Effects of urotensin II (UII) on paraventricular nucleus (PVN) neurons of hypothalamus from brain slices of rats were examined by using extracellular recording technique. The results are as follows: (1) In response to application of UII (0.3, 3.0, 30.0, 300.0 nmol/L, n=39) into the perfusate for 2 min, the spontaneous discharge rates (SDR) of 32/39 (82.05% ) neurons were significantly decreased in a dose-dependent manner; (2) Pretreatment with bicuculline (BIC, 100 μmol/L), a specific GABAA receptor antagonist, led to a marked increase in SDR of 5/7 ( 71.43% ) neurons in an epileptiform pattern. The increased discharges were not significantly changed after UII ( 30.0 nmol/L ) was applied into the perfusate for 2 min; (3) Pretreatment with picrotoxin ( PIC, 50 μmol/L ), a selective blocker of Cl- channel, led to an increase in the SDR of all 12/12 (100%) neurons. The increased discharges were not influenced by the applied UII (30.0 nmol/L) for 2 min in 11/12 (91.67%) neurons; (4) Application of nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME, 50 μmol/L ) into the perfusate could significantly augment the SDR of 11/12 ( 91.67% ) neurons , while UII ( 30.0 nmol/L ) applied into the perfusate for 2 min led the augmented SDR of all (12/12, 100%) neurons decrease. The results suggest that UII decreases the excitability of PVN neurons of hypothalamus by potentiating GABAA receptor-mediated Cl- current.

OBJECTIVE: Although the therapeutic method of stroke is progressed very quickly in recent years, the incidence of its post-depression is up to 40%. Poststroke depression many affect neural function recovery, for which, to understand it is advantageous of improving living quality of stroke patients.DATA SOURCE: The literatures relevant to poststroke depression were looked up from China medical nuclear journals and studies at home and abroad in recent 5 years on www.google.com, Medline. The Retrieval words: stroke, depression, incidence, relevant factors.STUDY SELECTION: Totally 42 relevant papers were selected on experimental and clinical studies on poststroke depression. The original literatures of non-randomized study were excluded and those of nonblind study were not excluded.DATA EXTRACTION: Of 42 papers, 10 papers were deleted because of repetition of various degrees and 32 papers were sorted out in category and 10 of those were selected as reference.DATA SYNTHESIS: The incidence of poststroke depression is about 40%, resulting from the co-factors of society, psychology and biology.It is viewed generally that the high risk phase of depression is in a couple of year after stroke and the duration of poststroke depression is various. The severity of neural functional deficits in recovery phase is affected by poststroke depression. Moderate and severe depression may delay the recovery of neural function and poststroke depression can also result in poor recovery of daily living capacity of patients, affect patients' cognition and increase the incidence of dementia. Concerning to clinical observation, a remarkable progression has been achieved on treatment of poststroke depression.CONCLUSION: The incidence of poststroke depression is very high,associated with multiple factors. Poststroke depression influences harmfully on neural function, cognition and daily living capacity. Active intervention and treatment provide a certain action on reducing the incidence of poststroke depression.

Objective To study the relation between chronic stressful, the neural changes in prefrontal cortex and depression. Methods Adapt chronic unpredictable stress with separate model to make depression model rats. After 22 days all the rats were killed and use immunohistochemistry method and computer image analysis to detect BDNF. To analysis the date with SPSS11.5 software. Results After 21 days stress, body weight ( t =2.915, P < 0.05), ambulation ( t = 6. 245, P < 0. 01 ), rearing( t = 2.693, P < 0. 05 ) and grooming ( t = 2. 685, P<0.05) decreased and stopping time in center( t=2. 388, P<0. 05) ,defecation( t =3. 846, P<0. 01 ) increased in experimental group. BDNF expressed obviously in control group and the prefrontal cortex expressed highly than that of the experimental group. BDNF expressions of experimental group were lower than that in control group ( P< 0.01 ) especially in right prefrontal cortex. Conclusion There was no difference of BDNF distribution in prefrontal cortex between both groups ,but after 21 days stress ,the BDNF levels of experimental rats obviously descent,especially in right prefrontal cortex.

OBJECTIVE To introduce the methods of hospital disease prevention and control and advance the level of infection management.METHODS We constituted and administered thoroughly hospital regulations of infection prevention and control according to our country and PLA′s laws and statutes.RESULTS To eliminate effectively the outbreak and epidemic of the hospital infection and cross infection,and complete the work of hospital disease prevention and control that leads appointed us.CONCLUSIONS Disease prevention and control are the key to the infection control in hospitals.

Objective To detect PAH gene mutations in classical PKU patients by HRM analysis. MethodsMutation scanning of PAH gene were performed in 17 classical PKU patients by HRM analysis ( LightScanner), covering the 13 exons and exon-intron boundaries. The HRM results were further confirmed by DNA sequencing, and the sensitivity and specificity of HRM method in PKU diagnosis were also evaluated. In addition, prenatal diagnosis was performed in two fetuses at risk for classical PKU. Results In the 17 patients, two mutations were identified in 16 patients, three mutations were identified in 1 patient.In this subject, a total of 22 different pathogenic mutations : 194V( c. 280A ＞ G), IVS4nt-1 G ＞ A( c. 442-1G ＞ A), R158Q( c. 4736 ＞ A), Q160X( c. 478C ＞ T), W187X( c. 561G ＞ A), E6nt-96A ＞ G( c. 611A ＞G), G239D( c. 716G ＞ A), R241 C( c. 721C ＞ T), R243Q( c. 728G ＞ A), G247R (c. 739G ＞ C), G247V (c. 740G＞T), R261X(c. 781C ＞T), PR261Q(c. 782G ＞ A), H264R (c. 791A ＞ G), F302fsX39 (c. 904delT), E305K( c. 913G ＞ A), G312V( c. 935G ＞ T), Y356X( c. 1068C ＞ A ), V399V ( c. 1197A ＞T), R408Q(c. 1223G ＞ A), T418P(c. 1252A ＞ C) , A434D(c. 1301C ＞ A), 3 silent mutations Q232Q (c. 696G ＞ A), V245V(c. 735G ＞ A), L385L(c. 1155C ＞ G), and one single nucleotide polymorphism rs2280615 ( c. 402A ＞ C) were identified, of which 194V ( c. 280A ＞ G), Q160X ( c. 478C ＞ T), H264R (c. 791A ＞ G), G312V( c. 935G ＞ T) and E305K ( c. 913G ＞ A) were novel mutations identified in PAH gene. The prenatal diagnosis results of the two fetuses : one was diagnosed as normal, the other was diagnosed as a carrier. In this study, the sensitivity and specificity for mutation detection by HRM were 100％, and the HRM results were consistent with DNA sequencing results. Conclusions HRM analysis is a simple,accurate, rapid, high-throughput and low-cost genetic analysis approach. It could be applied to mutation scanning of classical PKU of PAH gene and rapid prenatal diagnosis in parents with known mutations.

AIM To study the central role of genistein (GST) in regulating cardiovascular function of nervous center by examining the effects of GST on the electrical activity of rat paraventricular nucleus neurons in slice preparation and to elucidate the mechanism involved. METHODS Using extracellular single-unit discharge recording technique to examine discharges of neurons in paraventricular nucleus of hypothalamic slices at the resting potential level. RESULTS ①In response to the application of GST 10, 50 and 100 μmol·L-1, respectively, in the perfusate for 2 min, the spontaneous discharge rates (SDR) of neurons in 25/26 hypothalamic slices were significantly decreased in a concentration-dependent manner. ②Pretreatment with L-glutamate 0.2 mmol·L-1 led to a marked increase in the SDR of slices in an epileptiform pattern. GST 50 μmol·L-1 significantly attenuated the increased SDR in all 7 slices. ③In 8/8 slices, the G protein-coupled inwardly rectifying K+ channels (GIRKs) antagonist, tetraethylammonium 1 mmol·L-1 completely blocked the inhibitory effect of GST 50 μmol·L-1. ④Pretreatment with nitric oxide synthase inhibitor Nω-nitro-L-arginine methyl ester 50 μmol·L-1 increased SDR in all 7 slices, but did not affect the inhibitory effect of GST 50 μmol·L-1. CONCLUSION GST can inhibit the electrical activity of paraventricular neurons, and play a protective role on the central neurons. The inhibitory effect of GST may be related to the activation of GIRKs which induce K+ outward current and then engender the cell membrane hyperpolarization, but be not due to the NO release.

Objective To discuss the appropriate timing of providing enteral nutrition through nasojejunal tube for patients with severe craniocerebral injury.Methods 126 cases of patients were divided into 3 groups randomly,providing enteral nutrition through naso-jejunal tube for the first group,the second group and the third group within 12～24 hours,48 hours later and 72 hours later after injury respectively.The nutrition situation of 3 groups was recorded 6 hours later,48 hours later,on the 5th day and the 10th day,including indicators such as total serum protein,blood albumin,serum creatinine,etc and complication cases of diarrhea,hemorrhage of digestive tract,palirrhea,aspiration,inhalation pneumonia and so on within 2 weeks after injury.Results In terms of indicators of albumin,creatinine 48 hours after injury and total protein,albumin and creatinine on the 5th day and 10th day,the first group were better than the second and third group,there were statistic differences between the three groups.Complication comparison within 2 weeks after injury:the difference of palirrhea cases among the three groups was significant,the third group had a higher ratio than the first and second group.And there was no statistic difference in the other indicators like diarrhea,hemorrhage of digestive tract,aspiration and inhalation pneumonia.Conclusions It is high time that patients with simple severe craniocerebral injury are provided with enteral nutrition through naso-jejunal tube within 12 to 24 hours,which can improve patients nutrition situation without the increase of the complications.

Objective To explore the influence of feeding styles in early stage on children′s weight in different stages.Methods A complete record of 918 healthy infants was selected and then divided into 3 feeding groups:breast feeding, mixed feeding and artificial fee-ding, according to the way of feeding in the first 6 months after birth. Their weights and heights were measured in the 3rd,5th,8th,12th,18th,24th,60th month to conduct the Z score of weight for age (WAZ), weight for height (WHZ) and the body mass index (BMI) of 60-month-old infants.An investigation on the time of adding auxiliary food was conducted.Results The heavier,WAZ and WHZ of breast feeding group in the 3rd month were higher than the other groups,and the differences were statistially significant(F=4.12, 5.66, 5.79 Pa

Extracellular single-unit discharge recording technique was used to examine the effects of Ginkgolide B (BN52021) on the discharges of neurons in CAI area of hippocampal slices and to elucidate the mechanisms involved.The results showed that:(1) In response to the application of ginkgolide B (0.1,1,10 βμmol/L; n =43) into the perfusate for 2 rain,the spontaneous discharge rates (SDR) of 42/43 (97.67%) neurons were significantly decreased in a dose-dependent manner; (2) Pretreatment with L-glutamate (L-Glu,0.2mmol/L) led to a marked increase in the SDR of all 10 (100%) neurons in an epileptiform pattern.The increased discharges were suppressed significantly after ginkgolide B (1 μmol/L) was applied into the perfusate for 2 rain; (3) In 8 neurons,perfusion of the selective L-type calcium channel agonist,Bay K 8644 (0.1 μmol/L),induced a significant increase in the discharge rate of 8/8 (100%) neurons.Ginkgolide B (1 μmoL/L) applied into the perfusate inhibited the discharges of 7/8 (87.5%) slices; (4) In 8 neurons,the broad potassium channels blocker,tetraethylammonium (TEA,1 mmol/L) completely blocked the inhibitory effect of ginkgolide B (1 μmol/L).These results suggest that ginkgolide B can inhibit the electrical activity of CAI neurons.The inhibitory effect may be related to the blockade of L-type voltage-activated calcium channel and may be concerned with delayed rectifier potassium channel (KDR),which indicated that ginkgolide B play a protective role on the central neurons.

Objective To investigate the effect of X-ray irradiation on neurites growth of primary hippocampal neurons in vitro.Methods Primary hippocampal neuron culture in vitro were irradiated with 0,2,4,8,10,12 Gy of X-rays.In the first day and the third day after irradiation,the cell death of primary hippocampal neurons was detected by MTT method,and the morphological changes of primary hippocampal neuronal neurites were detected with immunofluorescence staining method.Results In the first day and third day after irradiation,the cell death of hippocampal neurons increased significantly (F =123.068,43.370,P ＜0.05),but there were no significant difference among 4,8,10,and 12 Gy irradiation groups.Immunofluorescence staining showed that,in the first day after irradiation,the neurite length and total dendritic branch length (TDBL) were significantly changed (F =9.169,7.856,P ＜0.05),and in the third day after radiation,the neurite length,TDBL and total dendritic branch tip number (TDBTN) were also altered (F =23.797,6.565,6.021,P ＜ 0.05).Conclusion X-ray irradiation can inhibit the growth of neurites in the primary hippocampal neurons in vitro.