Objective To examine the clinical application of ultrasonography to detection of mesenteric lymph nodes in chil‐dren with intermittent abdominal pain.Methods A total of 196 children who underwent abdominal ultrasonography for differ‐ent reasons were divided into the intermittent abdominal pain group and non‐abdominal pain group.The location ,size and num‐ber of mesenteric lymph nodes were recorded.Results Statistical difference in the long‐axis diameter(P=0.005)and ratio of short‐to‐long‐axis diameter was found among patients with different ages in non‐abdominal pain group(P= 0.015) ,while no significant difference was seen in short‐axis diameter(P=0.773).No significant difference was observed in the diameter of each axis between different genders in non‐abdominal pain group.There was a statistical difference between abdominal pain group and non‐abdominal pain group in the incidence of lymph nodes with short‐axis diameter of 6 mm and larger(P=0.002)and long‐axis diameter of 14 mm and larger(P=0.007).Conclusion Mesenteric lymph node with short‐axis diameter larger than 6 mm should be considered enlarged in children ,but should not be diagnosed with mesenteric lymphadenitis.It’s common to find en‐larged mesenteric lymph nodes in children without abdominal pain.Further investigations with a larger number of patients are required to confirm these findings .

OBJECTIVETo explore the possible neurophysiologic mechanisms of propofol and N-methyl-D- aspartate (NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs.

METHODSModels of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups (with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal (ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups (n=10 per group): ip injection of 5 ml saline; ip injection of 5 ml of 10 mg/kg MK-801; ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock; ip injection of 5 ml of 200 mg/kg propofol; ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock; and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis.

RESULTSPropofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock.

CONCLUSIONElectroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.

Animals ; Depression ; psychology ; Dizocilpine Maleate ; pharmacology ; Electroshock ; Glutamic Acid ; analysis ; Learning Disorders ; prevention & control ; Male ; Memory Disorders ; prevention & control ; Phosphorylation ; Propofol ; pharmacology ; Rats ; Rats, Sprague-Dawley ; tau Proteins ; metabolism

Brucellosis ; diagnosis ; therapy ; Female ; Humans ; Malta ; Middle Aged ; Spondylitis ; diagnosis ; therapy

Objectives: To observe the efficacy of encephalo-duro-arterio-synangiosis (EDAS) or in combination with endovascular embolization in the treatment of patients with moyamoya disease complicating intracranial aneurysms and to investigate the therapeutic strategy for moyamoya disease complicating intracranial aneurysms. Methods: A total of 27 patients (28 aneurysms) with moyamoya disease complicating intracranial aneurysms confirmed by cerebral angiography were recruited. Nineteen patients were presented as hemorrhagic disease and 8 patients were presented as cerebral ischemic disease. For 10 patients with arterial trunk aneurysms, they were treated with endovascular embolization, and then were treated with unilateral EDAS 7-10 days after embolization. Three months later the contralateral EDAS were performed. As for the aneurysms located in the peripheral arteries (n = 17) , if the embolization could be performed (n =9), the aneurysms were obliterated with coils or ONYX glue, otherwise the ipsilateral EDAS should be performed (n = 8). Results: Circled digit oneEighteen aneurysms in 19 patients (20 aneurysms) were embolized successfully and 2 patients were failed (one aneurysm in lenticulostriate artery and the other in posterior choroidal artery). After embolization, 3 patients with peripheral aneurysms had contralateral limb weakness, and recovered within 1 week to 3 months. Circled digit twoThere was no bleeding and rebleeding for 10-60 months follow-up after EDAS. Among the patients with cerebral ischemia, 2 had recurrence of TIA within 3 months after EDAS, but they had no recurrence of the symptom after 3 months. Circled digit threeThe angiography of 21 patients (21 aneurysms) 3 to 15 months after EDAS showed that the aneurysms treated with embolization did not reoccur (12 aneurysms); 8 of 9 peripheral aneurysms without eml)olization were disappeared; and significant retention of contrast agent in 1 aneurysm was found. All 21 patients showed better communication between the superficial temporal artery and intracranial angiogenesis. Conclusion: Endovascular embolization is one of the important means for the treatment of moyamoya disease complicating intracranial aneurysms. EDAS may promote the occlusion of peripheral aneurysms.

Adult ; Aged ; Female ; Heart Failure ; complications ; therapy ; Humans ; Hypothyroidism ; complications ; therapy ; Middle Aged

Objective To explore the possible neurophysiologic mechanisms of propofol and N-methyl-D-aspartate (NMDA) receptor antagonist against learning-memory impairment of depressed rats without olfactory bulbs.
Methods Models of depressed rats without olfactory bulbs were established. For the factorial design in analysis of variance, two intervention factors were included: electroconvulsive shock groups (with and without a course of electroconvulsive shock) and drug intervention groups [intraperotoneal (ip) injection of saline, NMDA receptor antagonist MK-801 and propofol. A total of 60 adult depressed rats without olfactory bulbs were randomly divided into 6 experimental groups (n=10 per group):ip injection of 5 ml saline;ip injection of 5 ml of 10 mg/kg MK-801;ip injection of 5 ml of 10 mg/kg MK-801 and a course of electroconvulsive shock;ip injection of 5 ml of 200 mg/kg propofol;ip injection of 5 ml of 200 mg/kg propofol and a course of electroconvulsive shock;and ip injection of 5 ml saline and a course of electroconvulsive shock. The learning-memory abilities of the rats was evaluated by the Morris water maze test. The content of glutamic acid in the hippocampus was detected by high-performance liquid chromatography. The expressions of p-AT8Ser202 in the hippocampus were determined by Western blot analysis.
Results Propofol, MK-801 or electroconvulsive shock alone induced learning-memory impairment in depressed rats, as proven by extended evasive latency time and shortened space probe time. Glutamic acid content in the hippocampus of depressed rats was significantly up-regulated by electroconvulsive shock and down-regulated by propofol, but MK-801 had no significant effect on glutamic acid content. Levels of phosphorylated Tau protein p-AT8Ser202 in the hippocampus was up-regulated by electroconvulsive shock but was reduced by propofol and MK-801 alone. Propofol prevented learning-memory impairment and reduced glutamic acid content and p-AT8Ser202 levels induced by electroconvulsive shock.
Conclusion Electroconvulsive shock might reduce learning-memory impairment caused by protein Tau hyperphosphorylation in depressed rats by down-regulating glutamate content.

Objective To investigate the effects ofamiodarone (AMD) on simvastatin (SV) in human liver microsomes and the possible underlying mechanisms. Methods Time-, NADPH- and concentration-dependent inhibitions were tested in HLM. The logarithm of relative inhibition values was plotted versus preincubation time (0, 5, 10, 15, 20min) for a series concentration of AMD used (0, 2, 5,25, 50 μ mol/L), and the slopes determined by linear regression. These slope values represente the observed inactivation rate constants (kobs). A double-reciprocal plot was then constructed using the reciprocal of the ko～ (y-axis) and the reciprocal of the associated inhibitor concentration (x-axis) to estimate the values ofkinact and K, which were two principal kinetic constants that were specific for mechanism-based inhibition (MBI).drug-drug interactions (DDI) potential was predicted based on in vitro data and by using the in vitro-in vivo extrapolation. Results The time-, concentration- and NADPH-dependent charactga'istics confirmed that when SV was the substrate of CYP3A4, the inhibition of AMD to CYP3A4 is MBI. Kj and kinact value were calculated to be 5.1 μ mol/L and 0.018min-1 The Clint of SV was reduced 2.96-5.63 fold when it was administrated with AMD. Conclusion Based on the results, AMD would inhibit SV metabolism via the mechanism-based manner, which would lead to DDI when they are taken together. Careful clinical observation is recommended when AMD and SV have to be simultaneously prescribed.

Objective To evaluate the effect and safety of pseudomonas aeruginosa injection (PA-MSHA) combined with ulinastatin (UTI) injection in the treatment of patients with malignant pleural effusion and/or ascites.Methods 52 patients were randomly divided into PA-MSHA group and PA-MSHA combined with UTI group,each group including 26 patients.All patients were given ultrasonic testing before treatment.The single drug group was given PA-MSHA 10 ml intrapleural and/or intraperitoneal injection.The two-drug combination group was given PA-MSHA 10ml and UTI 300 000 U,twice per week.Evaluation of the efficacy and adverse reaction was performed after 4 times.Results The effective rate of single PA-MSHA group was 34.6 ％ (CR 1 case,PR 8 cases),while the effective rate of PA-MSHA combined with UTI group was 61.5 ％ (CR 2 cases,PR 14 cases).The effective rate of PA-MSHA combined with UTI group was statistically higher than that of single PA-MSHA group (P ＜ 0.05).8 cases got fever in single PA-MSHA group,3 cases in PA-MSHA combined with UTI group got fever,side effect had no statistical significance (P ＞ 0.05).Conclusion PA-MSHA combined with UTI has better effect in the treatment of patients with malignant pleural effusion and/or ascites compared with single PA-MSHA,and both treatments have low side effects.

OBJECTIVE:To prepare anti-tumor drug H6(lactone compound)polymeric micelles,and to investigate its in vitro anti-tumor effects. METHODS:Using mPEG2000-PCL4000 as carrier,H6/mPEG2000-PCL4000 micelles were prepared. Using particle size, PDI and 48 h whether to produce precipitation as indexes,feeding ratio,H6 concentration,volume ratio of organic solvent were screened. The encapsulation efficiency and drug-loading amount of micelle were all detected. MTT assay was used to detect the tox-icity of micelles and H6 solution to human non-small cell lung cancer cell A549 and human lung cancer cell H460. RESULTS:The screened formulation was as follows as feeding ratio of 1∶25,H6 concentration of 2 mg/mL,the ratio of ethanol to chloroform of 1∶1(V/V). The parameters of prepared H6/mPEG2000-PCL4000 micelles were as follows as particle size of(40.74±0.116 3)nm,PDI of(0.101±0.006),encapsulation efficiency of(94.87±0.016 3)%,drug-loading amount of(7.07±0.001 5)%(n=3). IC50 of mi-celles and H6 solution to A549 cell were 15.62 and 12.57 nmol/L;IC50 of micelles and H6 solution to H460 cell were 27.68 and 15.19 nmol/L. CONCLUSIONS:H6/mPEG2000-PCL4000 micelles are prepared successfully and show in vitro anti-tumor effects.