Objective To investigate the protective effects of Bauhinia championii Benth flavones(BCF) on oxidative stress of neonatal rat cadiocytes induced by H2O2.Methods Cadiocytes of neonate rat was cultivated for 72 hours and divided into six groups: a normal control group, a H2O2 group, BCF(60, 120 and 240μg/ml)+H2O2 groups and aShuxueninginjection (100μg/ml)+H2O2 group (n=8). 6 hours after the drugs were given, the morphology changes was observed and the survival rate was detected; the content of AST, CPK, LDH in culture medium were detected; the activity of SOD, CAT, GSH-Px and the content of MDA in cardiomyocytes were also determinted; the apoptosis rate were detected, and the expression of caspase-3 in cardiomyocytes was detected by Western blot.Results Compared with the H2O2 group, the activity of AST(28.8 ± 6.1 U/ml, 24.5 ± 5.3 U/mlvs. 36.2 ± 6.7 U/ml), CPK(1.8 ± 0.4 U/ml, 1.5 ± 0.3 U/mlvs. 2.5 ±0.4 U/ml), LDH(805.2 ± 160.9 U/L, 671.5 ± 128.7 U/Lvs. 916.5 ± 168.4 U/L) in culture medium were significantly decreased (P<0.05,P<0.01), the activity of SOD(84.8 ± 17.4 U/mg, 95.3 ± 18.2 U/mgvs. 55.7 ± 13.1 U/mg), CAT(23.4 ± 3.1 U/mg, 26.3 ± 3.5U/mgvs. 15.2 ± 3.0 U/mg) in cardiomyocytes were significantly increased and the content of MDA(8.1 ± 1.7 nmol/mg, 6.8 ± 1.5 nmol/mgvs. 11.1 ± 2.3 nmol/mg) were significantly decreased (P<0.05,P<0.01), the expression of c caspase-3(1.64 ± 0.16, 1.30 ± 0.12vs. 2.06 ± 0.25) and the apoptosis rate (24.2% ± 5.5%, 13.4% ± 3.9%vs. 51.2% ± 9.1%) were significantly decreased (P<0.05,P<0.01); the activity of GSH-Px (3.6 ± 0.9 U/mg vs. 2.4 ± 0.7 U/mg) in cardiomyocytes of BCF 240μg/ml treatment group was increased (P<0.05).Conclusions BCF could effectively improve the morphology of neonatal rat cadiocytes induced by H2O2, increase the survival rate, improve the activity of antioxidase, down-regulate the expression of caspase-3 and decrease the apoptosis rate, suggesting that BCF had dose-dependent protective effects on oxidative stress of neonatal rat cadiocytes induced by H2O2.

Objective To investigate the effect of moderate pain on attentional bias towards emotional pictures among healthy subjects.Methods Thirty-two healthy college students aged from 17 to 26 (21.8±2.2;16 males and 16 females) participated in this study.A tourniquet was tied to each subject's left upper arm 1 to 2cm above the cubits horizontal grain.Pain was inflicted by inflating the tourniquet,and the pressure was maintained at 26.66kPa.While tourniquet was inflated (with pain) or not (no pain),each subject was asked to finish a pictorial dot-probe task with three kinds of pictures-emotionally positive,negative and neutral.In experiment 1,subjects performed the dot-probe tasks with the contralateral hand while the tourniquet was tied on the left upper arm without inflation.In experiment 2 the tourniquet was inflated until the subject completed the dot-probe task (for about 10min).The reaction times (RTs) and the error rates (Ers) in the recognition task were recorded,and the intensity of the subject's pain and discomfort were measured using a verbal rating scale.Results The subjects reported moderate to severe pain with the tourniquet inflated.The RT and ER data were analyzed using two-way analysis of variance (ANOVA) which showed a significant difference between the average RTs of the males (482±73ms without pain and 466±82ms with pain) and those of the females (536±90ms without pain and 519±100 ms with pain).The average ER was significantly different between the pain (2.38±1.49)％ and no pain (1.09±0.82)％ conditions in both groups.Holn-Sidak multiple comparison testing showed significant differences in both groups' average ER between the negative picture (3.81±1.73)％ and the positive picture (1.66±0.97)％,and between the negative and neutral pictures (1.68±0.8) ％ in the pain condition.Mild attentional avoidance was observed with the positive [pain condition (-5.1±4.8) ms and no pain (-4.6±4)ms] and negative pictures [pain condition (-3.43±6) ms and no pain (-0.79±4.1)ms],but no significant difference was found between the pain and no pain conditions.Conclusion The error rate in a pictorial dot-probe task is influenced by pain,especially with negative pictures.

Objective To explore the role of calcium/calmodulin-dependent protein kinase Ⅱ ( CaMK Ⅱ ) in the development of cerebral hypoxic preconditioning(HPC). Methods Healthy male BALB/c mice were randomly divided into 7 groups as follows; normoxic control (H0) , early(H1～H4) and delayed (H5～H6) hypoxically preconditioned mice groups. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to quantitatively analyze the level of CaMK Ⅱ phosphorylation and protein expression level in the brain of mice. Results Compared with H0 group, the phosphorylation level of CaMK Ⅱ increased in cortex and hippocampus of mice in H3～H5 hypoxically preconditioned groups (P<0.05). However, there was no significant changes in total CaMK Ⅱ protein expression in cortex and hippocampus of hypoxic preconditioned mice. Similarly, enhanced p-Thr286 CaMK Ⅱ was also observed in the hippocampus and cortex of mice by immunostaining following hypoxic exposures (H3 and H6). Conclusion The increased phosphorylation of CaMKⅡ may be involved in the development of cerebral HPC in mice.

Objective:To study and analyze the relationship between slow coronary flow (SCF) and vascular endothelial func‐tion .Methods:A total of 88 patients ,who received coronary angiography in our hospital from Jan 2014 to Dec 2014 ,were selected .TIMI blood flow classification was used to assess coronary flow velocity of all patients .The CTFC (corrected TI‐MI frame count ) >27 frames was regarded as slow flow .The patients with slow flow were regarded as SCF group (n=43) , and those with normal blood flow were regarded as normal control group (n=45) .Levels of blood pressure ,blood glucose and blood lipids ,and vascular endothelial function were measured and compared between two groups .Logistic regression a‐nalysis was used to analyze the relationship between SCF and vascular endothelial function .Results:There were no signifi‐cant difference in levels of blood pressure ,blood glucose and blood lipids between two groups , P>0. 05 all .Compared with normal control group , there were significant reductions in fore brachial artery flow‐mediated vascular diastolic function [FMD ,(8. 33 ± 2. 04 )% vs . (7. 06 ± 1. 78 )% ] and nitroglycerin mediated vasodilation [NMD , (20. 39 ± 4. 13 )% vs . (16.10 ± 5.22)% ] in SCF group ,P<0.01 both .Logistic regression analysis indicated that reduced FMD (OR=1.069 ,P=0.011) and NMD (OR=1.183 ,P=0.014) were risk factors for SCF .Conclusion:The vascular endothelial dysfunction is a risk factor of slow coronary flow .

To adapt to the system reformation of medical laboratory science from five academic years to four academic years and to meet the new professional technology-oriented requirements, the medical laboratory science institute of Guangdong Medical College has carried out a comprehensive reform of curriculum system. This paper has analyzed the current problems in the school medical ex-amination and explored the curriculum system reform from three respects such as adjusting curriculum by restructuring and integrating programs, implementing modular teaching to build its characteristics and strengthening practice teaching.And it has also explored the full assessment mode by optimizing the traditional one-stop assessment.

Objective:To investigate any change in the effective connectivity between the bilateral anterior central gyruses after transcranial magnetic stimulation (TMS).Methods:Twenty-one healthy subjects were examined using resting state functional magnetic resonance imaging (rs-fMRI) before and after receiving continuous theta burst stimulation (cTBS). The brain atlas of the Institute of Automation of the Chinese Academy of Sciences was used for fine partitioning of the bilateral anterior central gyruses. Granger causality analysis was used to compare any changes in the effective connectivity between them.Results:After the cTBS inhibited the right M1 area, significant changes in effective connectivity among the sub-regions of the bilateral M1 area were observed. The effective connectivity of the right upper limb to the left upper limb and the left head to face were weakened, while that of the left upper limb to the right head, as well as of the face to the right upper limb was enhanced.Conclusion:For people whose right M1 area has been inhibited by cTBS, the effective connectivity changes in both upper limb functional areas of the M1 region reflect inter-hemispheric inhibition. Opposite changes were found in the trunk and upper limbs.

Objective To investigate the risk factors related to progressive intracranial hemorrhage (PIH) in patients with acute traumatic brain injury (TBI) and analyze their clinical significance.Methods PIH was validated by comparing the initial and repeated CT scans. Data including gender,age, injury causes, Glasgow Coma Score (GCS) on admission, time interval from injury to the first CT scan, initial CT scan manifestations, prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fg), thrombin time (TT), platelet (PLT) and D-dimer (D-D) in both groups were compared with Logistic regression analysis to observe the risk factors related to PIH. Results The study involved 498 patients with acute TBI, of which 139 (27.91%) patients suffered from PIH. There were 116 patients (83.45%) with PIH who received the initial CT scan within two hours post injury.There was statistical difference in aspects of age, GCS on admission, time interval from injury to the first CT scan, initial CT scan manifestations ( including fractures, subarachnoid hematoma, contusion and onset hematoma), PT, Fg and D-D values in both groups (P ＜0.01 ). Logistic regression analysis showed that CT scans (subarachnoid hemorrhage, brain contusion and primary hematoma) and plasma D-D values were predictors of PIH ( P ＜ 0.01 ). Conclusions For patients with the initial CT scan manifestations including subarachnoid hemorrhage, brain contusion, primary hematoma together with D-D value increase within two hours post injury, a continuous CT scan should be performed promptly to detect PIH early.

Objective:To evaluate the role of autophagy in morphine preconditioning-induced reduction of oxygen-glucose deprivation and restoration (OGD/R) injury in primary cortical neurons of mice and the relationship with c-Jun N-terminal kinase (JNK).Methods:Primary cortical neurons extracted from C57BL/6 neonatal mice within 24 h after birth were divided into 9 groups ( n=24 each) using a random number table method: control group (C group), OGD/R group, morphine preconditioning group (M group), autophagy inhibitor 3-methyladenine (3-MA) group (3-MA group), 3-MA+ morphine preconditioning group (3-MA+ M group), autophagy inhibitor chloroquine group (Ch group), chloroquine + morphine preconditioning group (Ch+ M group), JNK inhibitor SP600125 group (SP group) and SP600125 + morphine preconditioning group (SP+ M group). Morphine preconditioning: morphine was added at a final concentration of 3 μmol/L before OGD/R, and the cells were incubated for 2 h in OGD/R group. In 3-MA, Ch and SP groups, 3-MA 5 mmol/L, chloroquine 50 μmol/L and SP600125 25 μmol/L were added, respectively, and the cells were incubated for 150 min. In 3-MA+ M, Ch+ M and SP+ M groups, 3-MA 5 mmol/L, chloroquine 50 μmol/L and SP600125 25 μmol/L were added, respectively, at 30 min before morphine preconditioning. Then the cells were subjected to oxygen-glucose deprivation for 1 h followed by restoration of oxygen-glucose supply for 24 h. CCK-8 assay was used to detect the neuronal viability. The expression of JNK, phosphorylated JNK (p-JNK), microtubule-associated protein 1 light chain 3 (LC3), p62, Beclin1, caspase-3, and cleaved-caspase-3 was determined by Western blot. The autophagosomes and autolysosomes were counted using LC3-double fluorescent adenovirus transfection, and the neuronal apoptosis rate was determined by TUNEL staining. Results:Compared with C group, the neuronal viability was significantly decreased, the expression of Beclin1 was up-regulated, the expression of p62 was down-regulated, and the LC3Ⅱ/LC3Ⅰ ratio, p-JNK/JNK ratio, the number of autophagosomes and autolysosomes, cleaved-caspase-3/caspase-3 ratio and neuronal apoptosis rate were increased in OGD/R group ( P<0.001). Compared with OGD/R group, the neuronal viability, p-JNK/JNK ratio, LC3Ⅱ/LC3Ⅰ ratio and the number of autophagosomes and autolysosomes were significantly increased, the expression of Beclin1 was up-regulated, and the expression of p62 was down-regulated in M group, the LC3Ⅱ/LC3Ⅰ ratio was significantly decreased, and the expression of p62 was down-regulated in 3-MA group, the LC3Ⅱ/LC3Ⅰ ratio was significantly increased, and the expression of p62 was up-regulated in Ch group ( P<0.001), and no significant change was found in the parameters mentioned above in SP600125 group ( P>0.05). Compared with M group, the neuronal viability was significantly decreased, the LC3Ⅱ/LC3Ⅰ ratio was decreased, and the expression of p62 was up-regulated in M+ 3-MA group, the neuronal viability was significantly decreased, the LC3Ⅱ/LC3Ⅰ ratio was increased, and the expression of p62 was up-regulated in M+ Ch group, and the neuronal viability, LC3Ⅱ/LC3Ⅰ ratio and p-JNK/JNK ratio were significantly decreased, the expression of p62 was up-regulated, the number of autophagosomes and autolysosomes was decreased, the expression of Beclin1 was down-regulated, and the cleaved-caspase-3/caspase-3 ratio and neuronal apoptosis rate were increased in M+ SP group ( P<0.001). Conclusions:Morphine preconditioning can attenuate OGD/R injury by activating JNK, enhancing autophagy and inhibiting apoptosis in primary cortical neurons of mice.

Objective To explore the ef fi cacy and safety of long-term use of low dose glucocorticoids in acute respiratory distress syndrome (ARDS). Methods Fifty ARDS patients were randomly divided into two groups. The control group(25 patients)received non-invasive or invasive mechanical ventilation,antibiotics and support treatments. The glucocorticoids group(25 patients)received the same treatments plus long-term use of low dose glucocorticoids. Results The mortality in glucocorticoids group(32％(8/25))was much lower than that in the control group(60％(15/25))(P < 0.05). The ventilator-free days and organ failure-free days within 28d in glucocorticoids group were significantly higher than those in the control group (P < 0.05). The oxygenation index and the serum IL-8 levels in glucocorticoids group at 14d and 28d were higher than those in the control group(P<0.05). Compared to the control group ,long-term use of low dose glucocorticoids in ARDS did not increase fasting blood-glucose at 7d,gastrointestinal bleeding and hospital infections within 28d. Conclusions Long-term use of low dose glucocorticoids in ARDS could reduce the serum IL-8 levels and improve the prognosis.

Alcoholic liver disease (ALD) is a growing global health concern, and its early pathogenesis includes steatosis and steatohepatitis. Inhibiting lipid accumulation and inflammation is a crucial step in relieving ALD. Evidence shows that puerarin (Pue), an isoflavone isolated from Pueraria lobata, exerts cardio-protective, neuroprotective, anti-inflammatory, antioxidant activities. However, the therapeutic potential of Pue on ALD remains unknown. In the study, both the NIAAA model and ethanol (EtOH)-induced AML-12 cell were used to explore the protective effect of Pue on alcoholic liver injury in vivo and in vitro and related mechanism. The results showed that Pue (100 mg·kg^-1) attenuated EtOH-induced liver injury and inhibited the levels of SREBP-1c, TNF-α, IL-6 and IL-1β, compared with silymarin (Sil, 100 mg·kg^-1). In vitro results were consistent within vivo results. Mechanistically, Pue might suppress liver lipid accumulation and inflammation by regulating MMP8. In conclusion, Pue might be a promising clinical candidate for ALD treatment.