Search

Styrene and the styrene-additive mixtures (kerosene, dioxane, ethylene dichloride, or dioctylphthalate) were soaked into a poly(vinylchloride) film and then styrene was polymerized. Subsequently, poly(styrene) was extracted with CCl4 and the microporous membrane was obtained, of which the morphology was studied. It is elucidated that the additives affect the morphology of the resultant composite films.

Anion exchange membranes (ferricyanide ion type) prepared by the “paste method” were treated with an aqueous solution of hydrogen peroxide, and the resultant microporous membranes had no ion exchange capacity but water permeability. By measuring the water permeability of the membranes and observing the electron microphotographs of the membrane surfaces, it was elucidated that the anion exchange membranes contained microheterogeneity of colloidal dimension.

The authors discuss laser surgery of meningiomas which are difficult or impossible to remove by conventional methods. The CO2 laser surgical unit (scalpel), Medilaser-S, Model MEL-442, was originally developed for neurosurgery by Takizawa and his team. One of the conspicuous advantages of the CO2 laser scalpel is its ability to remove highly vascularized tumors with minimum bleeding. Another advantage is that it enables a surgeon to remove a firm tumor precisely without using mechanical force. The cases included in this paper are highly vascularized sphenoid ridge meningioma, giant falx meningioma, firm tuberculum sellae meningioma, tentorial meningioma, ventricular meningioma and orbital meningioma. Disadvantages of the CO2 laser scalpel and methods to offset them are also discussed. These disadvantages may be surmounted by the combined use of the electrosurgical unit, cryosurgical unit, CUSA system, etc. The CO2 laser scalpel is not ideal, but it is no doubt a break through in surgery of brain tumors which are difficult to remove by conventional methods.

Intracellular and voltage-clamp recordings were made from neurons in rabbit vesical parasympathetic ganglia (VPG) maintained in vitro. Norepinephrine (NE, 10 nM-10 μM) reduced the Ca 2+ component of the action potential and the afterhyperpolarization. Clonidine and UK14304, the selective α 2 -adrenoceptor agonists, mimicked the inhibitory effects of NE on the action potential. NE and UK14304 blocked the Ca 2+ spike elicited in the presence of tetrodotoxin and tetraethylammonium. UK14304 suppressed the inward Ca 2+ current induced by depolarizing step command under the voltage-clamp condition. These inhibitory actions were antagonized by yohimbine and idazoxan but not by prazosin and propranolol. It is suggested that α 2 -adrenoceptors mediate the inhibition of voltage-dependent Ca 2+ entry during the action potential.

Intracellular recordings were made from neurons in rabbit vesical pelvic ganglia (VPG), in vitro. Increasing the frequency of preganglionic-nerve stimulations from 0.1–1 Hz to 10–20 Hz facilitated fast excitatory postsynaptic potentials (EPSPs), resulting in a generation of action potentials. Acetylcholine-induced response was not altered during the facilitation of the fast EPSP. Serotonin blocked action potentials elicited by preganglionic-nerve stimulations at 0.1 Hz, while it caused no blockade at 10 Hz. Serotonin may potentiate the feature of high-pass filter [1] in transmission of VPG. Immunohistochemical study demonstrated serotonin-like varicose terminals in rabbit VPG.

Intracellular recordings were made from neurons of rabbit vesical pelvic (parasympathetic) ganglia (VPG). Application of 5-hydroxytryptamine (5-HT, 0.3-30 microM) produced an initial depression followed by a long-lasting facilitation of the fast excitatory postsynaptic potential (e.p.s.p.) evoked by stimulation of the pelvic preganglionic nerve. The facilitation of nicotinic transmission lasted for 30-120 min, even when 5-HT was removed from the superfusing solution. 5-HT (0.3-30 microM) did not change the depolarization induced by a direct application of acetylcholine (ACh) to the VPG neurons pretreated with 1 microM atropine. 5-HT also caused an initial depression followed by an increase in the quantal content of the fast e.p.s.p. It is, therefore, suggested that diphasic effect of 5-HT on the nicotinic transmission is due mainly to a modulation of the ACh-release from presynaptic nerve terminals. Methysergide (5 microM), mianserin (5-30 microM) and ICS 205-930 (100-300 nM) did not antagonize the presynaptic actions of 5-HT on the nicotinic transmission, suggesting that the presynaptic 5-HT receptor may belong to a class of 5-HT1 subtypes. Spiperone (1 microM), a selective 5-HT1A antagonist, blocked the 5-HT-induced inhibition of the fast e.p.s.p. Under the effect of spiperone, the facilitation appeared soon after application of 5-HT. The facilitation of the fast e.p.s.p. may be mediated through a 5-HT1B or 5-HT1C subtype. Lowering temperature of the external solution eliminated the 5-HT-induced facilitation of the nicotinic transmission. Forskolin produced a presynaptic facilitation of the fast e.p.s.p., without producing an initial depression. 3-Isobutyl-1-methylxanthine (10 microM) potentiated the facilitatory action of 5-HT. Bath-application of dibutyryl cyclic adenosine monophosphate (cAMP) (1-6 mM) and 8-bromo-cyclic AMP (2-5 mM) mimicked the effect of 5-HT in producing the facilitation of the fast e.p.s.p.s. All data presented are consistent with the hypothesis that 5-HT, acting on presynaptic 5-HT1 receptors, causes a facilitation in the release of ACh from preganglionic nerve terminals possibly mediated through an activation of adenylate cyclase.

Intracellular recordings were made from neurons of vesical pelvic (parasympathetic) ganglia (VPG) isolated from the rabbit urinary bladder. Spontaneous hyperpolarizations (SH), occurring at intervals of 30 s to 5 min, could be recorded from 53% of VPG neurons in Krebs solution. The action potential was associated with inward sodium and calcium currents and was followed by fast and slow afterhyperpolarizations (AHPs). The action potential also evoked an additional hyperpolarization which was identical to the SH. The SH and the AHPs were associated with a decrease in the input resistance and reversed their polarity close to the potassium equilibrium potential. Intracellular cesium ions blocked the AHPs and the SH. Superfusing the preparation with a calcium-free solution produced a depolarization associated with an increased input resistance. The outward rectification activated at the resting membrane potential was depressed in the calcium-free solution. The removal of extracellular calcium ions also depressed both the SH and the spike AHPs. Bath-application of caffeine (1–3 mM) increased the frequency of the appearance of the SH. Injection of EGTA into VPG neurons caused a depolarization due to a blockade of the outward rectification. EGTA also depressed the slow AHP and the SH. These results suggest that the neuronal membrane of the rabbit VPG is endowed with a calcium-dependent potassium conductance (gKCa). Apamin (0.3–5 nM) and (+)-tubocurarine (30–300 μM) blocked the slow AHP and the SH without affecting the fast AHP and the resting membrane potential. Tetraethylammonium (TEA, 0.3–5 mM) suppressed the fast AHP and the SH without affecting the outward rectification. TEA augmented the slow AHP. Barium ions (0.1–1 mM) depressed the AHPs, the SH and the outward rectification. These pharmacological properties imply that at least 3 kinds of gKCa systems underlie the generation of the outward rectification, the spike AHPs and the SH.

Intracellular recordings were made from vesical pelvic ganglion cells of the rabbit in a Krebs solution containing tetrodotoxin (1 microM). Experiments were carried out during complete suppression of the calcium-dependent potassium conductance by tetraethylammonium (greater than or equal to 20 mM) and/or intracellular injection of cesium ions. The action potential was followed by a depolarizing afterpotential which lasted for 0.3-10 s and had a peak amplitude of 5-20 mV at about -50 mV. The afterdepolarization (ADP) could not be observed when the preceding calcium-dependent action potential was blocked in a nominally calcium-free solution. Intracellular injection of ethyleneglycol-bis(beta-aminoethyl ether)N,N'-tetraacetic acid (EGTA) or total substitution of extracellular calcium ions with barium ions selectively blocked the ADP. The ADP, associated with an increased membrane conductance, reversed its polarity at -17 mV, when ganglion cells were impaled with microelectrodes filled with potassium chloride or cesium chloride. This reversal level was similar to that of the depolarization induced by gamma-aminobutyric acid. The reversal potential shifted to about -50 mV when acetate or sulphate were injected as counter anions. The peak amplitude and the total duration of the ADP was increased by substitution of external sodium chloride with sucrose or sodium isethionate. These results suggest that the ADP results from calcium entry during the spike and subsequent opening of chloride channels in parasympathetic neurons of the rabbit.

Brainstem function in patients with Chiari-II malformation was evaluated by brainstem auditory-evoked potentials (BAEPs). All cases had associated hydrocephalus, some of which were shunted. The effect of the shunting operation on the wave forms was examined as well as the age-wave relationships. Although the shunting operation resulted in shortened brainstem conduction time, the overall postshunt responses were still far from normal. Another significant finding was that whereas there were remarkable abnormalities in recorded wave-forms in cases younger than 8 years, normal or almost normal responses were obtained in all cases older than 8. BAEP abnormalities could not be correlated with the severity of meningomyelocele, nor was the predictive value of response in assessing potential risk of symptomatic Chiari malformation established.

Substance P (0.5-5 microM) depressed the spike peak and after-hyperpolarization of action potentials of bullfrog sympathetic ganglion cells. It also depressed the after-hyperpolarization and prolonged the falling phase in Ca2+ spikes. The voltage-dependent K+ currents, both the delayed rectifier K+ current (Ik1) and the M current (Ik2), were suppressed by substance P, suggesting that the depression of the after-hyperpolarization may be due to suppression of these K+ currents.

Intracellular recordings were made from parasympathetic neurons of the rabbit vesical pelvic ganglia (VPG) maintained in vitro. 5-Hydroxytryptamine (5-HT) inhibited cholinergic transmission in the VPG by reducing the fast excitatory postsynaptic potential (EPSP) evoked by stimulations of pelvic nerves. 8-Hydroxy-2-(di-n-propyl-amino) tetralin hydrochloride mimicked the inhibitory effect of 5-HT on the ganglionic transmission. 5-HT-induced inhibition of the fast EPSP was antagonized by spiperone. The results suggest that 5-HT1A receptor subtypes mediate the inhibition of cholinergic transmission in the rabbit VPG.

Intracellular recordings were made from neurons in bullfrog sympathetic ganglia. Orthodromic, intracellular and antidromic stimulations evoked recurrent depolarizing responses accompanied by a spontaneous firing of the action potential in type 2 neurons. The depolarizing response elicited by intracellular and antidromic stimulations was selectively blocked by propranolol (1 μM), but not by yohimbine and phenoxybenzamine. Propranolol did not block the ‘nicotinic’ fast excitatory postsynaptic potential evoked by orthodromic stimulation. These results suggest that excitatory β-adrenoceptors mediate the recurrent synaptic facilitation of nicotinic transmission in type 2 neurons of bullfrog sympathetic ganglia.

The spike peak and after-hyperpolarization of the action potential of bullfrog sympathetic ganglion cells were depressed during the late slow excitatory postsynaptic potential (EPSP). These changes in the action potential were mimicked by luteinizing hormone-releasing hormone (LH-RH), a neurotransmitter candidate for the late slow EPSP. LH-RH (5 microM) suppressed the voltage-dependent K+ currents, both the delayed rectifier K+ current (IK1) and the M current (IK2). It is suggested that the depression of the after-hyperpolarization of the action potential during the late slow EPSP may be due to suppression of IK1 and IK2.

Effects of adenosine triphosphate (ATP) and dibutyryl cyclic adenosine monophosphate (dbc AMP) on the Na+ -K+ pump of cell membrane were studied by testing the effects of these nucleotides on the 22Na+-efflux from frog skeletal muscle fibres. The rate coefficient of 22Na+-efflux was found to be significantly increased by ATP 3 mM. Dbc AMP 3 mM showed no demonstrable effect. These results support the concept that ATP facilitates the electrogenic Na+ pump, but do not support the concept that the electrogenic Na+ pump is stimulated by cyclic AMP.

Multiple-input multiple-output (MIMO) systems employ advanced signal processing techniques. However, the performance is affected by propagation environments and antenna characteristics. The main contributions of the paper are to investigate Doppler spectrum based on measured data in a typical meeting room and to evaluate the performance of MIMO systems based on an eigenbeam-space division multiplexing (E-SDM) technique in an indoor time-varying fading environment, which has various distributions of scatterers, line-of-sight wave existence, and mutual coupling effect among antennas. We confirm that due to the mutual coupling among antennas, patterns of antenna elements are changed and different from an omnidirectional one of a single antenna. Results based on the measured channel data in our measurement campaigns show that received power, channel autocorrelation, and Doppler spectrum are dependent not only on the direction of terminal motion but also on the antenna configuration. Even in the obstructed-line-of-sight environment, observed Doppler spectrum is quite different from the theoretical U-shaped Jakes one. In addition, it has been also shown that a channel change during the time interval between the transmit weight matrix determination and the actual data transmission can degrade the performance of MIMO E-SDM systems.