Objective To explore the changes of Nogo-A mRNA and Nogo receptor(Ng-R) mRNA expressions in hippocampus of immature rats after febrile seizures(FS).Methods One hundred and twenty-seven male SD rats(15 days) were randomly divided into control group(immersed in 37 ℃ water,n=40)and hyperthermia treated group(immersed in 44.5 ℃ water,n=87).The latter was further divided into febrile control group(n=42) and FS group(n=45) according to whether seizures occurred or not.Each group was further divi-ded into 5 groups according to different therapies(1,3,5,7,10 times treatment).Then 5 cases of the 8 rats were randomly used to observe the expressions of Nogo-A mRNA,Ng-R mRNA in hippocampus by using reverse transcriptase polymerase chain reaction(RT-PCR).Three of the 8 rats were randomly used to observe the changes of neurons and mossy fiber sprouting(MFS) in hippocampus by Nissl and Timm staining.Results 1.No seizures occurred in normal control group.Seizures occurred in 2 rats of febrile control group.In FS group,various seizures occurred such as nodding spasms,tonic seizures,clonic seizures and tonic-clonic seizures,2 rats died of drowning and 3 rats died of status epilepticus.2.The expressions of Nogo-A mRNA,Ng-R mRNA in the immature rats′ hippocampus became up-regulated after the 7th and 10th seizure,significantly higher than those of the other 2 control groups(Pa

Objective To summarize the diagnostic and therapeutic experience of a patient with chronic graft versus host disease (cGVHD) related polymyositis (PM) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).Methods A patient with acute lymphocytic leukemia in com- plete remission received sibling allo-HSCT,and cyclosporine and methotrexate were adopted to pre- vent GVHD.Results Eleven days after HSCT,WBC＞0.5?10~9/L,13 days after HSCT,PLT＞20?10~9/L;27 days after HSCT,chromosome analysis of bone marrow cells showed 99% donor type. Seventeen days after HSCT,Ⅰ~0 acute GVHD of skin occurred,and it was cured by intravenous injec- tion of dexamethasone and methotrexate.Eight months after HSCT,cGVHD of liver happened.Al- though treated by tacrolimus and azathioprine,enzymes of liver were still elevated.At last,tacrolimus combined with sirolimus were used,and enzymes of liver subsided gradually.However,the serum creatine phosphokinase (CK) began to rise from 9 U/L to 3010 U/L,and fatigue all over the patient occurred.Finally,the symptom relapsed,and disability involved with the origin of limbs appeared. The electromyogram and magnetic resonance imaging of concerned muscles confirmed the PM diagno- sis.Although treated with methylprednisolone and plasma exchange,the patient died due to asphyxia, while the CK as high as 21 010 U/L.Conclusion PM is a rare kind of manifestations of cGVHD. When the key muscle tissue was involved,the prognosis is poor.

Objective To create a model with simple expression of mechanical characteristics of the human chest for the development of a manikin. Methods A simplified Gruben-model was proposed based on the anatomical structure and physical characteristics of the materials, and perfect coefficients were computed. The model feasibility was proved by the coefficient of determination and residual analysis.Results The mathematic form of the model provided had three fewer terms than Gruben′s. The coefficient of determination approximated 1, the residue was small, and the perfect coefficients of "a typical human" were determined.Conclusion The hypothesis of the model makes the coefficients physically meaningful, which provides a new method to study the force-displacement relationship of the thorax. Also the simple form makes it easy to create the model and provide some guidance for the design of a manikin′s chest.

Objective To explore the activition and polarization of microglia in the epileptic rats induced by lithium chloride-pilocarpine. Methods One hundred male SD rats were randomly divided into five groups: control group and different time points model groups including 1d,3d,7d and 14d. Epilepsy models were established by lithium chloride-pilocarpine intraperitoneal injection. The control group was given the same dosage of normal saline. The morphology change was detected by immunofluorescence,and the expressions of iNOS and Arg-1 were determined by IHC at respective time points. Results Compared the model groups with control group,microglia was activated,synapsis was shorten,volume got bigger,most of them seemed as amoebocyte,the expression of iNOS increased and Arg-1 decreased,especially at 3d.ConclusionThe results from this study indicated that microglia was activated and polarized in epileptic rats induced by pilocarpine.

Objective To observe the influence of nandrolone phenylpropionate(NP) on the ultrastructure of aorta in rats with or without movement training,and investigate the side effects of NP on the cardiovascular system. Methods Forty male SD rats were randomly divided into sedentary control group,sedentary+medicine group,exercise control group and exercise+medicine group.For the groups with medical treatment,NP of 10 mg/kg one time every three days was injected into the rats via gluteus for eight weeks.For the exercise groups,rats were trained to run on treadmill five days per week for eight weeks.The aortae were sampled and specimens were obtained for transmission electron microscopy. Results The ultrastructure of aorta was normal in sedentary control group.For sedentary+medicine group,mitochondrial swelling,vacuolated cytoplasm and lysis of endothelial cells were observed,disruption of intercellular conjunctions,widening of subendothelial spaces and furcation and breakage of internal elastic lamina were found,and smooth muscle cells changed into synthesis type.For exercise control group,no obvious morphologic change was observed,except that part of the internal elastic lamina disrupted.In exercise+medicine group,breakage and lysis of endothelial cells were observed,widening of subendothelial spaces and lysis of internal elastic lamina were found,and autophagosome and myelinoid body were seen in smooth muscle cells. Conclusion NP may lead to the impairment of endothelial cells and the change of smooth muscle cells into synthesis type.Exercise with NP administration may result in more severe impairment in vessel wall.

BACKGROUNDPeripheral T-cell lymphoma (PTCL) is generally characterized by poor prognosis after conventional chemotherapy. The place for high-dose chemotherapy and autologous stem cell transplantation (ASCT) in these patients is still not clear. In this study, we presented the outcomes of PTCL patients followed these treatments in our centre.

METHODSWe retrospectively analyzed the outcomes of 39 patients with PTCL received the two treatments between 1999 and 2010.

RESULTSThe 3-year overall survival (OS) of 61.9% and 3-year progression free survival (PFS) of 35.7% were observed in the 39 patient. Twenty-one patients received Hyper-CVAD chemotherapy with 3-year OS of 46.2% and 3-year PFS of 27.9%. Eighteen patients received ASCT with 3-year OS of 70.3% and 3-year PFS of 44.2%. Further analysis revealed that patients with elevated lactate dehydrogenase, at least 2 international prognostic index (IPI) points, and extranodal involvement had a poorer outcome compared with the control group.

CONCLUSIONThese findings might suggest that Hyper-CVAD chemotherapy and ASCT could offer a durable survival benefit for patients with aggressive PTCL.

Adolescent ; Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Cyclophosphamide ; therapeutic use ; Dexamethasone ; therapeutic use ; Doxorubicin ; therapeutic use ; Female ; Hematopoietic Stem Cell Transplantation ; methods ; Humans ; Lymphoma, T-Cell, Peripheral ; drug therapy ; therapy ; Male ; Middle Aged ; Retrospective Studies ; Vincristine ; therapeutic use ; Young Adult

AIMTo investigate protective effects of ginkgolide B (GB) in different administration modes on glutamate-induced neuronal damage.

METHODSEssential GB were obtained by supercritical CO2 fluid extraction. Glutamate excitotoxicity were examined in primary cultures from neonatal Wistar rat, by using of Trypan blue dye staining, testing the lactate dehydrogenase leakage from cultured neurons and terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) method. The protective effects of GB in different administration modes (pre-treatment and post-treatment) were adopted and compared with the NMDA receptor uncompetitive antagonist-MK-801 in acute-treatment.

RESULTSTreatment with GB in two administration modes both could increase ratio of surviving neuron, decrease LDH efflux and reduce ratio of neuron apoptosis in different degree, depended on dose in certain range. The protective effect of pre-treatment was superior to post-treatment, but inferior to MK-801.

CONCLUSIONGB can protect neurons against glutamate damage, and preventive using has more efficiency. The potential mechanism of its neural protection may be not only related to PAF receptor. If the predominant protection effect of GB in pretreatment is considered, precautionary intervention to high-risk population could have more value.

Animals ; Cells, Cultured ; Dizocilpine Maleate ; pharmacology ; Ginkgolides ; administration & dosage ; pharmacology ; Glutamic Acid ; adverse effects ; Hippocampus ; drug effects ; metabolism ; Lactones ; administration & dosage ; pharmacology ; Neurons ; drug effects ; metabolism ; Rats ; Rats, Wistar

OBJECTIVETo investigate the risk factors causing tracheal stenosis after tracheotomy for mechanical ventilation.

METHODSA retrospective study was carried out to review the clinical data of 560 patients who had been tracheotomy for mechanical ventilation in the First Affiliated Hospital of Sun Yat-sen University from 1990 to 2006. The clinical relevant factors causing tracheal stenosis included age, sex, preoperative intubation, preoperative intubation time, postoperative mechanical ventilation duration, airway infection, multiple changes of intubation tube, cricothyroidotomy, previous tracheotomy, gastroesophageal reflux, diabetes, etc. Multivariate stepwise logistic regression model was used for the analysis.

RESULTSFifty-four cases (9.6%) presented tracheal stenosis in 560 patients after tracheotomy. With multivariate analysis, it was confirmed that the following variable correlated to tracheal stenosis. i.e, preoperative intubation time (chi2 = 4.323, P = 0.038), postoperative mechanical ventilation duration (chi2 = 14.062, P = 0.000), airway infection (chi2 = 8.604, P = 0.004), diabetes (chi2 = 5.237, P = 0.014). The effect degree of these risk factors was as below, postoperative mechanical ventilation duration (OR = 10.818), airway infection (OR = 6.349), diabetes (OR = 3.019), intubation time preoperative (OR = 2.156).

CONCLUSIONSAmong patients who received tracheotomy for mechanical ventilation, the clinical relevant factors causing tracheal stenosis were various. Statistical analysis showed that preoperative intubation time, postoperative mechanical ventilation duration, diabetes, airway infection were main risky factors which may cause tracheal stenosis.

Adolescent ; Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Logistic Models ; Male ; Middle Aged ; Multivariate Analysis ; Respiration, Artificial ; adverse effects ; Retrospective Studies ; Risk Factors ; Tracheal Stenosis ; etiology ; Tracheotomy ; adverse effects ; Young Adult

OBJECTIVETo investigate the clinical relevant factors causing laryngeal stenosis after partial laryngectomy.

METHODSA retrospective study was carried out to review the history clinical data from 138 patients of partial laryngectomy in the First Affiliated Hospital of Sun Yat-Sen University between January 1994 to October 2004. The clinical relevant factors causing laryngeal stenosis were included as follows: age, sex, TNM stage, tumor site, extension of thyroid cartilage defect, extension of larynx parenchyma defect, reconstruction method, laryngeal dilator, duration of using antibiotics, postoperative radiotherapy, lung infection, gastroesophageal reflux, diabetes. Multivariate stepwise logistic regression model was used for the analysis.

RESULTSOf 138 cases after partial laryngectomy, stenosis developed in 25 cases. The occurrence rate was 18.1%. In multivariate analysis, it was confirmed that the following factors correlated to laryngeal stenosis, i. e, extension of thyroid cartilage defect (chi2 = 4.323, P = 0.038), postoperative radiotherapy (chi2 = 6.002, P = 0.014), lung infection (chi2 = 4.220, P = 0.040), and gastroesophageal reflux (chi2 = 5.614, P = 0.018).

CONCLUSIONSThe clinical relevant factors causing laryngeal stenosis after partial laryngectomy were multiple. Statistical analysis showed that extension of thyroid cartilage defect, postoperative radiotherapy, lung infection and gastroesophageal reflux were the risk factors which may cause laryngeal stenosis.

Adult ; Aged ; Aged, 80 and over ; Female ; Humans ; Laryngeal Neoplasms ; pathology ; surgery ; Laryngectomy ; adverse effects ; Laryngostenosis ; etiology ; pathology ; Logistic Models ; Male ; Middle Aged ; Neoplasm Staging ; Postoperative Complications ; Retrospective Studies ; Risk Factors

OBJECTIVETo study DNA damages of liver cells in rats exposed to vinyl chloride monomer (VCM), and the expressions of DNA damage repair enzymes including O(6)-methyl guanine-DNA methyl transferase (MGMT), X-ray repair cross-complementing group 1 (XRCC1) and X-ray repair cross-complementing group 3 (XRCC3); and to explore the repair mechanism of DNA damage induced by VCM.

METHODSRats were exposed to VCM by intraperitoneal injection. DNA damages were detected by single cell gel electrophoresis (comet assay). The expressions of DNA damage repair enzymes were measured by immunohistochemical methods.

RESULTSThe percentages of comet cells in low, moderate, and high dose groups (11.75%, 12.38%, and 17.63%, respectively) were greater than that of control (5.67%). The latter two groups were significantly different from that of control (P < 0.05, P < 0.01). The expressions of MGMT and XRCC1 decreased, and XRCC3 increased with the dose of VCM increased. DNA damage was correlated with the expression of XRCC3 (r = 0.438, P = 0.067).

CONCLUSIONVCM can cause DNA damage of liver cells with dose-response relationship. DNA damage repair enzymes take part in the repairing of DNA damage induced by VCM.

Animals ; Carcinogens ; toxicity ; DNA Damage ; drug effects ; DNA Repair ; DNA-Binding Proteins ; genetics ; metabolism ; Dose-Response Relationship, Drug ; Liver ; cytology ; metabolism ; Male ; O(6)-Methylguanine-DNA Methyltransferase ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Vinyl Chloride ; toxicity ; X-ray Repair Cross Complementing Protein 1