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.

Objective To explore the causes and treatment of the complications after laparoscopic surgery in neonate and infants.Methods From January 2003 to June 2007,totally 287 neonates and infants received laparoscopic surgeries in our hospital, 10 of them developed postoperative complications.Results The complications included 7 cases of gastric mucosa rupture during pyloric resection,1 case of delayed rupture of the pylorus,1 case of intestinal malrotation complicated with duodenal stenosis,and 1 case of incisional hernia.The former 9 cases were cured by open surgery,and the last one recovered spontaneously in 4 months. Conclusions Mucosarupture caused by pyloric resection is the most common complication after laparoscopic surgery in neonates and infants,open surgery should be performed in such a situation.Delayed rupture of the bowel after laparoscopic surgery can be potentially fatal,and should be treated as soon as possible.Intestinal malrotation may lead to a high rate of malformation,which can be avoided by early diagnosis and treatment.

Objective To investigate the value of lapa ro scopic surgery in the diagnosis and treatment of bile duct diseases in newborns and infants. Methods Clinical records of 9 newborns or infants with bile duct diseases diagnosed and treated under laparoscope from January 20 03 to August 2004 in this hospital were reviewed retrospectively. Resul ts Laparoscopic exploration in the 9 cases found 2 cases of congenital choledochal cyst, 5 cases of biliary atresia, 1 case of cholestasis, and 1 case of congenital bile duct hypoplasia. Cholangiography was successfully performed i n 8 cases. Two patients with choledochal cyst received an excision of the cyst a nd Roux-en-Y hepatico-jejunostomy. Among the 5 patients with biliary atresia, he patic porto-enterostomy was performed via open approach in 3 patients and via la paroscopic approach in 1, and surgery was refused in 1 patient. Open hepatic por to-enterostomy was also used in the patient with bile duct hypoplasia. The patie nt with cholestasis underwent a biliary tract irrigation. Conclusions Laparoscopy is simple and reliable in the diagnosis of bile duct disease s in newborns and infants. For the treatment of bile duct diseases, laparoscopic techniques have advantages of minimal invasion, good cosmetic results, less blo od loss, quick recovery, and reliable clinical effects.

Objective To explore the feasibility of tw o- port laparoscopy in the treatment of congenital hypertrophic pyloric stenosis. Methods A total of 21 infants with confirmatively diagnosed con genital hypertrophic pyloric stenosis were given a two-port laparoscopic pylorom yotomy. The procedure was performed using two trocars: a 5 mm trocar at the lowe r border of the umbilical ring was placed for the insertion of camera, and a 3 m m trocar was introduced below the costal margin at the midclavicular line to pas s the hook electrode and curved forceps. Results No conversion s to open surgery were required. The operation time was 23~65 min (mean, 31.3 mi n). The patients were discharged from hospital at 4~6 postoperative days. No com plications occurred. Follow-up for 2~7 months (mean, 3.2 months) showed a norma l development in all the 21 patients. Conclusions Two-port lap aroscopic treameat for congenital hypertrophic pyloric stenosis in infants is ef fective.

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.

Total glucosides of paeony root ( TGPs ) ( 5 ~40mg/kg, ip ) had a dose-related hypothermal effect in mice and rats, which was related to the environment temperature. But TGPs ( 40mg/kg, ip or iv ) showed no significant hypothermal effect in guinea-pigs or rabbits. TGPs ( 2, 4 mg/kg, icv ) had a potential hypothermal effect in rats. Chlopheniramine had antagonist effect on hypothermal effect of TGPs in mice and rats.

Influences of the concentrations of luminol, zymosan & cells and opsonizing time of zymosan on luminol-dependent chemiluminescence( LDCL ) of peritoneal macrophages ( PM?) in rats were investigated by the method of orthogonal analysis. The result showed that the best levels were 100?mol/L of luminol, 10 mg/ml of zymosan, 5? 10~6/ml of cells and 45 min for opsonizing time. The LDCL of PM? was enhanced by incubation with TGP for 12 h in a concentration-dependent manner in the range of 0.09-2.25 ?g/ml of TGP, but LDCL was diminished with the concentration of 11.25 ?g/ml of TGP . The concentration-effect curve seems to be bell-shaped. The data suggested that TGP had two-sided regulatory effects on the LDCL of PM? in rats, depending on the concentration used.

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.