The pathophysiology of allergic disease such as asthma and allergic rhinitis tell the similar story: when the endogenous and exogenous inflammatory mechanisms occur disorder, the body may begin with inflammatory cell activation, namely through the release of cytokine and inflammatory mediator role in the corresponding target cells, activate the sensory nerve fiber, acting on the cell organ specificity effect, clinical symptoms. This article is divided into the following five parts focused on the research progress of allergic inflammatory diseases: (1) inflammatory cells; (2) staphylococcus aureus superantigen; (3) small molecules (cytokines, inflammatory mediators, lipid classes medium); (4) nerve fibers and effect cells; (5) genetic and epigenetic factors.
Asthma ; physiopathology ; Cytokines ; immunology ; Humans ; Hypersensitivity ; physiopathology ; Inflammation ; physiopathology ; Respiratory System ; physiopathology ; Rhinitis, Allergic ; physiopathology

Medical imaging teaching depends on support from multimedia database which is constructed with image information provided by PACS/HIS ( Picture archiving and communication system/Hospital information system ).This paper evaluated construction,administration and application of the multimedia database,and illustrated the importance of PACS/HIS in construction of the database,as well as of the database in medical imaging teaching.

AIM:To establish a new rat model of depression by the antagonistic relationship of antagonizing pairs of neurotransmitters in the brain.METHODS:Dopamine D1 receptor antagonist SCH23390 was injected into the hippocampus of the rats by microinjection at low, medium and high doses (1, 2 and 4 g/L) to establish a depression model.After modeling, the sucrose consumption, open-field and novelty suppressed feeding tests were used to evaluate the behaviors of the rats, and screen out the best modeling drug dose.The model of depressive rats was induced using the best modeling drug dose and the model rats were observed for 2 weeks.The stability of the model was evaluated by behavioral tests, and the contents of IL-1β and TNF-α in cerebrospinal fluid (CSF) were measured by ELISA to evaluate the safety of the model.The levels of the antagonizing pairs of neurotransmitters in the cerebral cortex and hippocampus were analyzed by the method of high-performance liquid chromatography-mass spectrometry (HPLC-MS), so as to evaluate the pathological characteristics of neurotransmitter imbalance in the brain of the model rats.RESULTS:After modeling, the rat weight, sucrose preference rate, and horizontal motion and vertical motion scores of open-field test were significantly decreased in eACh dose model group, and feeding latent periods of novelty suppressed feeding test were significantly increased, indicating a typical depressive behavior.The rats with the medium dose (2 g/L) of SCH23390 had the most significant depressive behavior.At 2 weeks after modeling, compared with the normal control group, the weight, sucrose preference rate, and horizontal motion and vertical motion scores in medium dose group were significantly decreased (P<0.01), while the feeding inhibition time was significantly increased (P<0.05).No significant difference in the content of IL-1β and TNF-α in the CSF of normal control group, blank control group and medium dose group was observed, indicating that the model did not cause obvious inflammatory injury, and the modeling method was safe.Compared with blank control group, the contents of 5-HT, NE and Glu in the left hippocampus of rats in medium dose group were significantly increased (P<0.01), and the content of DA and ACh showed decreasing trends.The contents of 5-HT, NE and Glu in the right hippocampus of the rats were significantly increased (P<0.05), and the contents of DA and ACh showed decreasing trends.The content of Glu in cerebral cortex was significantly increased (P<0.05), the contents of 5-HT and NE showed increasing trends, and the contents of DA and ACh showed decreasing trends, indicating that the model was basically consistent with the pathological features of neurotransmitter imbalance in the brain of depression.CONCLUSION:This method can successfully replicate the rat model of depression, which has the characteristics of typical and persistent symptoms, fast modeling, and safe and easy operation.Using the dosage of 2 g/L is more suitable.

0.05),but it was significantly lower than that in LTP group (P

AIM To develope a reversed phase high performance liquid chromatography method to determine free concentrations of morphine (M) in the solution of human haemoglobin (Hb). To study the binding of M to haemoglobin, and evaluate the binding parameters of M to Hb. METHODS An ultrafiltration technique was used to recover morphine from the samples. Morphine was analyzed using a kromasil column (150 mm?4 6 mm) and a mobile phase of 0 1% tyiethylamine methanol (75∶25,v/v). The mobile phase pH was adjusted to 7 0 by phosphoric acid. The detection was set at 283 nm. RESULTS The ultrafiltration recovery of morphine was 98 5%. The Hb binding of M was concentration dependent of Hb and M. There were single typed binding sites for M to human Hb. The parameters determined were 4 1 for N and 340 mol?L -1 for K when the concentration of M and Hb were added from 8 50?10 -5 ～1 17?10 -2 mol?L -1 and 1 29?10 -4 ～8 57?10 -4 mol?L -1 respectively. CONCLUSION An ultrafiltration technique has proved to be simple and rapid for free drug determination. It is suitable for drug protein binding study.

Objective To construct the expression plasmid of human PAK4 gene and identify its recombinant protein expression.Methods Total RISA was extracted from human breast cancer MCF-7 cells.The hPAKA coding sequence was amplified by polymerase chain reaction (PCR) method and subcloned into pEBG vector.After the target region was sequenced.the plasmid was transfected into HEK293 cell line.The expression of the recombinant plasmid in HEK293 cells was proved by Western blot.Results hPAKA had been constructed into the expressing vector pEBG successfully.The length of the fragment was 1 800 bp,identified by restriction enzymes digestion.The expression of pEBG-hPAK4 fusion protein was detected by Western blot,with a molecular weight 94 KDa and was pulled down by Qutathione Sepharose 4B.Conclusion The recombinant plasmid was successfully cloned into eukaryotic expressing vector,and the expression of pEBG-hPAK4 fusion protein was identified and pulled down by Glutathione Sepharose 4B.

Objective To determine the risk factors for postoperative respiratory complications and establish a preoperative risk scoring system.Methods Patients,aged ≥ 18 yr,scheduled for elective surgery or undergoing emergency operation under total intravenous anesthesia or field block anesthesia,were studied.The general data of patients,preoperative SpO2,and conditions of respiratory infection,anemia or cough tests within 1 month before surgery were recorded.The operative sites (thorax,upper abdomen,other sites),duration of operation,type of surgery (emergency operation/elective operation),and methods of anesthesia (general anesthesia/field block) were also recorded.According to the development of respiratory complications within 1-7 days after operation,the patients were divided into either postoperative respiratory complication group or non-postoperative respiratory complication group.The risk factors of which P values were less than 0.05 would enter the multivariate logistic regression analysis to pick out the risk factors for postoperative respiratory complications and to establish a preoperative risk scoring system.Results Two thousand and thirty-seven patients completed the study.A total of 493 patients developed postoperative pulmonary complications,and the incidence was 24.20％.Statistical analysis showed that the risk factors associated with postoperative respiratory complications included age ＞ 50 yr,preoperative SpO2 ≤90％,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,respiratory infections at one month before operation,preoperative anemia,upper abdominal and intrathoracic operations,duration of operation ＞ 2 h.A preoperative risk scoring system was established for postoperative respiratory complications based on 6 independent risk factors:preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.The incidence of postoperative respiratory complications was 61.9 ％,52.8 ％ and 17.2 ％ in high-risk,medium-risk and low-risk groups,respectively,and there was significant difference between the three groups (P ＜ 0.01).Area under the ROC curve was 90％ for subsamples and 87％ for the validation subsamples.Conclusion Age ＞ 50 yr,high ASA physical status,duration of smoking ＞ 1 yr,positive cough tests,preoperative SpO2 ≤90％,anemia,respiratory infections at one month before operation,duration of operation ＞ 2 h,upper abdominal and intrathoracic operations are risk factors for postoperative respiratory complications.A preoperative risk scoring system is successfully established for postoperative respiratory complications based on preoperative SpO2,anemia,respiratory infections,age,duration of operation and operative sites.

Objective To investigate the productive effects of baicalin on the male rats with ischemic brain injury and its effects on serum progesterone level in rats; To explore the possible mechanism of baicalin in brain protection. Methods Adult SD male rats were used to create a permanent left middle cerebral artery occlusion model. The rats were evenly divided into model group, baicalin group, inhibitor group, and sham-operation group (without inserted into the intraluminal thread) according to the neurological function scores. At different time points after modeling, the neurological function scores and the grip strength of double foreleg were measured, and the reduction rate of grip strength was calculated. Serum progesterone and adrenocorticotrophic hormone (ACTH) were detected by ELISA. Results Compared with the sham-operation group, the neurological function of rats in the model group was impaired, the grip strength of double foreleg was significantly reduced. 7 days after treatment, compared with the model group, the neurological function score of baicalin group was lowered, grip strength of double foreleg was recovered, reduction rate of grip strength was reduced (P<0.05); compared with the baicalin group, protective effects of baicalin on neurological function was lowered in inhibitor group (P<0.05). 7 days after treatment, compared with the model group, the serum progesterone level in baicalin group was significantly higher (P<0.01), and ACTH level showed an increasing trend; compared with the baicalin group, serum progesterone and ACTH levels in the inhibitor group decreased (P<0.05). Conclusion The protective effects of baicalin on the male rats with ischemic brain injury may be related to the regulation of progesterone.

Objective To investigate the effects of baicalin on serum progesterone and related hormones in female normal and cerebral ischemia rats; To explore whether baicalin plays a role in cerebral protection of neurological functions by regulating progesterone levels.Methods With vaginal smear method, the adult estrus female SD rats were selected and divided into normal group, baicalin normal group, and molding groups. The left side of the middle cerebral artery of rats in the molding groups was blocked to establish the permanent middle cerebral artery occlusion (pMCAO). After modeling, the rats were randomly divided into model group, baicalin treatment group, progesterone treatment group and progesterone inhibitor group. The baicalin normal group and baicalin treatment group were given intraperitoneal injection of baicalin solution; the normal group and model group were given normal saline of the same quantity; progesterone treatment group was given intramuscular injection of progesterone; progesterone inhibitor group was given intraperitoneal injection of baicalin solution and intragastric administration of mifepristone solution.The neurological function deficit scores were evaluated and rat forelimb holding power was detected by Grip Strength Meter respectively at different time points. Serum was taken from the rats and the progesterone and related hormones levels in the serum of every group were measured by ELISA. Results Compared with normal group, neurological functions of rats in molding groups were damaged, and neural functional behavior scores of different time points were the most strongly increased (P<0.001), and rat forelimb holding power was the most strongly reduced (P<0.001). 5 days after treating, baicalin showed the trend of improvement of neurological functions (P>0.05) and more significant improvement of the forelimb holding power (P<0.01); 10 days after modeling, baicalin treatment group significantly increased neural functional behavior scorce (P<0.001) and the most significantly improved the forelimb holding power (P<0.001). Compared with baicalin treatment group, the progesterone inhibitor group had a significant inhibitory effect on neural functional recovery (P<0.05) 10 days after modeling, and the group also had a significant inhibitory effect on the recovery of holding power (P<0.05) 5 days and 10 days after treating. At the same time, compared with the model group, progesterone level in baicalin treatment group increased significantly (P<0.05), and FSH and LH decreased (P>0.05).Conclusion After applying mifepristone to block progesterone, baicalin neurologic protection is significantly inhibited. The results demonstrated that baicalin may play a role in cerebral protection via up-regulating serum progesterone level.

OBJECTIVE To investigate the effects of lead exposure on the permeability,secretion and transportation function of blood-cerebro-spinal fluid barrier (BCB)of rats in order to provide the theo-rical basis for elucidating the mechanis m of lead induced neurotoxicity.MEHTODS 60 SPF SD rats were rando mly divided into 4 groups,including a control group and three doses lead exposed groups. Rat in the lead exposure groups were given drinking water containning 0.05%,0.1 % and 0.2% lead acetate (at dose of 80,160,320 mg·kg -1 )for 8 weeks.Laser scanning confocal microscopy was uti-lized to determine the lead content in seru m,cerebrospinal fluid (CSF)and choroid plexus sa mples. Morris maze was used to test learning and me mory.Fe moral artery perfusion of Evans blue (EB)and fluorescein sodiu m (NaFI)was performed to measure BCB permeability function.Confocal laser scan-ning was applied to detect junction adhesion molecule (JAM)and occludin protein expression in choroid plexus.ELISA was used to measure the concentration of transthyretin (TTR)and leptin in seru m and CSF.RESULTS The lead content in seru m,choroid plexus and CSF significantly increased,especially the lead level in CSF.Morris water maze data showed that escape latency of rat in lead acetate 160 and 320 mg·kg -1 group were 52 ±12,(89 ±19)s,respectively,longer than that of control group 〔(28 ±7)s, P<0.05〕.The ti mes across platform of rats in lead acetate 160 and 320 mg·kg -1 group were lower than that of control group(P <0.05).The NaFI content in CSF of rats in all lead acetate exposure groups were 0.94 ±0.09,1 .02 ±0.03 and (1 .08 ±0.18)mg·L -1 ,respectively,and were higher than those of control group〔(0.74 ±0.04)mg·L -1 〕;While the EB content in CSF of rat in lead acetate 160 and 320 mg·kg -1 group were higher than the control group(P <0.05),which indicated that lead acetate exposure at low dose can lead to the increase of permeability of BCB.Laser scanning confocal micro-scope i mages showed that the JAM protein expression of choroid plexus in lead acetate 160 and 320 mg·kg -1 group were 44.9% and 42.9% of the control group.Sa me decline was seen in terms of occludin expression.The TTR content of CSF of rats in lead acetate 80 mg·kg -1 group was (32.3 ± 1 1 .7)ng·g -1 protein,lower than that of the control group,and the difference was significant.This decline was also noted in lead acetate 160 and 320 mg·kg -1 group.The data of TTR in CSF suggested that the low dose lead acetate exposure can disrupt the BCB secretion function.The leptin levels in CSF of lead acetate 160 and 320 mg·kg -1 group were lower than that in the control group (P <0.05 ). CONCLUSION Lead exposure did disrupt the permeability,transportation and secretion function of BCB.Our data suggest that BCB dysfunction might be involved in the mechanis m of lead induced neurotoxicity.