[A study on the F ion concentration of the drinking water in Chonnam mine area].
Explore the source record for details and available documents.
Fluorides↗
Biomedical subjects
S J Hong
Publications and source records attributed to S J Hong.
Pre- and postsynaptic effects of nicotine on the mouse phrenic nerve-diaphragm preparation.
Nicotine at less than or equal to 33 microM enhanced the single twitch response to indirect stimulation but potentiated the blocking effect of tubocurarine. Failure of tetanic contraction (tetanic fade) occurred on stimulation at 100 Hz. At 76 microM, nicotine induced a first phase rapid (10 min) inhibition of twitch response followed later (60-90 min) by a second phase complete block. Neostigmine partially restored the response at either phase of block whereas diaminopyridine completely antagonized the blockade. The end-plate was depolarized maximally by only 10-15 mV within 30 min with 43 microM nicotine. The depolarization was maintained but was antagonized by tubocurarine. The twitch response induced by direct stimulation was unchanged indicating no depolarization block ensued. The amplitudes of both EPP (0.7 Hz) and MEPP were markedly depressed in parallel indicating a curare-like postsynaptic inhibition without an effect on the release of transmitter. It is concluded that nicotine blocks the neuromuscular transmission by a dual mechanism by its partial agonist action. At higher frequencies of transmission, nicotine (greater than or equal to 22 microM) also produced a remarkable run-down of EPP just like other receptor antagonists suggesting that the nerve terminal acetylcholine receptors are not particularly sensitive to nicotine as those on the autonomic ganglia.
4-Aminopyridine↗
A regenerating release of acetylcholine from mouse motor nerve terminals treated with anticholinesterase agents.
It was found by intracellular recording with glass microelectrodes that train stimulation (50-200 Hz) of the phrenic nerve of intact or cut mouse diaphragm induced an accumulative depolarization of the endplate and triggered after a few pulses an 'all-or-none' regenerative depolarization lasting for 300-900 ms when acetylcholinesterase was inhibited by neostigmine or diisopropylfluorophosphate. This depolarization was associated with a noise of the membrane potential and a failure of the end plate potential. Low Ca2+ prolonged whereas high Ca2+ shortened the duration of regenerative depolarization which needed no further stimulation once triggered. d-Tubocurarine abolished the depolarization while restoring the end plate potential. A regenerative release of acetylcholine due to an activation of presynaptic cholinoceptors is speculated.
Acetylcholine↗
Pharmacological identification of saxitoxin-like toxins in the cultured purple clam, Hiatula diphos.
An outbreak of poisoning from ingestion of purple clam (Hiatula diphos), obtained from a brackish fish-culture pond, occurred in southern Taiwan in early January 1986. The extract blocked the twitch responses and generation of the action potential of the mouse diaphragm without an effect on the resting membrane potential or the miniature endplate potential. The depolarizations and spontaneous firings of the diaphragm induced by veratridine and crotamine were effectively antagonized by the toxic clam extract, indicating the presence of saxitoxin-like substances, which may have amounted to 0.013% tetrodotoxin equivalent.
Animals↗
Mechanisms of the inhibition by neostigmine of tetanic contraction in the mouse diaphragm.
Neostigmine (0.5-2 microM) caused fade of tetanic contractions (Wedensky inhibition) evoked by repetitive nerve stimulation. The mechanism underlying this action was studied in intact and cut isolated phrenic nerve-diaphragm preparations of mice. The fade was brought about by failure to elicit muscle action potentials. During fade, the muscle was unable to conduct directly evoked action potentials across the central endplate zone. Recovery of excitability occurred in 5 s with continued stimulation. In the presence of neostigmine, the resting membrane potential at endplate areas during repetitive stimulation decreased from -80 mV to less than -50 mV within the first 10 pulses at 75-200 Hz and thereafter recovered gradually to about -60 mV in the following 5 s during continuous stimulation. The quantal content of endplate potentials evoked by single stimulation was not reduced by neostigmine whereas that evoked by high frequency stimuli (75 Hz) was reduced to about 1/3 in 10 pulses. It is concluded that the fade of tetanic contraction caused by inhibition of acetylcholinesterase is induced by the inactivation of sodium channels in the area surrounding the endplates and that the sustained fade is due to a decrease of transmitter release. Both effects are the result of acetylcholine accumulation.
Action Potentials↗
A comparison of the antagonisms by neostigmine and diaminopyridine against the neuromuscular block caused by cobrotoxin and (+)-tubocurarine.
Cobrotoxin was about 11-fold more potent than (+)-tubocurarine on a weight basis in blocking neuromuscular transmission in mouse isolated phrenic nerve-diaphragm preparations. Neostigmine and diaminopyridine increased the concentrations of cobrotoxin for 70% inhibition of indirect contraction by 290 and 320%, and increased those of (+)-tubocurarine by 180 and 230%, respectively. More than additive increases were obtained when neostigmine and diaminopyridine were used simultaneously. Cobrotoxin, however, was only 6-fold more toxic than (+)-tubocurarine after intraperitoneal injection in mice. The lethal dose of (+)-tubocurarine was increased by 80% when both antidotes were used together, but only by 15-20% when used alone. In contrast, the lethality of cobrotoxin was not decreased by these drugs. Unexpectedly, the time to death after treatment with cobrotoxin was shortened when mice were pretreated with these antidotes.
4-Aminopyridine↗
Morphological changes of horseshoe crab amebocytes during in vitro cultivation.
Explore the source record for details and available documents.
Animals↗
Acetylcholine hydrolysis during neuromuscular transmission in the synaptic cleft of skeletal muscle of mouse and chick.
Inhibition of acetylcholinesterase (AChE) by more than 80% by neostigmine or physostigmine resulted in a failure of tetanic contraction (100 Hz) in the isolated mouse nerve-diaphragm preparation. In the chick biventer cervicis muscle, however, the tetanic contraction was well maintained and even outlasted the period of nerve stimulation after inactivation of AChE. The concentration of (+)tubocurarine for 70% block of the indirect twitch response of the mouse diaphragm at 0.1 Hz was increased from 0.67 to 0.99 to 1.21-2.03 microM in the presence of neostigmine (0.15-1.5 microM) which inhibited AChE by 70% or more, while that to depress the tetanic contraction (50 Hz) was increased from 0.38 to 0.42 to 0.53-0.69 microM. In the chick muscle, physostigmine at 2.4 microM increased the concentration of (+)tubocurarine for 70% block of the twitch response from 1.68 to 4.14 microM, whereas that for block of the response to exogenous acetylcholine (ACh) was increased from 1.47 to 74.6 microM. On single stimulation, the relative peak concentrations of acetylcholine (ACh) at the postsynaptic receptor site of the mouse diaphragm and chick biventer cervicis were estimated to be increased by about 110 and 120% respectively, after complete inhibition of AChE. In the chick muscle, physostigmine increased the relative concentration of ACh by about 40-fold at the receptor site for exogenously applied ACh. It is concluded that the intrinsic ACh released from the nerve terminal is hydrolyzed by about 50% during the time of diffusion across the synaptic cleft whereas most of exogenous ACh is hydrolyzed before reaching the target.
Acetylcholine↗
Electrophysiological studies of myotoxin a, isolated from prairie rattlesnake (Crotalus viridis viridis) venom, on murine skeletal muscles.
Myotoxin a reduced the resting membrane potential of mouse and rat diaphragms from about -80 mV to -60 mV, induced spontaneous repetitive firing and enhanced the contractile force in response to single stimulations. The depolarizing effect was reversed noncompetitively by tetrodotoxin, local anesthetics or low Na+ solution, but was augmented by ouabain or low Cl-solution while being unaffected by high K+ solution or electrical stimulation of the muscle. The duration of muscle action potential was prolonged by only 20-30%, whereas the rate of rise (dV/dt) was unaffected. About a 40% increase of membrane conductance was observed, be abolished by the Na+-channel blocker tetrodotoxin. By contrast, K+ conductance was unaffected. Effects on caffeine-induced contracture, quantal release of neurotransmitter and the amplitude of miniature endplate potential were not appreciably affected. These effects of myotoxin a indicate that the toxin affects the muscle, but not the nerve, by acting specifically on the Na+-channel of the sarcolemma or T-tubule, like crotamine, rather than on the sarcoplasmic reticulum. The effects of sea anemone toxin II on the Na+-channel (marked depolarization and prolongation of action potential) could not be prevented by saturating the muscle with myotoxin a. On the other hand, the effect of veratridine, a member of another group of toxins acting on the Na+-channel, was enhanced. These results suggest that myotoxin a acts on the Na+-channel at a site which is discrete from those of tetrodotoxin, veratridine and sea anemone toxin II.
Action Potentials↗
[An evaluation of communal water fluoridation in Korea].
Explore the source record for details and available documents.
Fluoridation↗
Potentiation between neostigmine and 3,4-diaminopyridine in antagonizing the neuromuscular block induced by D-tubocurarine.
The antagonisms to the d-tubocurarine-induced neuromuscular blockade by neostigmine and 3,4-diaminopyridine (DAP) were studied quantitatively in the isolated phrenic nerve-diaphragm preparation of mice in vitro and in lethality of mice in vivo by assaying concentrations of d-tubocurarine needed to produce 70% block of indirect muscle contraction and LD50, respectively. The "antagonist efficacies", defined as the ratio of d-tubocurarine concentration (dose) after pretreatment with antagonistic agents over that of control, were 1.87, 2.24 and 14.7, respectively, for neostigmine, DAP and both agents combined when the stimulus pulses were at 0.1 Hz. Under 50 Hz train stimulation, the antagonist efficacies were lower, being 1.85, 1.64 and 5.33, respectively. For the lethality to d-tubocurarine, the values were still lower, being only 1.21, 1.33 and 1.84, respectively. The synergism between neostigmine and DAP, as evident from the marked increase of antagonist efficacy in vitro, is more than expected from the possible interaction of the major pharmacological actions of these two agents.
4-Aminopyridine↗
Potentiation by crotamine of the depolarizing effects of batrachotoxin, protoveratrine A and grayanotoxin I on the rat diaphragm.
The interactions between crotamine and tetrodotoxin and group II sodium channel toxins, including batrachotoxin, protoveratrine A and grayanotoxin I, were studied on the rat diaphragm muscle. When the diaphragm was pretreated with 0.1 micrograms crotamine/ml for 45 min (a condition known to depolarize the muscle by less than 3 mV, which is only 20% of the maximal depolarization induced by a saturating concentration of crotamine), the rate of depolarization by group II toxins was markedly enhanced and the time to reach the steady state depolarization was greatly shortened. The maximal depolarizations induced by each of the group II toxins, however, were not increased. Pretreatment with saturating concentrations of crotamine also caused no change of the steady state depolarization induced by batrachotoxin or grayanotoxin I. Moreover, pretreatment of the diaphragm with a high concentration of grayanotoxin I, whose effect is reversible, did not impede the depolarizing effect of crotamine. Tetrodotoxin restored the membrane potential, depolarized by crotamine, with 50% restoration at a concentration of 16 ng/ml, no matter whether a high (20 micrograms/ml) or a low (2 micrograms/ml) concentration of crotamine were used. The above results indicate that there is no competition between crotamine and group II toxins or between crotamine and tetrodotoxin. However, crotamine may affect the binding of group II toxins allosterically, increasing their affinity although the intrinsic activity may not be changed.
Animals↗
A study on the membrane depolarization of skeletal muscles caused by a scorpion toxin, sea anemone toxin II and crotamine and the interaction between toxins.
Quinquestriatus toxin (QTX) isolated from the venom of a scorpion (Leiurus quinquestriatus) and sea anemone (Anemonia sulcata) toxin II enhanced the twitch response of the rat and mouse diaphragms and like crotamine (isolated from the venom of Crotalus durissus terrificus) caused spontaneous fasciculation of the muscle. Trains of action potentials in muscles at 70-250 Hz, which could not be antagonized by (+)-tubocurarine, were triggered by single stimulation or occurred spontaneously after treatment with these toxins. QTX and toxin II prolonged the rat muscle action potential 3 to 4 fold whereas crotamine prolonged the action potential by only 30%. The membrane potential was depolarized from about -82 mV to -55 mV by crotamine 2 micrograms ml-1, -41 mV by toxin II 5 micrograms ml-1 and to -50 mV by QTX 1 microgram ml-1. The concentrations to induce 50% maximal depolarization (K0.5) were 0.07, 0.15 and greater than 0.4 microgram ml-1, respectively, for QTX, crotamine and toxin II, whereas the rates of depolarization were in the order toxin II greater than or equal to crotamine greater than QTX. The depolarizing effects of crotamine and QTX, but not of toxin II, were saturable. The depolarizing effects of all three toxins were irreversible whereas the membrane potential could be restored by tetrodotoxin non-competitively. Simultaneous treatment with crotamine and QTX or crotamine and toxin II at concentrations below K0.5 caused only additive effects on depolarization. When the muscle was depolarized by pretreating with a saturating concentration of crotamine, the onset of depolarization by QTX was greatly retarded whereas that by toxin II was unaffected. Action potentials were further prolonged in both cases. 8 It is inferred that all three peptide toxins act at sites on the sodium channel and the binding sites for QTX and crotamine overlap to a considerable extent. On the other hand, the site for toxin II appears not to overlap with that of crotamine but may overlap with that of QTX.
Animals↗
Cystadenocarcinoma of the ovary in a 4-year-old: benign transformation during therapy.
Ovarian tumors comprise only 1% of all tumors in females below the age of 17 years. Of these, the epithelial tumors are the least common, being particularly rare before puberty and then increasing in frequency with advancing age after puberty. The youngest girl previously reported in the literature with an epithelial ovarian tumor was a 9-year-old child with an ovarian papillary cystadenocarcinoma. This is the only case thus far reported of a malignant ovarian epithelial tumor occurring before puberty. Only histologically benign appearing glands were detected in the resected tumor masses, on a second-look laparotomy following the use of multiagent chemotherapy.
Antineoplastic Agents↗
Electron spin resonance spin label studies of intercalation of nitrobenzene in DNA.
Explore the source record for details and available documents.
Animals↗
Activity-dependent changes in voltage-dependent calcium currents and transmitter release.
Voltage-dependent Ca2+ channels are important in the regulation of neuronal structure and function, and as a result, they have received considerable attention. Recent studies have begun to characterize the diversity of their properties and the relationship of this diversity to their various cellular functions. In particular, Ca2+ channels play a prominent role in depolarization-secretion coupling, where the release of neurotransmitter is very sensitive to changes in voltage-dependent Ca2+ currents. An important feature of Ca2+ channels is their regulation by electrical activity. Depolarization can selectively modulate the properties of Ca2+ channel types, thus shaping the response of the neuron to future electrical activity. In this article, we examine the diversity of Ca2+ channels found in vertebrate and invertebrate neurons, and their short- and long-term regulation by membrane potential and Ca2+ influx. Additionally, we consider the extent to which this activity-dependent regulation of Ca2+ currents contributes to the development and plasticity of transmitter releasing properties. In the studies of long-term regulation, we focus on crustacean motoneurons where activity levels, Ca2+ channel properties, and transmitter releasing properties can be followed in identified neurons.
Animals↗
Inflammatory myofibroblastic tumor of the stomach with peritoneal dissemination in a young adult: imaging findings.
Inflammatory myofibroblastic tumors are lesions that most often affect young adults and children. These tumors have been found in numerous extrapulmonary sites but rarely in the stomach. It is unknown whether this process is reactive or neoplastic. They are infiltrative lesions and often extend through the gastric wall, sometimes reaching adjacent organs including the esophagus, duodenum, peritoneal cavity, spleen. pancreas, and liver. These features mimic malignancy on endoscopy and radiology. We report the ultrasound, color Doppler ultrasound, and helical computed tomographic findings of a gastric inflammatory myofibroblastic tumor with peritoneal dissemination in a young adult. To our knowledge, this is the first report of color Doppler ultrasound and helical computed tomographic findings of this rare disease entity.
Adult↗
Transrectal color Doppler ultrasonography for postejaculation hematuria.
A case involving an adult man with postejaculation hematuria (PEH) is described. We used transrectal color Doppler ultrasonography to evaluate periprostatic or intraprostatic vascular anomalies. We confirmed a vascular anomaly by angiography and embolized it. Periprostatic vascular anomaly may be a cause of PEH, and color Doppler ultrasonography is helpful for the initial studies of this entity.
Arteriovenous Malformations↗