ABSTRACT
This study aimed to establish a new technology for health insurance reimbursement evidence-based decision-making framework on the basis of EVIDEM. Literature review,focus group discussion and qualitative inter-view were used to construct the preliminary decision-making framework,and expert consultation was adopted to deter-mine the necessity and weight of the criteria. The established evidence-based decision-making framework consists of guidelines of normative universal and contextual aspects. The normative aspect included following criteria, need for intervention (i.e. disease severity, size of affected population, benefit type of technology, unmet needs of reim-bursed technology),comparative outcomes of technology (i.e. comparative effectiveness,comparative safety/tolera-bility,comparative patient-perceived/patient-reported outcomes), and economic consequences of technology (i.e. cost,results of economic evaluation). The contextual aspect reflects the mission and mandate of medical insurance, population priorities and the accessibility,common goal and specific interests, political context, and affordability of medical insurance.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of exposure of paraquat and maneb on the behavior, the morphology and electrical activity of the Substantia nigra and striatum, and to discuss the relationship between this two pesticides and Parkinson's disease.</p><p><b>METHODS</b>37 rats were divided randomly into 3 groups: control group (n = 11), paraquat (10 mg/kg) group (n = 13) and combinative group of paraquat (10 mg/kg) and maneb (30 mg/kg) (n = 13), and were exposed twice a week for 6 weeks by intraperitoneal injection. The behavior of animals in the declined-plane, the vertical-grid and the open-field test were observed. The morphology of substantia nigral neurons were investigated by HE pathology. The spontaneous discharge of striatum neurons were recorded after exposure.</p><p><b>RESULTS</b>Compared to the control group and the pre-exposure group, both the numbers of animals sliding down from the declined-plane and the latency of rats' moving on the vertical-grid significantly increased, and the animals' autonomic movement decreased significantly (P < 0.05, P < 0.001). After the combinative exposure, the neurons of the Substantial nigra pars compacta (SNPc) were progressively impaired, the cell density of the paraquat group [(82.17 ± 12.91) n/mm(2)] and the combined group [(41.15 ± 6.44) n/mm(2)] were lower than that in control group (143.10 ± 20.85 n/mm(2)] (P < 0.01). In the paraquat group (5.97 ± 7.30 Hz) and the combined group [(6.95 ± 9.87) Hz], the average discharge rates of the striatum neurons were increased significantly compared to the control group [(1.78 ± 5.05) Hz] (P < 0.01). The bursting discharge was increased significantly in the combined group (22.3%) compared to the control group (9.8%) and the paraquat group (5.6%) (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>The co-exposure of paraquat and maneb could induce similar symptoms to Parkinsonism syndrome of rats such as rigidity, moving reduction and etc, and the combined exposure had a certain enhanced effect compared to alone paraquat exposure. The combinative exposure of paraquat and maneb could cause neural loss in SNPc and it is involved with the enhanced electrophysiological activity in striatum. The synergy toxicity of paraquat and maneb in nigrostriatal system is related to Parkinson's disease.</p>
Subject(s)
Animals , Male , Rats , Corpus Striatum , Maneb , Toxicity , Paraquat , Toxicity , Parkinsonian Disorders , Pesticides , Toxicity , Rats, Sprague-Dawley , Substantia NigraABSTRACT
Experiments were performed on Sprague Dawley rats with multibarrel microelectrode technique. The effects of acoustic response of A I cortex neurons produced by electrical stimulation of lateral amygdaloid nucleus (LA) and the influence of GABA were observed. Experimental results showed that iontophoretic administration of GABA caused a pronounced inhibition of the electrical activity of A-I neurons. Blockade of GABA(A) with bicuculline (BIC) facilitated the acoustic response. The acoustic response of A-I neurons was inhibited when the LA was stimulated. Iontophoretic application of GABA resulted in a similar inhibitory effect as that of LA stimulation. Blockade of GABA(A) with bicuculline reversed the inhibitory effect of LA stimulation on the acoustic response of A-I neurons. In contrast, application of strychnine, a glycine receptor antagonist, could not reverse the inhibitory effect of LA. Baclofen, a GABA(B) agonist, did not affect the acoustic response of the auditory neurons. These results indicate that GABA is the ultimate transmitter which mediates the LA stimulation-induced inhibition of the acoustic response of A-I neurons in rats, possibly via the GABA(A) receptor.