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X Zong

Publications and source records attributed to X Zong.

31 records · Page 2Linked to original sources
PubMed1998

Speckle reduction and contrast enhancement of echocardiograms via multiscale nonlinear processing.

This paper presents an algorithm for speckle reduction and contrast enhancement of echocardiographic images. Within a framework of multiscale wavelet analysis, we apply wavelet shrinkage techniques to eliminate noise while preserving the sharpness of salient features. In addition, nonlinear processing of feature energy is carried out to enhance contrast within local structures and along object boundaries. We show that the algorithm is capable of not only reducing speckle, but also enhancing features of diagnostic importance, such as myocardial walls in two-dimensional echocardiograms obtained from the parasternal short-axis view. Shrinkage of wavelet coefficients via soft thresholding within finer levels of scale is carried out on coefficients of logarithmically transformed echocardiograms. Enhancement of echocardiographic features is accomplished via nonlinear stretching followed by hard thresholding of wavelet coefficients within selected (midrange) spatial-frequency levels of analysis. We formulate the denoising and enhancement problem, introduce a class of dyadic wavelets, and describe our implementation of a dyadic wavelet transform. Our approach for speckle reduction and contrast enhancement was shown to be less affected by pseudo-Gibbs phenomena. We show experimentally that this technique produced superior results both qualitatively and quantitatively when compared to results obtained from existing denoising methods alone. A study using a database of clinical echocardiographic images suggests that such denoising and enhancement may improve the overall consistency of expert observers to manually defined borders.

Algorithms↗
PubMed1998

[The analysis of the causes of postoperative deaths in intracranial meningiomas in the elderly department of neurosurgery].

OBJECTIVE: Analysis the postoperative death reason of elderly patients with meningioma. METHOD: We analysised the death reason of 18 elderly patients with meningioma who died after operation in recent 16 years, Reviewing of document is also included in this review study. RESULT: 7 patients died of postoperative cerebral infarction (3 cases sufferd heamorrage of gastric-instinal tract). 3 cases died of cardiac infarction. 2 cases renal failure and 2 cases preoperative cerebral hernia. 1 case inhalant pneumonia, 1 case postoperative cerebral hematoma, 1 case hypothamamus injury and 1 case respiration failure. CONCLUSION: Operation is not prompt to patients whose KS scale is less than 50.

Acute Kidney Injury↗
PubMed1997

Blockade of neuromuscular transmission by huwentoxin-I, purified from the venom of the Chinese bird spider Selenocosmia huwena.

Huwentoxin-I (HWTX-I) is a neurotoxic peptide purified from the venom of the Chinese bird spider Selenocosmia huwena. The effects of HWTX-I on neuromuscular transmission of vertebrate skeletal muscle have been investigated by means of twitch tension and electrophysiological techniques. On isolated mouse phrenic nerve-hemidiaphragm preparations, HWTX-I blocked the twitch responses to indirect, but not to direct, muscle stimulation. The time needed for complete block of the neuromuscular transmission was dose dependent. The transmission could be mostly restored by prolonged repeated washing with Tyrode's solution. If the preparation was pretreated with D-tubocurarine and then immersed in a mixed solution of D-tubocurarine and HWTX-I, the washout time necessary to restore the neuromuscular transmission was significantly decreased. Intracellular recording at the end-plate region of frog sartorius muscle revealed that HWTX-I could synchronously reduce the amplitude of the acetylcholine potential induced by ionophoretic application of acetylcholine as well as the amplitude of the end-plate potential evoked by nerve stimulation. Both of these effects eventually disappeared; however, both could be restored by prolonged washing. Experiments on Xenopus embryonic myocytes indicated that HWTX-I reduced the open probability of acetylcholine-induced channel activity, and finally blocked the channel. All of these results demonstrated that HWTX-I was a peptide neurotoxin and the postsynaptic nicotinic acetylcholine receptor was its site of action.

Acetylcholine↗
PubMed1996

Molecular cloning and expression of the Modulatory subunit of the cyclic nucleotide-gated cation channel.

The cDNA of three variants of a cyclic nucleotide-gated (CNG) channel modulatory subunit (CNG4c-CNG4e) has been cloned. CNG4c, CNG4d, and CNG4e differ slightly from each other within an amino-terminal sequence that was originally reported as part of the bovine retinal glutamic acid-rich protein (GARP). The core region of CNG4 is homologous to the second subunit of the human rod photoreceptor channel (hRCNC2b), suggesting that both proteins are alternatively spliced products of the bovine and human homologue of the same gene. CNG4 transcripts are present in retina, testis, kidney, heart, and brain. Expression of CNG4 in HEK293 cells did not lead to detectable currents. Coexpression of CNG4 with the principal subunit of the bovine testis CNG channel (CNG3) resulted in currents which differed in several aspects from that induced by CNG3 alone. The heterooligomeric CNG3/CNG4 and the homooligomeric CNG3 channels were modified by Ca2+-calmodulin and some calmodulin antagonists. The results suggest that CNG4 forms functional heterooligomeric channels with CNG3 in vitro and probably also in intact tissues.

Amino Acid Sequence↗
PubMed1996

Ca(2+)-dependent inactivation of the class C L-type Ca2+ channel is a property of the alpha 1 subunit.

The stably expressed Ca2+ channel alpha 1C-a and alpha 1C-b subunit were used to investigate the molecular basis for Ca(2+)-dependent inactivation of the L-type current. The Ba2+ current (IBa) of both channels had similar kinetics and inactivated with one time constant of about 400 ms at +20 mV, whereas the Ca2+ current (ICa) could be fitted only with a bi-exponential function. The fast (tau f) and the slow (tau s) time constant were about 20 ms and 400 ms, respectively. The inactivation of ICa strongly depended on the entry of Ca2+ as shown by prepulses and variation of the intracellular Ca2+ chelator. Coexpression of the alpha 1C subunits with the auxiliary alpha 2/delta and beta subunits accelerated the voltage-dependent but not the Ca(2+)-dependent inactivation of the channels. These results suggest that the alpha 1C subunit of L-type Ca2+ channels itself mediates the Ca(2+)-dependent inactivation of the current.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Molecular diversity of cyclic nucleotide-gated cation channels.

Cyclic nucleotide-gated cation channels (CNG channels) form a multi-gene family consisting of at least five distinct members (CNG1-5). Expression studies have indicated that only CNG1-3 are able to form functional homooligomeric channels. Although structurally related, the cDNAs of CNG4-5 fail to induce cyclic nucleotide-dependent currents when expressed alone. However, when co-expressed with CNG1-3 they confer some of the physiologically observed properties of native CNG channels which are absent from the homooligomeric CNG1-3 channels. CNG channels are expressed in several tissues and cell types pointing to a general function of these channels in a wide variety of cellular systems. There is now increasing evidence that a major function of CNG channels may consist in providing a second messenger-regulated pathway for Ca2+ influx.

Amino Acid Sequence↗
PubMed1995

On the regulation of the expressed L-type calcium channel by cAMP-dependent phosphorylation.

The Ca2+ channel subunits alpha 1C-a and alpha 1C-b were stably expressed in Chinese hamster ovary (CHO) and human embryonic kidney (HEK) 293 cells. The peak Ba2+ current (IBa) of these cells was not affected significantly by internal dialysis with 0.1 mM cAMP-dependent protein kinase inhibitor peptide (mPKI), 25 microM cAMP-dependent protein kinase catalytic subunit (PKA), or a combination of 25 microM PKA and 1 microM okadaic acid. The activity of the alpha 1C-b channel subunit expressed stably in HEK 293 cells was depressed by 1 microM H 89 and was not increased by superfusion with 5 microM forskolin plus 20 microM isobutyl-methylxanthine (IBMX). The alpha 1C-a.beta 2.alpha 2/delta complex was transiently expressed in HEK 293 cells; it was inhibited by internal dialysis of the cells with 1 microM H 89, but was not affected by internal dialysis with mPKI, PKA or microcystin. Internal dialysis of cells expressing the alpha 1C-a.beta 2.alpha 2/delta channel with 10 microM PKA did not induce facilitation after a 150-ms prepulse to +50 mV. The Ca2+ current (ICa) of cardiac myocytes increased threefold during internal dialysis with 5 microM PKA or 25 microM microcystin and during external superfusion with 0.1 microM isoproterenol or 5 microM forskolin plus 50 microM IBMX. These results indicate that the L-type Ca2+ channel expressed is not modulated by cAMP-dependent phosphorylation to the same extent as in native cardiac myocytes.

Animals↗
PubMed1994

Another member of the cyclic nucleotide-gated channel family, expressed in testis, kidney, and heart.

Cyclic nucleotide-gated cation channels are essential in visual and olfactory signal transduction. An additional member of the cGMP-gated channel family, termed CNG-3, has been cloned from bovine kidney. Its deduced amino acid sequence is 60% and 62% identical with the CNG-channel proteins from bovine rod outer segment and bovine olfactory epithelium, respectively. Northern analysis and sequences amplified by the PCR showed that the CNG-3 mRNA is present in testis, kidney, and heart. Calcium permeated the expressed channel in the presence of extracellular Mg2+ and Na+ at membrane potentials from -100 to +45 mV. It is likely that CNG-3 protein is responsible for cGMP-induced Ca2+ entry in cells other than sensory cells.

Animals↗
PubMed1994

Augmentation of calcium channel currents in response to G protein activation by GTP gamma S in chick sensory neurons.

G protein-mediated downregulation of current through neuronal voltage-gated Ca2+ channels is well known. We now report that G protein activation by GTP gamma S increases the Ba2+ conductance of high-voltage-activated Ca2+ channels of chick dorsal root ganglion (DRG) cells. This occurs with a delay of minutes during which the channels are inhibited by the activated G proteins. The Ba2+ current (IBa) showed an absolute enhancement by a factor near 2, 15 min after GTP gamma S application. However, by utilizing prior observations of the voltage dependence of the inhibitory action we could demonstrate that the G protein-inhibited component of IBa, was still present. Moreover, the achieved amount of IBa disinhibition showed little variation throughout the experiments. This indicates that the increase in IBa is not due to a relief of the inhibitory action of activated G proteins but to the slow appearance of a distinct upregulating action, probably through a different pathway. Augmentation of IBa was eliminated by pertussis toxin (PTX) infusion or pretreatment, but was also prevented by intracellularly infusing protein kinase C (PKC) inhibitors together with GTP gamma S. The upregulation of neuronal Ca2+ channels thus appears to be exerted through a messenger pathway upstream of PKC activation that involves G proteins. Augmentation of Ca2+ currents (ICa) was observed only with strong intracellular [Ca2+] buffering, which suggests a control of the upregulating action by even moderate increase in intracellular [Ca2+].

Animals↗
PubMed1993

Whole cell and single channel analysis of the kinetics of glycine-sensitive N-methyl-D-aspartate receptor desensitization.

1. The kinetics of glycine-sensitive, N-methyl-D-aspartate (NMDA) receptor desensitization were investigated in cultured neurones with the patch clamp technique. 2. The degree of fast NMDA-receptor desensitization was inversely related to glycine concentration. Thus, increasing concentrations of glycine from 30 nM to 2.5 microM potentiated desensitized NMDA responses (873% +/- 101%) to a greater degree than peak responses (260% +/- 27%). 3. The desensitization was due to a decrease in the affinity of glycine for the strychnine-insensitive, glycine modulatory site (glycineB site) following activation of the NMDA-receptor complex. Thus, the A50 for glycine in potentiating peak responses (77 nM, 95% confidence limited 58-104 nM) was five fold lower than that for plateau responses (399 nM, 340-468 nM). 4. The rate of desensitization was related to glycine concentration such that a reciprocal plot of desensitization rate (1/tau S-1) against glycine concentration had a slope of 9.5* 10(6) M-1 S-1. 5. Recovery from desensitization following step increases in glycine or L-alanine concentration in the continuous presence of NMDA (200 microM) reflected the association kinetics of the glycineB agonist used. 6. The rate and degree of NMDA receptor desensitization was independent of holding potential. 7. NMDA receptor desensitization was also evident at the single channel level. 8. The glycineB antagonist 7-chlorokynurenic acid (7-Chl-Kyn 3 and 10 microM) concentration-dependently induced an identical form of desensitization in the presence of 1 microM glycine. 9. In contrast, the competitive NMDA antagonist (+/-)-amino-phosphonovaleric acid (APV 30 to 300 microM) concentration-dependently antagonized and slowed the onset kinetics of NMDA responses.

2-Amino-5-phosphonovalerate↗
PubMed1984

Antimuscarinic action of quinidine on the heart? A study in myocardial preparations from cat hearts.

Quinidine exerts anticholinergic effects which have been ascribed to atropine-like properties of the drug. We have examined the effects of acetylcholine on the force of contraction in isolated heart muscle preparations from cats and compared the inhibitory effects of atropine with those of quinidine. The effects of acetylcholine were antagonized competitively in the presence of atropine. The Schild-plot yielded a straight line; the slope was not significantly different from unity. In the presence of quinidine, the concentration-response curve of acetylcholine was shifted to the right as with atropine, however, the Schild-plot yielded a regression line which was not linear; the slope was statistically different from unity. The negative inotropic response to acetylcholine in cat ventricular heart muscle (revealed in the presence of the phosphodiesterase inhibitor, papaverine) was antagonized by atropine but not influenced by quinidine. We conclude that the inhibitory action of quinidine on the effects of acetylcholine in atrial heart muscle is not merely antimuscarinic. The antagonistic effects of acetylcholine and quinidine on atrial heart muscle may also be due to the opposite effects of the drugs on potassium conductance of the myocardial cell membrane.

Acetylcholine↗
PubMedDate not supplied

Evaluating the evidence of effectiveness for preventive interventions: using a registry system to influence policy through science.

In order to deal with the serious problems of drug use, delinquency, and mental health problems in this country, policy makers, communities, practitioners, and advocates need to identify prevention programs that have empirical support and at the same time meet their own community needs regarding acceptability, cost, and training, and supervision. An "evidence-based" approach to prevention, one that identifies the scientific knowledge about what prevention programs work, for whom, and under what circumstances, should play a critical part in this process. The premise of this evidence-based approach is that the wide adoption of prevention programs that have been found to be successful in rigorous evaluations, will lead to successful population-based prevention strategies. A web-based registry, or database that describes the available scientific information on individual preventive trials, would be of high potential use to policy makers engaged in prevention planning for their communities. This presentation describes a model registry based on descriptions of 167 preventive trials aimed at children aged 0-6. Empirical findings are presented regarding two critical components of the registry, the measurement of the quality of the trial and the strength of evidence for a beneficial effect produced by each intervention. Implications for the use of such a registry are also discussed.

Adolescent↗