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.

Air ; analysis ; Air Pollutants, Occupational ; analysis ; Ethane ; analogs & derivatives ; analysis ; Nitroparaffins ; analysis ; Uncertainty ; Workplace

Objective To assess the reliability and validity of the Tree-Drawing Test in medical college students.Methods The study randomly selected 312 aged 19 to 23-year-old medical students to take part in TreeDrawing Test.In addition,a total of 275 college students were selected to receive re-test,30 days late and Pearson correlation coefficient of two tests were calculated.The three raters were invited to assess 30 trees painting score,analyzing the Kendall coefficient of concordance between the scores to verify raters' reliability; parts of students also participated in the 16PF test,SAS,SDS test,analyzing the correlation coefficient between the various test results,in order to assess the effectiveness of the Tree-Drawing Test.Results The re-test reliability in different time was 0.570-0.733 and 0.341-0.713 (P＜0.05),the raters' reliability was 0.491 ～ 0.626(P＜0.05),there are some correlations between Tree-Drawing Test and 16PF,SAS,SDS.Conclusion The Tree-Drawing Test has good reliability and validity; it can be applied to the detection of college students' psychological assessment and psychological problems.

BackgroundRecent studies showed that diabetic retinal neuropathy is an earlier and more dangerous complication and neurotrophin has a protective effect on retina.ObjectiveThe present study was to observe the changes of brain derived neurotrophic factor (BDNF),its receptor TrkB,signal pathway protein phosphatized extracellular signal-regulated protein kinase1/2 (p-ERK1/2) and c-fos in the retina after injection of BDNF into the vitreous in STZ induced Wistar diabetic rats.MethodsWistar rats aged 9 weeks-old were randomly divided into BDNF injection group,diabetes mellitus (DM) control group and normal control group and 20 rats for each group.STZ was intraperitoneally injected in the rats of BDNF injection group and DM control group to create the experimental DM.BDNF was intravitreously injected in the rats of BDNF group 2 weeks after administration of STZ in three-day interval for 5 times,and BSS containing O.1％ bovine serum albumin (BSA) was used at the same way in the DM control group and normal control group.The retina was isolated for hybridization in situ for BDNF,and TrkB,p-ERK1/2 and c-fos.Levels in retina were detected using sandwich method ELISA.ResultsThe number of BDNF positive cells and the gray scale were lower obviously in the rat retina of DM control group than those of BDNF injection group and normal control group,showing significant differences among the 3 groups ( F =102.36,92.55 ;P＜0.05 ).ELISA assay showed that TrkB,p-ERK1/2 and c-fos values in retina were statistically significantly different among the 3 groups ( F =92.54,95.46,94.84,P＜0.05 ).The TrkB level in retina was statistically reduced,but the p-ERK1/2 and c-fos levels in retina were increased statistically in DM control group compared with BDNF injection group and normal control group( P＜0.05 ).No statistical difference was found in TrkB,p-ERK1/2 and c-fos values between the BDNF injection group and normal control group(P＞0.05).ConclusionsThe injection of BDNF into the vitreous cavity can protect retina from downregulating BDNF and TrkB levels and up-regulating the p-ERK1/2 and c-fos protein levels in the early stage of DM.