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The impact of sluice operations on the distribution and fate of perfluoroalkyl acids (PFAAs) remains poorly understood. In this study, the distribution of PFAAs was investigated in water, suspended particles, sediment, and pore water from the upstream and downstream sections of six sluice gates along the Wangyu River, China. The target PFAAs were widely distributed in the dissolved phase (∑PFAAs: 447.61 ± 180.26 ng/L), particle phase (∑PFAAs: 2040.95 ± 1870.88 ng/g dw), sedimentary phase (∑PFAAs: 39.42 ± 35.38 ng/g dw), and pore water phase (∑PFAAs: 8172.54 ± 4278.60 ng/L). Our data suggest predominant detections of short-chain PFAAs such as perfluorobutanoic acid (PFBA) and perfluorohexanoic acid (PFHxA) in the four environmental media. Sediment pore water appeared as an essential repository and potential source for PFAA re-release to the river environment. The levels of PFAAs in the dissolved and suspended particle phase upstream of the sluices were significantly lower than those downstream, while the situation in the sediment and pore water phase was the opposite. Sluice operation caused PFAA redistribution among the multi-environment media but did not change the PFAA composition, which had the significant effect on the partition behavior of perfluoroalkyl carboxylic acids (PFCAs) between particles and water, as well as changed the migration pattern of PFOA, PFNA and PFOS from equilibrium to the migration state. Quantitative prediction models were developed for simulating fate of PFAAs in gate-controlled river, and the major factors affecting the distribution and fate of PFAAs were identified. Our findings provide insights into the redistribution mechanisms of PFAAs and an understanding of their environmental fate.

Arachidonic acid (AA) and its metabolites are involved in the development and progression of inflammation and tumors in various tissues. We investigated the protein-protein interaction network (PPIN) of key enzymes in AA metabolism and their interacting proteins, as well as their expression patterns in different types of esophageal disease, involving esophagitis, Barrett’s esophagus, adenocarcinoma and squamous cell carcinoma. PPINs were constructed to illustrate the key enzymes and their interacting proteins along the metabolic cascade. The network also showed key enzymes that could connect or cross-talk with at least one partner protein. The inflammation-related gene RELA (NF-kB) was found to interact with both PLA2G4A and ALOX5. Expression levels of the PPIN proteins, as well as their expression correlations, in different esophageal diseases were analyzed and integrated into the PPIN to illustrate a dynamic change. At least six significant pairs of expression relationships were identified across different esophageal diseases. The expression levels of eight enzymes (ALOX5, ALOX5AP, CYP2C8, CYP4F11, LTA4H, PLA2G4A, CYP2D6, PTGES2) correlated with the survival time of ESCC patients. In summary, we constructed an AA metabolic PPIN to explore AA metabolism-related gene expression patterns in esophageal diseases, showing their dynamic change and potential for therapeutic targeting from inflammation to cancer.

Background: Lysyl oxidase-like 2 (LOXL2), a copper-dependent enzyme of the lysyl oxidase family, promotes tumor progression and metastasis. We previously revealed that the tumor-promoting role of LOXL2 is mediated by perturbing the architecture of the actin cytoskeleton in esophageal squamous cell carcinoma (ESCC). However, the molecular mechanisms underlying LOXL2-driven ESCC progression remain elusive, and the cytoskeletal proteins that directly interact with LOXL2 remain uncharacterized. Methods: Knockdown LOXL2 in ESCC cells was used by a lentivirus shRNA targeting LOXL2 and analyzed by RNA-sequencing and bioinformatics analysis. Proteomic analysis following by co-immunoprecipitation and immunofluorescence were applied for identification and validation of interacting partners of LOXL2 and its splicing isoform L2Δ13. Cell migration and invasion were measured by wound healing and transwell assays. By risk score calculations, immunohistochemistry of tissue microarrays were adopted to evaluate the prognosis of ESCC patients. Results: We found that knockdown of LOXL2 in ESCC cells suppresses cell migration and invasion, whereas re-expressions of LOXL2 and its non-enzymatic splicing isoform L2Δ13 rescue these cell behaviors. Silencing of LOXL2 inhibits filopodia formation, and induces changes in the expression of cytoskeleton-associated genes. Our interactome analysis identified four actin-binding proteins, i.e. ezrin (EZR), facsin (FSCN1), heat shock protein beta-1 (HSPB1) and tropomodulin-3 (TMOD3), as novel interactors of LOXL2 and L2Δ13. These novel LOXL2/L2Δ13 interaction networks carry important prognostic values in ESCC, as molecular signatures of combinations of LOXL2/L2Δ13 and their cytoskeletal interactors are associated with clinical outcome in ESCC patients. Mechanistically, the ezrin-LOXL2 interaction promotes PKCα-stimulated phosphorylation of ezrin at Thr 567 (T567), an essential residue for ezrin activation, which enhances cell motility and cell invasion in ESCC. Correlating with this, double-high expression of LOXL2 and phosphorylated ezrin-T567 predicts significantly shorter overall survival in ESCC patients. Conclusion: In conclusion, our findings have uncovered a novel molecular mechanism underlying the tumor-promoting role of cytoplasmic LOXL2, which may open new avenues for the therapeutic targeting of LOXL2 in ESCC. (This study is supported by the Natural Science Foundation of China (No. 81472613) and Li Ka Shing Foundation). Citation Format: Xiuhui Zhan, Jiwei Jiao, Haifeng Zhang, Jianzhong He, Runliu Li, Haiying Zou, Zhiyong Wu, Shaohong Wang, Xiue Xu, Jianyi Wu, Liandi Liao, Yinwei Cheng, Kai Zhang, Gera Neufeld, Liyan Xu, Enmin Li. Cytoplasmic LOXL2 regulates actin cytoskeletal organization in esophageal squamous cell carcinoma progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4594.

Thirteen novel chiral ionic liquids (CILs) containing the (−)-menthyl group can be easily prepared from isonicotinic acid with yields of 35–90%. The properties and characterization of these compounds were discussed and the alternation of optical rotation was analyzed.

Antidepressant drug (R)-rolipram was readily prepared on a large scale from isovanilline via a succinct route. The key reaction was carried out using a 1 mol% loading of nickel(II)-bis[(S,S)-N,N′-dibenzylcyclohexane-1,2-diamine]Br2 complex as the catalyst. The ee% could reach to 99%, and the catalyst could be recovered and used in the next reaction cycle with high ee%.

We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations.The nature of the reentrant circuit that underlies VT during acute MI is not well understood.Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI.Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P.01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P.05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P.05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P.05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT.The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.

This study reports the comparative quantitative, morphological, and electrophysiological properties of two pacemaker cell types, spider and spindle-shaped cells, isolated from the rabbit sinoatrial node. Isolated nodal cells were studied with perforated and ruptured patch whole cell recording techniques. The basic spontaneous cycle length of the spider cells was 381 ± 12 ms, and the basic spontaneous cycle length of the spindle cells was 456 ± 17 ms ( n = 12, P < 0.05). The spider cells had a more positive maximum diastolic potential (−54 ± 1 mV) compared with the spindle cells (−68 ± 1mV, P < 0.05). The overshoot and action potential amplitudes were also smaller in the spider cells. The hyperpolarization-activated inward ( I f) current density, measured from their tail currents, was 15 ± 1.3 pA/pF for the spider cells and 9 ± 0.7 pA/pF for the spindle cells ( P < 0.01). I f current activation voltage was more positive in the spider cells than the spindle cells. Isoproterenol (1 μM) decreased the spontaneous cycle length of the spider cells by 28 ± 3% and the spindle cells by 20 ± 1.5% ( P < 0.05). Acetylcholine (0.5 μM) hyperpolarized the membrane potential of the spider cells to −86 ± 0.7mV and the spindle cells to −76 ± 0.8 mV ( P < 0.05). In summary, there are at least two distinct pacemaker cell types in the sinus node with different electrophysiological characteristics.

Ezrin is involves in multiple cancer cell functions. In this study, differentially expressed genes (DEGs) identified from mRNA expression profiling following Ezrin knockdown in esophageal squamous cell carcinoma (ESCC), were analyzed by multiple bioinformatics methods for a comprehensive understanding. Gene Ontology enrichment found significant terms related to immunity, stimulus response, extracellular matrix-binding and signal transduction. Functional Annotation Chart showed except GO categories, these DEGs were annotated by 72 functional category terms. Subpathway analyses revealed the DEGs were involved in 36 subpathways, overwhelming the traditional pathway enrichment. Promoter analyses showed specific sequence patterns and transcription factors correspond to the co-downregulation and co-upregulation of DEGs. MNB1A, DOF2, PBF, YY1, PRRX2, UBX and ARNTAHR co-regulate the downregulated genes, whereas GATA2, ZNF42, deltaEF1, MYCN and ARNT co-regulate the upregulated genes. This paper provides a workflow for a better understanding the roles of Ezrin knockdown in ESCC by the bioinformatics analyses of its DEGs.

The antidepressant drug (R)-rolipram (VI) is readily prepared on kilogram scale from isovanillin via a straightforward route.

Sarcolemmal Phospholipid Alterations and Arrhythmogenesis. Myocardial ischemia in vivo is associated with dramatic electrophysiologic alterations that occur within minutes of cessation of coronary flow and are rapidly reversible with reperfusion. This suggests that subtle and reversible biochemical alterations within or near the sarcolemma may contribute to the electrophysiologic derangements. Our studies have concentrated on two amphipathic metabolites, long-chain acylcarnitines and lysophosphatidylcholine (LPC). which have been shown to increase rapidly in ischemic tissue in vivo and to elicit electrophysiologic derangements in normoxic tissue in vitro. Incorporation of these amphiphiles into the sarcolemma at concentrations of 1 to 2 mole %, elicits profound electrophysiologic derangements analogous to those observed in ischemic myocardium in vivo. The pathophysiological effects of the accumulation of these amphiphites are thought to be mediated by alterations in the biophysical properties of the Sarcolemmal membrane, although there is a possibility of a direct effect upon ion channels. Inhibition of carnitine acyltransferase I (CAT-I) in the ischemic cat heart was found to prevent the increase in long-chain acylcarnitines and LPC and to significantly reduce the incidence of malignant arrhythmias including ventricular tachycardia and fibrillation. This review focuses on the electrophysiologic derangements that are observed during early ischemia and presents data supporting the concept that accumulation of these amphiphiles within the sarcolemma contributes to these changes. The potential contribution of these amphiphiles to the increases in extracellular potassium and intracellular calcium are examined. Finally, recent data pertaining to the accumulation of long-chain acylcarnitines on cell-to-cell uncoupling are presented. In addition to the events reviewed here, there are many other alterations that occur during early myocardial ischemia, but the results from multiple studies over the past two decades indicate that the accumulation of these amphiphiles contributes importantly to arrhythmogenesis and that development of specific inhibitors of CAT-I or phospholipase A may be a promising therapeutic strategy to attenuate the incidence of lethal arrhythmias associated with ischemic heart disease in man.

Electrophysiological and biochemical sequelae of myocardial ischemia occur within minutes of the onset of myocardial ischemia in vivo. Both conduction delay and conduction block occur rapidly within the same time interval as the accumulation of long-chain acylcarnitines. In the present study, double whole-cell voltage-clamp procedures were used to assess the influence of long-chain acylcarnitines on gap junctional conductance in isolated pairs of canine ventricular myocytes. Long-chain acylcarnitine (5 microM) decreased gap junctional conductance from 153 to 48 nS in a time-dependent and reversible manner. Although the amplitude of junctional current was reduced by 68%, the current continued to demonstrate a linear current-voltage relation. The extent of endogenous accumulation of long-chain acylcarnitines in junctional regions of the sarcolemma was assessed in isolated myocytes in which endogenous free, short-chain, and long-chain acylcarnitine pools had been equilibrated with [3H]carnitine. Under normoxic conditions, long-chain acylcarnitines were not detectable in junctional sarcolemma of myocytes as assessed using electron microscopic autoradiography. Exposure of myocytes to hypoxia (PO2, < 15 mm Hg) for 10 minutes resulted in the preferential accumulation of endogenous long-chain acylcarnitines in junctional sarcolemma (173 +/- 5 x 10(5) molecules/microns 3), a concentration that was sevenfold greater than that found in nonjunctional sarcolemma. Therefore, endogenous long-chain acylcarnitines accumulate preferentially in junctional regions of the sarcolemma during short intervals of hypoxia. Exogenously supplied long-chain acylcarnitines can markedly decrease cellular coupling in a reversible manner, suggesting that this amphiphile may contribute to the marked slowing in conduction velocity in the ischemic heart in vivo, not only by suppressing the rapid Na+ inward current directly, as has been shown previously, but also by decreasing cellular coupling.

“I should know this!” These words, or ones conveying a similar meaning, are often uttered by a physician who is given a sick patient's electrocardiogram (ECG) that shows a wide QRS complex tachycardia (WCT). Despite a wealth of established criteria, the diagnosis of a WCT remains difficult for the practicing physician. Making the correct diagnosis is important not only for choosing appropriate initial therapy to terminate the arrhythmia episode but also for subsequent management. For example, many physicians assume that a WCT in a patient who is alert and hemodynamically stable must be supraventricular tachycardia (SVT) because “the condition of patients with ventricular tachycardia (VT) is always unstable.” If the rhythm is actually VT in a patient with reduced systolic function and an injection of verapamil is given for treatment of presumed SVT, severe and prolonged hypotension may result, and a stable situation can quickly become very unstable. An incorrect initial diagnosis can also set the wrong course for chronic therapy with potentially disastrous results. Thus, arriving at the correct diagnosis of the cause of WCT is more than an intellectual exercise.

The mechanisms responsible for ventricular tachyarrhythmia (VT) initiation have been studied extensively since the beginning of the last century. Multiple approaches including clinical observations; experiments in vivo, in vitro, and at cellular and genetic levels; theoretical analysis; and numeric simulations have been used. Most VTs are initiated by spontaneous discharge(s) at one or several sites in the ventricle, which can contribute to, or precipitate, reentry that then maintains the VT. Although most VTs occur in abnormal hearts such as in patients with coronary artery diseases, cardiomyopathy, abnormal ionic currents, or other problems, VT can also be functional, occurring in seemingly normal hearts when the conditions for its initiation are met. Because of the possible outcome of sudden cardiac death and the increasingly aging population in the industrialized countries, managing VT is a significant and important clinical task. Understanding the mechanisms of its initiation is one of the key steps in developing clinical strategies to prevent and treat VT. However, the mechanisms of VT initiation are still not fully understood and are the topic for a brief overview in this chapter.

We report the case of a patient in whom transvenous left ventricular pacing lead placement at the time of a biventricular upgrade led to an exacerbation of clinical monomorphic ventricular tachycardia (MVT). At implant, slow left ventricular pacing repeatedly induced sustained MVT. However, testing of the biventricular pacing showed no MVT inducibility, and the system was implanted. The patient was readmitted due to multiple episodes of the MVT observed at implant. The MVT was controlled with pharmacotherapy, allowing the patient to continue with biventricular pacing. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1245-1247, November 2003)

The findings of multiple nondiscrete AV nodal pathways and asymmetric transitional zone provide a biophysical basis for understanding normal and abnormal AV node electrophysiology. Unidirectional block occurring at the transitional zone transforms the nondiscrete pathways model into a classic dual pathways physiology for AVNRT.

摘要 以 2,7-二羟基萘为起始原料, 经与 8-(对甲苯磺酰氧基)-3,6-二氧-1-辛醇醚化, 再与对甲苯磺酰氯酯化得 7, 7 最后 与 2,7-二羟基萘在碳酸铯为碱作用下得基于 2,7-二羟基萘基块新型的冠醚, 三步总收率为 35%. 利用单晶 X衍射研究其 结构, 晶体为三斜晶系, P-1 空间群, a=8.165(3) A, b=13.435(4) A, c=14.083(3) A, γ=64.11(2)°, β=80.40(3)°, γ= 88.19(3)°, V=1368.9(7) A 3 , Z=2, Dc=1.331 g/cm 3 , λ=0.071070 nm, μ(Mo Kα)=1.331 mm -1 Abstract A Novel naphthalene-based crown ether has been synthesized by the etherification of 2,7-dihydroxynaphthalene with 8-tosyloxy-3,6-dioxaoctanol in the presence of K2CO3, followed by reaction with p-toluenesufonyl chloride to give 7. Compound 7 was further reacted with 2,7-dihydroxynaphthalene in the presence of cesium carbonate to give 1 in 38% total yield. Its crystal structure was determined by X-ray diffraction method. The crystal is of triclinic, space group P-1 with a= 8.165(3) A, b=13.435(4) A, c=14.083(3) A, α=64.11(2)°, β=80.40(3)°, γ=88.19(3)°, V=1368.9(7) A 3 , Z=2, Dc=1.331 g/cm 3 , λ=0.071070 nm, μ(Mo Kα)=1.331 mm -1 , Mr=353.22, F(000)=584. The crystal structure of 1 shows that two nap- thalene units are linked two tri(ethylene glycol) bridges to form dinapthalzo(30)crown-8 cavity and one Z-like central cavity with size of ca. 8.2 A×12.0 A. The host 4 was proved to be a efficient host for the complexation with paraquat derivatives in solution by 1 H NMR.

A novel naphthalene-based open-chain crown ether has been synthesized by the etherification of 2-bromo- N-phenylacetamide with 3,6-dibromo-2,7-dihydroxynaphthalene, followed by reduction with sodium borohydride and boron trifluoride ether solution, in 95% total yield. Its crystal structure was determined by X-ray diffraction method. The crystal is of triclinic space group P-1 with a=9.588(3) A, b=10.898(3) A, c=13.060(4) A, α=103.190(4)°, β=93.953(4)°, γ= 115.622(5)°, V=1176.0(6) A 3 , Z=2, Dc=1.571 g/cm 3 , λ=0.71075 A, μ(Mo Kα)=3.472 mm -1 , Mr=353.22 and F(000)= 560. In the structure, one of the N—H groups forms bifurcated N—H…Br and N—H…O hydrogen bonds. These link the molecules into inversion related dimers. The centrosymmetric dimers are aggregated via pairs of C—H…π interactions into two-dimensional sheets parallel to (110). Keywords open-chain crown ethers; synthesis; crystal structure

Long-chain acylcarnitines increase within 2 min in ischemic myocardium in vivo and induce delayed afterdepolarizations (DADs) and complex oscillations of membrane potential in vitro. This study was performed to assess the ionic currents underlying these electrophysiological alterations in isolated rabbit ventricular cells using whole cell voltage-clamp procedures. Palmitoyl carnitine (10 microM, for 6-10 min) elicited a transient inward current (Iti) in the presence of blockade of Ca2+ and K+ channels. The effect of palmitoyl carnitine was reversible after washout (n = 6). The amplitude of Iti was dependent on the amplitude of the preceding depolarization step. Palmitoyl carnitine (10 microM, for > 2 min) also induced another inward current, which was activated spontaneously at potentials between -120 and -20 mV with a linear current-voltage relationship (1.0 +/- 0.1 nA at -80 mV). This current was abolished by replacing extracellular Na+ with tetraethylammonium chloride, indicating that Na+ was the charge carrier. Inactivation of this current was slow (gamma = 885.9 +/- 89.1 ms, n = 12) or incomplete, indicating the appearance of a slow-inactivating Na+ inward current [INa(s)]. Palmitoyl carnitine always induced INa(s) before the appearance of Iti. Intracellular ethylene glycol-bis(beta-amino-ethyl ether)-N,N,N',N'-tetraacetic acid (10 mM) abolished Iti but did not suppress INa(s) (n = 4), indicating that INa(s) was not activated by intracellular Ca2+ (Cai2+). Tetrodotoxin (10 microM) also decreased the amplitude of INa(s). Thus palmitoyl carnitine induces INa(s), which likely leads to an increase in Na+ influx, thereby eliciting an increase in Cai2+ via the Na(+)-Ca2+ exchanger and leading to the development of Iti, DADs, and triggered activity.

Torsades de pointes (TdP) is defined as a polymorphic ventricular tachycardia (VT) with a twisting QRS morphology associated with a prolonged QT interval and/or increased U wave amplitude in the ECG.1,2⇓ Patients with acquired or congenital long-QT syndrome (LQTS) can develop TdP that results in sudden cardiac death. Fifty or more drugs, both typical antiarrhythmic agents such as quinidine as well as other classes of drugs such as some antibiotics, affect membrane ionic currents, prolong the duration of the QT interval in the ECG, and have been associated with the acquired LQTS.3 Similarly, inherited genetic defects in the cardiac membrane ion channels can cause congenital LQTS. Some patients with apparent acquired LQTS may actually have mild congenital forms and remain asymptomatic until exposed to one of the drugs noted above.4 Congenital LQTS can be divided into multiple subtypes depending on the affected membrane ionic currents (eg, LQT1, LQT2, and LQT3 for alterations in I Ks, I Kr, and the inactivation process of I Na+). Due to the possible fatal outcome and involvement of many drugs, it is important to understand the mechanism of TdP, predict its occurrence, and manage it clinically. See p 770 It has been suggested that an early afterdepolarization (EAD) exceeding the activation threshold, arising from the endocardium (including the Purkinje network)5 or from the mid-myocardial region,6 could initiate TdP.2,7⇓ EADs have been observed experimentally in monophasic action potential recordings at multiple epicardial and endocardial sites.8 Increased dispersion of repolarization preceding the TdP induction has been noted in an isolated rabbit heart model of LQT2.9 Long intervals between activations, ie, slow rates, prolong the duration of the action potential and increase the transmural dispersion of …

Long-chain acylcarnitines (LCAC) increase 3.5-fold within 2 min in ischemic myocardium in vivo, and previous studies have suggested, through indirect evidence, that LCAC can stimulate the voltage-dependent L-type Ca2+ current [ICa(L)] in both cardiac and smooth muscle cells. In the present study, whole cell voltage-clamp procedures were performed in isolated adult guinea pig ventricular myocytes to assess the direct effect of LCAC on ICa(L). The intracellular solution contained (in mM) 80 CsCl, 40 K-aspartic acid, and 5 ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Maximal current density of ICa(L) at 0 mV was 10.1 +/- 0.5 pA/pF (n = 22) at extracellular Ca2+ concentration ([Ca2+]o) = 2.7 mM. LCAC induced a concentration (1-25 microM, n = 23)- and time-dependent, reversible decrease in ICa(L). When delivered extracellularly for 10 min, LCAC (5 microM) inhibited the maximal current of ICa(L) by 48.1 +/- 1.3% (n = 9, P less than 0.01) and shifted the half-maximal voltage of steady-state activation and inactivation from -13.1 +/- 0.5 to -6.8 +/- 0.4 mV (n = 4; P less than 0.05) and from -21.8 +/- 0.2 to -16.5 +/- 0.6 mV (n = 4; P less than 0.01), respectively. Intracellular delivery of LCAC (5 microM) also suppressed ICa(L) to a similar degree (47.5 +/- 1.5%, n = 4; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Whole cell voltage-clamp techniques were used to study the effects of extracellular Mg2+ on T- and L-type Ca2+ currents recorded from single atrial myocytes from cat heart. T and L currents were distinguished primarily by their voltage dependence. With 5.4 mM Ca2+ as charge carrier, maximal T- and L-current densities were 1.0 +/- 0.06 and 9.7 +/- 0.4 pA/pF, respectively. Nickel (Ni2+, 50 microM) inhibited maximal T current (-65.6 +/- 5.9%) more than L current (-15.7 +/- 2.4%), and 10 microM cadmium (Cd2+) inhibited L current (-65.5 +/- 5.9%) without significant effect on T current (-8.7 +/- 8.1%). Mg2+ elicited a dose-dependent inhibition of both T and L currents. Mg2+ less than 8.4 mM inhibited T current more than L current. At Mg2+ greater than or equal to 8.4 mM, T-current inhibition reach a plateau at approximately 52%, whereas L current was further inhibited (-65%) at 16.8 mM Mg2+. Mg2+ elicited a dose-dependent positive shift in half-maximal voltages of activation and inactivation for both T and L currents. Mg2(+)-induced inhibition of both T and L currents was greater in lower (2.7 mM) external Ca2+. Finally, 4.2 mM Mg2+ and 50 microM Ni2+ elicited a similar decrease in the late diastolic slope of subsidiary pacemaker action potentials, whereas 10 microM Cd2+ markedly inhibited action potential amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

X-ray generator is mainly used for non-destructive testing, security check areas and so on. In order to accurately adjust cross voltage and through current of the X-ray tube, this paper adopts full-digital PID algorithm to control PWM output waveforms.The tube voltage adjustable range is 40 to 120 kV and the tube current range is 0.1 to 1.5 mA. We can set up work parameters and get the working status by LCD and Console on the generator. It also can be fully controlled by a computer so as to enhance the safety of the operator, simplify operation and so on.

The X-ray source is a key part for public security detection applied in airport, custom and many public security detection places. In this paper, it introduces how to design X-ray source system and its X-ray source controller.

Abstract —The reentrant pathways underlying different types of atrioventricular (AV) nodal reentrant tachycardia have not yet been elucidated. This study was performed to optically map Koch’s triangle and surrounding atrial tissue in an isolated canine AV nodal preparation. Multiple preferential AV nodal input pathways were observed in all preparations (n=22) with continuous (73%, n=16) and discontinuous (27%, n=6) AV nodal function curves (AVNFCs). AV nodal echo beats (EBs) were induced in 54% (12/22) of preparations. The reentrant circuit of the slow/fast EB (36%, n=8) started as a block in fast pathway (FP) and a delay in slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP through the atrial tissue located at the base of Koch’s triangle. The reentrant circuit of the fast/slow EB (9%, n=2) was in an opposite direction. In the slow/slow EB (9%, n=2), anterograde conduction was over the intermediate pathway (IP) and retrograde conduction was over the SP. Unidirectional conduction block occurred at the junction between the AV node and its input pathways. Conduction over the IP smoothed the transition from the FP to the SP, resulting in a continuous AVNFC. A “jump” in AH interval resulted from shifting of anterograde conduction from the FP to the SP (n=4) or abrupt conduction delay within the AV node through the FP (n=2). These findings indicate that (1) multiple AV nodal anterograde pathways exist in all normal hearts; (2) atrial tissue is involved in reentrant circuits; (3) unidirectional block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask the existence of FP and SP, producing continuous AVNFCs.