevated calcium of black widow spider venom activity at frog neuromuscular junctions.

Frog neuromuscular junctions were treated with both concentrated black widow spider venom (BWSV) and elevated extracellular calcium (5-50 mM). This procedure causes a dramatic increase in the frequency of spontaneous miniature endplate potentials (mepps) which persists for only a few minutes. In contrast, BWSV-induced mepp activity, the venom effect (VE), continues for 20 min-1 h at junctions in elevated calcium Ringer solutions treated with doses of dilute venom or at junctions in normal calcium (1.91 mM) Ringer solution treated with concentrated venom. Following the disappearance of the VE in elevated extracellular calcium, only a few normal amplitude mepps and a few giant amplitude mepps are observed. The disappearance of the VE in these preparations is irreversible and occurs whether exposure to elevated extracellular calcium precedes or follows exposure to BWSV. Electron microscopy indicates that the major structural alterations produced by exposure to concentrated BWSV and 20 mM calcium Ringer solution are the swelling of nerve terminal mitochondria and the clumping of synaptic vesicles, large numbers of which remain in the terminals. Exposure to 20 mM calcium Ringer solution alone produces no ultrastructural modifications in these preparations. These observations can best be explained if one of the effects of BWSV is to increase the permeability of the nerve terminal membrane to calcium. Only doses of concentrated venom can sufficiently elevate intracellular calcium to a concentration at which synaptic vesicles clump together, thus interruping the transmitter release process.

Action Potentials↗
PubMed1976

Regulation of purine metabolism. Adenylosuccinate synthetase from Novikoff ascites tumor cells.

Adenylosuccinate synthetase has been partially purified from Novikoff ascites tumor cells. The properties of the protein are quite different from the enzyme from rat liver in that the Km for asparate is higher and the K1 for the feedback inhibitor AMP is also higher. The antibiotic hadacidin has a preferential inhibitory effect on the tumor enzyme. These results suggest that the Novikoff ascites tumor enzyme is less sensitive to normal feedback controls but may be more sensitive to specific antitumor drugs.

Adenosine Monophosphate↗
PubMed1976

Changes in the structure of neuromuscular junctions caused by variations in osmotic pressure.

Neuromuscular junctions of the frog, Rana pipiens, were examined for structural modifications produced by exposure to increased and reduced osmotic pressure (pi). Preparations exposed to increased pi for varying lengths of time were fixed with either OSO4-Veronal with and without calcium, glutaraldehyde-phosphate, or glutaraldehyde-formaldehyde-phosphate as primary fixatives. The greatest difference between the fixatives was seen in preparations exposed to increased pi for 5 min, corresponding to the time when miniature endplate potential frequency is highest. The 5-min OSO4 calcium-free preparations appeared comparatively normal, while those fixed with OSO4 and 2 mM CaCl2 or aldehyde-phosphate had wide infoldings of the presynaptic membrane and a reduced number of synaptic vesicles. Aldehyde-phosphate had the same effect on mouse diaphragm. Another series of frog preparations were conditioned to elevated pi and then returned to normal Ringer's for varying times before fixation in OSO4-phosphate. Preparations fixed 2 min after their return to normal Ringer's showed marked disruption of the presynaptic membrane as well as apparently rupturing vesicles. If fixed after 10 min, terminals were depleted of vesicles although the presynaptic membrane had returned to its normal position and appearance.

Animals↗
PubMed1976

Possible active enhancement of a human cadaver renal allograft with antilymphocyte serum (ALS) and donor bone marrow: case report of an initial attempt.

Nonspecific immunosuppression of transplant patients frequently leads to complications which might be circumvented by inducing donor-specific immune unresponsiveness. Such specific immunosuppression has been produced experimentally, with use of donor antigen and antilymphocyte serum (ALS) for active enhancement. A case is presented in which the recipient of a cadaveric renal allograft (zero antigen match, cross-match negative) was given ALS (first 14 days after operation) and 11 X 10(9) donor bone marrow cells (twenty-fifth postoperative day) along with conventional doses of prednisone and Imuran in an attempt to produce donor-specific immune unresponsiveness. There were no rejection episodes, and serum creatinine remained less than 1.0 mg. per 100 ml. By the second month after transplantation there was no evidence for the persistence of donor erythrocytes or white cells. The conventional immunosuppressive agents were tapered and renal function was normal 8 months after transplantation, when the patient developed fatal peritonitis secondary to perforated sigmoid diverticulitis. At autopsy the renal allograft showed only minimal evidence of rejection. The present case illustrates an attempt to use ALS and donor bone marrow cells for active enhancement of a human cadaveric renal allograft. The infusion of stored donor marrow cells after transplantation is a particularly applicable technique for human cadaveric organ transplantation. The rejection-free course of this patient suggests that attempts to produce active enhancement clinically deserve further trial.

Adult↗
PubMed1972

"Ischaemic" colitis in young adults.

Four cases of transient haemorrhagic colitis seen in young adults resemble 10 others in the literature. The 14 cases are distinguished from the classical transient ischaemic colitis syndrome by their youth, the low incidence of stricture formation, and the prevalence of right-sided lesions.

Acute Disease↗
PubMed1972

Changes in the fine structure of the neuromuscular junction of the frog caused by black widow spider venom.

Application of black widow spider venom to the neuromuscular junction of the frog causes an increase in the frequency of miniature end-plate potentials (min.e.p.p.) and a reduction in the number of synaptic vesicles in the nerve terminal. Shortly after the increase in min.e.p.p. frequency, the presynaptic membrane of the nerve terminal has either infolded or "lifted." Examination of these infoldings or lifts reveals synaptic vesicles in various stages of fusion with the presynaptic membrane. After the supply of synaptic vesicles has been exhausted, the presynaptic membrane returns to its original position directly opposite the end-plate membrane. The terminal contains all of its usual components with the exception of the synaptic vesicles. The only other alteration of the structures making up the neuromuscular junction occurs in the axon leading to the terminal. Instead of completely filling out its Schwann sheath, the axon has pulled away and its axoplasm appears to be denser than the control. The relation of these events to the vesicle hypothesis is discussed.

Animals↗