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Biomedical subjects

C Edwards

Publications and source records attributed to C Edwards.

At least 217 records · Page 12Linked to original sources
PubMed1988

A possible role for the acetylcholine transport system in non-quantal release of acetylcholine at the rodent myoneural junction.

The effects on the spontaneous, non-quantal release of acetylcholine (ACh) from motor nerve terminals of substances known to inhibit the ACh transport system present in cholinergic synaptic vesicles have been investigated. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine (dTC) in muscle endplates that had been treated by an anticholinesterase was partly or completely abolished by 2-(4-phenylpiperidino) cyclohexanol (AH5183, 10(-7)-10(-6)M), quinacrine (10(-7)M) and tetraphenylborate (10(-6) M). Since the sensitivity of the endplate to ACh was not changed, the block of the dTC induced hyperpolarization indicated an inhibition of the spontaneous, non-quantal release of ACh. This was confirmed by direct measurement of the ACh released by rat diaphragm. The release of ACh from the innervated diaphragm was decreased by about 50% by AH5183 (10(-8)-10(-6) M) and by 42% by quinacrine (10(-7)-10(-6) M). The ACh released was presumably neural, since the release of ACh from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The results indicate that the spontaneous release of ACh from the motor nerve terminals is probably mediated by a carrier which may be the vesicular transport system responsible for moving ACh into the vesicle. The transport system is likely incorporated into the membrane of the nerve terminal during exocytosis.

Acetylcholine↗
PubMed1987

Mechanically induced electrical responses in murine mammary epithelial cells in primary culture.

In mouse mammary epithelial cells in primary culture, mechanical stimulation of a cell induced in other cells within the same colony a short depolarization of less than 15 mV with a duration of 1-8 s and a subsequent, prominent hyperpolarization of 6 mV lasting 10-40 s. Epidermal growth factor induces a spontaneous hyperpolarizing response in cultured mammary cells, and in cells treated with EGF mechanical stimulation produced a greater hyperpolarization, while the amplitude of the depolarizing response was not affected. The amplitude of the mechanically induced hyperpolarization was markedly reduced by quinine and tetraethylammonium, blockers of the Ca2+ -dependent K+ channel. The results suggest that the Ca2+ -dependent K+ channel was involved in the hyperpolarization.

Animals↗
PubMed1987

Buoyant density fluctuations during the cell cycle of Bacillus subtilis.

A simple rapid method for preparing synchronous cultures of Bacillus subtilis has been used to investigate changes in density during the cell cycle. Asynchronous cells separated on a stepped Percoll density gradient had a mean cell density of 1.117 g ml-1 +/- 0.004. Samples from a synchronous culture exhibited variation (ca. 1.5%) in mean cell density which was greatest at the onset of cell division. An asynchronous control culture showed little variation in density. These results are discussed in relation to previous work on Escherichia coli.

Bacillus subtilis↗
PubMed1987

A study on early post-denervation changes of non-quantal and quantal acetylcholine release in the rat diaphragm.

The d-tubocurarine (dTC) induced hyperpolarization of antiesterase-treated muscles at the endplate zone, miniature endplate potentials (mepps), resting membrane potentials (RMPs) and the input resistances of single muscle fibres (Rin) were measured in rat diaphragm at various times after denervation. The dTC-induced hyperpolarization decreased in two phases: 2 h after denervation it decreased transiently to 25%, after 4 h it had partially recovered to 60% and from 6 h it progressively decreased up to 12 h after which time it changed to depolarization. The initial fall and recovery were also present in muscles from sham-operated animals. The frequency of mepps decreased by 25% and the amplitude diminished by 10% within the first 2-4 h. After 10 h the frequency had decreased by 35% and the amplitude by 65%. After 12 h no mepps were present. The RMP was not significantly changed during the first 16 h after denervation. From 16 to 24 h the membrane became depolarized at a rate of about 1 mV/h. The input resistance of a single muscle fibre was constant for 12 h after denervation and from 12 to 24 h it increased by 25%. It is concluded that the early decrease in the dTC-induced hyperpolarization is probably due to the desensitization of acetylcholine (ACh) receptors caused by stress-activated non-quantal ACh release. The later decrease of dTC-hyperpolarization reflects a fall in the non-quantal ACh release. The depolarization of the resting membrane after denervation is related to the decrease in passive membrane permeability which is a secondary consequence of transmission failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

Malignant melanotic schwannoma of the bronchus.

A case of malignant melanotic schwannoma arising in the right upper lobe bronchus of a 27 year old man is presented. Tumours of this type most commonly occur in spinal nerve roots and are generally considered to be benign. The behaviour of those originating elsewhere is less predictable. As far as we are aware this is the first reported case affecting the respiratory tract.

Adult↗
PubMed1987

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice.

Uterine blood flow was assessed in mice by measuring organ uptake of intravenously injected [14C]butanol. In ovariectomized mice, injection of 100 ng oestradiol-17 beta increased blood flow 5-fold over that of untreated controls. The injection of oestradiol-17 beta in progesterone-treated mice also increased uterine blood flow at the time of maximal sensitivity to a decidual stimulus, but not 4 days later. Absolute values of blood flow increased during development of the decidual cell reaction in proportion to the increase in uterine weight, reaching maximal values 96 h after decidual induction. When progesterone injections were stopped 72 h after decidual induction, a rapid decrease in absolute and relative blood flow values preceded the decrease in uterine weight. This decrease in uterine blood flow occurred within 12 h of removing a subcutaneous implant containing progesterone. These results are consistent with the view that increased uterine blood flow during decidual development may be necessary to support the rapid increase in uterine weight at implantation and the subsequent decrease in both relative and absolute uterine blood flow on withdrawal of progesterone may promote decidual regression in the mouse.

Animals↗
PubMed1987

In-vitro production of nitrosamines by bacteria isolated from the operated stomach.

Evidence is presented of in-vitro catalysis of nitrosation by organisms isolated from the hypoacidic operated stomach. Subjects taking part in a prospective study of potential premalignancy after benign ulcer surgery underwent endoscopy, and samples of gastric juice were obtained aseptically. The organisms present were identified using the API system and tested for their ability to catalyse the nitrosation of the secondary amine, morpholine, at neutral pH and 37 degrees C. Four of the five species tested were found to be capable of the catalysis. Cellular disruption and denaturation of protein abolished the catalytic ability, suggesting that the catalysis is mediated by an enzymic system. Osmotic shock experiments indicate that the enzyme site may be on the inner membrane.

Female↗
PubMed1986

Involvement of the Ca2+-dependent K+ channel activity in the hyperpolarizing response induced by epidermal growth factor in mammary epithelial cells.

Epidermal growth factor (EGF) induces a hyperpolarizing response of 5-20 mV amplitude in mouse mammary epithelial cells in culture. The amplitude of the hyperpolarizing response was reduced by more than 60% within several minutes after addition of blockers of voltage and/or Ca2+-dependent K+ channels such as tetraethylammonium (7 mM) or quinine (0.29 mM). Both nifedipine (0.15 mM), a blocker of the Ca2+ channel, and ruthenium red (2 mM), an inhibitor of the Ca2+-binding site, also reduced the amplitude of the hyperpolarizing response by more than 60%. The Ca2+ ionophore, A23187 (3.8 microM), induced a large hyperpolarization, which was 25-40 mV and lasted about 3 min. These data suggest that activity of the Ca2+-dependent K+ channel was involved in the EGF-induced hyperpolarizing response of the mammary epithelial cells.

Animals↗
PubMed1986

The anion selectivity of the gamma-aminobutyric acid controlled chloride channel in the perfused spinal ganglion cell of frog.

The selectivity of the GABA-controlled Cl- channel in the membrane of the dorsal root ganglion cell of the frog has been measured in internally perfused cells by means of current and voltage clamp. When Cl- was replaced by various anions, the 10(-5) or 10(-4) M GABA-induced reversal potentials (EGABA) for Br-, I-, NO3-, ClO4-, SCN-, BF4- and ClO3- were more negative than that for Cl-, despite the fact that, in solution, the test anions are either larger than or similar in size to Cl-.

Animals↗
PubMed1986

Induction of distinct types of spontaneous electrical activities in mammary epithelial cells by epidermal growth factor and insulin.

Electrophysiological measurements of the membrane potentials of mouse mammary epithelial cells in primary culture revealed the presence of spontaneous-oscillating-hyperpolarizing potentials in cells incubated with epidermal growth factor. The hyperpolarizing potentials were 5-20 mV in amplitude and about 10 sec in duration. The peak height of the response was reduced by hyperpolarization, and the input membrane resistance decreased during the response. The response was probably due to activation of K+ channels. The latency period for the epidermal growth factor induction of the hyperpolarizing potential was approximately 3 hr. In contrast, insulin induced spontaneous-depolarizing potentials that were about 5 mV in amplitude and 1 sec in duration. The depolarizing potentials were attributed to activity of ion channels, since the peak height was dependent on the membrane potential and the depolarizing potential was accompanied by a decrease of input membrane resistance. The time lag for the induction of the depolarizing potential was 6-12 hr. Other hormones involved in mammary cell differentiation, such as cortisol and prolactin, neither induced the depolarizing potentials nor changed the induction of depolarizing potential by insulin. In addition, other growth factors, such as nerve growth factor and fibroblast growth factor, elicited no electrical activity.

Animals↗