Narcolepsy is a rare sleep-wake rhythm disorder in clinic practice, mainly characterized by recu-rrent unstoppable sleep during the day and often accompanied by cataplexy, sleep paralysis and hypnagogic hallucinations.Clinicians′ insufficient knowledge about narcolepsy is one of the main causes of misdiagnosis and delayed diagnosis.Moreover, narcolepsy may get easily confused by epilepsy because of complex and diverse types of epileptic seizures.Therefore, it is necessary to distinguish the two forms each other.When they are comorbidity, the diagnosis and treatment will be much more difficult.In this article, the clinical characteristics of narcolepsy and the causes of delayed diagnosis were analyzed, differential diagnosis between narcolepsy and epilepsy was investigated, and practical expe-rience in diagnosis and treatment of comorbidities were summarized, so as to raise clinicians′ awareness of narcolepsy and its comorbidity with epilepsy and improve patients′ prognosis and their quality of life.

Objective To investigate the changing trend of incidence and the relevant factors in fetal macrosomia. Methods 84 883 newborns during Jan. 1,1970 to Dec. 31,1999 were used to analyze the incidence of fetal macrosomia,the average birth weight,the percentage of superior fetal macrosomia, the distribution of gestational age, the rate of cesarean section and the vaginal delivery, the relevant factors of fetal macrosomia. Results All the cases were divided into 3 groups, one group from 1970 to 1979, the second one from 1980 to 1989, the third one from 1990 to 1999. The incidence of fetal macrosomia for three groups were 2. 6%, 6. 9% and 13 2% ( P

OBJECTIVE To discuss the possibility of HBV contaminating environment and transmission through the polluted surroundings. METHODS On the basis of that ascertain the contaminated environment by HBV marker(HBVM) and the relationship between HBVM and HBV infectivity in the blood,to discuss the probability of HBV contaminating and be spreading through the circumstance. RESULTS The positive rate of HBsAg and HBeAg was 26.39% and 11.11%,respectively in these specimens.While all of samples in control group were negative.The HBV DNA positive rate was 73.72% and 100.00%,respectively in the positive blood specimens of HBsAg and HBeAg.The infectivity was 0-10~9 and 10~2-10~9 ID/ml,respectively. CONCLUSIONS The blood worktable surface is contaminated by HBVM.The pollution is from patients′ blood.So the probability exists that HBV is transmitted through environment pollution.

Objective To study the clonal heterogeneity in differentiation potential of immortalized mesenchymal stem cells in vitro and in rive.Methods The monoclonal cell lines were performed with limiting dilution cloning,and were induced to adipocytic,asteogenic and neuronal differentiation in vitro.After transplanted the monoclonal cell lines into SCID mice,the xenotransplants were removed and evaluated by immunohistochemistry.Results From the parental HMSC-TERT,32 single-cell derived clones were established,of which the differentiation properties varied considerably in vitro.The cells grow in different plating densities during expansion in culture:HMSC-TERT-2 expressed more strongly in LCA,GFAP and vimemin;HMSC-TERT-C19 expressed more strongly in keratinose than HMSC-TERT-2,HMSC-IERT-20,and MSC-H;HMSC-TERT-C2 expressed more strongly in actin than HMSC-TERT-2.Conclusions The HMSC-TERT monoclone cells are heterogeneity in differentiation petential in vitro and in vivo,suggesting that standard in vitro culture and in vivo inoculate procedure phy an important role in the clinical application of stem cells.

BACKGROUND: As unspecific antagonist of opiate receptor, naloxone is widely used for multiple diseases which are related with abnormal release of endogenous opium. At present, researches suggest that large dosage of naloxone is used at early period can decrease death rate of patients with acute craniocerebral injury and promote neural functional recovery.OBJECTIVE: To investigate the effect of naloxone on improving the nervous function of rats with acute craniocerebral injury and to analyze effectively.DESIGN: Randomized grouping design based on the experimental animal.SETTING: Beijing Neurosurgical Institute.MATERIALS: Totally 250 SD rats were divided randomly into 0.3, 1.0,3.0, 9.0 mg/kg naloxone group, positive control group and negative control group.METHODS: Craniocerebral injured model was established with Feenly free fall struck, and the medicine was given 30 minutes after injury. The rats of the first four experimental group were injected transpeniponeally with naloxone hydrochloride by 0.3 mg/kg, 1.0 mg/kg, 3.0 mg/kg and 9.0 mg/kg respectively once a day; meanwhile, the control groups were given 2 mg citicoline sodium for injection and 0.5 mL normal saline per rat respectively. The longest time was 14 days.MAIN OUTCOME MEASURES: MNSS neural functional score was used every day. The brain edemas of 8 rats in each group were measured with wet-dry weight methods on the second and the fourth day after head trauma.RESULTS: Among 250 rats, 172 entered the final analysis. The nervous function of rats in naloxone groups was better than the two control groups (P ＜ 0.01), and that in 1, 3 and 9 mg/kg naloxone group were better than 0.3 mg/kg group (P ＜ 0.05), but there were no significant differences a mong the three naloxone groups (P ＞ 0.05). The brain edemas of rats in naloxone groups were lighter than that in the control groups (P ＜ 0.05), and that of 1, 3 and 9 mg/kg groups were lighter than 0.3 mg/kg (P ＜ 0.05), but there were no significant differences among these three groups (P ＞ 0.05).CONCLUSION: Naloxone can decrease the brain edemas of rats with traumatic brain injury, promote the nervous function recovery, and the treatment effect changes with the dosage during some range.Therefore, the experiment illustrates that naloxone can decrease the brain edemas of experimental brain injury in SD rats and improve the nervous function, but the effect of naloxone is associated with the dosages in some range.

This study is to assess the efficacy of BPCBG on the decorporation of uranium (VI) and protecting human renal proximal tubular epithelial cells (HK-2) against uranium-induced damage. BPCBG at different doses was injected intramuscularly to male SD rats immediately after a single intraperitoneal injection of UO2(CH3COO)2. Twenty-four hours later uranium contents in urine, kidneys and femurs were measured by ICP-MS. After HK-2 cells were exposed to UO2(CH3COO)2 immediately or for 24 h followed by BPCBG treatment at different doses for another 24 or 48 h, the uranium contents in HK-2 cells were measured by ICP-MS, the cell survival was assayed by cell counting kit-8 assay, formation of micronuclei was determined by the cytokinesis-block (CB) micronucleus assay and the production of intracellular reactive oxygen species (ROS) was detected by 2',7'-dichlorofluorescin diacetate (DCFH-DA) oxidation. DTPA-CaNa3 was used as control. It was found that BPCBG at dosages of 60, 120, and 600 micromol kg(-1) resulted in 37%-61% increase in 24 h-urinary uranium excretion, and significantly decreased the amount of uranium retention in kidney and bone to 41%-31% and 86%-42% of uranium-treated group, respectively. After HK-2 cells that had been pre-treated with UO2(CH3COO)2 for 24 h were treated with the chelators for another 24 h, 55%-60% of the intracellular uranium was removed by 10-250 micromol L(-1) of BPCBG. Treatment of uranium-treated HK-2 cells with BPCBG significantly enhanced the cell survival, decreased the formation of micronuclei and inhibited the production of intracellular ROS. Although DTPA-CaNa3 markedly reduced the uranium retention in kidney of rats and HK-2 cells, its efficacy of uranium removal from body was significantly lower than that of BPCBG and it could not protect uranium-induced cell damage. It can be concluded that BPCBG effectively decorporated the uranium from UO2(CH3COO)2-treated rats and HK-2 cells, which was better than DTPA-CaNa3. It could also scavenge the uranium-induced intracellular ROS and protect against the uranium-induced cell damage. BPCBG is worth further investigation.

Objective To observe the effects of transplantation of bone marrow stromal cells(BMSCs)on expression of vascular endothelial growth factor(VEGF)after local brain injury in rats.Methods The animal model of local brain injury in rat was established.The human BMSCs(hBMSCs)were transplanted into the local brain.The immunohistochemistry,real-time quantitative PCR,and ELISA were used to observe the changes of VEGF and VEGF mRNA in tissues of local brain.Results After the hBMSCs were transplanted into the animal model,the quantities of the VEGF positive cells increased;real-time quantitative PCR showed that VEGF mRNA of local brain was enhanced.Conclusion The BMSCs transplantation can improve expression of endogenous VEGF and raise the content of VEGF in injured tissues of brain.

ObjectiveTo observe the effects of bone marrow stromal cells (BMSCs) on vessel endothelial cells proliferation and microvessel formation in vitro.MethodsBMSCs and brain vessel endothelial cells were separated from adult and divided into co-culture group of BMSCs and endothelial cells, medium group of BMSCs, comparison group. Endothelial cells proliferation and microvessel formation were observed. ResultsEndothelial cells were promoted to proliferate and formate the microvessel in medium group and co-culture group. And the effect was prominence in co-culture group.ConclusionBMSCs can promote the proliferation and microvessel formation of endothelial cells.

One hundred and thirty seven pafients diagnosed by coronary angiography were recruited in the study and divided into coronary heart disease group(CAD)and control group.Relationship between serum apolipoprotein M levels and the severity of stenosis of coronary arteries was analyzed.In covariate analysis,serum apolipoprotein M levels were significantly lower in CAD group than those in control group adjusted for sex,age,body mass index(BMI)(P＜0.05).By stepwise muhiple regression,serum levels of apolipoprotein M were correlated positively with BMI(r=0.65,P＜0.01),and correlated negatively with total cholesterol(TC)(r=-0.53,P＜0.01)and low density lipoproteins(LDL-C)(r=-0.42,P＜0.01).Serum levels of apolipoprotein M were correlated negatively with the score of coronary stenosis(r=-0.62,P＜0.01).The results suggest that apolipoprotein M might be related to the development of coronary artery disease.

Objective:To explore the effect of pregabalin on sleep structure in rats with temporal lobe epilepsy induced by pilocarpine.Methods:Twelve adult SD rats (half male and half female) were injected intraperitoneally with pilocarpine to establish a chronic temporal lobe epilepsy model.According to the principle of gender matching, they were divided into model group and pregabalin group, with 6 rats in each group(half male and half female). Another 6 SD rats (half male and half female) were taken as the control group.The skull electrodes were placed in the brain areas of rats to monitor the cerebral electrical activity, then recorded the data after resting for 1 week.Rats in pregabalin group were intraperitoneally injected with 50 mg/kg pregabalin while the rats in model group and control group were intraperitoneally injected with equal volume of normal saline.Fifteen minutes later, video electroencephalogram(EEG) and electromyogram(EMG) of rats in each group were recorded.The recording time was from 10∶00 to 17∶00 for 2 consecutive days.The seizure frequency, EEG and EMG were obtained.SPSS 25.0 was used for data analysis, one-way ANOVA was used for multi group comparison, and Tukey test and Games-Howell test were used for further pairwise comparison.Results:(1)The frequency of seizures in the pregabalin group (0.0(0.0, 1.0)times) were significantly lower than that in the model group(2.5(1.0, 4.8)times)( Z=-3.0, P<0.05). (2)During the 7 h recording period, the analyzed data showed that there were significant differences in the sleep-wake transition frequency, slow-wave sleep(SWS) phase duration, rapid eye movement (REM) sleep phase duration, total SWS time, total REM time and total sleep time among the three groups( F=10.5, 4.1, 13.0, 7.8, 4.4, 9.3, all P<0.05). The frequency of sleep-wake transitions in the pregabalin group ((66.3±18.0) times) and the control group ((87.8±14.1) times) were less than that in the model group ((106.7±20.8) times) (both P<0.05). The duration of SWS phase ((11.2±4.0) min) in pregabalin group was significantly longer than that in model group ((5.9±1.8) min) ( P<0.05), while that in model group was shorter than that in control group ((7.7±1.2) min) ( P<0.05). The duration of REM phase in the model group ((1.9±0.4) min) was shorter than that in the control group ((2.5±0.4) min) ( P<0.05). There was no significant difference in the duration of REM phase between the pregabalin group and the model group ( P>0.05). Within 7 h of observation, the total SWS time ((296.5±37.1) min) and total sleep time ((338.4±33.3) min) in pregabalin group were longer than those in model group ((258.1±38.4) min, (288.9±41.0) min) (both P<0.05). The total REM time ((30.4±11.1) min) and total sleep time ((288.9±41.0) min) in the model group were significantly shorter than those in the control group ((50.2±8.5) min, (339.0±19.6) min) (both P<0.05). Conclusion:Pregabalin alone can reduce seizures and change the sleep structure disorder caused by epilepsy, which is mainly manifested in reducing the number of sleep-wake transitions, prolonging the duration of SWS, increasing sleep duration, increasing SWS and total sleep time and improving sleep quality.