Child ; Humans ; Inflammatory Bowel Diseases ; etiology ; pathology

Objective To evaluate the role of oxidative stress in the spinal neurotoxicity induced by ropivacaine in rats.Methods Ninety pathogen-free male Sprague-Dawley rats,weighing 250-320 g,aged 3 months,in which intrathecal catheter was successfully implanted into L5,6 interspace without complications,were randomly divided into 3 groups (n =30 each) using a random number table:control group (group C),ropivacaine group (group R),and antioxidant Tempol group (group T).The rats received 1％ ropivacaine 1.2 μg/g for 8 times at 1.5 h intervals through the catheter in R and T groups,while the rats received the equal volume of normal saline instead in group C.In T group,Tempol 20 μg/g was injected intrathecally at 4,8,12,24,48 and 72 h after the last injection of ropivacaine.The rats were sacrificed at 1,3,5,7 and 14 days after the end of ropivacaine injection,and their lumbar enlargements were removed for TUNEL staining to detect the cell apoptosis.SOD activity was determined by colorimetry and MDA content was measured using TBA photoelectric colorimetry.Apoptosis index was calculated.Results Compared with group C,apoptosis index and MDA content were significantly increased,and SOD activity was decreased in R and T groups.Compared with group R,apoptosis index and MDA content were significantly decreased,and SOD activity was increased in group T.Conclusion Oxidative stress is involved in the development of spinal neurotoxicity induced by ropivacaine in rats.

Objective To develop a new method, the bone marrow stromal cells (BMSCs)-mediated tissue engineering technique combined with mosaicplasty, for repair of osteochondral defects and integration of gaps. Methods BMSCs from 12 Chinese goats were cultured and proliferated in vitro. Prior to the BMSCs harvest, osteochondral defects, 5 mm in diameter and 3 mm in depth, were created in the femoral medial condyles of both the goat's hind limbs. When the mosaicplasty (osteochondral autograft transplantation) was performed, the BMSCs, which had been harvested and compounded with hyaluronic acid, were injected into the gaps between the osteochondral autografts in the left hind limb. The right hind limb which only received osteochondral autograft transplantation without BMSCs served as a control. At four, eight and 16 weeks post-operatively, samples of the repaired defects were harvested and assessed by histological evaluation, immunohistochemical analysis and glycosaminoglycan (GAG) quantification. In both groups 16 weeks post-operatively, the GAG quantification was analyzed by one-way ANOVA and least significant difference (LSD) method. Results At all the time points, the cartilage autografts in both groups survived as hyaline cartilage and presented no significant difference from the surrounding native cartilage. In the group filled with BMSCs compound, the gaps were replaced by regenerated hyaline cartilage and disappeared; however, in the control group, the osteochondral autografts were still distinct from the surrounding normal cartilage, though the gaps were replaced by fibrous tissue or fibrous cartilage. Immunohistochemical analysis of typeⅡcollagen showed positive staining in the matrix of transplanted and regenerated cartilage. The Alcian blue method also confirmed a significantly less GAG content in the regenerated tissue in gaps in the control group than in the treatment group and in the normal cartilage. Conclusion Since tissue engineering combined with mosaicplasty can promote gap integration and cartilage healing, the method can be an ideal way for osteochondral defect repair.

The metabolic profile of pseudolaric acid B (PB) was investigated by using in vivo and in vitro tests. Pseudolaric acid C2 (PC2) was identified as the specific metabolite of PB in plasma, urine, bile and feces using HPLC and HPLC-ESI/MS(n) after both oral and intravenous administration to rats, and almost no prototype was detected in all kinds of samples. The metabolic behaviors of PB orally administered in rats treated with antibiotics to eliminate intestinal microflora were identical with those in untreated rats, demonstrating that the metabolism of PB is independent of intestinal microflora. PB was stable in 48 h respective incubation with artificial gastric juice and artificial intestinal juice, suggesting that neither pepsin nor trypsin is in charge of metabolism of PB, and also demonstrating that PB is stable in both pH environments of gastric tract and intestinal tract. In vitro research on metabolism of PB in rat liver microsomes incubation revealed that little PB was metabolized and that the proposed metabolites were the demethoxy and demethoxydecarboxy products of the prototype. The amount of metabolites was extremely low compared with the prototype, indicating that liver microsomes are not responsible for the metabolism of PB either. PB was gradually metabolized into PC2 during 1 h in whole blood incubation in vitro, and the metabolic process showed dynamically dependent manner with incubation time. Once absorbed into blood, PB was quickly metabolized into PC2, accordingly, little prototype was detected in all kinds of samples. The metabolism was attributed to the rapid hydrolysis of C-19 ester bond by plasma esterase. These results clarified the metabolic pathway of PB for the first time, which was of great significance to identify the in vivo active form and interpret acting mechanism of the active compounds of P. kaempferi.

The preliminary metabolic profile of total diterpene acid (TDA) isolated from Pseudolarix kaempferi was investigated by using in vivo and in vitro tests. Pseudolaric acid C2 (PC2) was identified as the predominant metabolite in plasma, urine, bile and feces after both oral and intravenous administrations to rats using HPLC-UV and HPLC-ESI/MS(n), and demethoxydeacetoxypseudolaric acid B (DDPB), a metabolite proposed to be the glucoside of PC2 (PC2G), as well as pseudolaric acid C (PC), pseudolaric acid A (PA), pseudolaric acid A O-beta-D glucopyranoside (PAG), pseudolaric acid B O-beta-D glucopyranoside (PBG) and deacetylpseudolaric acid A (DPA) originated from TDA could also be detected. It was demonstrated by tests that the metabolism of TDA is independent of intestinal microflora, and neither of pepsin and trypsin is in charge of metabolism of TDA, TDA is also stable in both pH environments of gastric tract and intestinal tract. The metabolites of TDA in whole blood in vitro incubation were found to be PC2, DDPB and PC2G, which demonstrated that the metabolic reaction of TDA in vivo is mainly occurred in blood and contributed to be the hydrolysis of plasma esterase to ester bond, as well as the glucosylation reaction. These results clarified the metabolic pathway of TDA for the first time, which is of great significance to the in vivo active form and acting mechanism research of P. kaempferi.

Objective To evaluate the efficacy and safety of bicyclol tablet on hepatic lesions caused by Epstein-Barr virus( EBV) infection in children.Methods A single-center controlled retrospective study was conducted in 121 children with hepatic lesions caused by EBV infection for evaluating safety,tolerability, and efficacy of treatment with bicyclol tablets or Glycyrrhizin capsules.Childer n in bicyclol group ( n=63 ) were treatedw ith bicyclol at blets and cotn rol group ( n =58 ) were treated with Glycyrrhizin capsules.The course of the treatment were both 8 weeeks for two groups.The level of the EBV load pretreatment and plas-ma aminotransferase,blood routine,urine routine pretreatment and 1 week,4 weeks and 8 weeks after treat-mentw ere analyzed er trospectively.Rse ults (1) The pal smaA LT level sigin ficantly decreased in theb icy-clol group compared with that in the contro l group(P<0.01), se pecai lly the levle after 8 weeks treatm ent. (2) Bicycol l was more effce tive in the bicyclol group than Glycyrrhizin capslu se in the control group( P<0.01).(3) Both grousp had no significantlya dvesr e events.Conclusion Bicyclol tablet can derc ease plas-ma aminotransferase level,espce ially ALT,inc hildren caused by EBV infection with better efficiency and safety.

Purpose To assess the left ventricular global systolic function changes using three-dimensional speckle tracking imaging (3D-STI) in female patients with subclinical hypothyroidism (SHT) undergoing L-thyroxine treatment. Materials and Methods Thirty-eight female patients with SHT and 40 healthy female volunteers of the same age (control group) were selected, all the SHT patients received L-thyroxine therapy and were followed for 1 year after euthyroid status was achieved; all the participants underwent blood biochemical examinations, complete conventional echocardiographic and 3D-STI examinations, left ventricular end-diastolic diameter (LVEDd), left ventricular end-systolic diameter (LVEDs), interventricular septal depth (IVSd), left ventricular posterior wall depth (LVPWd), left atrial diameter (LAD), diastolic mitral flow spectrum of A peak, left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular ejection fraction (LVEF) of the two groups were compared, and the correlation of parameters of three dimensional left ventricular global longitudinal strain (GLS), global circumferential strain (GCS), global radial strain (GRS), global area strain (GAS), and thyroid stimulating hormone (TSH) with each parameter was analyzed. Results IVSd and LVPWd in the study group were higher than those of the control group (t=3.30 and 3.64, P<0.05). Compared with the control group, GLS, GCS, GRS and GAS of left ventricular of SHT patients in the study group were significantly lower (t=8.60, 11.95, 9.78 and 5.92, P<0.05) before treatment. GLS, GCS, GRS and GAS of SHT patients improved after L-thyroxine therapy, and the difference was statistically significant (t=6.91, 9.41, 6.46 and 4.31, P<0.05).TSH level was negatively correlated with E/A ratio and E (r= - 0.39 and - 0.42, P<0.05), and also negatively correlated with GLS, GCS, GRS and GAS (r= - 0.38, - 0.56, - 0.33 and - 0.41, P<0.05). Conclusion Left ventricular global systolic function changes of SHT patients before and after L-thyroxine treatment can be evaluated properly using 3D-STI.

Cytochrome P450 (CYP450) is a key element in the Ganoderma triterpenoid biosynthetic pathway. The catalytic reaction process for CYP450 requires NADPH / NADH for electron transfer. After searching the genome dataset of Ganoderma lucidum, the unique sequence encoding CYP450 and NADPH were discovered, separately. The open reading frames of GLCYP450 and GLNADPH were cloned separately using RT-PCR strategy from G lucidum. The appropriate restriction enzyme cutting sites were introduced at the 5' and 3' ends of gene sequence. The genes of GLCYP450 and GLNADPH were recombined into the yeast expression vector pESC-URA, leading to the formation of the yeast expression plasmid pESC-GLNADPH-GLCYP450. This study provides a foundation for researching Ganoderma triterpene biosynthesis using the approach of synthetic biology.

Objective To research the functional role of thyroidal motilin and the effects of electric excitation of the paraventricular nuclei(PVN) on gastric motility and the levels of motilin in thyroid and plasma.Methods The expression of motilin in rat and human thyroid was detected by immunofluorescence staining.A phase Ⅲ-like contraction was recorded before and after thyroidectomy and after PVN excitation.The changes in concentrations of plasma FT3,FT4 and motilin were determined via radioimmunoassay (RIA).c-Fos expression of PVN after thyroidectomy and motilin expression in thyroid after PVN excitation were observed by immunohistochemical staining.Results There were motilin immunoreactive cells in rat and human thyroid.The phase Ⅲ-like contraction and concentration of motilin in plasma decreased significantly when measured on the second and fourth days after thyroidectomy(2d,P＜0.01 ;4d,P＜0.05).The expression of c-Fos in PVN after thyroidectomy was significantly increased(P＜0.05).An electric excitation of PVN could increase the concentration of motilin in plasma and thyroid and increase corresponding gastric motility in rats (P ＜0.05).The increased phase Ⅲ-like contraction by PVN excitation could be partially inhibited by administration of motilin receptor antagonist,GM-109 (P＜0.05).Excitation of PVN in thyroidectomized rats resulted in lower plasma motilin and less intense phase Ⅲ-like contraction of stomach,as compared with the sham operated control group(P＜0.05).Conclusion Motilin from the thyroid may be secreted into the peripheral plasma to affect gastric motility and PVN may modulate gastric motility and motilin expression in the thyroid.

Objective To report the MRI findings of brain damage obsenrved in neonatal patients who suffered from isolated hypoglycemia and to explore the value of diffusion-weighted imaging(DWI) inearly detection of neonatal hypoglycemic brain iniun,. Methods Twelve neonates with isolated hypoglycemia(10 of the 12 were diagnosed to suffer from hypoglycemic encephalopathy)were enrolled in this study.They were first scanned at age from 3 days to 10 days with Tl WI,T,WI and DWI(b is 0 s/mm2,1000 s/mm2),and 4 of them were then scanned from 7 days to 10 days following the initial scan.All acquired MR images were retrospectively analysed.Results First series of DWl images showed distinct hyperintense signal in 11 cases in several areas including bi lateral occipital cortex(2 cases),right occipital cortex(1 case),left occipital cortex and subcortical white matter(1 case),biIateral occipital cortex and flubcortical white matter(2 cases),bilateral parieto-occipital cortex(2 cases),bilateral parieto-occipital cortex and subcortical white matter(2 cases),the splenium of corpus catlosum(4 cases),bilateral corona radiata(2 cases),left eaudate nucleus and globus pallidus(1 case),bilateral thalamus(1 case),bilaterally posterior limb of internal capsule(1 ease).In the initial T1 WI and T2,WI images,there were subtle hypointensity in the damaged cortical areas(3 cases),hyperintensity in the bilaterally affected occipital cortex(1 case)on T1 weighted images,and hyperintensity in the affected cortex and subcortieal white matter with poor differentiation on T2 weighted images.The followed-up MRI of 4 cases showed regional encephalomalaeia in the affected occipital lobes(4 cases),slightly hyperintensity on T2 weighted images in the damaged occipital cortex(2 cases),extensive demyelination(1 case).disappearance of hyperintensity of the splenium of corpus callosum(1 case),and persistent hyperintensity in the splenium of corpus callosum (1 case)on T2 weighted images.Conclusion The findings suggest that posterior parieto-occipital regions are most frequently injured in neonatal period due to severe hypoglycemia.DWI is a useful technique in the early detection and evaluation of hypoglycemic brain injury of neonates.