Objective To study patients' characteristics in the early phase from Weachuan Earthquake.Method Totally 576 patients from Wenchuan Earthquake were received by the emergence department of WestChina Hospital between 14:28 May 12, 2008 and 14:28 May 15, 2008. The patients were recorded the detailednames, age, living places,time and way to hospital. Injury severity score (ISS) was used to judge the severity of the injury. T test was used to analyze these acquired data, while X2 test was for count data. Results From the first to third 24-hour period, our hospital accepted 199, 111 and 256 patients respectively. Their average ISS scorewere 7.16±4.75, 10.24±5.79, and 8.55±4.96 respectively. The average number of patients per hour ac-cepted by the hospital was(7.90±11.75). The second peak time for accepting patients was the 53rd (70 pa-tients) and 54th(58 patients) hour after earthquake.The patients accepted by the hospital on the second 24 hourshad the highest ISS score (10.24±5.79), and on the first and third 24 hours the ISS score was (7.16±4.75)and (8.55±4.96), respectively. There existed significant difference on ISS score between the second 24 hoursand the first, third 24 hours (P<0.05). Conclusions According to the study, patients accepted by the hospitalon the second 24-hour period had the most serious injury, and on the third 24-hour period, the number of patients accepted by the hospital reached its peak.

Uric acid is an end product of purine degradation in humans and normally depends upon renal excretion for the majority. Hyperuricemia is likely to cause gout, renal disease, or stones, and associated with cardiovascular impairment over the long term. The prevalence of gout and hyperuricemia appears to be on the increase in recent years. The present paper reviews the relationships between hyperuricemia and insulin resistance,purine metabolism and uric acid elimination , the genetics study and the mechanisms of hyperuricemia.

Hyperuricemia is induced by the mechanism of the elevated production of uric acid or the decreased renal excretion of uric acid. At present, there are three major methods to establish models for hyperuricemia: first, it will elicit pronounced hyperuricemia when feeding or injecting the animal with hypoxanthine 600～1000 mg?kg -1 , xanthine 600 mg?kg -1 , adenine 150～300 mg?kg -1 , yeast 15～30 g?kg -1 , uric acid 250 mg?kg -1 or 350～700 mg?kg -1 because of the elevated serum uric acid. Such effect will be also observed as administrating the animal with the inhibitors of uric acid excretion such as ethambutol 250 mg?kg -1 , nicotinic acid 100 mg?kg -1 at the same time of the above steps. Second, being an uricase inhibitor, when fed the rats 0 4 g?d -1 and uric acid 0 6 g?d -1 for 3～4 weeks, oxonic acid is able to cause the continuously elevated serum uric acid. Similarly, when potassium oxonate 300 mg?kg -1 ip only once, the serum uric acid in mice will be also elevated. Third, to destruct the urate oxidase gene (EC 1.7.3.3) in the mouse by homologous recombination in embryonic stem cells, and then the oxidase deficient mutant mouse as the hyperuricemia model, is generated by gene recombination.The rats and the mice have urate oxidase, which can decompose the uric acid to allantoin, while the avian (such as chicken, coturnix and so on) have not.

AIM To study the anti inflammatory and immunomodulatory actions of total glucosides of Mudan cortex(TGM)on adjuvant arthritis(AA)rats and its mechanisms. METHODS To observe the change of secondary inflammation and immune function on AA rats treated with TGM and to detect the effect of TGM on immune function in normal and AA rats in vitro. RESULTS TGM (25,50,100 mg?kg -1 ig) could significantly inhibit secondary inflammatory reaction(secondary inflammatory swelling, multiple arthritis, pathologic change of AA rats ankle arthrosis)of AA rats. Among them, TGM 50 mg?kg -1 ig had the best therapeutic effect, and could make the weight of atrophied thymus of AA rats restore to normal. Treated with TGM ig, not only the lower response of splenocytes to Con A and decreased IL 2 synthesis of AA rats were restored to normal but also the elevated IL 1 synthesis and PGE 2 release of PM? were reduced. The production of IL 1 by LPS induced PM? from normal rats were enhanced by in vitro treatment with lower concentrations (0 4～10 mg?L -1 )of TGM, but diminished with higher concentrations(50～250 mg?L -1 )of it. The production of PGE 2 were increased with dose independent manner(TGM 0 4～250 mg?L -1 ). In the range of 10～250 mg?L -1 TGM in vitro could significantly decreased the production of IL 1 and PGE 2 from AA rats and enhanced Con A induced proliferative response of splenocytes and IL 2 synthesis from splenocytes of AA rats. CONCLUSION TGM has anti inflammatory and immunomodulatory actions on AA rats mainly through inhibiting cell mediated immunity.

After icv administration, the analgesic action of Hyp was found on the tail-flick and hot-plate tests. The analgesic action potency of icv Hyp was approximately equal to 1 ~20 of morphine and was about 100 times as potent as sc administration. No effect was seen on the analgesic action of Hyp after ip naloxone, the analgesic action of Hyp was no concern of L-enkephalin contents in discrete regions of rat brain either. But icv EGTA markedly enhanced while icv CaCl2 antagonized the analgesic action of Hyp. It was also found that calcium ion content in mice brain markedly reduced when the analgesic action of Hyp appeared. These results suggest that Hyp have significant central analgesic action and the central analgesic action of Hyp may relate to reducing of calcium ion in brain.

The inhibitory effects of total glucosides of Moutan Cortex (TGM) and to talglucosides of Paeony Lactiflora (TGP) on osmotic hemolysis and oxidative hemolysis induced by hydrogen peroxide were studied. TGM at lower concentration and TGP could inhibit osmotic hemolysis significcantly, but higher concentration (100mg ? L-1) of TGM had a hemolytic activity. TGM and TGP could inhibit hemolysis induced by H2O2 significantly,but TGM was more effective than TGP. TGM .TGP and Vit E all could inhibit lipid peroxidation and glutathione depletion, induced by H2O2, on erythrocytes.

Pinealectomy (PX), zymosan-in-duced-luminol-dependent-chemiluminescence (CL) and PGE2 radioimmunoassay were used to determine the effects of the pineal gland and melatonin ( MT ) on CL of peritoneal macrophages (PM?s) and PGE2 content in the hypothalamus and spleen in rats. It was suggested that the CL value of PM?s was decreased and PGE2 contents in the hypothalamus and spleenwere increased significantly after PX, which could be restored respectively by 10~ 1 000 ?g? kg-1MT and 10 ?g?kg-1MT. 10 ?g?kg-1MT could also inhibit PGE2 in the hypothalamus and spleen in normal rats.

Total glucosides of paeony (TGP, 50 mg/kg 7d, ig) could enhance the episode duration of slow-wave sleep (SWS) in normal rats, and restore the sleep parameters in the insomniac rats induced by caffeine ( 1 2. 5 mg/kg 7 d,ip)nearly to the normal level. It (50 mg/kg 3 d,ig) also increased significantly thetotal time of SWS and paradoxical sleep (PS) in the swimming rats (water temperature 25?1℃, swimming time 30 min). These results suggest that TGP probably improve the sleep of rats under the different states.

The protective effects of total glucosides of paeony (TGP) on eoperimental hepatitis were studied in mice. The elevation of SGPT and the decrese of serum protein and hepatic glycogen contents in D-Galactosamine or CCl4-induced hepatitis were significantly improved by pretreatment with TGP (10, 20mg ? kg-1d-1?7d,ip). It also remarkably diminished the hepato-cellular degeneration and necrosis induced by D-Galactosamine or CCI4.Moreover, ultrastructural studies showed that TGP markedly restored the structures of mitochondria, lysosome and endoplasma reticulum of hepatocvtes injured by D-Galactosamine. These results indicate that TGP has obviously protective effects on acute hepatitis. The mechanisms of its actions remain to be furthes studied.

A postulated suppression of T lymphocyte function by clonidine (an adrenogic receptor agonist) was explored by utilizing mitogen induced lymphocyte transformation of mouse spleen cells in vitro. Added at the onset of the culture or 24h later, clonidine (10-(?)-10-8 M ) did not suppress T lymphocyte transformation induced by ConA or PHA. It implies that there is a difference in the sensitivity for clonidine between T and B lymphocyte, as clonidine has been suggested to suppress the SRBC induced primary immune response of mouse spleen cells in a dose dependent manner.