The application of resonance charging circuit to electro-hydraulic impulse apparatus for treating wastewater is introduced in this paper.The circuit permits the graduating increase of current without influence from time.The unique change of voltage on capacitor is favorable for the recovery of electric strength of electro-hydraulic impulse apparatus.The theory and design method of resonance charging circuit are provided.

BACKGROUND: It is indicated in a large amount of basic researches that compound danshen di wan has a certain action on removing carotid atherosclerotic plaques (CAP), but there is lack of large sample data in randomized, controlled, multi-central clinical experiment.OBJECTIVE: To observe the removing action of compound danshen di wan on CAP, compared with aspirin.DESIGN: Multi-central, randomized controlled experiment was designed.SETTING: Research Center of Traditional Chinese Medicine and Ultrasonic Department of Xinjing Hospital, Fourth Military Medical University of Chinese PLA; Department of Traditional Chinese Medicine of Second Clinical Hospital, Xi' an Jiaotong University and Department of Cardiac Internal Medicine of Xi' an Hospital of Traditional Chinese Medicine.PARTICIPANTS: Totally 162 cases were selected from the clinic of Research Center of Traditional Chinese Medicine, Fourth Military Medical University of Chinese PLA; Department of Traditional Chinese Medicine, Second Clinical Hospital, Xi' an Jiaotong University and Department of Cardiac Internal Medicine of Xi' an Hospital of Traditional Chinese Medicine from 2002 to 2004, aged varied from 40 to 80 years, the thickness of carotid internal media ≥ 1.2 mm. They were randomized into two groups, named danshen di wan group of 89 cases(cases of soft plaque and hard plaque were 49 and 40 respectively) and aspirin group of 73 cases(cases of soft plaque and hard plaque were 42 and 31 respectively).METHODS: In danshen di wan group: compound danshen di wan was administrated orally(10 pills/time, 3 times/day), in aspirin group, enteric soluble aspirin table was administrated orally(75 mg/time, once a day),continuously for 6 months. The alternations of thickness of carotid internal media were determined with ultrasonic B of high resolving power before and after treatment.MAIN OUTCOME MEASURES: Changes in thickness of carotid internal media before and after treatment.RESULTS: By practical measuring analysis, 143 cases accomplished nation of thickness of carotid internal media in the patients with soft plaque:In danshen di wan group, the thickness was remarkably decreased after treatment[ (2. 12 ± 0. 34), (2.44± 0.40) mm, t = 4. 267, P ＜ 0.01 ] . In aspirin group, it was also reduced relatively after treatment[ (2.25 ± 0. 3),of carotid internal media in the patients with hard plaque: The changes were not significant no matter in danshen di wan group or aspirin group in the comparison before and after treatment[in danshen di wan group: (2.46 ±0.42),(2.34 ± 0. 40) mm; in aspirin group: (2.42 ± 0. 44), (2. 36 ± 0. 38) mm,P＞ 0.05].CONCLUSION: Compound danshen di wan acts on removing soft atherosclerotic plaque and its effect is similar to aspirin.

Plasticity in the glutamatergic synapses on striatal medium spiny neurons (MSNs) is not only essential for behavioral adaptation but also extremely vulnerable to drugs of abuse. Modulation on these synapses by even a single exposure to an addictive drug may interfere with the plasticity required by behavioral learning and thus produce impairment. In the present work, we found that the negative reinforcement learning, escaping mild foot-shocks by correct nose-poking, was impaired by a single in vivo exposure to 20 mg/kg cocaine 24 h before the learning in mice. Either a single exposure to cocaine or reinforcement learning potentiates the glutamatergic synapses on MSNs expressing the striatal dopamine 1 (D1) receptor (D1-MSNs). However, 24 h after the cocaine exposure, the potentiation required for reinforcement learning was disrupted. Specific manipulation of the activity of striatal D1-MSNs in D1-cre mice demonstrated that activation of these MSNs impaired reinforcement learning in normal D1-cre mice, but inhibition of these neurons reversed the reinforcement learning impairment induced by cocaine. The results suggest that cocaine potentiates the activity of direct pathway neurons in the dorsomedial striatum and this potentiation might disrupt the potentiation produced during and required for reinforcement learning.