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J Jing

Publications and source records attributed to J Jing.

At least 55 records · Page 3Linked to original sources
PubMed1997

Serotonin-immunoreactivity in peripheral tissues of the opisthobranch molluscs Pleurobranchaea californica and Tritonia diomedea.

The distribution of serotonin (5-HT)-immunoreactive elements in peripheral organs of the sea-slugs Pleurobranchaea californica and Tritonia diomedea was studied in cryostat sections. For Pleurobranchaea, 5-HT-immunoreactive (5-HT-IR) neuron cell bodies were found only in the central nervous system (CNS); 5-HT-IR cell bodies were not observed in foot, tentacles, rhinophores, oral veil, mouth, buccal mass, esophagus, gills, salivary glands, skin, reproductive system, and acidic glands, nor in peripheral tentacle and rhinophore ganglia. However, 5-HT-IR neuronal processes were widely distributed in these structures and the patterns of 5-HT-IR elements were characteristic for each particular peripheral tissue. 5-HT-IR elements were most dense in the sole of the foot and the reproductive system, followed by rhinophores, tentacles, oral veil, mouth, buccal mass, and esophagus. The sensory epithelium of rhinophores, tentacles, and mouth showed a highly structured glomerular organization of 5-HT-IR fibers, suggesting a role for 5-HT in sensory signaling. A much lower density of 5-HT-IR innervation was observed in gills, skin, salivary, and acidic glands. 5-HT-IR was observed in neuropil of tentacle and rhinophore ganglia with many transverse 5-HT-IR axons running to peripheral sensory areas. The distribution of 5-HT-IR elements in Tritonia was similar to that of Pleurobranchaea. A significant suggestion of the data is that central serotonergic neurons may modulate afferent pathways from sensory epithelia at the periphery.

Animals↗
PubMed1997

Inactivation of a voltage-dependent K+ channel by beta subunit. Modulation by a phosphorylation-dependent interaction between the distal C terminus of alpha subunit and cytoskeleton.

Kv1.1/Kvbeta1.1 (alphabeta) K+ channel expressed in Xenopus oocytes was shown to have a fast inactivating current component. The fraction of this component (extent of inactivation) is increased by microfilament disruption induced by cytochalasins or by phosphorylation of the alpha subunit at Ser-446, which impairs the interaction of the channel with microfilaments. The relevant sites of interaction on the channel molecules have not been identified. Using a phosphorylation-deficient mutant of alpha, S446A, to ensure maximal basal interaction of the channel with the cytoskeleton, we show that one relevant site is the end of the C terminus of alpha. Truncation of the last six amino acids resulted in alphabeta channels with an extent of inactivation up to 2.5-fold larger and its further enhancement by cytochalasins being reduced 2-fold. The wild-type channels exhibited strong inactivation, which could not be markedly increased either by cytochalasins or by the C-terminal mutations, indicating that the interaction of the wild-type channels with microfilaments was minimal to begin with, presumably because of extensive basal phosphorylation. Since the C-terminal end of Kv1.1 was shown to participate in channel clustering via an interaction with members of the PSD-95 family of proteins, we propose that a similar interaction with an endogenous protein takes place, contributing to channel connection to the oocyte cytoskeleton. This is the first report to assign a modulatory role to such an interaction: together with the state of phosphorylation of the channel, it regulates the extent of inactivation conferred by the beta subunit.

Amino Acid Sequence↗
PubMed1996

Deletion of the N-terminus of a K+ channel brings about short-term modulation by cAMP and beta 1-adrenergic receptor activation.

On deletion of the N-terminus of RCK1 K+ channel, acute modulation of the channel by cAMP-elevating treatments is revealed. This modulation is studied in Xenopus oocytes using two-electrode voltage-clamp, site-directed mutagenesis, and SDS-PAGE analyses. Treatments by Sp-8-Br-cAMPS, a membrane-permeant cAMP analog, and by isoproterenol, a beta 1-adrenergic receptor (beta 1R) agonist, both increased the current amplitudes with no effect on the voltage dependency of activation. The effect of isoproterenol was blocked by coexpression of either G alpha S or G alpha i3 proteins. The channel protein is phosphorylated on the Sp-8-Br-cAMPS treatment at Ser446; however, a phosphorylation-deficient variant in which this site has been altered is still modulated by Sp-8-Br-cAMPS and isoproterenol. Expression of the full-length channel with Kv beta 1.1 auxiliary subunit renders the channel at the same modulation as that of the truncated one. Taken together, the RCK1 channel can be acutely modulated by cAMP and beta 1R activation possibly through protein kinase A (PKA) activation, but not through direct channel phosphorylation; the involvement of the N-terminus in this modulation is discussed.

Adrenergic beta-Agonists↗
PubMed1996

Safety and immunogenicity of a recombinant hepatitis B vaccine administered to infants at 2, 4 and 6 months of age. The Kaiser-UCLA Vaccine Study Group.

A recombinant hepatitis B vaccine was administered to over 5000 infants in a prospective, randomized and blinded study. Infants were given either recombinant hepatitis B vaccine (Engerix-B, SmithKline Beecham Pharmaceuticals, 10 micrograms dose-1) or a Haemophilus influenzae type b (Hib) conjugate vaccine at 2, 4 and 6 months of age simultaneously with diphtheria-tetanus-pertussis and oral polio vaccines. Adverse reactions were ascertained by parental reports and interviews, and review of medical records. Blood specimens collected from 269 infants given hepatitis B vaccine were assayed for antibody to hepatitis B surface antigen (anti-HBs) by enzyme immunoassay. Infants given hepatitis B vaccine experienced low rates of adverse reactions that were similar or lower than the rates in infants given Hib conjugate vaccine. The geometric mean anti-HBs concentrations were 9.6 mIU ml-1 after one dose, 333 mIU ml-1 after two doses and 1812 mIU ml-1 after three doses (99% had levels > or = 10 mIU ml-1). Antibody responses to diphtheria and tetanus toxoids were unaffected by simultaneous administration of hepatitis B or Hib conjugate vaccine. Engerix-B vaccine was safe and immunogenic when given with other routine childhood immunizations at 2, 4 and 6 months of age, and should provide long-term protection against hepatitis B virus infection.

Antibodies, Bacterial↗
PubMed1995

Interstitial space, electrical resistance and ion concentrations during hypotonia of rat hippocampal slices.

1. The degree to which mammalian brain cells swell in hypotonic environments has not previously been determined. We exposed hippocampal tissue slices prepared from anaesthetized rats to artificial cerebrospinal fluid from which varying amounts of NaCl had been deleted. Interstitial volume (ISV) change was determined from the volume of dilution of the marker ions tetramethylammonium (TMA+) or tetraethylammonium (TEA+). Tissue electrical resistance was measured as the voltage generated by constant current pulses. 2. ISV decreased as a function of lowered extracellular osmolality (osmotic pressure, pi o), indicating cell swelling. After reaching a minimum, ISV recovered partially, suggesting regulatory volume decrease of cells. After restoring normal pi o the ISV expanded, indicating post-hypotonic cell shrinkage. The electrical resistance of the tissue (Ro) increased when pi o was lowered, due to the reduced ionic strength, as well as restricted ISV. 3. To control for low NaCl concentration, reduced NaCl was replaced by mannitol or fructose. In isosmotic, NaCl-deficient solution, ISV showed inconsistent change, and Ro corrected for ionic strength tended to decrease. 4. Extracellular K+ concentration decreased slightly in low pi o except when spreading depression caused it to increase. Extracellular Ca2+ concentration decreased substantially, consistently and reversibly. Administration of isosmotic low-NaCl concentration solutions caused a similar decrease in extracellular Ca2+ concentrations. We propose that low Na+ concentration in extracellular fluid impaired the extrusion of Ca2+. 5. In severely hypotonic solution, ISV was reduced to 25% of its control volume, corresponding to a mean cell volume increase of at least 11%, probably more. From plotting relative changes in ISV against osmolarity we concluded that, within the range tested, hypotonic cell swelling was not opposed by the close approach of plasma membranes of neighbouring cells.

Animals↗
PubMed1995

Factors influencing reflectance spectrophotometric measurements of gastrointestinal mucosal blood flow.

Although the technique of endoscopic reflectance spectrophotometry has been applied in clinical studies, factors that modify the reproducibility of measurements have not been assessed systematically. To determine the limitations of the technique, measurements were made while endoscopic light intensity, systemic oxygen saturation, and orientation of the measuring probe were varied. The effects of hemorrhagic hypotension and exposure of the mucosa to 10% dextrose were also studied. When a large number (n = 480) of measurements in the human colon were considered, endoscopic light significantly decreased the index of oxygen saturation (ISO2) and increased the index of hemoglobin concentration (IHB). The decrease in ISO2, however, was small and unlikely to be of clinical importance despite being statistically significant. In one subject with chronic lung disease and baseline hypoxemia, administration of supplemental oxygen significantly increased oxygen saturation at the finger tip as measured by an oximeter and ISO2 of the buccal mucosa as measured by reflectance spectrophotometry. Varying the angle between the measuring probe and the gastric mucosa in rats from 90 degrees to 60 degrees did not affect ISO2 or IHB measurements. At 45 degrees, however, IHB but not ISO2 was significantly increased. Ischemia subsequent to induction of hemorrhagic hypotension and hyperemia induced by administration of 10% dextrose could be demonstrated reproducibly. We conclude that by lowering the intensity of endoscopic light and providing supplemental oxygen, errors in the measurement of IHB and ISO2, respectively, can be minimized. Minor deviations from the perpendicular orientation do not significantly affect ISO2 and IHB measurements. Attention to these details enhances the accuracy of endoscopic reflectance spectrophotometric recordings of ISO2 and IHB in clinical studies.

Animals↗
PubMed1995

Neuronal elements that mediate escape swimming and suppress feeding behavior in the predatory sea slug Pleurobranchaea.

1. The white, bilaterally paired A1 interneurons of the cerebropleural ganglion of Pleurobranchaea californica fire rhythmic bursts of action potentials during escape swimming behavior. We studied the role of the A1s in swimming behavior and pattern generation in whole animal and isolated CNS preparations. 2. The escape swim is a cyclic sequence of dorsal and ventral flexions of the body. During the swim, A1 bursts precede and accompany the dorsal flexion phase of the cycle. Hyperpolarization of A1 to prevent spike activity interrupts swimming behavior in the whole animal and fictive swimming in the isolated CNS. Stimulated A1 activity was not observed to cause swimming in whole animals, and was only occasionally sufficient to trigger fictive swimming activity in the isolated CNS. 3. In quiescent whole animal preparations, stimulation of a single A1 normally causes a single dorsal flexion followed by body flexion to the side contralateral to the stimulated cell; characteristically, A1 spike activity stimulates feedback inhibition coinciding with the end of dorsal flexion and the onset of contralateral flexion. 4. A1 spike activity suppresses feeding behavior and causes proboscis retraction in whole animal preparations induced to feed. A1 activity also suppresses fictive feeding driven by stimulation of the critical phasic paracerebral neurons (PCps) of the motor network of feeding in the isolated CNS. Concomitantly, A1 spikes cause potent inhibition of the PCp interneurons. 5. The A1s are specifically excited by noxious mechanical and chemical stimuli, but are not affected by feeding stimuli or the occurrence of feeding behavior. 6. We conclude that the A1 neurons are elements of an escape swimming pattern generator, and that they are probably homologous to the similar C2 neurons of the nudibranch Tritonia diomedea. One of their functions outside of generating the swim pattern may be the suppression of feeding behavior in response to noxious stimulation. These observations provide a neural mechanism for the original observations of the dominance of escape swimming behavior over feeding.

Action Potentials↗
PubMed1994

Interstitial volume changes during spreading depression (SD) and SD-like hypoxic depolarization in hippocampal tissue slices.

1. Relative interstitial volume (ISV) was estimated from the concentration changes of iontophoretically administered tetramethyl- and tetraethylammonium (TMA+ and TEA+). Spreading depression (SD) was provoked by high K+, and hypoxic SD-like depolarization (HSD) was induced by withdrawing oxygen. 2. Probe ion concentrations increased dramatically and about equally during SD and HSD, except that in a few hypoxic trials signals became transiently smaller than control. Interstitial volume appeared to decrease on the average by approximately 70%. 3. The ISV that remains patent in CA1 region at the height of SD is < 4% of total tissue volume. Probe ions may occasionally have passed through cell membranes for a short time during hypoxic SD.

Animals↗
PubMed1993

Blockade of antidromic invasion of CA1 pyramidal cells during synaptic activation of NMDA receptors.

We have studied in situ the excitability state of the axon-soma membrane of CA1 pyramidal cells in the rat during synaptic activation of N-methyl-D-aspartate (NMDA) receptors. Repetitive activation (3-5 Hz) of Schaffer collaterals provoked a NMDA receptor-mediated component in the field excitatory postsynaptic potential (fEPSP) within 15 s. The generation of this component follows a characteristic self-limiting cycle, vanishing after 6-10 s. When alvear shocks were paired to the orthodromic volleys, the antidromic population spike (PS) was completely abolished only if the NMDA receptor-mediated fEPSP had occurred. This blockade of antidromic invasion lasted for 120-150 ms after each orthodromic shock. A reduction in the safety factor for axon-soma transmission is presumed during NMDA receptor synaptic activation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1993

Role of calcium channels in spreading depression in rat hippocampal slices.

In the CA1 region of rat hippocampal slices, spreading depression (SD) was provoked by a brief period of hypoxia or by localized application of high potassium solution. We measured extracellular DC voltage (Vo), extracellular potassium concentration ([K+]o) and/or extracellular Ca2+ concentration ([Ca2+]o). SD was provoked under control conditions and also when voltage-gated Ca2+ channels were blocked by application of 2 mM Ni2+ or Co2+. In some experiments, CPP, DNQX, or the two together were also applied to block glutamate receptor-coupled channels. When SD was provoked by hypoxia, these treatments significantly increased the latency of SD onset and decreased the amplitudes of the accompanying delta Vo, delta [Ca2+]o and delta [K+]o. Hypoxia-induced SD was never blocked completely, however and delta [Ca2+]o was reduced at most by 50%. When SD was provoked by application of high K+ solution near the recording site, Ni2+ or Co2+ partially suppressed the Vo and [Ca2+]o shifts but did not block SD altogether. When high K+ solution was applied at a distance, Ni2+ or Co2+ blocked the propagation of SD to the recording site. We conclude that during SD, a significant proportion of the calcium ions flowing into neurons does not pass through voltage-gated or glutamate receptor-linked channels.

Animals↗
PubMed1993

Effectiveness and safety of an Haemophilus influenzae type b conjugate vaccine (PRP-T) in young infants. Kaiser-UCLA Vaccine Study Group.

OBJECTIVE: To study the safety, immunogenicity, and protective efficacy of the Haemophilus influenzae capsular polysaccharide tetanus conjugate vaccine (PRP-T). DESIGN: Randomized, double-blind, controlled clinical trial. SETTING: Southern California Kaiser-Permanente Health Plan. PARTICIPANTS: 10,317 infants 6 to 15 weeks of age, with no known immune dysfunction, exposure to hepatitis B, or contraindication to diphtheria-tetanus-pertussis (DTP) vaccination were enrolled between August 1989 and September 1990. INTERVENTION: Infants were randomized to receive either PRP-T or a recombinant hepatitis B control vaccine (in addition to DTP) at approximately 2, 4, and 6 months of age. OUTCOME MEASURES: Adverse reactions occurring during the first 72 hours and between doses (including hospitalizations and outpatient visits) were measured using parental reporting/interviews and review of records. Invasive disease caused by H influenzae was ascertained from the time of enrollment until December 31, 1990. RESULTS: In October 1990, the study was prematurely terminated because of licensure of other H influenzae vaccines recommended for routine infant use. The rates of systemic and local reactions occurring within 72 hours of each vaccine dose were generally similar for infants given PRP-T and hepatitis B, but some reaction rates (local reactions, fever > or = 102 degrees F, irritability, crying) were significantly higher in the PRP-T group. In the month following receipt of vaccine, PRP-T-vaccinated infants experienced five definite seizures compared with three in the hepatitis B control group. Within 48 hours of vaccination, three seizures (two definite and one possible), which were thought to be related to vaccination, occurred in the PRP-T group, compared with none in the control group (P < .13). Overall morbidity, mortality, and hospitalization rates were similar in the two vaccine groups. Three cases of invasive disease caused by H influenzae occurred in the control group; none occurred in the PRP-T group. CONCLUSIONS: The PRP-T vaccine is safe and appears to be effective in preventing invasive disease caused by H influenzae type b.

Bacterial Vaccines↗
PubMed1993

Cellular physiology of hypoxia of the mammalian central nervous system.

We began this brief review with a condensed summary of the responses of mammalian central neurons to hypoxic insult and then described our recent studies aimed at solving the biophysical basis of these responses. We distinguished three main phases of cerebral hypoxia. First, withdrawal of oxygen is rapidly followed by failure of synaptic transmission. Second, there is massive depolarization of cells, resembling the SD of Leão. Timely reoxygenation can still restore function. If, however, SD-like depolarization continues beyond a critical time, the third phase, irreversible loss of responsiveness, sets in. Cell loss is initially highly selective. Finally, upon reoxygenation, some neurons, which at first appear normal, then undergo a sequence of changes leading to delayed neuron degeneration. The principal cause of early synaptic failure is the depression of synaptic potentials. This can be attributed to reduced release of transmitter substance, in turn caused by failure of the opening of voltage-dependent calcium channels in presynaptic terminals. Calcium-channel failure is probably caused either by a rise of intracellular free calcium activity, depletion of adenosine triphosphate (ATP) levels in presynaptic terminals, or a combination of both. Conduction block in presynaptic fiber terminals can, in some situations, contribute to synaptic failure. In some (postsynaptic) neuron membranes, conductance for potassium increases, raising the firing threshold and hastening the failure of excitatory synaptic transmission. Hypoxic SD-like depolarization is a complex but stereotyped and explosive event. The longer the depolarization lasts, the smaller the chance for functional recovery after reoxygenation. The least likely to recover are those cells that undergo SD the earliest. Prolonged intracellular accumulation of free calcium, admitted into the cells by the SD-like membrane change, plays a key role in causing neuron damage (Fig. 8). Some antagonists of NMDA receptors and blockers of sodium, calcium, and potassium channels influence the onset and magnitude of SD-like hypoxic depolarization, but no known drug prevents it. The irreversible neuron damage that occurs during hypoxia should be distinguished from delayed postischemic injury that occurs after initial apparent recovery. The delayed process can proceed even in the controlled environment of isolated hippocampal tissue slices, but it can be prevented in vitro by NMDA receptor antagonist drugs. In the clinical management of cerebral ischemia not only the intrinsic neuronal degenerative process, but also the deteriorating extracellular milieu, needs to be treated, and the latter may not be improved by NMDA receptor blockade.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Mechanism of spreading depression: a review of recent findings and a hypothesis.

Spreading depression of Leão (SD) can be provoked by numerous nonspecific mechanical, electrical, and chemical stimuli. A similar, if not identical, phenomenon can be provoked by hypoxia. SD is characterized by drastic depolarization of neurons, severe reduction of membrane resistance, and redistribution of ions across cell membranes. Glial cells also depolarize but retain membrane resistance. Tetraethylammonium hastens the onset of hypoxic SD but reduces the sustained potential shift and K+ outflow from cells; 4-aminopyridine also accelerates SD but has no effect on the voltage shift. N-Methyl-D-aspartate receptor antagonists delay the onset of SD, while nickel and cobalt reduce the amplitude of SD-related redistribution of Ca2+. Yet, no specific blocker of SD has been found. Microdialysis of high-K+ solution in hippocampal CA1 region induces recurrent waves of SD propagating semi-independently in adjacent tissue layers, and a prolonged unstable depressed state that has not previously been described. Neither the release of K+ ions nor of glutamate is the unique agent of SD propagation. On the basis of recent findings we propose a hypothetical sequence of events that reconcile many of the previously seemingly paradoxical observations.

Animals↗
PubMed1991

Lasting neuron depression induced by high potassium and its prevention by low calcium and NMDA receptor blockade.

Spreading depression-like neuron depolarization was induced in CA1 of hippocampal tissue slices by irrigation with artificial cerebrospinal fluid containing 133.5 mM K+ for 8-40 min. Evoked responses disappeared during irrigation with high-K+ solution. Following 8-20 min irrigation orthodromic responses showed a triphasic recovery cycle: early partial return with evidence of neuron hyperexcitability, then secondary depression and finally slow partial recovery. After 30 min or more of high-K+ exposure, ortho- and antidromic responses remained severely depressed for at least 5.5 to 6.5 h. When, however, the tissue was deprived of calcium, or N-methyl-D-aspartate (NMDA) receptors were blocked by 10 microM 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), then evoked responses recovered partially after a 30- or 40-min high-K+ exposure. Post-exposure hyperexcitability was not prevented by CPP. We conclude that prolonged depolarization by elevated K+ causes irreversible neuron damage, which is triggered or accelerated by influx of calcium ions into neurons, mediated in part by NMDA receptor activation.

Animals↗
PubMed1991

Ion channel involvement in hypoxia-induced spreading depression in hippocampal slices.

Rat hippocampal tissue slices were made hypoxic in control medium and in medium containing the ion channel blockers tetraethylammonium (TEA), 4-aminopyridine (4-AP), or tetrodotoxin (TTX). Postsynaptic evoked potentials, extracellular DC potential Vec, and in some experiments extracellular potassium concentration [K+]o were monitored in stratum pyramidale of the CA1 region. TEA (10 mM) decreased the latency of hypoxia-induced spreading depression (SD), and reduced the amplitudes of the changes in Vec and [K+]o. 4-AP (50 microM) also decreased the latency of SD but had no effect on the Vec shift. In most slices, TTX (1 microM) increased SD latency but had no effect on the Vec shift. In some slices, TTX blocked the occurrence of SD.

4-Aminopyridine↗
PubMed1991

Effect of 5-hydroxytryptamine and its antagonists on colonic smooth muscle of the rabbit.

The effect of 5-hydroxytryptamine (5HT) was studied in circular and longitudinal muscle from the proximal and distal colon of New Zealand white rabbits. 5HT stimulated a dose-dependent isometric contraction of distal and proximal circular muscle that was greater than in distal longitudinal muscle (P less than 0.01). 5HT did not stimulate taenia coli longitudinal muscle. The EC50 for 5HT stimulation of distal circular muscle (-7.0 +/- 0.1), distal longitudinal muscle, and proximal circular muscle was similar. Methysergide dose-dependently inhibited the 5HT stimulation of both proximal and distal circular muscle. The IC50 for methysergide inhibition of 5HT (5 x 10(-7) M) stimulation was -5.5 +/- 0.2. Ketanserine and ICS 205-930 did not inhibit 5HT stimulation of colonic muscle. Tetrodotoxin (TTX) decreased the potency, but not the efficacy of 5HT stimulation of proximal and distal circular muscle. Atropine decreased the potency (EC50 = -6.6 +/- 0.1) (P less than 0.05) and the efficacy by 40%. Electrical field stimulation (EFS) caused an on-contraction and off-contraction of distal circular muscle and an on-contraction of proximal circular muscle. 5HT decreased the off-contraction of the distal circular muscle but did not affect the on-contraction of the other muscle strips. 5HT receptor antagonists did not affect EFS of the tissue. The studies suggest: (1) 5HT stimulates circular colonic muscle with greater efficacy than longitudinal muscle, (2) 5HT stimulates circular muscle through a 5HT1 receptor, (3) there is atropine-sensitive and atropine-insensitive 5HT stimulation of circular colonic muscle, (4) 5HT inhibits neurons responsible for the off-contraction in distal circular muscle without affecting the on-contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗