Objective To clarify the effective location of propofol in central nervous system (CNS) by detection of the c-jun expression after propofol-induced anesthesia in rats. Methods Wistar rats were randomly divided into 6 groups: normal control (C), low-dose propofol group (50 mg/kg, P 1), middle-dose propofol group (100 mg/kg, P 2), high-dose propofol group (150 mg/kg, P 3), stimulation with tail broken group (S 1), and propofol + stimulation with tail broken group (S 2). The expressions of nucleoprotein JUN in the CNS were detected by immunohistochemisty. Results Rather weakly stained nucleoprotein JUN positive neurons were observed in the supraoptic nucleus, lateral septal nucleus, and lateral habenular nucleus in the control group. In groups P 1, P 2, and P 3, the expressions of nucleoprotein JUN were increased significantly as compared with those in the control group. The expressions were mainly located in the accumbent nucleus, lateral septal nucleus, periventricular hypothalamic nucleus, ventral lateral geniculalaten nucleus, dorsal lateral geniculate nucleus, supraoptic nucleus, suprachiasmatic nucleus, anteroventral preoptic nucleus, nucleus of the solitary tract, supramammillary nucleus, basolateral amygdaloid nucleus, paraventricular thalamic nucleus, lateral habenula nucleus, and islands of Calleja. The expressed positive neuron number was positively correlated with the doses of propofol. Conclusion Propofol anesthesia has the determined sites of action in rat CNS.

Objective To clarify the effective location of propofol in central nervous system (CNS). Methods Forty-two Wistar rats were ramdomized into control group,50 mg/kg propofol,100 mg/kg propofol,150 mg/kg propofol,tail shearing,propofol followed by tail shearing (n=7 in each group). The NOS expressions in the CNS were recorded by NADPH-d histochemistry after anesthesia by intraperitoneal injection of propofol. Results Rather widely stained NOS positive neurons were observed in the control group. In propofol groups,the NOS expressions were decreased significantly as compared with the control group,mainly located in ACB,LS,Pe,VLG,Den,SO,SCh,AVPO,Sol,SuM,BL,PV,LHb and Icj,showing a negative dose-effect relation with propofol. Conclusion Propofol has the determined sites of action in CNS and the decrease of NO synthesis by the inhibition of NOS may play a role in propofol-induced general anesthesia.

Objective An HPLC method was established for determination of paeoniflorin in plasma after ig compound decoction of Radix Paeoniae Rubra with Fructus Piperis to mice. Methods The conditions of chromatography: Kromasil C 18 column (250 mm ? 4.6 mm, 7 ?m) was used with a mobile phase of CH 3OH-H 2O ( 38∶ 62); flow rate was 0.5 mL/min; the detecting wavelength was 230 nm; external standard method was quantitative analysis method. Results Paeoniflorin was fully separated from the other components in plasma. The linear range was 5.0—250.0 ng/?L (r= 0.999 9 ), the lowest detectability was 1.49 ng/?L, the average recovery was higher than 90%. Conclusion This method specially provides an accurate and sensitive way in detecting the in vivo blood concentration of paeoniflorin in plasma.

OBJECTIVETo detect potential mutations of OTC gene in a male infant affected with ornithine transcarbamylase deficiency.

METHODSGenomic DNA were isolated from peripheral blood samples of family members and 100 healthy individuals. Potential mutations of the 10 exons of OTC gene were screened with PCR and Sanger sequencing.

RESULTSA homozygous missense mutation c.917G>C in exon 9, which results in p.R306T, was identified in the infant. Sequencing of the mother and two female members of the family indicated a heterozygous status for the same mutation. The same mutation was not found in other members of the family and 100 healthy controls.

CONCLUSIONA missense mutation c.917G>C in the OTC gene is responsible for the pathogenesis of the disease. Identification of the mutation can facilitate prenatal diagnosis and genetic counseling for the family.

Computational Biology ; Female ; Humans ; Male ; Mutation ; Ornithine Carbamoyltransferase ; genetics ; Ornithine Carbamoyltransferase Deficiency Disease ; diagnosis ; genetics ; Sequence Analysis, DNA