Biomedical subjects

Y L Shih

Publications and source records attributed to Y L Shih.

25 records · Page 2Linked to original sources

PubMed1992

[Cation channels formed in lipid bilayer by Pinellia ternata lectin].

Pinellia ternata lectin (PTL), a protein exhibiting hemagglutination activity and carbohydrate binding specificity to mannan was purified from rhizome of Pinellia ternata. In this work the actions of PTL on artificial lipid bilayer were investigated by means of the two-compartment system of Mueller and Rudin. The lipid bilayer with resistance more than 10G omega was formed by a solution of lecithin and cholesterol (20 mg/ml and 5 mg/ml respectively) in N-decane. The electrical properties of the lipid bilayer were investigated in voltage clamp mode. Several minutes after the addition of PTL (2 micrograms/ml) in one compartment the channel-like noise as well as a decrease of the resistance of the bilayer were observed. These actions were inhibited by mannan significantly. The resistance increase of the bilayer with PTL-channels could be observed from 2G omega to control level (greater than or equal to 10 G omega) immediately after addition of 40 micrograms/ml mannan. The discrete conduction steps were recorded at low concentration of PTL and at low holding potential. The predominant unit conductance was 35pS in symmetric KCl solution of 100 mmol/L. The selectivity of PTL-channel was estimated from Goldman-Hodgkin-Katz equation by measurement of the reversal potential in an asymmetrical salt solution. The results showed that PTL-channels were cation selective.

Cations↗

PubMed1991

[Effects of aureofuscin on muscle cell membrane and quantal release of acetylcholine (ACh) from the motor nerve terminals].

By means of the intracellular recording technique, the effect of aureofuscin (20 micrograms/ml, oversaturation solution) on the ACh release from motor nerve terminals and on muscle cell membrane potential were investigated in phrenic nerve diaphragm preparations of the mice. The results showed that (a) aureofuscin reduced the resting membrane potential of the muscle cell slightly; (b) the frequency of miniature end-plate potentials and the mean quantal content of end-plate potentials increased at first and then recovered approximately to the control level; (c) the depolarization produced by aureofuscin in the muscle cell membrane was reversible and the aureofuscin-invoked facilitation in miniature end-plate potential discharges was Ca(2+)-dependent; and (d) aureofuscin did not block neuromuscular transmission.

Acetylcholine↗

PubMed1990

Tropic effect of dexamethasone on goldfish melanocytoma cells: induction of calcium-dependent but protein synthesis-independent morphological changes.

Treatment of melanocytoma cells of goldfish origin with dexamethasone leads to rapid morphological changes, flattening of cell body and extension of dendrites. This effect is independent of protein synthesis but requires the presence of extracellular calcium, indicating that it is a "tropic effect" distinct from the typical "trophic effects" of steroid hormones that involve de novo protein synthesis.

Animals↗

PubMed1989

[Experimental analysis of membrane potential changes during maturation of Bufo bufo gargarizans oocytes].

The full-grown oocytes obtained from toad (bufo bufo gargarizans) submitted in hibernation state or reared at 25-30 degrees C for several months, named hibernation oocyte or high temperature oocyte, had a membrane potential of -41.51 +/- 0.77 mV and -43.83 +/- 1.39 mV in Ringer's solution respectively. The hibernation oocytes underwent GVBD (germinal vesicle breakdown) and membrane depolarization at 19 +/- 1 degree C after progesterone stimulation. The membrane potential was about -20 mV at the period of GVBD, and -10 mV or so at 20 hours after the hormone treatment. However, the high temperature oocytes did not undergo GVBD, their membrane potential decreased before the fourth hour after treatment with progesterone and then recovered. If the hibernation oocytes were preincubated at 37-38 degrees C for 13 hours prior to the culture in the medium containing progesterone (10(-6)M, 37-38 degrees C), no GVBD was observed and the membrane depolarized before the fourth hour after treatment with progesterone then recovered, but MPF was detectable in the cytoplasm (unpublished). Both GVBD and membrane depolarization appeared in the hibernation oocytes and high temperature oocytes after injection of MPF. The time required for the hibernation oocytes injected MPF to attain the membrane potential about -20 mV was 4 hours earlier than that of progesterone treatment. It was just the time required for the appearance of MPF in the cytoplasm of oocytes treated with the hormone. It was noticed in our precedent article that a factor which appeared in the cytoplasm of high temperature oocytes differed from MPF. The factor was called Hibernation Oocyte Mature Promoting Factor (HOMPF).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Sequencing and synthesis of pardaxin, a polypeptide from the Red Sea Moses sole with ionophore activity.

Pardaxin, an amphipathic polypeptide secreted by the Red Sea flatfish Pardachirus marmoratus whose sequence is NH2-G-F-F-A-L-I-P-K-I-I-S-S-P-L-F-K-T-L-L-S-A-V-G-S-A-L-S-S-S-G-G-Q-E, was synthesized by the solid-phase method. The structure was verified by sequencing. The synthetic polypeptide changed the resistance of lipid bilayers by forming pores. At 10(-7)-10(-8) M, the synthetic pardaxin increased the frequency of the spontaneous release of quanta of acetylcholine at the neuromuscular junction by up to 100-fold, resembling the native product. Synthetic pardaxin seems to be a suitable tool for investigating the molecular structures underlying channel selectivity.

Acetylcholine↗

PubMed1986

Abolishment of non-quantal release of acetylcholine from the mouse phrenic nerve endings by toosendanin.

The hyperpolarizing effect (H-effect) of d-tubocurarine on the end-plate of the isolated diaphragm pretreated with an anticholinesterase was irreversibly abolished by toosendanin (1 X 10(-5) g/ml), indicating the blockade of spontaneous non-quantal release of acetylcholine (ACh). The H-effect was also inhibited, but temporarily, when toosendanin (a dose of 0.6 LD50) was subcutaneously injected into the mouse and the diaphragm was isolated 40-120 min after injection. During such an inhibitory period, however, spontaneous release of ACh remained facilitated. It is concluded that the effect of toosendanin on non-quantal release of ACh was different from its effect on quantal release not only at the direction but also at the time course.

Acetylcholine↗

PubMed1983

Anti-botulismic effect of toosendanin and its facilitatory action on miniature end-plate potentials.

The time for blocking neuromuscular transmission by botulinum toxin is lengthened in phrenic nerve-diaphragm preparation of rats sacrificed at various times after subcutaneous injection of toosendanin (7 mg/kg). This effect of toosendanin manifests itself 15 min after injection and lasts for 3 days. During this period the frequency of miniature end-plate potentials is increased.

Action Potentials↗