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Biomedical subjects

W Jin

Publications and source records attributed to W Jin.

At least 127 records · Page 7Linked to original sources
PubMed1995

Influence of the compliance of the pump housing and cannulas of a paracorporeal pneumatic ventricular assist device on transient pressure characteristics.

The dependence of transient pressure characteristics of a ventricular assist device (VAD) on the compliance of its housing and cannulas was investigated in a mock circulation. The peak rate of change of pressure (dP/dtmax) values was greater in the cannulas than other compartments and was associated with valve closure-induced pressure oscillations. When cannula compliance was increased from 0.0057 to 0.0129 cm3/mm Hg, these values decreased by approximately 20%, and outflow cannula pressure oscillation frequency decreased from 17.5 Hz by 35%. This trend was also apparent in the inflow. A VAD housing compliance increase from 0.0162 to 0.0483 cm3/mm Hg caused a dP/dtmax decrease of 30% in both the blood chamber and the outflow cannula. The effect of this change on the inflow was weaker implying that housing absorbs the energy associated with outflow deceleration more effectively than the inflow. These findings suggest that increasing VAD housing and cannulas compliance can improve hydrodynamic performance.

Biocompatible Materials↗
PubMed1995

[Anti-lipid peroxidation effects of sini decoction and its components on ischemic myocardium and the dose- and time-effects].

The complete Sini Decoction can significantly reduce the content of MDA in ischemic myocardium. Single ingredients of the decoction, such as Radix Aconoti Praeparata or Radix Glycyrrhizae, except Rhizoma Zingiberis, also have similar effect but inferior to that of the complete decoction. Under the present conditions of experiment, anti-lipid peroxidation of Sini Decoction is significant at doses ranging from 0.05 to 0.2ml/20g administered for 2-7 days at 0.1ml/(20g.d).

Animals↗
PubMed1994

U73122 inhibits phospholipase C-dependent calcium mobilization in neuronal cells.

The aminosteroid U73122 inhibited phospholipase C (PLC)-mediated intracellular Ca2+ release in differentiated and undifferentiated NG108-15 cells, as well as rat dorsal root ganglion (DRG) neurons grown in primary culture. 1 microM U73122 blocked bradykinin (BK)-induced increases in the intracellular free Ca2+ concentration ([Ca2+]i) measured in single cells with indo-1-based dual emission microfluorimetry. A close structural analog, U73343, was without effect. The effects of U73122 were time and concentration-dependent. 1 microM drug produced half maximal inhibition in approximately 3 min. The IC50 for a 20-min exposure was approximately 200 nM. The effects of the compound were irreversible for the duration of experiments as long as 1 h. Treatment with 1 microM U73122, but not U73343 produced a small but significant increase in [Ca2+]i which resulted from Ca2+ release from an intracellular store. It is not clear whether this [Ca2+]i increase resulted from inhibition of PLC or an action on the store directly. In differentiated NG108-15 cells U73122 blocked completely depolarization-induced Ca2+ influx. In contrast, in DRG neurons U73122 inhibited only slightly voltage-sensitive Ca2+ channels. Thus, we caution that U73122 may not be selective at concentrations required for maximal block of PLC and that the selectivity of U73122 is dependent on cell type. Overall, our results are consistent with U73122 inhibiting PLC in neuronal cells and indicate that under the appropriate conditions, this compound is a useful tool for studying inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ mobilization.

Animals↗
PubMed1994

Experimental investigation of the motions of the pumping diaphragm within a sac-type pneumatically driven ventricular assist device.

The motions of the pumping diaphragm within a sac-type pneumatically driven ventricular assist device (VAD) were monitored non-intrusively using a laser Doppler anemometer (LDA) working in the back-scattering mode. The interaction between the diaphragm and the flow, and the causative factors of the motions were investigated. The motions of a number of points on the diaphragm were determined by analysing the timing of interruption of the Doppler signals due to intrusion of the diaphragm on the LDA sampling volume. The position-time relationships for the identified diaphragm points were then interpolated into two-dimensional surfaces to reconstruct the moving patterns of the diaphragm at selected instants. The motion is strongly affected by the orientation of the device with respect to gravity due to hydrostatic pressure gradients on the liquid side, which are generally large compared with those associated with the fluid accelerations. Hence, during ejection, the part of the diaphragm experiencing the lowest hydrostatic pressure is always set in motion first, while during filling, the part with the highest hydrostatic pressure moves first. Consequences of these non-symmetrical motions on local flow behaviour are discussed, and methods of controlling diaphragm shape during pumping are outlined.

Acceleration↗
PubMed1994

Pressure development within a sac-type pneumatically driven ventricular assist device.

Intrinsic features of the pumping process of a pneumatically driven ventricular assist device (VAD) and the effects of different types of pneumatic drivers upon its performance were investigated in vitro by analysing the pressure distributions within the device and the motions of the prosthetic valves. It was found that the stretching of the flexible, elastic diaphragm in both late systole and diastole initiates a pressure oscillation which directly affects the timing of the pumping process. The timing was also found to be dependent on the length and stiffness of the cannulae which link the VAD to the model circulation system. During the stretch-induced oscillation in late systole, the VAD housing experiences partial collapse due to fluid momentum effects, which tends to increase the effective stroke volume of the device, and reduce the amplitude of the pressure oscillation. Reducing the rising (falling) rate of driving pressures (dpd/dt) may not necessarily reduce the maximum rate of change of the blood chamber pressure (dpch/dtmax) but may upset the stability of the pumping process. This is because a minimum dpch/dtmax exists, which is determined by the stretch-induced oscillation. In order to minimize dpch/dtmax and to provide the device with a stable working condition, dpd/dt should match the dpch/dtmax.

Algorithms↗
PubMed1994

Supravalvular aortic stenosis associated with a deletion disrupting the elastin gene.

Supravalvular aortic stenosis (SVAS) is an inherited vascular disease that can cause heart failure and death. SVAS can be inherited as an autosomal dominant trait or as part of a developmental disorder, Williams syndrome (WS). In recent studies we presented evidence suggesting that a translocation disrupting the elastin gene caused SVAS in one family while deletions involving the entire elastin locus caused WS. In this study, pulsed-field, PCR, and Southern analyses showed that a 100-kb deletion of the 3' end of the elastin gene cosegregated with the disease in another SVAS family. DNA sequence analysis localized the breakpoint between elastin exons 27 and 28, the same region disrupted by the SVAS-associated translocation. These data indicate that mutations in the elastin gene cause SVAS and suggest that elastin exons 28-36 may encode critical domains for vascular development.

Aortic Stenosis, Subvalvular↗
PubMed1994

Opioids mobilize calcium from inositol 1,4,5-trisphosphate-sensitive stores in NG108-15 cells.

Opioids elicit an increase in the intracellular free Ca2+ concentration ([Ca2+]i) in neuroblastoma x glioma hybrid NG108-15 cells, which, depending upon growth conditions, results from either Ca2+ influx in differentiated cells or Ca2+ release from internal stores in undifferentiated cells (Jin et al., 1992). In this report we describe fura-2-based digital imaging studies that demonstrate that opioid-evoked Ca2+ release in these cells results from the activation of phospholipase C (PLC) and subsequent mobilization of the inositol 1,4,5-trisphosphate (IP3)-sensitive store. D-Ala2-D-Leu5-enkephalin (DA-DLE) evoked concentration-dependent increases in [Ca2+]i (EC50 approximately equal to 4 nM). The response was blocked by naloxone (1 microM). In single cells, sequential application of selective opioid agonists (10 nM) evoked responses of the rank order DADLE = D-Pen2, D-Pen5-enkephalin (DPDPE) > trans-(+/-) 3,4-dichloro-N-methyl-N-(2-[1- pyrrolidinyl]cyclohexyl) benzeneacetamide (U50488) > D-ala2, N-Me-Phe4, Gly5-ol-enkephalin (DAMGO), consistent with activation of a delta-opioid receptor. Forty percent (n = 198) of the cells responded to 100 nM DADLE with a net [Ca2+]i increase of 483 +/- 40 nM. Bradykinin (100 nM) elicited a response in 91% of the cells with a mean net amplitude of 707 +/- 36 nM. The DADLE-evoked responses were not blocked by removal of extracellular Ca2+; instead, they were abolished by treatment with 10 nM thapsigargin, an agent that depletes and prevents refilling of IP3-sensitive Ca2+ stores. A 1 microM concentration of U73122, an aminosteroid inhibitor of PLC, completely blocked the DADLE-evoked [Ca2+]i increase, while an inactive analog, U73433, was without effect. To explore the possible role of G-proteins in mediating opioid-induced [Ca2+]i increases in NG108-15 cells, we pretreated cells with pertussis or cholera toxin; pertussis toxin blocked the opioid-induced response while cholera toxin was without effect, consistent with a Gi- or Go-mediated effect. Activation of the opioid inhibitory pathway previously described for these cells appears to stimulate the phosphoinositide (PI) cascade as well. Including the PI cascade among the multiple second messenger systems modulated by opioids may be key to understanding the biochemical events that underlie acute and chronic opioid action.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

Opioid-induced inhibition of voltage-gated calcium channels parallels expression of omega-conotoxin-sensitive channel subtype during differentiation of NG108-15 cells.

Depolarization-induced increases in intracellular free calcium concentration ([Ca2+]i) were measured in single NG108-15 cells using indo-1 based microfluorimetry. In cells differentiated for 6 days in serum-free forskolin (5 microM) supplemented media, application of micromolar concentrations of [D-Ala2-D-Leu5]enkephalin (DADLE) inhibited Ca2+ influx mediated by voltage-gated Ca2+ channels. Inhibition of 50 mM K(+)-induced Ca2+ influx by DADLE was concentration-dependent over the range of 0.1 to 10 microM and blocked by 100 microM naloxone. Differentiation increased the amplitude of depolarization-induced [Ca2+]i transients from 78 +/- 21 nM in undifferentiated cells to 1,282 +/- 318 nM after 6 days. One microM nitrendipine inhibited Ca2+ influx by at least 65% at all stages of differentiation, while sensitivity to omega-conotoxin GVIa (omega-CgTx) did not appear until day 3. omega-CgTx inhibited a dihydropyridine-sensitive Ca2+ channel. DADLE inhibition of Ca2+ channels did not appear until 3 days of differentiation. Thus, opioid inhibition of depolarization-induced Ca2+ influx paralleled the expression of omega-CgTx sensitive voltage-gated Ca2+ channels.

Calcium Channel Blockers↗
PubMed1993

Experimental investigation of unsteady flow behaviour within a sac-type ventricular assist device (VAD).

The flow behaviour of human blood in a pneumatically driven sac-type ventricular assist device (VAD) has been simulated by a non-Newtonian polymer (Separan) solution, and investigated by both a one-component laser Doppler anemometer (LDA) in back-scattering mode and flow visualisation. The device was driven by a pneumatic driver with a squarewave output pressure, and was operated at a pumping rate of 70 bpm, and a systolic duration of 35% of the pumping cycle. The preload and the average afterload to the device were set at 10 mmHg and 100 mmHg, respectively. The output flowrate was 4.05 l min-1. The wall of the peripheral and the central parts of the blood chamber of the VAD were well 'washed' by a main vortex developed during filling and the flow components perpendicular to the base of the VAD produced by the diaphragm motions, respectively. Flow recirculation regions were found at several locations. Around the junction between the tube sections and the blood chamber, the recirculation with an associated fluid particle deposition indicates an underlying risk of thrombus formation. This risk will be reduced by modifying the device design. The maximum turbulent shear stress estimated from the maximum turbulent normal stress (74 N m-2), is unlikely to cause significant damage to blood for the exposure times found. The maximum particle residence time was found to be closely related to the heart rate and the degree of completion of ejection/filling. At a given flow rate, the operating conditions which produce the highest stroke volume give the shortest residence times.

Adult↗
PubMed1993

Hemizygosity at the elastin locus in a developmental disorder, Williams syndrome.

Williams syndrome (WS) is a developmental disorder affecting connective tissue and the central nervous system. A common feature of WS, supravalvular aortic stenosis, is also a distinct autosomal dominant disorder caused by mutations in the elastin gene. In this study, we identified hemizygosity at the elastin locus using genetic analyses in four familial and five sporadic cases of WS. Fluorescent in situ hybridization and quantitative Southern analyses confirmed these findings, demonstrating inherited and de novo deletions of the elastin gene. These data indicate that deletions involving one elastin allele cause WS and implicate elastin hemizygosity in the pathogenesis of the disease.

Adult↗
PubMed1992

Quantitative phase analysis of myocardial wall thickening by technetium-99m 2-methoxy-isobutyl-isonitrile SPECT.

Regional wall thickening was assessed by ECG-gated SPECT using technetium-99m 2-methoxy-isobutyl-isonitrile (99mTc-MIBI). For myocardial segments with an optimal short axis, regional count changes from end-diastole to end-systole were used to calculate the regional wall thickening. Functional images displaying amplitude, % wall thickening (% WT), and phase were generated by a fundamental Fourier analysis. In the control subjects, % WT analysis showed heterogeneous contraction among the left ventricular wall segments. The amplitude values showed a similar pattern to the %WT values. Phase images demonstrated that the timing of ventricular contraction was almost homogenous between the various wall segments. In the CAD patients, regional decreases in amplitude and %WT corresponding to zones of reduced perfusion were shown in the ischemic segments. Phase images also indicated asynchronous contraction in these segments. Phase analysis of regional wall thickening in 99mTc-MIBI scintigraphy seems to be useful for understanding regional myocardial function in combination with perfusion scanning.

Aged↗
PubMed1992

Perfusion and mechanical analysis with technetium-99m 2-methoxy-isobutyl-isonitrile in a case of dilated cardiomyopathy.

With technetium-99m 2-methoxy-isobutyl-isonitrile (99mTc-MIBI), regional wall thickening in a patient with dilated cardiomyopathy was analyzed by the first component Fourier method. The regional wall thickening was compared with thallium-201 and 99mTc-MIBI SPECT imaging. Thallium-201 SPECT images showed mildly reduced perfusion in the posterior wall and redistribution in the septum, whereas 99mTc-MIBI images showed heterogeneous accumulation around the left ventricular circumference. By means of phase analysis, diffusely decreased wall thickening and discontinuity of percent wall thickening in neighboring segments were observed throughout the left ventricle. Regional wall motion and wall thickening correlated roughly. However, discrepancies between the mechanical function and myocardial perfusion, and discrepancies in regional myocardial perfusion between thallium-201 and 99mTc-MIBI were observed.

Aged↗