As an important branch of system biology,metabolomics is an emerging discipline following with genomics,proteomics and transcriptomics,which studies the variety of endogenous and exogenous metabolites in physiological or pathological state.With the rapid development of technology,metabolomics has been widely used in clinical researches.

During radiation for head and neck cancers,part of parotids are contained in planning target volume(PTV),which lead to parotids receiving radiation as the same as PTV.Radiation for head and neck cancers will influence the parotids.In the period of radiation,many factors will influence parotids,such as age,primary parotid volume,V10-40,weight and mean radiation dose et al.These factors will result in that the parotid volume reduces nearly 50％ and moves toward the middle line of the body.As a result,the real dose of the parotid receiving is higher than prescription dose.The excretion function of the parotid will be severely damaged after radiation,which will lead to xerostomia and influence the quality of patients life.

AIM: To explore the characteristics of motor evoked potential(MEP) and cortical excitability in Parkinson's disease by transcranial magnetic stimulation(TMS).METHODS: 20 normal volunteers were enrolled as control(group A),with the average age of(62.3?16.7) year old ranged from 52 to 79 years including 12 males and 8 females.MEP were assessed and compared separately between left and right hemispheres.21 patients with Parkinson's disease(PD) in asymmetry symptoms were performed in this study(group B),with the average age of(63.3?16.7) year old ranged from 46 to 80 years including 12 males and 9 females.UPDRS motor scores(UPDRSⅢ) were assessed before the check of cortical excitability(MEP).Motor evoked potentials(MEP) was assessed and compared separately on the minor and the serious bodyside,compared to control group.RESULTS: The indexes of MEP from both sides of normal control had no significant diversity.Amp was increased and both rest motor threshold(RMT) and cortical latency(CL) were also decreased significantly in PD patient compared to the normal control.On the serious side of PD,RMT decreased significantly compared to the minor side.Amp,CL and central motor conduct time(CMCT) changed without significant diversity between minor and serious bodyside.CONCLUSION: The motor cortical excitability is increased in PD patients.The excitability is higher with the more serious symptom side.The character of MEP in PD patients may be helpful to make a diagnosis and evaluate the severity of symptoms.

AIM: To construct the recombinant adenovirus carrying fusion suicide gene CDglyTK with the C promoter(Cp),one of the key factors in controlling Epstein-Barr virus latent gene expression,and to investigate if the Cp mediates the expression of CDglyTK in CNE1 cells and kills the cancer cells specifically.METHODS: The tk,cd,Cp sequences were amplified by PCR and subcloned into corresponding sites of pDC316 vector with directional cloning method to construct the pDC316-CP-CDglyTK.The plasmid was analyzed by DNA sequencing and enzyme digestive method.The recombinant adenovirus of Ad-Cp-CDglyTK was packaged,amplified and purified in 293 cells,and the virus titre was determined by TCID50 method.The CDglyTK gene expression in CNE1 and NP69 were examined by reverse transcription-polymerase chain reaction(RT-PCR) after in vitro transfection in CNE1 and NP69 cells.The killing effect of Ad-Cp-CDglyTK/GCV+5-FC on CNE1 cells was detected by MTT method.RESULTS: The results of restriction enzyme digestion and DNA sequencing showed that the tk,cd,and Cp gene were inserted into the pDC316 plasmid in correct orientations.The titer of the recombinant adenovirus was 5.6?1012 TCID 50/L.The Cp fragment was amplified from the total RNA of the transfected CNE1 cells by RT-PCR.The mRNA of CDglyTK gene expression was not detected in NP69 cells.The MTT results showed that after administration of GCV and 5-FC,the killing effects of fusion gene were much better than those of single gene therapy.CONCLUSION: The C promoter specifically mediates the expression of CDglyTK in CNE1 cells.The Ad-Cp-CDglyTK/GCV+5-FC has much better killing effects on CNE1 cells than single gene.

Objective To investigate the effect of penehyclidine hydrochloride ( PHC) pretreat?ment on nuclear factor erythroid 2?related factor 2∕heme oxygenase?1 ( Nrf2∕HO?1) signaling pathway in re?nal tissues of rats with rhabdomyolysis?induced acute kidney injury ( AKI) . Methods Thirty?six pathogen?free male Sprague?Dawley rats, weighing 200-220 g, were assigned into 3 groups ( n=12 each) using a random number table: control group (group C), group AKI and PHC pretreatment group (group PHC). Rhabdomyolysis was induced by intramuscular injection of 50% glycerol 10 ml∕kg in bilateral hindlimbs. PHC 0?2 mg∕kg was injected intraperitoneally at 30 min before glycerol was injected intramuscularly in group PHC. At 1 and 6 h after glycerol injection, serum was collected for determination of blood urea nitro?gen ( BUN) and creatinine ( Cr) concentrations, and bilateral kidneys were harvested for pathological ex?amination and for determination of HO?1 activity and expression of Nrf2 mRNA and HO?1 mRNA ( by quan?titative real?time polymerase chain reaction) , Nrf2 in nucleoprotein and total protein and HO?1 in total pro?tein in renal tissues ( by Western blot) . The damage to the renal tubules was scored. Results Compared with group C, the BUN and Cr concentrations in serum and renal tubular damage scores were significantly increased, the expression of Nrf2 in nucleoprotein and total protein and HO?1 in total protein was signifi?cantly up?regulated, and HO?1 activity was significantly increased in AKI and PHC groups, the expression of HO?1 mRNA was significantly up?regulated in group AKI, and the expression of Nrf2 mRNA and HO?1 mRNA was significantly up?regulated in group PHC (P<0?01 or 0?05). Compared with group AKI, the BUN and Cr concentrations in serum and renal tubular damage scores were significantly decreased, the ex?pression of Nrf2 in nucleoprotein and total protein and HO?1 in total protein was significantly up?regulated, and HO?1 activity was significantly increased in group PHC ( P<0?01 or 0?05) . Conclusion The mecha?nism by which PHC pretreatment attenuates rhabdomyolysis?induced AKI may be related to activation of Nrf2∕HO?1 signaling pathway in renal tissues of rats.

Objective To study the reason and preventive measures of inconformity of the extraction appeared in the process of transfusion blood specimens with the patient's blood type.Methods The reasons of transfusion errors why extracting required blood type was not consistent with the patient's blood type examplesa in Zhengzhou transfusion of hospital from 2008 to 2012 were retrospectively analyzed.Results The experimental results showed that blood specimen inconformity was 49.60%,the error rate of blood extraction and blood infusion was 31.20%,infusion error only was 15.20%,blood type change after stem cell transfusion was 4.00%.Reasons of blood type change after stem cell transplantation to extract blood samples mainly included the blood center or blood did not accord with logo type blood stations provided (16.13%),blood use application form to fill in error(20.97%),check the wrong blood type (6.45%),blood samples taken(29.03%),the blood sample tag(27.42%).Conclusion In order to ensure the safety for clinical use must adopt measures to prevent resolutely put an end to a blood transfusion errors.

Objective To evaluate the effect of anisodamine on endoplasmic reticulum stress during acute kidney injury (AKI) in rats.Methods Forty-two nale Sprague-Dawley rats,weighing 200-220 g,were randomly divided into 3 groups:control group (group C,n =6),AKI group (n =18) and anisodamine group (group AD,n =18).AKI was induced by intramuscular injection of 50％ (v/v) glycerol 10 ml/kg into bilateral hind limbs in groups AKI and AD.In addition,anisodamine 10 mg/kg was injected intraperitoneally 20 min before intramuscular injection of glycerol in group AD.In group C the rats received intramuscular injection of normal saline 10 ml/kg into bilateral hind limbs.Six rats were chosen immediately after injection of normal saline in group C or at 1,6 and 24 h after glycerol injection in groups AKI and AD and then anethetized with intraperitoneal pentobarbital.The animals were sacrificed and kidney specimens were obtained and cut into sections which were stained with hematoxylin and eosin for pathological examination.The pathological changes of the renal tubules were scored.The expression of glucose-regulated protein 78 (GRP78) and oxygen-regulated protein 150 (ORP150) in renal tissues was determined by immuno-histochemistry and Western blot.Results Compared with group C,the pathological scores were significantly increased and the expression of GRP78 and ORP150 was up-regulated at all time points in groups AKI and AD (P ＜ 0.01).Compared with group AKI,the pathological scores were significantly decreased and the expression of GRP78 and ORP150 was down-regulated at all time points in group AD (P ＜ 0.05 or 0.01).Conclusion Anisodamine can ameliorate AKI through inhibiting endoplasmic reticulum stress in renal tubular epithelial cells and decreasing endoplasmic reticulum stress-induced cell apoptosis in rats.

Objective To investigate the effects of Inula Britannica on myocardial caspase-3 and cytochrome c ( cyt c) following overtraining-induced acute myocardial injury in rats.Methods Forty-eight male Wistar rats weighing 200-220 g were randomly divided into 3 groups:group control (group C,n =8) ; group exhausting swim (group E,n =24) and group Inula Britannica (group IB,n =16).The animal model of overtraining-indnced acute myocardial injury was developed by exhausting swim.The animals were forced to swim until they were exhausted.The animals sank to the bottom and no righting reflex or escape response was elicited when they were taken out of water in groups E and IB.In group IB oral Inula Britannica 25 ml/kg was given 24 h and immediately before overtraining.Blood samples were taken from inferior vena cava immediately and at 6,24 h after overtraining in group E and at 6,24 h after overtraining in group IB for determination of serum cardiac troponin I (cTnI) concentration (by ELISA).The animals were sacrificed after blood sampling and myocardial specimens were obtained for microscopic examination and determination of caspase-3 and cyt c expression (by immuno-histochemistry).Results Overtraining significantly increased serum cTnI concentration and up-regulated myocardial caspase-3 and cyt c expression in group E as compared with group C.Oral Inula Britannica significantly attenuated overtraining-induced increase in serum cTnI concentration and myocardial caspase-3 and cyt c expression in group IB as compared with group E.Conclusion Inula Britannica can reduce overtraining-induced acute myocardial injury by down-regulating caspase-3 and cyt c expression.

Objective To evaluate the effect of penehyclidine hydrochloride pretreatment on rhabdomyolysis-induced acute kidney injury (AKI) in rats.Methods Forty-two pathogen-free male SpragueDawley rats,weighing 200-220 g,aged 2 months,were randomly divided into 3 groups using a random number table:control group (group C,n =6),AKI group (n =18),and penehyclidine hydrochloride group (group PH,n =18).The model of rhabdomyolysis-induced AKI was established by injecting 50％ glycerol 10 ml/kg into the lateral muscle of bilateral hindlimbs in AKI and PH groups.The equal volume of normal saline was given in group C.Penehyclidine hydrochloride 0.2 mg/kg was injected intraperitoneally at 30 min before administration of glycerol in group PH.Six rats were selected at 1 h after administration of normal saline in group C,or at 1,6 and 24 h after administration of glycerol,blood samples were collected from the inferior vena cava for determination of the serum blood urea nitrogen (BUN) and creatinine (Cr) concentrations by enzymic colorimetric method.The animals were sacrificed,and kidney specimens were obtained for pathologic examination and for determination of the expression of DJ-1 and phosphatase tensin homolog deleted on chromosome 10 (PTEN) encoding protein (by immuno-histochemistry and Western blot).The damage to the renal tubules was scored.Results Compared with group C,the serum BUN and Cr concentrations and renal tubular damage score were significantly increased,the expression of D J-1 was down-regulated,and the expression of PTEN protein was up-regulated in group AKI (P＜0.05 or 0.01).Compared with group AKI,the serum BUN and Cr concentrations and renal tubular damage score were significantly decreased,the expression of DJ-1 was up-regulated,and the expression of PTEN protein was down-regulated in group PH (P＜0.05 or 0.01).Conclusion Penehyclidine hydrochloride pretreatment can reduce rhabdomyolysis-induced AKI probably by up-regulating the expression of DJ-1 and down-regulating the expression of PTEN protein in rats.

[ ABSTRACT] AIM:To investigate the transient outward potassium channel protein expression in paraventricular nucleus (PVN) and its contribution to renal sympathetic nerve activity (RSNA) in rats with chronic heart failure (CHF). METHODS:A rat model of CHF was prepared by acute myocardial infarction that was induced by ligation of the left ante -rior descending coronary artery .Four weeks after heart failure , echocardiogram was applied to identify the CHF model and plasma norepinephrine (NE), serum NH2-terminal pro-brain natriuretic peptide (NT-proBNP) were detected by ELISA. The expression of ransient outward potassium channel proteins Kv 4.2 and Kv4.3 at mRNA and protein levels was deter-mined by real-time PCR and Western blot .The mean arterial pressure ( MAP) , heart rate ( HR) and RSNA were measured in anesthetized rats with PVN microinjection of potassium channel blockers 4-AP.RESULTS:In CHF group , the rat car-diac function and Kv4.2 and Kv4.3 expression in PVN were obviously lower while plasma NE and serum NT-proBNP were obviously higher than those in sham group .Microinjection of 4-AP into PVN induced an increase in MAP , HR and RSNA in both sham and CHF rats , while the CHF rats exhibited smaller responses to 4-AP than sham-operated rats .CONCLU-SION:Downregulation of Kv4.2 and Kv4.3 expression in the PVN may be a potential mechanism for sympathoexciation in the rats with chronic heart failure .