Objective To investigate the effects of short-term sleep deprivation(SD)at different time during night on serum cortisol level and emotion state of healthy men,and to find out the influence of work shift onto human circadian rhythm.Methods Two periods of sleep-time were deprived in the present study:the late-night SD(permitted to sleep from 0:00 to 3:00 each day)and the early-night SD(permitted to sleep from 3:00 to 6:00 each day).Ten healthy male adults were chosen to undergo the late-night SD first,followed by normal sleeping for eight nights for washout,and then underwent early-night SD.Each SD period lasted 6 days,i.e.1 day before SD,4 days of SD and 1 day after SD for recovery.Fasting blood samples,for detection of serum cortisol,were collected at 7:00 am every SD day,and the state anxiety inventory(S-AI)scoring was done at the same time.Results The cortisol levels were lowered after 2 types of SD(P0.05).Dependability analysis showed that the cortisol level during the late-night SD period was negatively related to the SD days(r=-0.954 7,P0.05).Both types of SD could elevate anxiety scores,which positively correlated with the SD days(late-night SD:r=0.990,P

Chronic insomnia is a severe disease that seriously influence the human health,and about 10%-15% of the adults suffer from it.No definite conclusion has been made about its etiology up to now,possibly associated with heredity,hormone secretion and living habits.Insomnia not only decreases the patients' quality of life,but also adds burden to society,families and individuals.The diagnosis of chronic insomnia should be based on the patients' sleep history,medication history,psychiatric history and necessary examinations.International diagnosis criteria should be combined if possible.Presently the treatments for chronic insomnia mainly include the OTC medicine,prescription drugs,self-medication with alcoholic beverage,cognitive behavior therapy,melatonin and some traditional herbal therapies.Limited information is available presently about insomnia and a large amount of laboratory and clinical research need to be done to further understand and solve this public problem.

Objective To discuss the protective effect of Tongsaimai pellets(TSMP) and butylphthalide(NBP) on PC12 cell in the hypoxia/hypoglycemia model.Methods Two ischemia models including hypoxia,hypoglycemia models were used to assay the anti-ischemic roles of TSMP and NBP in cultured PC12.Results TSMP and NBP possessed obvious protective effects on PC12 cells from two injured models.Both of them could increase the number of living cells and decrease LDH activity significantly,particularly in hypoglycemia injured model.Conclusion TSM and NBP have protective effect on PC12 cells from two injured models effectively in vitro.

The transformation from the biomedical mode to socio-psycho-biological mode requires higher demands for medical education and comprehensive quality for the medical talents.The existing method of neurology education has disadvantages and cannot meet the needs of modern social life for doctors.By analyzing the neurology education situation that can not be adapted to progression of society,some measures to enhance neurology education are put forward.

Objective To study the releasing properties and mechanism in vitro of the active ingredients of the gastric floating sustained-release tablet containning Zuojin Pellet extraction(ZJ-GFST).Methods The release rates of berberine,palmatine,evodiamine,and rutaecarpine from ZJ-GFST in vitro within 8 h were measured by using rotating basket method in Chinese Pharmacopeia.The cumulative curve of drug release data was fitted to zero order,first-order and Higuchi equation to ascertain the kinetic modeling of drug release.Release mechanism was ascertained using Peppas equation.Results The similar factors of the cumulative release curve of all the four ingredients mutually compared were more than 80%,indicating that the release of the four ingredients were similar.The cumulative release rate of all the four ingredients fitted Higuchi equation.The value of slopes of Peppas models of all the four ingredients were more than 0.45,indicating that drug released by concurrent action of diffusion and matrix erode(non-fickian diffusion).Conclusion The releasing properties in vitro of the active ingredients of ZJ-GFST is consistent.

AIM To establish a quantitative analysis of multi-components by single-marker (QAMS) method for the simultaneous content determination of four saikosaponins in Xiaozheng Pellets (Bupleuri Radix,Cyperi Rhi-zoma,Rhei Radix et Rhizoma,etc.).METHODS The analysis of 5％ ammonia-methanol extract of this drug was performed on a Waters Xbridge C18column (250 mm ×4.6 mm,5 μm),with the mobile phase comprising of acetonitrile-water flowing at 1.0 mL/min in a gradient elution manner,and the detection wavelengths were set at 210 nm and 254 nm.With saikosaponin a as a internal standard,the relative correction factors of saikosaponins b1,b2 and c were calculated,followed by the determination of their contents.RESULTS Four saikosaponins showed good linear relationships within their own ranges (r ≥ 0.999 5),whose average recoveries were 98.08％-102.94％ with the RSDs of 0.85％-1.82％.The results obtained by QAMS approximated those obtained by external standard method.CONCLUSION This simple,precise and feasible method can be used for the quality control of Xiaozheng Pellets.

Objective To investigate the effect of rapid eye movement (REM) sleep deprivation on spatial memory and hippocampal cellular prion protein (PrPC) expression and to explore the underlying mechanism of cognitive impairment induced by sleep deprivation.Methods Adult Sprague-Dawley rats were sorted by weight,randomly divided into three groups:the cage control (CC) group,the tank control (TC) group,and the sleep deprivation (SD) group.Rats were deprived of REM sleep for 72 h using the modified multiple platform method.The Morris water maze task was used to assess hippocampal-dependent spatial memory.After sleep deprivation,the rats were sacrificed and their brain tissue was analyzed for PrPC protein expression via Western blotting.Hippocampal neuron axon elongation was examined as well after lentivector-mediated RNA interference (RNAi) of PrPC in primary cultured rat hippocampal neurons.Results REM sleep deprivation for 72 h resulted in spatial memory impairment.The number of times of rats passing through the platform was decreased significantly in the SD group (3.17 ±0.95) compared with the CC (7.17 ±0.95) and TC (6.50 ±0.62) groups (Z =2.026 6,Z =2.026 6,P ＜0.05),the mean value of proximity to the platform (mm) was greater for rats of the SD group (711.74 ± 33.99) compared to those of theCC (592.32±31.31) andTC (580.86±11.36) groups (Z=-2.001 6,Z=-2.4820,P ＜ 0.05).REM sleep deprivation for 72 h resulted in reduced PrPC level in the hippocampus (0.33 ± 0.10) compared with the CC (1.01 ±0.33) and TC (0.96 ±0.27) groups (Z=2.152 9,Z=2.152 9,P ＜ 0.05).In primary cultured hippocampal neurons,axon elongation(μm) was inhibited 7 days in infected neurons (326.28 ± 12.53) compared with normal (555.00 ±30.43) or negative control (558.70 ±23.10) cells (Z =4.768 4,Z =4.877 0,P ＜ 0.05).Conclusion These findings suggest that PrPC-mediated hippocampal neuron axon elongation inhibition is probably involved in spatial memory impairment induced by sleep deprivation in rats.

Objective To observe changes in the working memory and brain functional imaging on functional magnetic resonance imaging(fMRI) after 36 hours sleep deprivation (SD) in healthy volunteers and to explore the possible mechanism of the changes.Methods FMRI scannings were performed in ten male healthy young volunteers before and after 36 hours SD and results were analyzed using SPM2 software.Subjects were also tested LTR and PLUS task to measure the persistence and operation of working memory before and after 36 hours SD.Results The reaction time of LTR task after 36 hours SD ( (866 ± 102) ms)was significantly longer than that before SD ( (754 ± 91 ) ms, t = 2.59, P < 0.01 ).The reaction time of PLUS task after SD ( (848 ± 94) ms) was significantly longer ( t = 2.37, P < 0.05 ) than that before SD ( (756 ± 79) ms).The error rate of LTR task after SD (95.3% ± 3.56% ) was significantly higher (t=3.52,P < 0.01 ) than that before SD (84.8% ± 8.71% ).The error rate of PLUS task after SD (95.7% ±4.72% ) was significantly higher (t =3.38 ,P <0.01 ) than that before SD (84.2% ±9.66% ).There were no significant differences between the two tasks.The frontal and parietal lobes, anterior cingulate gyrus and thalamus were activated during memory tasks testing before SD.Brain activation was broader and stronger in PLUS task than in LTR task.After SD, activation in parietal lobe was decreased and activation in prefrontal and thalamus was increased significantly.Conclusions The working memory performance decreased after SD.Both LTR and PLUS tasks of working memory activate frontal and parietal lobes, anterior cingulate gyrus and thalamus.The activation of parietal lobe decreased and the activation of prefrontal lobe and thalamus increased after 36 hours SD.This is the possible mechanism of SD to causes the cognition decline.

Objective To evaluate the efficacy of eszopiclone for patients with acute insomnia and the impact of premedication with eszopiclone on sleep structure of patients with acute insomnia.Methods In an open-label,self-control trial was conducted at Changzheng Hospital Sleep Centers,and patients (n =32) with acute insomnia (12 men,20 women; mean age,36.2 years) were administered eszopiclone 3 mg for three consecutive nights.Sleep was monitored via polysomnography.The insomnia severity index (ISI),and mini-mental state examination (MMSE) were used to assess the degree of insomnia and impact of drugs on cognitive function during the day.Results Eszopiclone can shorten sleep latency ( before treatment:(52.92 ± 11.71 ) min,after treatment:(28.2 ± 10.11 ) min; t =-4.376,P ＜0.01 ),prolong total sleep time(before treatment:(365.22 ±30.13) min,after treatment:(429.18 ±26.93 ) min; t =4.102,P ＜ 0.01 ),decrease wake up times( before treatment:( 5.00 ± 1.92 ) times,after treatment:( 2.73 ± 0.91 )times; t =- 4.592,P ＜ 0.01 ),improve sleep efficiency ( before treatment:72.69％ ± 6.32％,after treatment:82.67％ ± 4.16％ ; t =3.371,P ＜ 0.01 ),reduce awake time ( before treatment:( 88.51 ±17.48) min,after treatment:(65.93 ±21.l0)min; t =-4.592,P ＜0.01 ),decrease light sleep ( NREM1 period) the percentage of time ( before treatment:12.54％ ± 2.10％,after treatment:7.30％ ± 2.90％ ;t=-3.155,P ＜ 0.01 ),and increase the percentage of slow wave sleep (before treatment:8.03％ ±5.37％,after treatment:9.31％ ±5.29％; t =4.228,P ＜0.01).No effect was observed on the percentage of NERM2 period (t =0.731,P ＞0.05) and REM period (t =-0.813,P ＞0.05).Eszopiclone can improve the quality of subjective assessment of sleep ( ISI score decreased,t =- 2.551,P ＜ 0.05) and has no significant effect on cognitive function on first the morning after patients taking the medication.Conclusion Eszopiclone can positively regulate the sleep structure in patients with acute insomnia and improve subjective assessment of sleep quality.It is safe and has no significant effect on cognitive function.