H1 H2 Research Articles

Different effects on gating of three myotonia-causing mutations in the inactivation gate of the human muscle sodium channel.

1. Three mutations at the same site in the inactivation gate of the alpha-subunit of the human muscle Na+ channel, G1306E, G1306V and G1306A, cause three phenotypes of K(+)-aggravated myotonia: G1306E as the most severe and G1306A as the most benign form. 2. Recombinant wildtype (WT) and mutant (G1306E, G1306V and G1306A) human Na+ channels were expressed in human embryonic kidney cells (HEK293). G1306E and G1306V channels showed a distinct increase in the time constants of inactivation (tau h1 and tau h2) and in the ratios of steady-state to peak currents (Iss/Ipeak) (e.g. at 0 mV, G1306E vs. WT; tau h1, 1.29 +/- 0.10 vs. 0.52 +/- 0.01 ms; Iss/Ipeak, 2.90 +/- 0.40 vs. 0.93 +/- 0.19%). G1306A channels showed only an increase in tau h1 (0.74 +/- 0.07 ms). For G1306E and G1306V channels, the steady-state inactivation curves, as well as the voltage dependence of the rate of recovery from inactivation, were shifted by +15 mV. For G1306A the h infinity curve was shifted by only +5 mV. 3. G1306E and G1306V channels showed prolonged current rise times and later first openings suggesting slowing of activation. For G1306E channels only, the steady-state activation curve was shifted by -7 mV. For all mutants the deactivation time constants were increased. 4. We conclude that (i) the combination of alterations in inactivation and activation produces the slowing of the current decay, (ii) the slowed inactivation is most responsible for myotonia, and (iii) the shift of the steady-state activation curve, seen only with G1306E channels, may explain the severity of this phenotype. 5. The results suggest that two of the mutations in the Na+ channel inactivation gate also alter channel activation and deactivation.

Acoustic and perceptual investigation of breathy voice

Although breathy voice is typically characterized by an increase in spectral noise, it is notoriously difficult to devise a computational method to distinguish breathy from clear (modal) voice. The present study successfully makes use of an algorithm, originally developed to quantify aspects of pathological voice quality [G. de Krom, J. Speech Hear. Res. 36, 254–266 (1993)], which computes a harmonics-to-noise ratio (HNR). The algorithm calculates the harmonics-to-noise ratio using a comb filter defined in the cepstrum domain to separate the harmonics from the noise. Performance of the algorithm was tested on three speakers (2 male, 1 female) of Javanese producing a word list of 31 minimal breathy/clear word pairs. Results showed that the algorithm reliably distinguished breathy from clear tokens for all three speakers, with higher HNRs for clear than for breathy tokens. Moreover, accurate performance was obtained for nearly all frequency ranges investigated (60–2000 Hz, 2000–3000 Hz, 3000–5000 Hz). A comparison to other methods (such as H1–H2) will also be presented. Finally, perceptual rating experiments will be conducted to determine if the algorithm’s performance correlates with perceived degree of breathiness.

Effect of histamine in autoimmune myocarditis mice

The contractile effect of histamine, as well as the H1 receptor population and H2 receptor-mediated cAMP production, were measured in cardiac tissue from control normal and autoimmune myocarditis mice. Histamine triggered positive chronotropy and negative inotropy at high concentrations in both control and autoimmune auricles, H2 receptors being the most important mediator of these responses. In contrast, in atria from autoimmune myocarditis mice, histamine at lower concentrations caused positive inotropy and negative chronotropy. These effects, not verified in the normal control atria, are mediated by H1 receptors. The expression of H2 and H1 receptors mediating the cardiac response to histamine was evaluated through histamine-stimulated cAMP level and binding of [ 3H] mephyramine, respectively. Both control and autoimmune myocardium were able to increase cAMP levels, an effect that was inhibited by H2 antagonist drug. The amount of cAMP was significantly higher in control myocardium than in those from autoimmune ones. Saturable binding of [ 3H] mephyramine occurs in autoimmune myocardium, with distinct high and low affinity binding sites. In control myocardium non-saturable binding was detected. These results suggest that H1 and H2 receptors coexist in heart from autoimmune myocarditis mice, whereas only H2 receptors are present in myocardium from control mice. The presence of H1 receptors in autoimmune myocardium could be an important factor in the regulation of its physiological behaviour.

Cooling effects on the histaminergic response of rabbit ear and femoral arteries: role of the endothelium

The effects of cooling on the isometric response of rabbit isolated central ear (cutaneous) and femoral (non-cutaneous) arteries to histamine were determined at 37 degrees C and 24 degrees C (cooling). Under resting tension, both types of arteries contracted to histamine (10(-7)-10(-3) M), and the sensitivity of ear arteries, but not of femoral arteries was lower at 24 than at 37 degrees C. Chlorpheniramine (10(-7) M) blocked the contraction of both types of arteries to histamine at both temperatures. In ear arteries, endothelium removal or treatment with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 10(-5) M) did not affect the contraction to histamine at 37 degrees C, but it reversed the decreased contraction at 24 degrees C. In femoral arteries, endothelium removal or L-NAME (10(-5) M) did not affect the response to histamine at 37 and 24 degrees C. Ear and femoral arteries precontracted with endothelin-1 (10(-8)-10(-7) M) and pretreated with chlorpheniramine (10(-5) M) relaxed to histamine (10(-7)-10(-4) M), and the sensitivity of this relaxation in ear arteries, but not in femoral arteries, increased at 24 degrees C. The relaxation of ear and femoral arteries to histamine was not modified by endothelium removal, L-NAME (10(-5) M) or meclofenamate (10(-5) M), but it was blocked by cimetidine (10(-6) M) at 37 degrees C and 24 degrees C. These results suggest: (1) ear and femoral arteries have contracting H1 and relaxing H2 receptors, probably located on smooth musculature, and (2) cooling reduces the contraction and increases the relaxation of cutaneous arteries to histamine: the reduction of this contraction could be caused by an augmented availability of endothelial nitric oxide, and the increment of this relaxation could be caused by an augmented sensitivity of H2 receptors of smooth musculature induced by cooling. These features do not seem to occur in deep vessels.

Kinetic mode switch of rat brain IIA Na channels in Xenopus oocytes excised macropatches

Na currents recorded from outside-out macropatches excised from Xenopus oocytes expressing the alpha subunit of the rat brain Na channel IIA show at least two distinguishable components in their inactivation time course, with time constants differing about tenfold (tau h1 = approx. 150 microseconds and tau h2 = approx. 2 ms). In excised patches, the inactivation properties of Na currents changed with time, favoring the faster inactivation kinetics. Analysis of the fast and slow current kinetics shows that only the relative magnitudes of tau h1 and tau h2 components are altered without significant changes in the time constants of activation or inactivation. In addition, voltage dependence of both activation and steady-state inactivation of Na currents are shifted to more negative potentials in patches with predominantly fast inactivation, although reversal potentials and valences remained unaltered. We conclude that the two inactivation modes discerned in this study are conferred by two states of Na channel the interconversion of which are regulated by an as yet unknown mechanism that seems to involve cytosolic factors.

Characterization of synaptically elicited GABAB responses using patch‐clamp recordings in rat hippocampal slices.

1. Tight-seal, whole-cell voltage clamp recording techniques were used to characterize monosynaptically evoked GABAB currents in adult rat brain slices maintained at 34-35 degrees C. Responses were recorded from granule cells of the dentate gyrus following the blockade of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-, D-2-amino-5-phosphonovaleric acid (D-AP5)- and picrotoxin-sensitive fast synaptic transmission, so that the remaining synaptic currents could be studied in isolation. 2. Under these conditions, stimulation in the molecular layer elicited a slow outward current which was blocked by the selective GABAB antagonist CGP 35348 in a concentration-dependent manner (200-800 microM). This current was absent in recordings made with pipettes containing 10-15 mM of the lidocaine derivative QX-314 or when caesium was substituted for K+. 3. Increasing the [K+]o e-fold (from 2.5 to 6.8 mM) shifted the reversal potential of the GABAB current from -97.9 to -73.2 mV, as predicted by the Nernst equation. Peak conductance was constant, but in 6.8 mM [K+]o at voltages hyperpolarized to EK (equilibrium potential for potassium), a small outward rectification was evident. 4. The time course of the current could be described by fourth-power exponential activation kinetics with double exponential inactivation. At 34-35 degrees C, the average activation time constant (tau m) was 45.2 ms, while the two inactivation time constants (tau h1 and tau h2) were 110.2 and 516.2 ms, with corresponding weighting factors (wh1 and wh2) of 0.84 and 0.16, respectively. The Q10 (temperature coefficient) values for these time constants were between 1.82 and 2.31. Neither tau m, nor tau h1 and tau h2 were voltage dependent in the range from -45 to -95 mV. 5. Paired-pulse depression of the GABAB current was studied by giving identical conditioning and test stimuli over a wide range (50-5000 ms) of interstimulus intervals (ISIs). The maximal depression (48%) occurred at 200 ms ISI, and the depression lasted for over 5 s. The magnitude of paired-pulse depression was not dependent on the postsynaptic membrane potential. 6. Application of the competitive antagonist CGP 35348 such that the peak current was diminished by approximately 50% had no effect on the activation or inactivation kinetics of the current. Similarly, during paired-pulse depression the kinetics of test currents were identical to those of conditioning currents. These findings support the hypothesis that the mechanism responsible for paired-pulse depression involves a reduction in neurotransmitter release without postsynaptic alterations in K+ channel activation/inactivation kinetics.(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of Cerebral Venous Congestion on the Pressure-Volume Index in the Evaluation of Intracranial Pressure Dynamics

Translocation of cerebrospinal fluid (CSF) between the intracranial and spinal subarachnoid space was blocked by ligating the cervical spinal core in eight cats under pentobarbital and nitrous oxide anesthesia, and the effects of cerebral venous congestion on the pressure-volume index (PVI), a measure relating the change in intracranial volume, and the logarithm of intracranial pressure (ICP) were evaluated. The changes in the volume-pressure response (VPR), a measure of intracranial elastance, were calculated simultaneously. Cerebral venous congestion was induced by lowering the head relative to the level of the heart by tilting the trunk of the animals to 20 degrees below horizontal. The presence of venous congestion was confirmed by an increase in the sagittal sinus pressure (SSP). The body position was shifted from horizontal prone (H1 group) to head-down tilt (D1 group) in four animals (group 1) and from head-down tilt (D2 group) to horizontal prone (H2 group) in the other four animals (group 2), and PVI and VPR were determined in each group. The changes in ICP and SSP with change of body position in group 1 were not significantly different from those in group 2, with both pressures changing by 7-8 mm Hg. PVI showed no significant differences between the H1 group and H2 group or between the D1 group and D2 group. The mean (+/- SEM) PVI for all measurements in the head-down tilt position (D1 and D2 groups) was significantly higher (0.50 +/- 0.02 ml; p < 0.01) than in the horizontal position (H1 and H2 groups; 0.35 +/- 0.02 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

A fast transient potassium current in thalamic relay neurons: kinetics of activation and inactivation.

1. Whole-cell voltage-clamp techniques were used to record K+ currents in relay neurons (RNs) that had been acutely isolated from rat thalamic ventrobasal complex and maintained at 23 degrees C in vitro. Tetrodoxin (TTX; 0.5 microM) was used to block Na+ currents, and reduced extracellular levels of Ca2+ (1 mM) were used to minimize contributions from Ca2+ current (ICa). 2. In RNs, depolarizing commands activate K+ currents characterized by a substantial rapidly inactivating (time constant approximately 20 ms) component, the features of which correspond to those of the transient K+ current (IA) in other preparations, and by a smaller, more slowly activating K+ current, "IK". IA was reversibly blocked by 4-aminopyridine (4-AP, 5 mM), and the reversal potential varied with [K+]o as predicted by the Nernst equation. 3. IA was relatively insensitive to blockade by tetraethylammonium [TEA; 50%-inhibitory concentration (IC50) much much greater than 20 mM]; however, two components of IK were blocked with IC50S of 30 microM and 3 mM. Because 20 mM TEA blocked 90% of the sustained current while reducing IA by less than 10%, this concentration was routinely used in experiments in which IA was isolated and characterized. To further minimize contamination by other conductances, 4-AP was added to TEA-containing solutions and the 4-AP-sensitive current was obtained by subtraction. 4. Voltage-dependent steady-state inactivation of peak IA was described by a Boltzman function with a slope factor (k) of -6.5 and half-inactivation (V1/2) occurring at -75 mV. Activation of IA was characterized by a Boltzman curve with V1/2 = -35 mV and k = 10.8. 5. IA activation and inactivation kinetics were best fitted by the Hodgkin-Huxley m4h formalism. The rate of activation was voltage dependent, with tau m decreasing from 2.3 ms at -40 mV to 0.5 ms at +50 mV. Inactivation was relatively voltage independent and nonexponential. The rate of inactivation was described by two exponential decay processes with time constants (tau h1 and tau h2) of 20 and 60 ms. Both components were steady-state inactivated with similar voltage dependence. 6. Temperature increases within the range of 23-35 degrees C caused IA activation and inactivation rates to become faster, with temperature coefficient (Q10) values averaging 2.8. IA amplitude also increased as a function of temperature, albeit with a somewhat lower Q10 of 1.6. 7. Several voltage-dependent properties of IA closely resemble those of the transient inward Ca2+ current, IT. (ABSTRACT TRUNCATED AT 400 WORDS)

Histamine influences the expression of the interleukin-6 receptor on human lymphoid, monocytoid and hepatoma cell lines

Based on our earlier data on the enhancing effect of histamine on the action of interleukin-6 (IL-6), we have studied the molecular mechanisms of these interactions. The effect of histamine was investigated on the binding of 125I-IL-6 by B lymphoma cell line CESS, monocytoid cell line U937 and hepatoma cell line HepG2. Histamine increases the IL-6 binding by CESS cells and inhibits that by U937 and HepG2 cells. Using H1 receptor (cetirizin and loderix) and H2 receptor (cimetidine and ranitidine) specific antagonists, an H1-dependent stimulation of IL-6 binding by CESS cells was found. In contrast, down-regulation of IL-6 binding by histamine was clearly mediated through H2 receptors. On U937 cells, using a monoclonal antibody reacting with the 80 kd chain of the human IL-6 receptor, and H2-receptor mediated inhibition of IL-6 receptor expression was found by FACS analysis.

Vowel acoustics in cochlear implant patients

Acoustic parameters were measured for vowels spoken in /hVd/ context by three postlingually deafened cochlear implant recipients. Two female subjects became deaf in adulthood; the male subject, in childhood. Recordings were made before and at intervals following processor activation. The measured parameters included formant frequencies, F0, SPL, duration, and amplitude difference between the first two harmonic peaks in the log magnitude spectrum (H1–H2). A number of changes were observed from pre‐ to post‐implant, with intersubject differences. The male subject showed changes in F1, vowel durations, and F0. These changes were consistent with one another; however, they were not necessarily in the direction of normalcy. On the other hand, the female subjects showed changes in F2, vowel durations, F0, and SPL, which were in the direction of normal values and, for some parameters, tended to enhance phonemic contrasts. For all three subjects, H1–H2 changed in a direction that was consistent with previously mad...

Role of histamine receptors in rabbit pancreatic exocrine secretion stimulated by cholecystokinin and secretin

An investigation was made of the effects of H1 and H2 receptor agonists and antagonists on rabbit pancreatic exocrine secretion stimulated by secretin and cholecystokinin (CCK). The H1 agonist 2-thiazolylethylamine elicited dose-dependent increases in the rate of secretion. Increases in pancreatic juice flow and enzyme output were also noted after H2 antagonist cimetidine. In contrast, the H1 antagonist chlorpheniramine and H2 agonist dimaprit caused reductions in flow and enzyme output. The results suggest that H1 receptors have stimulative effects and H2 receptors have inhibitory effects on exocrine rabbit pancreas.

Protective Potential of Colostrum and Early Milk Against Prospective Influenza Viruses

The incidence of infectious disease is markedly reduced in breast-fed infants yet the association of breastfeeding with reduced respiratory illness is less marked even though controlled studies have indicated a protective capability. Non-specific inhibitors (NSI) in colostrum occur naturally and may be atavistic remnants now present in man as natural resistant factors. This study was done to discover if NSI activity for avian influenza viruses (believed by some to be the precursors to pandemic influenza viruses with hemagglutinin subtypes H1 H2 and H3 in humans) occurs in colostrum and early milk. 72 primiparous and multiparous Chinese women who were long term residents of central Hong Kong and had minimal contact with animals were studied. The colostrum and early milk contained varying levels of NSI activity in the hemagglutination inhibition tests but had little viral infectivity neutralizing (VN) activity in ovo assays. 5 of 12 samples lacking detectable NSI did have VN activity and this activity was isolated with the lipid soluble fraction of the breast milk. The ability of colostrum and early milk to neutralize the potentially pandemic H4 influenza subtype emphasizes the variety of protective factors to be found in colostrum and milk and the importance of breastfeeding.

Experimental study of the evolution of a solitary wave at an abrupt junction

This paper describes physical and numerical experiments that were carried out to investigate the scattering of nonbreaking solitary waves of moderate amplitude on encountering an abrupt discontinuity in depth from h1 to h2. It is shown that in the neighborhood of the step from deeper to shallower depth the wave amplitude undergoes a rapid evolution which depends on the amount of reflection and energy losses and on dispersive and nonlinear wave effects. On the shallower shelf, the wave amplitude reaches a minimum value after the step. It is proposed that the wave characteristics (shape and volume) recorded at this point be used to predict the far field wave evolution on the shelf. From the experimental results an evolution modes diagram is drawn which distinguishes four types of wave evolution on the shelf: (1) fission, (2) fission and peaking of the first soliton, (3) transition, and (4) plunging. The diagram includes lines of constant breaking index ab/h2, where ab is the breaking wave amplitude and h2 is the shelf depth. Following Mei (1985), an energy loss coefficient fe is presented. For large values of a1/(h1–h2), the experimental data conform with the values given by the steady state formula of Daily and Harleman (1966).

A representation of recursively enumerable languages by two homomorphisms and a quotient

A new representation for recursively enumerable languages is presented. It uses a pair of homomorphisms and the left (or right) quotient: For each recursively enumerable language L one can find homomorphisms h1, h2: ∑∗A → ∑∗B, such that w ∈ ∑∗L is a word in L if and only if w =h1(α)h2(α) for some α∈∑+A. (Or, each recursively enumerable language can be given by L = O(h1h2) ∩ ∑∗L, where O(h1h2) is the so-called right overflow languaged defined as O(h1h2) = {h1(x)h2(x); x ∈ ∑∗A}.)

Implication of Prostaglandins and Histamine H 1 and H 2 Receptors in Radiation-Induced Temperature Responses of Rats

Exposure of rats to 1-15 Gy gamma radiation (60Co) induced hyperthermia, whereas 20-200 Gy induced hypothermia. Exposure either to the head or to the whole body to 10 Gy induced hyperthermia, while body-only exposure produced hypothermia. This observation indicates that radiation-induced fever is a result of a direct effect on the brain. The hyperthermia due to 10 Gy was significantly attenuated by the pre- or post-treatment with a cyclooxygenase inhibitor, indomethacin. Hyperthermia was also altered by the central administration of a mu-receptor antagonist naloxone but only at low doses of radiation. These findings suggest that radiation-induced hyperthermia may be mediated through the synthesis and release of prostaglandins in the brain and to a lesser extent to the release of endogenous opioid peptides. The release of histamine acting on H1 and H2 receptors may be involved in radiation-induced hypothermia, since both the H1 receptor antagonist, mepyramine, and H2 receptor antagonist, cimetidine, antagonized the hypothermia. The results of these studies suggest that the release of neurohumoral substances induced by exposure to ionizing radiation is dose dependent and has different consequences on physiological processes such as the regulation of body temperature. Furthermore, the antagonism of radiation-induced hyperthermia by indomethacin may have potential therapeutic implications in the treatment of fever resulting from accidental irradiations.

Inactivation of sodium channels in isolated myocardial mouse cells

Inactivation of sodium currents is investigated in single myocardial mouse cells by the use of a one suction pipette voltage clamp technique. Semilogarithmic plots of the decay phase of sodium currents show two phases and analysis yields a fast (tau h1) and a slow (tau h2) time constant. At increased depolarization the contribution of tau h2 is decreased. Increasing the temperature from 22.0 +/- 0.5 degrees C to 36.5 +/- 0.5 degrees C influences tau h1 and tau h2 to the same extent. The Q10 values were 2.28 +/- 0.32 for tau h1 and 2.46 +/- 0.35 (mean +/- SD) for tau h2. Between -50 and -20 mV the time course of current decay is substantially faster than inactivation induced by prepulses. Onset of inactivation by the prepulse protocol needs two time constants (tau c1, tau c2) for a satisfactory description. Both decrease steeply with increasing depolarization. For small depolarizations, tau c2 values are in the range of several seconds. Recovery from inactivation by short prepulses (40 ms) could be described by two exponentials (tau r1, tau r2). For longer prepulses (1,000 ms) a very slow component, tau r3, was observed indicating a history dependence of inactivation. Delay time constants for the onset of inactivation (tau dc) are determined between -50 and -20 mV. The more depolarizing voltages generate smaller delay times (0.55 +/- 0.10 ms at -20 mV, mean +/- SD) but larger deviations from the exponential time course. Delay in recovery from inactivation (time constant tau dr) has the value 2.0 +/- 0.7 ms (mean +/- SD) at -80 mV and decreases at more hyperpolarizing potentials. The remaining series resistance at maximum compensation was calculated as 80 k omega. Its influence on the sensitive delay in the double pulse inactivation is discussed.

Cell-attached patch clamp measurement of macroscopic rapid inward sodium current in cultured heart cell reaggregates

A megaohm seal, cell-attached patch clamp technique utilizing plastic suction pipettes for measuring macroscopic rapid inward sodium current (INa) was applied to cell membrane patches 30 to 100 micron2 in area at the periphery of reaggregates of myocardial cells from newborn rats cultured for 3 to 7 days. The reaggregates were composed of about 20 to several thousand of electrically well-coupled cells, the latter forming spheroidal reaggregates with a diameter of maximally 300 microns. This system was shown to guarantee satisfactory voltage-clamp control during ionic current measurements. The time and voltage dependence of the INa recorded during periods of up to 90 min was similar to that observed in single cardiac cell preparations from adult rats. INa inactivation was described by two time constants (tau h1, and tau h2). For maximal INa tau h1 and tau h2 had values of 1.5 +/- 0.25 ms and 8.7 +/- 3.9 ms (n = 4), respectively. The time course for recovery of INa from inactivation at the reaggregate resting potential exhibited also two time constants (tau re1 = 9.8 +/- 3 ms, tau re2 = 193 +/- 50 ms, n = 5). Estimated current density was about 10 pA/micron2. The concentration of tetrodotoxin needed to reduce maximal INa by 75% was 85 times lower in the reaggregates than it was in freshly isolated heart muscle cells from adult rats. The present system offers a combination of features that should make it well-suited for the study of both short- and long-term effects on the sodium channels in neonatal heart cells: Easy handling of the object, great electric stability, high time and amplitude resolution during ionic current measurements, and viability for at least one week.

The effect of temperature on Na currents in rat myelinated nerve fibres

Voltage clamp experiments were performed in single myelinated nerve fibres of the rat and the effect of temperature on Na currents was investigated between 0 degrees C and 40 degrees C. The amplitude of the peak Na current changed with a Q10 = 1.1 between 40 degrees and 20 degrees C and with a Q10 = 1.3 between 20 degrees and 10 degrees C. Below 10 degrees C the peak Na current changed with a Q10 = 1.9. The temperature coefficient for time-to-peak (tp), the measure for Na activation, and tau h1 and tau h2, the time constants for Na inactivation changed throughout the temperature range. Q10 for all of these kinetic parameters increased from 1.8-2.1 between 40 degrees and 20 degrees C to 2.6-2.7 between 20 degrees and 10 degrees C. Below 10 degrees C Q10 increased to 3.7 for tau h1 and tp, and to 2.9 for tau h2. When the series resistance artifacts were minimized by addition of 6 nM TTX, the Q10's at T less than 10 degrees C were 2.9-3.0. When the temperature was decreased from 20 degrees to 0 degrees C, both the curve relating Na permeability to potential, PNa(V), and the steady state Na inactivation curve, h infinity (V), were reversibly shifted towards more negative potentials by 6 mV and 11 mV, respectively. When the temperature was increased from 20 degrees to 37 degrees C no shifts occurred. The Hodgkin-Huxley rate constants alpha h(V) and beta h(V) were calculated from h infinity (V) and tau h (or tau h1) at 20 degrees and 4 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Hook-associated proteins essential for flagellar filament formation in Salmonella typhimurium.

The hooks of the flagella of Salmonella typhimurium were purified by a newly developed method, using a flaL mutant without a filament, and the hook components were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. As a result, we detected three protein species in addition to hook protein. We call these three proteins hook-associated proteins (HAPs). Their molecular weights were 59,000 for HAP1, 53,000 for HAP2, and 31,000 for HAP3. The HAP1/hook protein/HAP3/HAP2 molar ratio, calculated from their relative amounts and their molecular weights, was 1:10:1.1:0.53. The compositions of HAPs were analyzed in the hooks from the other filamentless mutants which were defective in H1 H2, flaV, flaU, or flaW. Hooks from the H1 H2 mutant had the same HAP composition as hooks from the flaL mutant. Hooks from the flaV mutants contained HAP1 and HAP3. Hooks from the flaU mutants contained HAP1. Hooks from the flaW mutants contained a very small amount of HAP3. From these results, the process of hook morphogenesis and the genes responsible for each step were postulated. Electron micrographs of hooks from the filamentless mutants showed that hooks which contained all three HAPs had a sharp clawlike tip, whereas hooks lacking any HAP had a flat tip. Electron micrographs of hooks treated with antibody against the hook protein showed that each claw-shaped end was not covered with antibody. These results strongly suggest that all three HAPs or at least some of them are located at the claw-shaped end and play an essential role in filament formation.

Fault Topography and Recent Faultings along the Shiroishi-Fukushima Fault System, Northeast Japan

The Shiroishi-Fukushima Fault System, located on the eastern fringe of the southern Ou Backbone Ranges, has been said to be active mainly during late Quaternary (e. g. Matsuda, 1973). Geomorophic surfaces in this area are classified into tweleve surfaces, namely H1 H2, M1, Older mud flow surface, M2, Younger pyroclastic flow surface, L1, L2, L3, L4, Small fan and Alluvial surfaces, descending order. Most of them except lower terraces (L4 and Alluvial surface) were deformed by many active faults. In order to consider a characteristics of recent faultings, the author investigated geology and topography, especially deformed landforms, of the western margins of the Shiroishi Basin, Kosugo Lowland and Fukushima Basin. The findings can be summarized as follows.1) The Shiroishi-Fukushima Fault System, 50km in length, is consisted of twentyone reverse faults in the NNE-SSW, NE-SW or E-W directions (Fig. 6).2) This fault system can be divided into four fault groups; Kosugo faults, Kori faults, Niwasaka faults and Sahara faults.3) The formative periods of several surfaces were dated by radiocarbon method. Developing above M2 surface and Younger pyroclastic flow surface are older than 35, 000 yr B. P. The formative periods of L1 surface is about 20, 000 yr B. P. That of L3 is about 5, 000 yr B. P. Other surfaces also can be distinguished in chronologic order.4) Judging from the periods of most recent faulting in this fault system, it was not all of the faults had been active at the same time. That is to say, Kosugo faults and Kori faults in the northern part of this fault system (1-14 fault) had been active after the formative period of L3 surface before that of Alluvial surface. On the other hand, Niwasaka faults and Sahara faults in the southern part (15-21 fault) had not been active since the formative period of L3 surface.