Search PubMed⌕ Search

Biomedical subjects

J M Fox

Publications and source records attributed to J M Fox.

At least 109 records · Page 6Linked to original sources
PubMed1978

Retained posterior horn of the medial meniscus.

The incidence of a symptomatic retained posterior fragment of the medial meniscus in 2 different groups of patients with medial meniscectomy is compared. If the original surgery was done through one capsular incision, there was a 9.5% incidence of symptomatic retained posterior fragment as compared to 0.2% incidence if the original surgery was performed through 2 capsular incisions. For total excision of the meniscus medial meniscectomy should be performed through 2 capsular incisions.

Humans↗
PubMed1977

Ultraviolet-induced alterations of the sodium inactivation in myelinated nerve fibres.

Ultraviolet radiation irreversibly reduces the sodium permeability in nerve membranes and, in addition, induces a change of the potential dependence of the kinetic parameters of sodium inactivation in the node of Ranvier. This second ultraviolet effect shifts the kinetic parameters of sodium inactivation h infinity (V), alpha h (V), and beta h (V) to more negative potentials (no changes of the slopes of the curves). The amount of the displacement delta V along the potential axis is equal for the three parameters and depends on the ultraviolet dose. It is about delta V = --10 mV after an irradiation dose of 0.7 Ws/cm2 at 280 nm. Both ultraviolet-induced effects depend on membrane potential and on the wavelength of the applied radiation. But while the potential shift is enhanced at more negative holding potentials, the ultraviolet blocking is diminished and vice versa. Further, the ultraviolet-induced potential shift is greater at 260 nm than at 280 nm, whereas a maximum sensitivity of ultraviolet blocking is found at 280 nm. Therefore, the two radiation effects are the result of two separate photoreactions. For explanation of the radiation-induced potential shift it is assumed that ultraviolet radiation decreases the density of negative charges at the inner surface of the nodal membrane. From this hypothesis a value for the inner surface potential psii was derived. --19 mV less than or equal to psii less than or equal to --14 mV.

Animals↗
PubMed1976

Block of gating currents by ultraviolet radiation in the membrane of myelinated nerve.

The effect of ultraviolet radiation on the asymmetrical displacement currents in the membrane of the node of Ranvier was measured and compared with the ultraviolet blocking of the sodium current. Ultraviolet radiation irreversibly reduced the peak sodium current and the charge displaced during a depolarizing test pulse, the relative reduction being independent of potential. The ratio of the ultraviolet sensitivities of the sodium and the asymmetrical displacement currents is 2.3+/- 0.2. This result suggests two independent identical gating particles per sodium channel in the membrane of myelinated nerve.

Animals↗
PubMed1976

Investigation of the relation between structure and function in myelinated nerve fibres with be aid of ultraviolet radiation.

Ultraviolet radiation induces two photochemical alterations relevant to excitability in the nodal membranes: A selective blocking of the sodium permeability and a potential translation of the voltage dependent kinetic parameters of sodium inactivation and activation along the potential axis in the negative direction. The underlying processes are two different photoreactions, since 1) the action spectrum of the blocking effect shows a marked peak near 280 nm and rapidly decreasing sensitivity towards higher and lower wavelengths, while the action spectrum of the potential shift increase with lower wavelengths; 2) the blocking effect is enhanced by a more positive holding potential, while the potential shift is decreased; 3) the potential shift can be prevented intraaxonal application of l-cysteine or 2-mercaptoethanol, but the blocking effect is not affected.

Membrane Potentials↗
PubMed1976

Ultra-slow inactivation of the ionic currents through the membrane of myelinated nerve.

(1) Voltage-clamp experiments were performed with myelinated fibres isolated from the sciatic nerve of the frog to study slow changes of the specific sodium and potassium currents as a function of membrane (holding) potential and time. (2) The level of the peak sodium current depends on holding potential VH. This dependence can be described by a sigmoidal function uinfinity(VH). The underlying process is called "ultra-slow sodium inactivation" and is different and separable from the short time steady-state inactivation, hinfinity(V), and from the slow inactivation depending on the extracellular potassium concentration (Adelman, Jr., W. J. and Palti, Y. (1969), J Gen. Physiol. 54, 589-606; Peganov, E. M., Khodorov, B.I. and Shishkova, L. D. (1973), Bull. Exp. Biol. Med. 25, 15-19; Khodorov, B. I. Shishkova, L. D. and Peganov, E. M. (1974), Bull. Exp. Biol. Med. 3, 10-14). (3) After a sudden change of the holding potential the sodium current reaches a new steady-state level (due to the transition of uinfinity(VH) to the corresponding value) within approx. 4 min. The kinetics of the transition cannot be described by a single exponential function. (4) A corresponding voltage- and time-dependent process of ultra-slow inactivation exists for the potassium current in the node of Ranvier. The kinetics are faster than those of the sodium system.

Animals↗
PubMed1976

Kinetics of the slow variation of peak sodium current in the membrane of myelinated nerve following changes of holding potential or extracellular pH.

(1) Changes of the holding potential applied to the membrane of myelinated nerve fibres induced slow variations of the peak sodium current, which are super-imposed on the effect of sodium inactivation. (2) These slow variations are transitions between various steady levels of available sodium conductance. Their time course can be described by the function erfc (square root t/tau) where tau is the time and erfc the error function complement. The characteristic time tau lies in the range 2-4 min and depends on the membrane potential. (3) Changes of extracellular pH cause a rapid change of the peak sodium current followed by a slow variation as observed after changes of the holding potential. This slow variation can be prevented by applying simultaneously an appropriate change of the holding potential, e.g. the effect of changing pH from 7.3 to 5.3 is balanced by changing the potential from --70 to --55 mV. (4) The results are interpreted by postulating charged components diffusion slowly within the nodal membrane. Their transverse distribution controls the number of sodium channels available at a given membrane potential. The equivalence between change of pH and voltage is explained by assuming negative fixed charges at the outer surface of the membrane, which are protonated at low pH and thus affect the intrinsic membrane potential. (5) It is concluded that effects which are ascribed to the action of agents on individual sodium channels have to be corrected for variations in the number of available channels if these agents influence the intrinsic membrane potential, e.g. changes of extracellular pH.

Animals↗
PubMed1975

The action of thiamine and its di- and triphosphates on the slow exponential decline of the ionic currents in the node of Ranvier.

Sodium and potassium currents in the node of Ranvier decrease exponentially with time during long lasting voltage clamp experiments. This decline is strongly dependent on temperature (Q10 approximately 3). Thiamine and, particularly, its diand triphosphoric acid esters are shown to prevent this exponential decline of the ionic currents. Thiamine acts from the outside and from the inside of the nodal membrane, but more potently from the inside. Thiamine diphosphate prevents the exponential decline of the ionic currents only when applied internally. Thiamine triphosphate, the most effective thiamine derivative was tested form the inside only. Bacterial thiaminases applied externally were not effective, presumably because they do not permeate the nodal membrane. Tetrodotoxin, that has been shown by other investigators to induce a release of thiamine from nerve membranes, does not alter the action of thiamine on the exponential decline of current and vice versa. It is concluded that: (1) thiamine diphosphate or thiamine triphosphate are the active thiamine compounds in nerve membranes; (2) the site of action is located at the internal suface of the membrane; (3) the reduction of the thiamine concentration in the membrane or in the axoplasm could cause the exponetial decline of currents; (4) the release of thiamine from nerve membranes induced by tetrodotoxin is interpreted as a side effect not even related to the mechanism by which tetrodotoxin blocks the sodium channels; (5) thiamine polyphosphates appear to stabilise the intrinsic electric field strength of the nodal membrane in the resing state. Threfore, as a working hypothesis, it is suggested that the thiamine derivatives control the number of functioning ionic channels by stabilising the density of negative surface charges at the inner side of the nerve membrane.

Animals↗
PubMed1975

Degeneration and rupture of the Achilles tendon.

An analysis was perfomed on 32 operative cases of Achilles tendon disease. Two patient classifications emerged. One group suffering an acute rupture of the Achilles tendon with no antecedent complaints, and the second group had a history of chronic pain, weakness and functional loss. This latter group could be further differentiated by the occurrence of tendon failure in 10 of 22 cases. Surgical exploration in the group with chronic complaints demonstrated a high incidence of diffuse reactive changes such as fibrinoid and myxomatous degeneration, fibroisis and metaplastic calcification. Degenerative disease of the Achilles tendon should be recognized and treated not as a simple injury but as a pathological lesion.

Achilles Tendon↗