Objective To evaluate the effects of dexmedetomidine on the expression of phosphor-cAMP response element binding protein (p-CREB) in isoloated hippocampal neurons of fetal rats.Methods SpragueDawley rats on 16-18 days of gestation were sacrificed and the fetal rats were obtained.The hippocampi of fetal rats were isolated and hippocampal neurons were seeded in culture medium for 8 days.The cells were then divided into 4 groups (n =12 each) using a random number table:control group (group C),dexmedetomidine 0.001 μmol/L group (group D1),dexmedetomidine 0.010 μmol/L group (group D2),and dexmedetomidine 0.100μmol/L group (group D3).In D1.3 groups,dexmedetomidine with the final concentrations of 0.001 μmol/L,0.010 μmol/L,and 0.100 μmol/L was added to the culture medium,respectively,and then the cells were incubated for 3.5 h.The apoptosis in hippocampal neurons was detected by flow cytometry.The expression of p-CREB in hippocampal neurons was determined by RT-PCR and Western blot.Results Compared with group C,apoptosis rate was significantly decreased and the expression of p-CREB was up-regulated in D1.3 groups.Conclusion Dexmedetomidine inhibits apoptosis in isolated hippocampal neurons of fetal rats by up-regulating the expression of p-CREB.

Objective To evaluate the effects of propofol on the proliferation of hippocampal neurons in fetal rats in vitro.Methods Pregnant Sprague-Dawley rats at 16-18 days of gestation,were sacrificed and the fetal rats were taken out from the abdominal cavity.The hippocampal neurons of the fetal rats were isolated and seeded in culture plates.After being cultured for 9 days,the neurons were divided into 7 groups using a random number table(n =36 each):control group (C group),intralipid group (I group) and propofol 0.1,1.0,10.0,100.0,1 000.0 μmol/L groups (P1-5 groups).In group I,10％ intralipid was added to the culture media until the final concentration reached 100 μmol/L.In P1-5 groups,propofol was added to the culture media until the final concentration reached 0.1,1.0,10.0,100.0 and 1 000.0 μmol/L,respectively.The neurons were then incubated for 3 h.The proliferation of hippocampal neurons was determined by MTT assay at 12,24,36,48,60 and 72 h after the end of incubation with propofol.Results Compared with group C,the proliferation of hippocampal neurons was significantly decreased in P1-5 groups (P ＜ 0.05),while no significant change was found in group I (P ＞ 0.05).Compared with group P1,the proliferation of hippocampal neurons was significantly decreased in group P5 (P ＜ 0.05),while no significant change was found in P2-4 groups (P ＞ 0.05).Conclusion Propofol can decrease the proliferation of hippocampal neurons in fetal rats in vitro.

Objective To explore the level of Th2 type cytokines including IL-4, IL-10 and IL-13, and the immunoreg-ulation of cytokines in patients with neurocysticercosis. Methods Lymphocytes in patients with neurocysticercosis were separated from the blood sample with density gradient centrifugation and the total RNA was extracted by guanidine isothiocynate method. cDNA was synthesized by reversed transcription reaction. The target gene was then amplified by PCR. The PCR products were analyzed by electrophoresis. Results Results of RT-PCR showed that cytokines mRNA in lymphocytes of peripheral blcod were detected in 27 patients with neurocysticercosis but not in the other 3 cases. Among the positive cases, mRNA of IL-4, IL-10 and IL-13 was detected in 16, 17 and 14 cases respectively and mRNA of IL-4, IL-10 and/or IL-13 was detected in all the 27 cases. In the detection of lymphocytes in peripheral blcod of 10 healthy subjects, expression of IL-4 and IL-10 was found in only one case at low level. Conclusion The study revealed that Th2 associated cytokines were expressed at high level and the humoral immunocompetence was relatively strong in patients with neurocysticercosis.

A 65-year-old woman presented with intermittent right hand numbness and elevated serum creatinine for more than 2 months. The histological examination of kidney biopsy showed renal arterioles occlusion and interstitial fibrosis. Pathological abnormality was originally considered as a part of systemic atherosclerosis. Thus, rosuvastatin 20 mg/d, fosinopril 10 mg/d, metoprolol 47.5 mg/d and aspirin 0.1g/d were administrated. No improvement of renal function was seen. Further Congo red staining was applied. Diffuse amorphous eosinophilic substance was deposited in interlobular artery and small arteriolar artery. Combined with the abnormal free light chain (FLC) level and ratio (serum κ 340 mg/L, κ/λ 10.932), the diagnosis of systematic light-chain amyloidosis was confirmed. The patient received 3 courses of chemotherapy regimen as BCD (bortezomib 2 mg d1, 8, 15, 22, cyclophosphamide 0.3 g d1, 8, 15, 22 and dexamethasone 40 mg d1, 8, 15, 22). A hematologic partial response was achieved and serum creatinine decreased to 180 μmol/L.

Objective To examine the circulating glucose and body weight in the transgenic MKR mouse model who expressed dominant-negative IGF-1 receptor and insulin receptor in skeletal muscle leading to systemic insulin resistance and diabetes. Methods MKR mice were genotyped by PCR analysis of tail DNA.And in these mice we examined the circulating glucose and body weight once a week from 1 to 16 weeks of age, and the circulating insulin and glucose tolerance at age of two-month-old by using C57 mice as controls. Results The descendents of MKR mice kept hereditary feature. And these mice had hyperglycaemia from 3 weeks of age,and an increasing body weight slowly(P<0.01).Twenty-fold significant hyperinsulinemia was observed in MKR mice,and they were glucose intolerant in 2-month-old male and female (P<0.01).Conclusions The MKR mouse is an excellent model of type 2 diabetes

In recent years, laser microdissection followed by mass spectrometry (LMD/MS) has been successfully applied to the proteomic studies of formalin-fixed paraffin-embedded (FFPE) renal tissues. This new technique improves the diagnosis of kidney diseases and has a better potential for future clinical application. The review focuses on the use of this methodology for exploring the mechanisms, diagnosis and classification of kidney diseases including renal amyloidosis and membrane proliferative glomerulonephritis.
Formaldehyde ; Humans ; Kidney ; pathology ; Kidney Diseases ; diagnosis ; Laser Capture Microdissection ; Mass Spectrometry ; Proteomics ; Tissue Fixation

Objective To observe the clinical effect of magnesium isoglycyrrhizinate on moderate and severe nonalcoholic steatohepatitis(NASH) and analyse its mechanism. Methods 42 cases with moderate and severe nonalcoholic steatohepatitis were selected in our study. All patients were divided into observation group and control group randomly. Control group were received simvastatin while the observation group were received simvastatin combined with magnesium isoglycyrrhizinate treatment. The course was 6 weeks.The changes of NASH classiifcation, clinical symptom, liver function, lipid levels and liver ifbrosis items in two groups before and after treatment were observed and recorded. Results All patients were received 6 week treatment, none of them dropped out. The clinical symptoms were improved in both two groups. There were 5 severe NASH improved to moderate NASH, 8 moderate NASH improved to mild NASH in observation group while only 3 severe NASH improved to moderate NASH in control group. The difference of NASH classiifcation between two groups was signiifcant(P<0.05). Compared to pre-treatment, the AST, ALT, TBIL,γ-GT were decreased in both two groups. But the liver function items in observation were lower than control group(P<0.05). The lipid level were decreased in both two group and there were no signiifcant differences between two groups after treatment. The level of PC III, HA, C-IV were decreased in observation group while had no changes in control group. Conclusion The magnesium isoglycyrrhizinate could decrease the AST, ALT and lipid level, improve the classiifcation of liver ifbrosis, and had low rate of side effect during treatment.

Objective To analyze serum amyloid protein A (SAA) subtype and amino acid mutation sequence of the renal biopsy specimens from patients with renal amyloidosis secondary to ankylosing spondylitis (AS) by laser microdissection combined with mass spectometry.Methods Kidney biopsy formalin-preserved paraffin-embedded (FFPE) specimen slices were stained by Congo red,the positive areas of Congo red staining were selected by microdissection,after trypsin hydrolysis and filtration,peptide samples were subjected to liquid chromatography tandem mass spectrometry.Analysis softwares were used to evaluate the results,and the patient's amino acid sequence of SAA protein was compared to mutant amino acid sequence reported by literature or deduced from mutant SAA gene to determine whether there was a variation.Results SAA1 and SAA2 proteins with high abundance were identified by mass spectrometry,serum amyloid P and apolipoprotein E were also detected.No variation of SAA1 and SAA2 protein was detected.Conclusions The SAA1 and SAA2 proteins in AA amyloidosis secondary to ASwere identified for the first time,which enriched the pathogenesis of amyloidosis secondary to AS and provided a new method for the accurate classification of AA amyloidosis.

OBJECTIVE:To study the bioequiavailability of domestic roxithromycin tablets and imported ones.METH?ODS:20male healthy volunteers took single dose of150mg roxithromycin tablet orally in a random crossover design,blood concentrations were determined by LC-MS.RESULTS:The main pharmacokinetic parameters of domestic and imported tablets were determined respectively as follows,AUC 0～72 were(72.81?23.85)(mg?n)/L and(72.63?20.86)(mg?h)/L,AUC 0～∞ were(74.41?24.45)(mg?h)/L and(74.42?24.45)(mg?h)/L,C max were(6.46?1.51)mg/L and(6.58?1.55)mg/L,t max were(1.9?0.5)h and(1.8?0.5)h,t 1/2 were(13.56?1.35)h and(14.18?1.50)h,the relative bioavailability of the homemade tablet to imported one was(99.8?11.2)%.CONCLUSIONS:Domestic and imported roxithromycin are bioequivalent.

AIM: To compare the pharmacokinetics and relative bioavailability of the domestic and imported sustained-release tablets of gliclazide in healthy volunteers. METHODS:The study was performed by an four-period crossover design with singledose and multiple-dose administration. The plasmadrug concentrations of twenty male healthy volunteers were determined by liquid chromatography with mass spectrum detector method (LC-MS). RESULTS:The pharmacokinetic parameters after a single oral dose of the domestic and imported gliclazide tablets were (7.2+s 1.5) h and (6.9 +1.4) h for tmax, (13.4 ±1.2) h and (13.7 +1.3) h for t1/2, (2.4 +0.8) mg ·L-1and (2.3 ±0.6) mg· L-1 forcmax, (48 ±14)mg · h · L-1 and (48 +14) mg· h · L-1 forAUC0-60,(51+15) mg· h· L-1 and (50±14) mg· h· L-1for AUC0-∞, (22.4 ± 1.9 ) h and (22.8 ± 1.9 ) h for MRT, respectively. The steady state pharmacokinetic parameters after multiple doses of the domestic and imported gliclazide tablets were (6. 1 ± 1.4) h and (6.5+1.4) h for tmax, (4.6±0.9) mg· L-1 and (4.7±1.1) mg· L-1 for cmax, (0.23 ±0.08) mg ·L-1and (0.26±0.08) mg· L-1 forcmin, (1.6±0.3) mg·L-1 and (1.6±0.3) mg · L-1 for mean value of steady plasma-drug concentration (cav),(94±19) mg· h · L-1 and (95 ±20) mg · h · L-1forAUCss, (282 ±33)% and (283 ±43)% for degree of fluctuation DF ), respectively. The relative bioavailability of the domestic gliclazide tablet to the imported gliclazide tablet following a single and multiple dose were ( 102 ± 9) % and (99 ± 10 ) %, respectively. Main pharmacokinetic parameters between the two formulations in both single and multiples dose studies showed no statistical difference ( P >0.05 ). CONCLUSION: The result of two one side t-test shows that the two formulations are bioequivalent.