Objective To study the proportion of cyclic vomiting syndrome(CVS) developing to migraine by the medium term prognosis,and explore the relationship between CVS and migraine.Methods Twenty-eight of 38 cases who had identified in our clinical records were traced ,each child was matched to a control,and they all conducted a telephone interview by a standardized question.Results Ninteen(46%) of the subject had continued CVS and(or) migraine,the prevalence of past or present migraine in subjects(46%)was significantly higher than that in control group(10.7%)(P=0.003).Conclusion The progonosis of CVS is closely related to migraine,many of the suffers of CVS tend to develop migraine.

ObjectiveTo evaluate the effects on serum homocysteine(Hcy) level,vascular function and carotid intima-media thickness(IMT) in metformin-treated diabetic patients with or without supplementation with folate and Vitamin B12.MethodsA total of 100 newly diagnosed diabetic type 2patients were divided into two groups by random digits table with 50 cases each,90 patients completed study.Forty-seven participants (control group) received a 6-month course of metformin treatment,43 patients (treatment group) received mefformin,folate and Vitamin B12 treatment.The levels of serum Hcy,endothelin-1 (ET-1),carotid IMT,large or small arterial elasticity index (C1,C2),flow-mediated dilatation (FMD) of the brachial artery were evaluated before and after treatment.ResultsThe level of serum Hcy in control group significantly increased compared with before treatment[ (13.4 ± 2.7)μ mol/L vs.(11.1 ± 1.9)μ mol/L],hut the level of serum Hcy in treatment group significantly decreased compared with before treatment [ (9.2 ± 1.8 ) μ mol/L vs. ( 11.3 ± 2.0) μ mol/L ],there was significant difference(P ＜ 0.05 ).A beneficial effect was observed in the serum ET-1,FMD,carotid IMT and C2 in treatment group[ (20.0 ± 6.2)ng/L,( 15.8 ± 7.6)％,(0.8 ± 0.2) mm,(4.1 ± 2.1 ) ml/mm Hg ( 1 mm Hg =0.133 kPa) × 100 vs. (31.3 ±10.1 ) ng/L,(9.7 ± 4.5)％,( 1.1 ± 0.4) mm,(2.3 ± 1.0) ml/mm Hg × 100 ] (P ＜ 0.05).The levels of ET-1,FMD,carotid IMT and C2 after treatment in control group [ (24.8 ± 6.8) ng/L,( 12.9 ± 6.3 )％,(0.9 ± 0.3)mm,(3.0 ± 1.4) ml/mm Hg × 100] had significant difference compared with before treatment [ (30.6 ± 8.7)ng/L,(9.8 ± 4.6)％,( 1.0 ± 0.3) mm,(2.2 ± 0.9) ml/mm Hg × 100](P＜ 0.05).However,the results were improved significantly in treatment group than those in control group (P ＜0.05).In treatment group,significant correlation were detected between changes of Hcy and ET- 1 (r =0.43,P ＜ 0.05 ),carotid IMT(r =0.56,P ＜ 0.05),FMD (r =-0.54,P ＜ 0.05 ),C2 (r =-0.37,P ＜ 0.05 ).ConclusionsAdministration of folate and Vitamin B12 can reduce the levels of serum Hcy and ET-1 in metformin-treated type 2 diabetic patients,which exert beneficial effect on carotid IMT,FMD and C2.

Protein kinase Cε (PKCε) is a transforming oncogene and plays an important role in many cellular processing. In the present paper, we review the development of experimental researches on the acute-chronic pain transformation. Results indicated that prostaglandin E2 (PGE2) / EP1 receptor-Gq-PKCε is an important signaling pathway to modulate chronic pain in peripheral dorsal root ganglion (DRG) neurons, and also plays a role in the later stage of hyperalgesia during transformation from acute to chronic pain. PKCε in DRG neurons induces mechanical and thermal hypersensitivity respectively by over expression of transient receptor potential vanilloid 1 (TRPV1) and TRP ankyrin-1 (TRPA1), further mediating the transformation from acute to chronic pain. Whereas, PGE2-evoked activation of EP1-Gq-PKCε signaling may be the key link in initiating the pain translation process through regulating downstream TRPA1 and TRPV1. Electroacupuncture (EA) has been used to effectively relieving various types of acute and chronic pain for decades, and can significantly inhibit the expression of PKCε and its upstream and downstream molecules. Therefore, it can be inferred that there exists a possibility of EA interventions in interfering the transformation from acute to chronic pain by regulating peripheral PKCε signaling pathway.

No abstract available.
Diagnosis* ; DNA* ; Polymerase Chain Reaction* ; Tuberculosis*

Child ; Female ; Humans ; Male ; Neurocirculatory Asthenia ; psychology ; Temperament

No abstract available.
Carcinoma, Non-Small-Cell Lung* ; Drug Therapy, Combination*

Objective To explore acute toxicity of succimer on mice.Methods Twenty Kunming mice(10 males and 10 females) weighting approximately (21.2?2.3)g were acclimatized for 3 days prior to dosing,then were divided into control group and experiment group with 10 mice in each group according to body weight.Fasted for 12 hours,the mice in experiment group received intragastric administration of 160mg DMSA in deionized water in 24 hours,and the control group received the same volume of deionized water,and then they were observed for 7 days.Blood was collected into heparinized-tubes by removal of eyeball.All mice were sacrificed and brain,heart,liver and kidney were removed and washed with normal saline.The activity or amount of BUN,Scr,AST,ALT,SOD, GSH-PX and MDA were analyzed.Results (1)Given 160rag DMSA in 24 hours,gastrointestinal symptoms were main side effects.During the observation,experiment group lost weight due to the decrease of food-intake ,and some mice had slight hydroabdomen.(2)High dose of DMSA caused a significant inhibition of GSH-PX(P0.05).The hepatic cell was damaged accord- ing to the significant raise of MDA in liver(P0.05),which was related to acute toxicity on liver.Conclusion Succimer could inhibit the antioxidarrt systems and could do damage to liver and kidney.

OBJECTIVETo examine modulations caused by cyclooxygenase-2 (COX-2) inhibitors on altered microenvironments and overbalanced neurotransmitters in pilocarpine-induced epileptic status rats and to investigate possible mechanisms.

METHODSCelecoxib (a COX-2 inhibitor) was administered 45 min prior to pilocarpine administration. The effects of COX-2 inhibitors on mIPSCs (miniature GABAergic inhibitory postsynaptic currents) of CA3 pyramidal cells in the hippocampus were recorded. Expressions of COX-2, c-Fos, newly generated neurons, and activated microgliosis were analyzed by immunohistochemistry, and expressions of alpha-subunit of gamma-amino butyric acid (GABA(A)) receptors and mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) activity were detected by Western blotting.

RESULTSPretreatment with celecoxib showed protection against pilocarpine-induced seizures. Celecoxib prevented microglia activation in the hilus and inhibited the abnormal neurogenesis and astrogliosis in the hippocampus by inhibiting MAPK/ERK activity and c-Fos transcription. Celecoxib also up-regulated the expression of GABA(A) receptors. NS-398 (N-2-cyclohexyloxy-4-nitrophenyl-methanesulfonamide), another COX-2 inhibitor, enhanced the frequency and decay time of mIPSCs.

CONCLUSIONThe COX-2 inhibitor celecoxib decreased neuronal excitability and prevented epileptogenesis in pilocarpine-induced status epilepticus rats. Celecoxib regulates synaptic reorganization by inhibiting astrogliosis and ectopic neurogenesis by attenuating MAPK/ERK signal activity, mediated by a GABAergic mechanism.

Animals ; Blotting, Western ; Celecoxib ; Cyclooxygenase 2 ; metabolism ; Cyclooxygenase 2 Inhibitors ; pharmacology ; Disease Models, Animal ; Fibrocystic Breast Disease ; metabolism ; Hippocampus ; drug effects ; enzymology ; pathology ; Immunohistochemistry ; MAP Kinase Signaling System ; drug effects ; Male ; Mitogen-Activated Protein Kinase Kinases ; metabolism ; Nitrobenzenes ; pharmacology ; Pilocarpine ; Proto-Oncogene Proteins c-fos ; metabolism ; Pyrazoles ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-A ; biosynthesis ; Status Epilepticus ; chemically induced ; enzymology ; pathology ; Sulfonamides ; pharmacology ; Synapses ; drug effects ; pathology

OBJECTIVETo establish a sensitive and specific multiplex RT-PCR(MRT-PCR) for the simultaneous detection of influenza virus types and subtypes.

METHODSPrimers were designed from highly conserved region of the hemagglutinin(HA) gene of influenza H1N1H3N2 and B virus and MRT-PCR was performed. Additional two pairs of primers were designed to determine the N1 and N2 subtypes of neuramidinase NA of influenza H1N1 and H3N2 virus.

RESULTSThe fragments of HA gene of all types of influenza virus were amplified and there was no cross reaction. The sensitivity of detection of influenza H1N1 and H3N2 virus was 0.10 TCID50/50 microliter by the second PCR and that was 0.01 TCID50/50 microliter for influenza B virus. The NA gene of influenza H1N1 and H3N2 virus was also amplified by this method.

CONCLUSIONThe sensitivity of detection of influenza virus from clinical patients' throat washing specimens by MRT-PCR was higher than that by MDCK cell culture or egg embryo isolation. This method was highly sensitive and timely for detection of influenza virus types and subtypes.

Animals ; Cell Line ; Chick Embryo ; Chickens ; DNA Primers ; Humans ; Influenza A Virus, H1N1 Subtype ; genetics ; isolation & purification ; Influenza A Virus, H3N2 Subtype ; genetics ; isolation & purification ; Influenza A virus ; genetics ; isolation & purification ; Influenza in Birds ; virology ; Influenza, Human ; virology ; RNA, Viral ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; methods

To observe the serum samples and the anti-inflammatory effect of Tripterygium wilfordii in treating RA by using the pharmacokinetic-pharmacodynamic model, make a correlation analysis on concentration-time and effect-time curves, and explore RORγt, IL-17, STAT3, IL-6 mRNA transcriptional levels in rats by PCR. Methotrexate, tripterine and high-dose T. wilfordii could down-regulate RORγt, IL-17, STAT3, IL-6 mRNA transcriptional levels in AA rat lymph nodes. The study on PK-PD model showed correlations between inflammatory factors and blood concentration of T. wilfordii. T. wilfordii and its main active constituent tripterine could show the inflammatory effect and treat RA by inhibiting IL-17 cytokine.
Animals ; Arthritis, Rheumatoid ; drug therapy ; immunology ; Biomarkers ; Female ; Interleukin-17 ; antagonists & inhibitors ; genetics ; Interleukin-6 ; genetics ; Phytotherapy ; Rats ; Rats, Sprague-Dawley ; Tripterygium ; Triterpenes ; pharmacokinetics ; pharmacology