Objective To investigate the value of 18F-FDG PET-CT in the diagnosis of adrenal metastasis.Methods 88 patients (107 adrenal lesions) with adrenal metastasis and benign tumor underwent 18F-FDG PET-CT,all adrenal lesions' short diameter,CT value and 18F-FDG maximum standardized uptake values (SUVmax) were measured.The t test,chi-square test and Pearson correlation test were used for data analysis.Meanwhile,receiver operating characteristic (ROC) curve was used to determine the ability of CT value and SUV~x to differentiate the adrenal metastasis and benign tumor.Results There were 73 adrenal metastases and 34 adrenal benign tumors of 107 adrenal lesions.The short diameter of adrenal metastasis was (2.17±1.14) cm,benign tumor was (1.76±1.00) cm,there was no statistical significant difference between the two groups (t =1.817,P =0.072).The CT value of adrenal metastasis and benign tumor were (29.65±10.29) Hu and (14.83±14.42) Hu (t =5.389,P =0.000),respectively.The SUVmax of adrenal metastasis was 9.28±5.33,while benign tumor was 2.81±1.14,statistical significant difference was found between the two groups (t =9.890,P =0.000).For adrenal metastasis,a significant positive correlation was found between short diameter and SUV~ (r =0.620,P =0.000),and it was also found between CT value and SUVmax (r =0.561,P =0.000).Among all patients with adrenal metastasis,32 (58.2 ％) patients' lesions were found in the left adrenal gland,and 5 (9.1％) in the right side (x2 =29.689,P =0.000).ROC curve analysis showed that using lesion' s SUVmax ＞ 4.1 and CT value ＞ 20 Hu as diagnostic criteria,the sensitivity,specificity,accuracy,PPV and NPV were 91.3 ％ (63/69),94.7 ％ (36/38),92.5 ％ (99/107),96.9 ％ (63/65) and 85.7 ％ (36/42),respectively.Conclusion 18F-FDG PET-CT has high sensitivity,specificity and accuracy in diagnosis of adrenal metastasis,and the adrenal lesion' s SUVmax ＞ 4.1 and CT value ＞ 20 Hu is a better diagnostic criteria.

Objective To investigate the risk factors in the outcome of neonatal pulmonary hemorrhage. Methods A total of 69 cases of neonatal pulmonary hemorrhage from January 2005 to December 2011 were studied. They were divided into 2 groups according to clinical outcome (death or alive). The data of the two groups were compared using single factor analysis. The risk factors were analyzed using multi-factor analysis. Results The death of neonates with pulmonary hemorrhage was correlated with aspiration pneumonia, coagulation abnormalities, DIC, heart failure and MPV. Multi-factor analysis showed that DIC (OR=6.90, 95%CI:1.514-31.419), heart failure (OR=9.62, 95%CI:1.710-54.150) and MPV<11 prior to pulmonary hemorrhage (OR=7.01, 95%CI:1.475-33.312) were the independent risk factors of neonatal pulmonary hemorrhage. Conclusions For the neonatal pulmonary hemorrhage with DIC, heart failure and low MPV, active intervention should be implemented.

Objective The antimicrobial peptide LL-37 ( LL-37) is the mature form of Human Cationic Antimicrobial Pep-tide of 18kD (hCAP18) and play a certain regulation role in the pathogenesis of asthma .However, the mechanism is unclear.The aim of this study was to investigate the role of inflammatory release from human eosinophils induced by the antimicrobial peptide LL -37 in the pathogenesis of asthma and the underlying mechanisms . Methods Sixteen mild or medium allergic asthma patients from January 2015 to January 2016 in Panzhihua college affiliated hospital were enrolled .Another 16 healthy volunteers were enrolled as control .Pri-mary eosinophils were isolated from peripheral blood .The cells were divided into two groups:asthma group and healthy control group . Cells were divided into blank , PAF, LL37, single cytokine ( IL-5, GM-CSF) and cytokines combined with LL-37 group based on in-tervention (cell treating factors) difference;Cells were divided into PTx, WRW4, suramin, and LL-37 combined with inhibitors group based on inhibitors difference;Cells were grouped into LTD 4 and LTB4 treatment based on leukotrienen difference;ELISA was applied to analyze cysteinyl leukotrienes ( cys-LTs) level in various treatment groups;Western blot was used to detect change of cPLA 2, p-cP-LA2, ERK1/2, p-ERK1/2 in the cells from the control group after PTx and WRW 4 treatment and the level of hCAP 18 after leukot-riene treatment. Results Compared with the control 15 μg/mL LL-37 sub group, the expression of Cys-LTs was increased in the control 30μg/mL LL-37 sub group 15 and 30 minutes after the LL-37 treatment [(54.02±7.15) pg/105 vs (37.86±6.33) pg/105, (53.30±6.99) pg/105 vs (36.27±6.46) pg/105, P<0.05].Compared with the control IL-5 sub group (26.18±4.86) pg/105, the ex-pression of Cys-LTs was increased in the control IL-5+15 μg/mL LL-37 sub group (59.97±6.83) pg/105 and the control IL-5+30μg/mL LL-37 sub group (81.44±13.70) pg/105(P<0.05).Compared with the control sub group , the expression of Cys-LTs was in-creased in the asthma 15 μg/mL LL-37 sub group and the asthma 30μg/mL LL-37 sub group ( P<0.05) .Compared with the control LL-37 sub group, the expression of Cys-LTs was decreased in the control PTx sub group , control WRW4 sub group, control suramin sub group, control PTx +LL-37 sub group, and control WRW4+LL-37 sub group (P<0.05).Western blot results indicated that LL-37 treatment induced the activation and phosphorylation of ERK 1/2 in eosinophil, and PTx and WRW4 blocked the upregulation of pERK1/2 induced by LL-37.Treatment with PD inhibited the phosphorylation of cPLA 2 and the release of Cys-LTs induced by LL-37. hCAP18 was higher in the asthma groups than the healthy control . Conclusion LL-37 was identified as an eosinophil-activating pep-tide that could trigger the release of inflammatory mediators , which might be involved in occurrence and development of asthma through regulating ERK1/2 phosphorylation, inducing cPLA2 phosphorylation and finally initiate synthesis of cys-LTs.This suggests that LL-37/hCAP18 and its signaling pathway might be potential therapeutic targets for asthma .

Objective To investigate the association between the C609T polymorphism of NAD (P)H:quinoneoxidoreductase (NQO1) gene and post operative cognitive dysfunction (POCD).Methods 90 ASA Ⅰ-Ⅱ patients of 59 to 78 years old, undergoing elective hip replacement with epidural anesthesia were enrolled.All patients were given a battery of 5 neuropsychological tests before operation and seven days after operation.Patients were divided into POCD group and control group according to test results (45 patients in each group).The single nucleotide polymorphism C609T of NQO1 gene was detected using real-time PCR by Taqman probes and subjected to odd ratio assessment.Results 5 samples in control group couldn' t be used in the real-time PCR analysis due to quality control.The frequency of C/C genotype in POCD control was lower than that of control group ( 30.0% vs 11.1% ) with statistical significance ( OR = 0.292,95 % CI 0.092 ～ 0.92 1, P ＜ 0.05 ).The C/T +T/T genotype frequency was significantly higher in group POCD than in the control group(88.8% vs 70% ).Patients presented with C/T + T/T genotype showed an evidently increased risk of POCD ( OR =3.42,95% CI 1.08 ～ 10.82,P ＜ 0.05 ).The frequency of C allele of NQO1 gene in group control was 56.2%, as compared with 40% in group POCD with significance ( OR = 0.519,95% CI 0.282 ～ 0.955, P ＜ 0.05 ).The frequency of T allele of NQOI gene in control group was 43.7% ,as compared with 60.0% in POCD group( OR = 1.93,95% CI 1.047 ～3.552,P＜O.05).Conclusion The NQO1 gene single nucleotide polymorphism C609T is evidently associated with the increased risk of POCD.

Objective To study clinical manifestations and imagine features (CT and MRI) on toxic encephalopathy after inhaling heroin. Methods 13 patients with toxic encephalopathy induced by inhaling heroin were observed and analyzed on its clinical and imagine features (CT and MRI).Results 13 patients all were male, and were intoxicated by way of inhaling heroin vapour. Nine cases had appearances of clinical manifestations during abrupt abstinence. The main clinical manifestations of the disease were of the sub-acute diffuse cerebral lesions, especially of early mental symptoms and cerebellum ataxia. The CT of all 13 cases showed multiple white matter lesions involving in the frontal, parietal, occipital,temporal, and cerebellum hemisphere dentate nucleus. There was no occupational mass shown in general. The MRI of 6 cases showing focus was the same as of the CT. Conclusion The diagnosis of HTE should be dependent on the definite inhaling heroin vapour and their clinical features and neuroradiological appearance. CT should be valuable for the diagnosis of HTE, and the MRI as well. Corticosteroids show less therapeutic effect on such diesease.

Increased evidences indicate that resistin is a new hormone secreted from adipose tissue, it is reported to be an important signal molecule linking between obesity,insulin resistance and type 2 diabetes. Many factors can affect the gene expression of resistin. However, the detailed function of resistin still remains mysterious and much work needs to be undertaken. [

AIM: To investigate the influence of ischemic preconditioning on heart function, the activities of lactate dehydrogenase(LDH), malondialdehyde(MDA), and heme oxygenase-1(HO-1) after ischemia/reperfusion in isolated rat heart. METHODS: The model of Langendorff was used in isolated rat heart perfusion. Ischemic preconditioning protocol: stopping perfusion for 5 minutes and reperfusion for 5 minutes, repeating three times. Ischemia protocol: stopping perfusion for 40 minutes and reperfusion for 20 minutes. Indexes of heart function were recorded in control group, ischemia and reperfusion group(IR), and ischemic preconditioning group(IPC). The content of LDH of coronary effluent was measured. Moreover, the content of MDA and activity of HO-1 in myocardium were also measured. RESULTS: The recovery percentage of heart function in IPC group was significantly higher than that in IR group(P

Objective To investigate the influence of early rehabilitation and defibrase on the hemodynamic cerebral vascular dynamic index (CVDI) of hemiplegic patients with acute cerebral infarction. Methods Ninety hemiplegic patients with acute infarction were randomly divided into a rehabilitation and a control group. Both groups received defibrase routine treatment. The rehabilitation group received systematic rehabilitation training in addition. The Fugl-Meyer assessment ( FMA) , the Scandinavian Scoring Scale ( SSS) and Barthel's index ( MBI) were employed to evaluate the functioning of the two groups. The CVDIs of all patients were quantified before and after treatment. Results The FMA, MBI and SSS scores as well as the CVDIs of both groups had improved after 4 weeks of treatment, but all were more improved in the rehabilitation group than in the control group. Conclusions Early rehabilitation was effective for relieving neurological impairment and improving ability in the activities of daily living for patients with acute cerebral infarction.

BACKGROUND: Angiotensin Ⅱ (Ang Ⅱ) can induce cardiac hypertrophy and platelet-derived growth factor(PDGF) also stimulates cardiac hypertrophy. Is AngⅡ responsible for the pathogenesis of cardiac hypertrophy by inducing PDGF receptor expression?OBJECTIVE: To investigate the effect of mitogen activated protein kinase (MAPK) on the role of cardiac hypertrophy induced by Ang Ⅱ in cardiac myocytes so as to provide theoretical basis for clinical prevention and cure of cardiac hypertrophy.DESIGN: Controlled experimental study taking cardiac myocytes of cultured neonatal rats as subjects.SETTING: Department of pathophysiology in a university.MATERIALS: The experiment was completed in the Department of Pathophysiology, Medical College of Peking University. A total of 80 Wistar rats of either gender, aged 1 - 3 days, were provided by the Animal Center of Medical College, Peking University. Their hearts were removed for myocyte culture in the Cell Culture Laboratory.INTERVENTIONS: The cultured neonatal rat cardiac myocytes treated with 10-7mol/L Ang Ⅱ were Ang Ⅱ group, and those preincubated with 10-5mol/L PD98059(an antagonist of MAPK) for 30 minutes and then treated with Ang Ⅱ were PD98059 group. Cardiac myocytes of normal neonatal rats were as control group. The expression of PDGF-β was detected by western blot at 24 hours.MAIN OUTCOME MEASURES: Content of PDGF-β receptor in neonatal rat cardiac myocytes.RESULTS: The expression of PDGF-β receptor induced by Ang Ⅱ at neonatal rat cardiac myocytes markedly increased at 24 hours (432.41 ± 54.08) compared with that of control group(197.65 ± 44. 10) ( q = 6.77, P< 0.01 ). PDGF-β receptor expression of PD98059 group(317.2 ± 21.12) decreased compared with that of Ang Ⅱ group(q = 3.91, P < 0.05) .However, the expression did not return to the level of control group, and there was significant difference between PD98059 group and control group( q= 3.85, P <0.05).CONCLUSION: The results indicate that angiotensin Ⅱ promotes cardiac hypertrophy through inducing expression of PDGF receptor, in which mitogen activated protein kinase participates in. Maybe it is another important mechanism for Ang Ⅱ -induced cardiac hypertrophy. The results can provide experimental data for the primary and secondary prevention in heart rehabilitation.

AIM: To investigate the crosstalk between angiotensin Ⅱ (AngⅡ)-mediated and platelet-derived growth factor (PDGF)-mediated signal transduction in vascular smooth muscle proliferation.METHODS: A model of renal hypertension was made by two kidney/one-clip operation. Level of PDGF receptor β subunit of aorta was measured by Western Blot analysis. The effect of Ang Ⅱ on PDGF receptor β subunit expression was investigated in culture rat aortic vascular smooth muscle cells (VSMC).RESULTS: Systolic blood pressure obviously increased at 8th week after operation, whereas the level of PDGF receptor β subunit of aorta significantly increased by 126.6% (P＜0.05) in 2K1C rats compared with control group. The expression of PDGF receptor β subunit in cultured VSMC stimulated by AngⅡ was higher than that of control by 192.74%(P＜0.01). The effect of AngⅡ was inhibited remarkably by pretreated with losartan, a kind of specific AngⅡ receptor 1 (AT1) subtype antagonist and U73122, a kind of phospholipase C inhibitor. The effect was partly blocked by PD98059, which inhibit the activity of mitogen-activated, ERK-activating kinase (MEK).CONCLUSION: AngⅡ-induced PDGF receptor β subunit expression is regulated by the AT1 and its downstream signal molecule-PLC and ERK, might participate in the intracellular signal transduction pathway.