PubMed HealthSearch

Biomedical subjects

W M Li

Publications and source records attributed to W M Li.

At least 19 recordsLinked to original sources

Electrodermal activity in schizophrenia: a quantitative study using a short interstimulus paradigm.

BACKGROUND: Electrodermal activity in response to short interstimulus interval (ISI) stimulation allows aspects of information processing to be examined, but such paradigms cause skin conductance responses (SCRs) to overlap. A signal decomposition method was developed and employed to score the overlapped SCRs. This is the first application of the method to the study of schizophrenia. METHODS: Electrodermal activity of 30 medicated patients with schizophrenia and 50 normal controls was obtained using a conventional auditory oddball paradigm with an ISI of 1.3 sec. Tonic skin conductance level (SCL), phasic SCRs, SCR temporal dynamics, and a range of SCR variables in response to target tones were examined. RESULTS: The schizophrenic group showed reduced response rate, proportion of responders, SCR amplitude, rise time, peak latency, and steady-state response amplitude, over the trial compared with controls. There were no between-group differences in SCL or SCR onset time. CONCLUSIONS: The combined use of a conventional short ISI paradigm and the new SCR scoring method demonstrated new facets of electrodermal hyporeactivity in medicated patients with schizophrenia. The hyporeactivity could not be attributed to changes in tonic arousal or dysfunctions in peripheral sympathetic nerve conductance.

Acoustic Stimulation

Acute and chronic oral administration of bis(maltolato)oxovanadium(IV) in Zucker diabetic fatty (ZDF) rats.

This is a preliminary study in which both acute and chronic oral administration of bis(maltolato)oxovanadium (IV) (BMOV) was examined in the Zucker diabetic fatty (ZDF) rat, an animal model that develops overt hyperglycemia in the presence of hyperinsulinemia followed by beta-cell depletion. At 9-10 weeks of age, in the presence of hyperglycemia, hyperinsulinemia and hyperlipidemia, an acute oral gavage dose response was conducted to determine glucose-lowering properties of BMOV, time of response and effect of BMOV on plasma insulin levels. Doses of BMOV greater than 0.2 mmol/kg resulted in plasma glucose levels of less than 9 mmol/l. The highest dose administered (0.8 mmol/kg) significantly reduced plasma insulin (initial: 2.83+/-0.2, final: 1.23+/-0.09 nmol/l, P<0.05) and plasma triglyceride (initial: 4.94+/-0.33, final: 1.55+/-0.07 mmol/l, P<0.05) levels. At 15 weeks of age, in the presence of hyperglycemia, hyperlipidemia and normal insulin levels, BMOV was administered orally in the drinking water for a 10-week period to determine the effect of treatment on glucose, insulin and lipid levels. BMOV treatment significantly reduced plasma glucose levels (final BMOV-treated: 13.25+/-1.43, untreated: 28.71+/-0.6 mmol/l, P<0.05) and effectively preserved pancreatic beta-cell function. These data suggest a role for BMOV as a therapeutic agent in non-insulin-dependent diabetes mellitus through improvement in glucose homeostasis and preservation of insulin reserves.

Administration, Oral

Time-related mapping of quantitative trait loci underlying tiller number in rice.

Using time-related phenotypic data, methods of composite interval mapping and multiple-trait composite interval mapping based on least squares were applied to map quantitative trait loci (QTL) underlying the development of tiller number in rice. A recombinant inbred population and a corresponding saturated molecular marker linkage map were constructed for the study. Tiller number was recorded every 4 or 5 days for a total of seven times starting at 20 days after sowing. Five QTL were detected on chromosomes 1, 3, and 5. These QTL explained more than half of the genetic variance at the final observation. All the QTL displayed an S-shaped expression curve. Three QTL reached their highest expression rates during active tillering stage, while the other two QTL achieved this either before or after the active tillering stage.

Chromosome Mapping

Late components of the event-related potentials and their topography in Parkinson's disease.

Late components of the event-related potential (ERP; N100, P200, N200, and P300) were elicited using an auditory oddball paradigm (with a button-press response to target stimuli) in 15 Parkinson's disease (PD) patients and 50 normal control subjects. Compared with control subjects, PD subjects showed a significant decrease in N200 amplitude. Between-group topographical differences in N200 amplitude were evident at central (C3, Cz, C4) and temporal (T5, T3, T4, T6) regions. The results may reflect a deficit in response selection in PD possibly resulting from a dysfunction associated with the abnormalities in the central and temporal regions found to have a decreased N200 amplitude compared with normal control subjects in this study.

Acoustic Stimulation

Insulin-induced Glut4 recruitment in the fatty Zucker rat heart is not associated with changes in Glut4 content in the intracellular membrane.

Impaired cardiac glucose metabolism and glucose transport have been shown in the insulin resistant fatty Zucker rat. The aim of the present study was to examine the translocation of the insulin-sensitive glucose transporter (Glut4) in the heart of the fatty Zucker rat under in vivo conditions. Insulin was injected into both lean (FA/?) and fatty (fa/fa) Zucker rats via the tail vein. The time course of cardiac Glut4 translocation was studied by determining the subcellular distribution of Glut4 using a newly developed ELISA quantitation method. Insulin (10 U/kg) caused a 30% and 37% increase in plasma membrane Glut4 content at 20 min after injection in lean and fatty rats respectively. The plasma membrane Glut4 contents in the basal and insulin-stimulated states were significantly lower in the fatty rat when compared to the lean control. The dose effect of insulin (2.5-10 U/kg) on Glut4 mobilization to the plasma membrane was similar in both phenotypes. The time course of Glut4 mobilization to the plasma membrane (5-30 min), which was similar in both lean and fatty Zucker rats, showed that maximal translocation was reached at 5 min post insulin injection and persisted throughout the remaining 25 min. However, in fatty Zucker rats, Glut4 content in the intracellular membrane remained unchanged at all insulin doses and all time points studied. Collectively, these results show that Glut4 recruitment to the plasma membrane is responsive to insulin in the fatty Zucker rat heart and that the maximal response was similar to that in lean Zucker rats. However, the recruitment of Glut4 to the plasma membrane was not associated with changes in the intracellular membrane Glut4 content.

Animals

Dysfunctions of automatic (P300a) and controlled (P300b) processing in Parkinson's disease.

P300 Event Related Potentials components (P300a and P300b) were investigated using an auditory oddball paradigm (with a button press response to target stimuli) in 15 Parkinson's disease patients and 50 normal controls whilst simultaneously measuring electrodermal activity. Cluster analysis showed that the first 10 target stimuli generated the largest skin conductance responses. The first 10 single-trial ERP epochs were therefore analysed as an ERP sub-average for each individual. The P300a component (associated with the automatic 'Orienting Reflex') was expected to be most prevalent in this sub-average (compared with sub-averages of subsequent blocks of 10 target stimuli). Twenty-nine out of 50 normal controls (58%) elicited a P300a in the first 10 target sub-average, compared with only 2 out of 15 Parkinson's disease subjects (13%). The conventional P300b component (associated with controlled processing) was found to be significantly delayed for all sub-averages for the Parkinson's disease group when compared with controls. These preliminary findings suggest a possible dysfunction in both automatic and controlled processing in this disorder.

Adult

Excitation of baroreceptors depresses A- and C-components of the somato-cardiac sympathetic reflex in anesthetized rats.

The effect of baroreceptor activation on somato-cardiac sympathetic reflex discharges was examined in urethane-anesthetized, vagotomized, and artificially ventilated rats. Single shock stimulation of myelinated (A) and unmyelinated (C) fibers in the tibial nerve of the left hindlimb elicited two separate excitatory reflex discharge components in a branch of the cardiac sympathetic nerve. They are termed the A- and C-components of the somato-cardiac sympathetic reflex discharges. When aortic nerves (AN) and carotid sinus nerves (CSN) were intact, a sudden increase in mean arterial blood pressure to about 150 mmHg induced by I.V. injection of phenylephrine (50 micro/kg) depressed the A- and C-components by up to 47 +/- 5.4 and 37 +/- 7.7% of the control values, respectively. However, bilateral sino-aortic denervation completely abolished the pressure-induced depression of both components. We conclude that baroreceptor afferent signals from the AN and CSN inhibit both A- and C-components of the excitatory somato-cardiac sympathetic reflex discharges. This and other previous evidence mentioned in the text indicate that inhibitory cardiac sympathetic reflexes originating from arterial baroreceptors and excitatory ones originating from somatic afferents interact, probably at the brainstem.

Anesthetics, Intravenous

Fast and slow reaction time changes reflected in ERP brain function.

A number of studies have examined the average late component Event Related Potential (ERP) and Reaction Time (RT) in response to multiple target stimuli (across-trial averages). This study demonstrates within-trial differences in ERP brain function associated with relatively fast and slow RTs in 50 normal subjects. A conventional auditory oddball paradigm (with a 1 ISI) was employed. Increased ERP N100 and N200 amplitude (and decreased P200 amplitude), as well as earlier P200, N200 and P300 latency were found in the fast compared with the slow ERP subaverages. These results show the potential to elucidate temporal and spatial dynamics of brain function associated with changes in performance, in conventional "cognitive" paradigms applicable to both health and disease states.

Acoustic Stimulation

Fast and slow reaction times and associated ERPs in patients with schizophrenia and controls.

A number of studies have examined across-trial averaged late component. Event Related Potentials (EPR) and Reaction Times (RT) in response to multiple target stimuli. In this study, within-trial relatively fast and slow sub averages are additionally examined, in 20 patients with schizophrenia and 20 age and sex matched controls. A conventional auditory oddball paradigm. Across-trial ERP average analysis showed smaller N200 amplitude and delayed latency (but larger P200 amplitude) in patients with schizophrenia compared with controls. Within-trial ERP analysis revealed a number of additional findings. Controls showed distinctive differences in fast compared with slow ERP sub averages (smaller P200 amplitude, increased N200/P300 amplitudes and earlier latencies). The schizophrenic group on the other hand, showed relatively similar fast versus slow subaverages (no differences in P200 amplitude and N200 latency). In addition, between-group (within-trial) analyses highlighted significant differences in earlier stages of processing (compared with across-trial averages) in both fast and slow subaverages (increased N100 amplitude in controls). The complementary within-trial (compared with across-trial) data are interpreted with respect to a possible disturbance in inhibitory function in patients with schizophrenia.

Adult

Partial preservation of pancreatic beta-cells by vanadium: evidence for long-term amelioration of diabetes.

Streptozotocin (STZ)-diabetic rats treated with vanadium can remain euglycemic for up to 20 weeks following withdrawal from vanadium treatment. In this study, we examined the effects of short-term vanadium treatment in preventing or reversing the STZ-induced diabetic state. Male Wistar rats were untreated (D) or treated (DT) with vanadyl sulfate for 1 week before administering STZ. Treatment was subsequently maintained for 3 days (DT3) or 14 days (DT14) post-STZ, after which vanadium was withdrawn. At 4 to 5 weeks post-STZ and following long-term withdrawal from vanadium, DT14 rats demonstrated levels of food and fluid intake and glucose tolerance that were not significantly different from those of age-matched untreated nondiabetic rats, and had significantly reduced glycemic levels in the fed state compared with D and DT3 groups. The proportion of animals that were euglycemic (fed plasma glucose < 9.0 mmol/L) was significant in DT14 (five of 10) relative to D (one of 10) and DT3 (one of 10) (P = .01). All euglycemic animals had an improved pancreatic insulin content that, albeit low (12% of control), was strongly linked to euglycemia in the fed state (r = -.91, P < .0001). Moreover, the highly significant correlation persisted with the analysis of untreated STZ-rats alone (r = -.95, P < .0001). Similarly, improvements in glucose tolerance and insulin secretory function in euglycemic rats were strongly correlated with small changes in residual insulin content. Hence, as vanadium pretreatment did not prevent STZ-induced beta-cytotoxicity, the vanadium-induced amelioration of the diabetic state appears to be secondary to the preservation of a functional portion of pancreatic beta cells that initially survived STZ toxicity. The partial preservation of pancreatic beta cells, albeit small in proportion to the total insulin store, was both critical and sufficient for a long-term reversal of the diabetic state. These results suggest that apparently modest effects in preserving residual pancreatic insulin content can have profound consequences on glucose homeostasis and may bear important implications for interventions that have "limited" protective effects on beta cells.

Animals

Quantitative methods for measuring the insulin-regulatable glucose transporter (Glut4).

This review article describes various quantitation methods for the insulin-regulatable glucose transporter (Glut4). Several methods including reconstituted glucose transport, cytochalasin B binding assays, immunocytochemistry, immunoblots, ELISA, and the more recently developed exofacial labels are discussed. Since Glut4 translocates from an intracellular compartment to the plasma membrane in response to the action of insulin, it is of particular interest to measure Glut4 changes in the membrane fractions. Hence, the measurement of Glut4 commonly involves the isolation of cell membranes using subcellular fractionation in combination with one of the quantitation methods. The limitations of each quantitation method due to the use of subcellular fractionation are discussed in this article. As well, the advantages and disadvantages in terms of isoform specificity and technical difficulties of each method are presented.

Affinity Labels

Automatic processing dysfunction in Parkinson's disease.

Simultaneous measures of Event Related Potentials (ERP) and electrodermal activity (EDA) allow the delineation of ERPs that did, and did not, evoke an electrodermal 'Orienting Reflex' (OR). The OR is an automatic reflex invoked by novel or significant stimuli. Our group have developed a model to quantify electrodermal OR activity acquired in conventional late component ERP paradigms with short interstimulus intervals. Target late component (N100, P200, N200, P300) ERPs (acquired in an auditory oddball paradigm) and EDA was examined in 15 Parkinson's disease (PD) subjects and 50 normal controls. Single-trial target ERPs were averaged according to whether or not they elicited an electrodermal OR. Compared with controls, the PD group showed significantly decreased N100 and N200 amplitudes in the OR related ERPs ('Orienting ERPs'). These preliminary findings suggest that conventional late component ERPs can be delineated according to whether or not they evoked an OR. The 'orienting ERPs' in PD showed more significant disturbances compared with controls, than ERPs that did not evoke an OR.

Acoustic Stimulation

Morphine microinjected into the nucleus tractus solitarius and rostral ventrolateral medullary nucleus enhances somatosympathetic A- and C- reflexes in anesthetized rats.

The modulatory effects of morphine microinjected into localized areas of the brainstem on somatosympathetic A- and C-reflexes were examined in urethane-anesthetized rats. Somatosympathetic A- and C-reflexes were elicited in a branch of the inferior cardiac nerve by electrical stimulation of myelinated (A) and unmyelinated (C) afferent fibers in the tibial nerve. Morphine (0.002-0.2 microgram/50 nl) was microinjected into the rostral, intermediate and caudal parts of the nucleus tractus solitarius (NTS), the rostral ventrolateral medullary nucleus (RVLM), the caudal ventrolateral medullary nucleus (CVLM), the locus coeruleus (LC), the raphe magnus (RM), the periaqueductal gray (PAG), and the accumbens nucleus (Acb). Microinjections of morphine (0.2 microgram) into the intermediate and caudal NTS produced significant augmentations of the A- and C-reflexes, C-reflexes being more markedly enhanced than A-reflexes. Microinjection of morphine (0.2 microgram) into the RVLM produced a prominent increase in the C-reflex, the threshold dose for a significant increase being 0.02 microgram morphine. Microinjection of morphine up to 0.2 micrograms/50 nl into the other areas mentioned above had no significant effect on either reflex component. All opiate-induced increases of the reflex discharges could be reversed by intravenous application of naloxone (2 mg/ kg). The reflex augmentation induced by microinjection of morphine into the NTS may be caused by suppressing inhibitory baroreceptor information or by enhancing excitatory chemoreceptor information in the NTS. Augmentation of the C-reflex induced by microinjection of morphine into the RVLM may be caused by facilitating C-reflex pathways or by suppressing inhibitory neural circuits involved in the C-reflex within the RVLM.

Afferent Pathways

Systemic hypoxia facilitates somato-cardiac sympathetic A- and C-reflexes in anesthetized rats.

In rats anesthetized with urethane, electrical stimuli applied to tibial nerve afferents produced a somato-sympathetic A-reflex of 41 +/- 2 (mean +/- SEM)ms latency and C-reflex of 210 +/- 13 ms latency recorded in the left inferior cardiac sympathetic nerve. Hypoxia was induced by switching room air to nitrogen/oxygen gas mixture in the inspiratory line reducing end-tidal oxygen from about 18% FETO2 to 10% FETO2 and 6% FETO2 for 60s, respectively. During 6% FETO2 hypoxia, the amplitude of the somato-cardiac sympathetic A-reflex increased significantly to 138 +/- 13% of the control, and that of the C-reflex increased to 186 +/- 18% of the control. During 10% FETO2 hypoxia, the A-reflex increased insignificantly to 117 +/- 8%; the amplitude of the C-reflex was augmented significantly to 149 +/- 11% of the control. Peripheral carotid chemoreceptor denervation abolished the facilitatory effects of systemic hypoxia. It is concluded that carotid chemoreceptor stimulation enhances the responsiveness of somato-cardiac sympathetic excitatory reflexes originating in the hind limb receptors.

Animals

Glutamate N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists administered into the brain stem depress the renal sympathetic reflex discharges evoked by single shock of somatic afferents in anesthetized rats.

The involvement of glutamate receptors in the central transmission of somatosympathetic reflexes was studied by examining, in anesthetized rats, the effects of MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, and CNQX, a non-NMDA receptor antagonist, on two reflex components, the A- and C-reflexes evoked in the left sympathetic renal nerve by a single shock to the left tibial nerve. The A-reflex elicited by myelinated A fiber stimulation and the C-reflex elicited by unmyelinated C fiber stimulation were depressed, in a dose-dependent manner, following administration of either MK-801 or CNQX into the cisterna magna (i.c.m.). Intrathecal (i.t.) administration of MK-801 did not have any effect on either A- or C-reflexes, while i.t. administration of CNQX had a slight effect on the A-reflex (significantly on the A-reflex only when treated with the highest dose of 100 ng) and the C-reflex. These results indicate that both NMDA and non-NMDA receptors, stimulated by glutamate released possibly as a neurotransmitter, are involved in the central transmission pathways of somatosympathetic reflexes at the level of the brain stem, but not the spinal cord.

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

The inhibitory role of nitric oxide (NO) in the somatocardiac sympathetic C-reflex in anesthetized rats.

The role of nitric oxide (NO) in the two somatosympathetic reflex arcs, i.e. A- and C-reflexes, was examined using NO synthase (NOS) inhibitor in anesthetized rats. The A- and C-reflex components were recorded from a cardiac sympathetic efferent nerve and elicited by stimulation of myelinated A and unmyelinated C afferent fibers in the left tibial nerve. NG-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, when administered by either intrathecal (i.t.) or into the cisterna magna (i.c.m.) routes, augmented only the C-reflex in a dose-dependent manner. The effective i.t. dose of L-NAME to augment the C-reflex was approximately 1000 times the i.c.m. dose. NG-nitro-D-arginine methyl ester (D-NAME), an isomer of L-NAME, had no effect on either A- or C-reflexes, when administered i.c.m. Neither i.c.m. pre-treatment nor post-treatment with L-arginine, a NOS substrate, influenced either A- or C-reflexes, but i.c.m. pre-treatment with L-arginine abolished the facilitatory effect of L-NAME on the C-reflex. These results suggest that NO, synthesized in the brain stem, plays an inhibitory role in the central modulation of the somatocardiac sympathetic C-reflex. The possibility of movement of L-NAME to the brain stem from the spinal cord is discussed.

Anesthesia

[Effects of composite xueliting on four gastric ulcer models in rats and mice].

Composite Xueliting (CXLT) was found to be an effective anti-ulcer agent in four experimental models in rats and mice, namely, the stress restraint-induced, histamin-induced, salicylic acid-induced and reserpine-induced ulcers. In above-mentioned models, CXLT (0.214-0.856 g/kg, 1/d x 5, per os) could inhibit gastric ulcer by 40%-63%, 48%-85%, 68%-87% and 27%-65% respectively. Among these, the salicylic acid-induced ulcer was more markedly inhibited. The result suggested that CXLT had the protective function against the gastric ulcer.

Animals