Objective To investigate the effect of naloxone on neuronal cells apoptosis induced by repeated febrile seizures(FS).Methods Warm water was used to induce 70 rats FS model 15 days after birth in this study; each rat was induced 7 times febrile seizures at one- day interval . Seventy rats were randomly divided into naloxone-treated group and FS control group, receiving injection of naloxone or saline at 5, 30, 60 min and 2 hours after FS each day respectively. The rats were sacrificed 24 hours after the last seizure. Neuronal cell apoptosis was determined by TUNEL methods in situ cell death kit. TUNEL positive cells(TPC) were stained and counted as apoptosis in hippocampus and cortex. Ultrastructural changes of apoptosis neurons were observed under the electron microscope(EM). Results Compared with the FS control group, naloxone treatment could significantly relieve neuron apoptosis induced by repeated FS when it was used at 5, 30, 60 min after the last FS. However there was no significant difference in neuron apoptosis between 2 groups when naloxone was used at 2 hours after FS. The comparison of different naloxone administration time showed that the earlier naloxone was injected,the fewer apoptosis neurons were induced by FS.Conclusion Naloxone,as early used in proper dosage,may significantly alleviate apoptosis after repeated FS ,and protect neurons.

Objective To investigate the effect of naloxone on c-fos expression in hippocampus induced by repeated febrile seizures(FS).Methods Warm water induced rat FS model was developed in this study. Each rat was induced 7 febrile seizures with the interval of one day. Naloxone-treated rats and FS control rats received injection of naloxone(1 mg/kg,2 mg/kg) or saline once FS occurrence every 2 day respectively. All rats were sacrificed 24 hours after the last seizure. In hippocampus, c-fos expression distribution and semi-quantitative analysis was determined by immuhischemical staining measure and western-blotting respectively.Results Compared with FS control group, naloxone treatment could significantly relieve c-fos expression in hippocampus induced by repeated FS, mainly in dentate gyrus(DG) and CA3 region. The comparison between 1 mg/kg and 2 mg/kg naloxone-treated group showed that 2 mg/kg naloxone could reduce c-fos positive expression more significantly.Conclusion Naloxone of proper dosage may significantly alleviate c-fos expression after repeated FS ,which further proved its antiepileptic function and also implied that endogenous opioid may be involved in the regulation of c-fos expression during seizure.

To report a boy with reflex seizures induced by micturition.He suffered from seizures during micturition for four yesrs.The clinical symptoms consisted of head backwards,limbs dithering,sometimes accompanying tumble.During the episodes of the seizure,his consciousness did not lose.Few seizures showed only eyes up-staring for several seconds.The livelong process of micturition was often interrupted by seizures for several times.When he finished or stoped micturition,the seizures did not occur again.His seizures could not be induced by free of micturition or other stimulative factors.The interictal EEGs showed that background asymmetry manifested as the lower amplitude and irregular rhythm in the left hemisphere,sharp or sharp and waves in right hemisphere,especially mid and back temporal.There also had sharp,spike,and spike and waves in many regions of double spheres in interictal EEGs.The other assistant check-ups were normal.while this disease was infrenquncy,it would be worthy to regard.

OBJECTIVETo improve the diagnosis and treatment of penile metastasis from rectal carcinoma.

METHODSWe reported a case of penile metastasis secondary to rectal adenocarcinoma, reviewed the relevant literature, and discussed the common origins, clinical features, pathogenic mechanisms, diagnosis and treatment of this disease.

RESULTSThe patient was a 54-year-old male, with metastatic penile tumors secondary to rectal adenocarcinoma, with serious adhesion to the surrounding tissue and metastasis to the liver. As treatment, we performed colostomy to relieve voiding difficulty, followed by combination chemotherapy with oxaliplatin, 5-fluorouracil, and levofolinate. The patient died 10 months later as a result of systemic failure.

CONCLUSIONPenile metastatic malignancy has a poor prognosis. Early diagnosis and combined and individualized therapies may improve the quality of life, relieve pain and prolong the life of the patient.

Adenocarcinoma ; secondary ; therapy ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Combined Modality Therapy ; methods ; Fluorouracil ; administration & dosage ; Humans ; Liver Neoplasms ; secondary ; therapy ; Male ; Middle Aged ; Organoplatinum Compounds ; administration & dosage ; Penile Neoplasms ; secondary ; therapy ; Quality of Life ; Rectal Neoplasms ; pathology

Objective To explore the changing regularity of nitric oxide synthase(nNOS) in recurrent febrile seizures (FS), and the influence of NOS/NO on brain damage induced by recurrent FS.Methods FS rats were induced in a bath of warm water.The ex-periments were divided into 2 groups. The contents of nNOS cDNA in the first group was measured by quantitative RT-PCR and the contents of nNOS protein was measured by Western blot.The mtensity , latency, duration and rectal temperature of the seizure in rats in the second group were recorded. Morphologic changes of hippocampal neurons were observed with HE stain.Results Alter recur-rent FS, the expression of nNOS mRNA in hippocampus was significantly inereased compared with those in control group and hyper-thermia group, associated with an increase of nNOS protein.With the increase of seizure number,thert were changes of seizure latency and gradually prolonged trend of the seizure duration. By using the inhibitor of NOS, the seizure latency was gradually prolonged and the prolonged trend of the seizure duration was significantly decreased than that in FS group.There was no significantly difference of seizure intensity and rectal temperature between 2 groups.After recurrent FS, histological changes of hippocampal neurons could be seen under light microscope.The inhibitor alleviated nearonal injury.Conclusions Recurrent FS can induce nNOS gent expression.The NOS/NO system may be involved in the development of brain damage induced recurrent FS.

Objective To explore the effect of nitric oxide (NO) on ?-aminobutyric acid B receptor (GABA_BR) subunits during recurrent febrile seizures (FS).Methods Twenty-four Sprague-Dawley rats aged 21 days were randomly divided into 4 groups: control group (37.0 ℃ water,n=8), FS group (45.2 ℃ water,n=8), FS + SNP group (45.2 ℃ water,n=8), FS+L-NMMA group (45.2 ℃ water,n=8). FS rats were induced 10 times in a warm-water bath, once every 2 days. The plasma level of NO was detected by the spectrophotometer. The expressions of GABA_BR subunit mRNA and c-fos gene were examined by in situ hybridization. The expressions of GABA_BR subunit and Fos protein were observed by immunohistochemistry. Results The plasma level of NO increased in FS + SNP group while decreased in FS+L-NMMA group compared with that in FS group. The expressions of GABA_BR_2 were down-regulated in FS+SNP group, while GABA_BR_1 hardly changed compared with those in FS group. In FS+L-NMMA group, both the expression of GABA_BR_2 and GABA_BR_1 up regulated compared with those in FS group. The expressions of c-fos gene and Fos protein were significantly enhanced after recurrent FS. SNP elevated the expressions of c-fos gene and Fos protein, while L-NMMA down regulated the expressions of them.Conclusion NO may play a regulatory role through modulating GABA_BR function in the pathogenesis of recurrent FS.

Objective To explore the influence of ?-aminobutyric acid B receptor(GABA_BR)on carbon monoxide (CO)/heme oxygenase(HO-1)system during recurrent febrile seizures (FS).Methods Sprague-Dawley rats aged 21 days were randomly divi- ded into 4 groups:control group and FS group,FS+baclofen group,FS+phaclofen group.FS in rats were induced 10 times in a bath of warm water, once every 2 days.The plasma level of CO was detected by the dual wave lengh spectrophotometer;the expressions of GABA_BR and HO-1 mRNA were examined by insitu hybridization;the expressions of GABA_BR and HO-1 protein were observed by immunohistochemistry.Results The plasma level of CO increased in FS+baclofen group,while decreased in FS+phaclofen group compared with FS group.The expressions of GABA_BR and HO-1 upregulated in FS+baclofen group,while decreased in FS+phaclofen group compared with FS group.There were significant difference (All P

OBJECTIVEThe brain damage caused by repeated febrile seizure (FS) during developing age is harmful to the intellectual development of children. So how to decrease the related damage is a very important issue. The main purpose of the present study was to find out whether the non-specific opiate antagonist naloxone at low dose has the neuroprotective effect on seizure-induced brain damage.

METHODSWarm water induced rat FS model was developed in this study. Forty-seven rats were randomly divided into two groups: normal control group (n = 10) and hyperthermic seizure groups (n = 37). The latter was further divided into FS control group (n = 13) and naloxone-treated group (n = 24). The dose of naloxone is different in two naloxone-treated groups (12/each group), in one group the dose was 1 mg/kg, in the other one 2 mg/kg. Seven febrile seizures were induced in each rat of hyperthermic seizure groups with the interval of 2 days. The rats were weighed and injected intraperitoneally with naloxone once the FS occurred in naloxone-treated group, while the rats of the other groups were injected with 0.9% sodium chloride. Latency, duration and grade of FS in different groups were observed and compared. HE-staining and the electron microscopy (EM) were used to detect the morphologic and ultrastructural changes of hippocampal neurons.

RESULTSIn naloxone-treated group, the rats' FS duration and FS grade (5.02 +/- 0.63, 2.63 +/- 0.72) were significantly lower (t = 5.508, P < 0.01; t = 8.439, P < 0.01) than those in FS control group (7.70 +/- 2.25 min, 4.52 +/- 0.49), although no significant gap was observed on FS latency between them. In FS control group, HE-staining pattern of hippocampal CA(1) and CA(2) showed lots of disordered neurons with confused polarity and vacuoles formed. Nuclei were with various size, some rounded and some oblong. While in naloxone-treated groups, the arrangement of neurons was regular, only a small quantity of neurons had changed polarity and vacuoles formed. Most nuclei were oblong and in the same size. In hippocampal CA(1) region and dentate gyrus of rats from FS control group, EM showed that the most mitochondrion volumes obviously increased with vacuoles formed, the matrix condensed, the ridge obscured or disappeared, apoptosis body emerged. Minor to moderate dilation of rough endoplasmic reticulum and Golgi's complex was also observed. However, in naloxone-treated groups, the number of neurons with swollen mitochondrion and endoplasmic reticulum was much fewer than that in FS control group. No apoptosis body was observed. The comparison between them showed much lighter brain damage in naloxone-treated groups than in FS control group.

CONCLUSIONAlthough low-dose naloxone could not totally stop the occurrence of febrile seizure, it could lighten the brain damage resulted from repeated FS to some extent.

Animals ; Brain ; drug effects ; pathology ; Male ; Models, Animal ; Naloxone ; pharmacology ; therapeutic use ; Narcotic Antagonists ; pharmacology ; therapeutic use ; Neuroprotective Agents ; pharmacology ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Seizures, Febrile ; drug therapy ; physiopathology ; Treatment Outcome

A phytochemical investigation on the aerial parts of a Tibetan medicine Meconopsis horridula, by solvent extraction, repeated chromatographies on silica gel, Sephadex LH-20, and preparative TLC techniques, led to the isolation of 9 compounds. By spectroscopic analysis and comparison of its 1H and 13C-NMR data with those in literatures, their structures were identified as oleracein E(1), N-( trans-p-coumaroyl) tyramine (2), chrysoeriol (3), apigenin (4), hydnocarpin (5), p-coumaric acid glucosyl ester (6), stigmast-5-ene-3beta-ylformate (7), 3beta-hydroxy-7alpha-ethoxy-24beta-ethylcholest-5-ene (8), and beta-sitosterol (9), respectively, among which compounds 6-8 were isolated from the genus for the first time,and 1,3 were isolated from the species for the first time. A MTT method was applied to evaluate the cytotoxic activity of compounds 14 against the human hepatocellular liver carcinoma cell line (HepG2), and compound 1 showed significant cytotoxicity against HepG2,with its inhibitory rate of 52.2% at 10 micromol x L(-1).
Medicine, Tibetan Traditional ; Molecular Structure ; Papaveraceae ; chemistry ; Plant Extracts ; chemistry ; Spectrometry, Mass, Electrospray Ionization

Objective To explore the effect of ? - aminobutyric acid B receptor(GABABR)on brain damage induced by recurrent febrile seizures (FS). Methods Rats were randomly divided into four groups: control group (37. 0 ℃ water, n = 8), FS group (45.2 ℃ water,n=8), FS + baclofen group (45.2 ℃ water,77 = 8), FS + phaclofen group (45. 2 ℃ water,n=8). FS in rats were induced for ten times in a bath of warm water, once every 2 days. The intensity, latency and duration of the seizure in rats were recorded. The expression of c - fos gene and Fos protein were examined by in situ hybridization and immunohistochemistry, respectively. Results Compared with those of FS group, the seizure latency gradually prolonged, and the seizure duration was shortened in FS + baclofen group. In FS+ phaclofen group, the seizure latency was shorter and the seizure duration was longer than those of FS group. The seizure intensity was lessened in FS + baclofen group while aggravated in FS + phaclofen group compared with that of FS group. The expression of c - fos gene and Fos protein increased significantly after recurrent FS. Baclofen down regulated the expression of c -fos gene and Fos protein, while phaclofen enhanced the expression of them. Conclusion The study by using the agonist and the inhibitor of GABABR showed that GABABR might play a crucial role in the development of FS- induced brain damage.