BACKGROUND To establish quicker cardiac arrest and less myocardial distension injury during heart procurement, we combined St. Thomas and histidine-tryptophan-ketoglutarate (HTK) solutions for donor heart preservation since June 2008. METHODS From June 2008 to March 2010, we enrolled 31 heart transplantation (HT) patients in this study. During heart procurement we initially infused 1,000 mL cold St Thomas cardioplegic solution to achieve cardiac arrest. After procurement, a further 2,000 mL of cold HTK solution was infused at low perfusion pressure. Another 1,000 mL cold HTK solution was perfused before donor heart implantation. We examined donor age, recipient preoperative characteristics, ischemia time, hospital stay, postoperative graft function, major cardiac events, and transplant vasculopathy (TCAD). RESULTS Twenty-two patients (71.0%) presented with dilated cardiomyopathy and 7 (23.3%) with ischemia cardiomyopathy. There were 23 (76.7%) male donors, and the mean donor age was 38.4 ± 13.8 years. Six patients underwent a redo sternotomy, 1 patient needed a third-do sternotomy, and 1 a seventh sternotomy (third HT) for repeated endocarditis and graft failure. The average ischemia time was 224.9 ± 71.0 minutes and the postoperative hospital stay was 57.7 ± 47.7 days. The surgical mortality (3.2%) was not accompanied by hospital or follow-up mortality. Patient left ventricular ejection fraction postoperative was 59.6 ± 2.3% with good functional status. Major cardiac events occurred in 8 patients (26.7%) without major complications. There were two subjects with TCAD but normal graft function. The correlation between ischemia time and hospital stay was insignificant (r = 0.21; P =.26). CONCLUSIONS Donor heart preservation combining St Thomas cardioplegic arest and low-pressure perfusion with HTK solution seemed to be safe with. short-term survival similar to other approaches.

Single photon emission computed tomography (SPECT) with Tc-99m TRODAT-1 as ligand can be used to evaluate striatal dopamine transporters (DAT) in young subjects. The purpose of this study was to evaluate the reproducibility of (99m)Tc-TRODAT-1 SPECT in DAT binding in healthy young men. Fourteen healthy young men were recruited. The test-retest studies were performed 1week apart. Specific uptake ratios (SUR) of the striatum (ST) and its subregions, the caudate (CA) and the putamen (PU), were measured using the occipital cortex as the reference tissue. The reliability of the two measurements between test and retest, showed significant correlations for the ST, CA and PU, was demonstrated by calculating the intraclass correlation coefficient (ICC). Thus,(99m)Tc-TRODAT-1 SPECT might provide a reproducible and reliable tool in clinical management of young patients with DAT-related disorders.

Baicalein is the flavonoids with multiple pharmacological activities. The aim of our study was to investigate the effects of baicalein on colorectal cancer (CRC) and to recognize the targets of baicalein treatment. To better understand baicalein's target, proteomic approaches were used to purify and identify the protein substrates using 2D difference gel electrophoresis (2D SDS-PAGE) to elucidate proteins differential display. Results from this study investigate that baicalein treatment of CRC cells results in reduced cell proliferation. As a result, differential protein displays between baicalein-treated and untreated CRC were determined and validated. There were 11 differentially expressed proteins between baicalein-treated and untreated CRC. Furthermore, we demonstrate that baicalein inhibits cancer cell proliferation and reduced reactive oxygen species (ROS) by up-regulating the levels of peroxiredoxin-6 (PRDX6). Knockdown of PRDX6 in baicalein-treated CRC cells by specific small interfering RNA resulted in ROS production and proliferation, opposite of the baicalein treatment scenario as indicated by cell cycle distribution. These results illustrate that baicalein up-regulates the expression of PRDX6, which attenuates the generation of ROS and inhibits the growth of CRC cells, whereas baicalein treatment have no effect on normal epithelial cells.

BACKGROUND: Cormobid developmental coordination disorder (DCD) in the patients with attention-deficit hyperactivity disorder (ADHD) often complicated the treatment strategy. Methylphenidate (MPH) improves the coordination problem in patients with ADHD. AIM: The study intended to investigate the pathophysiology and the mechanisms of MPH in comorbid DCD of the adolescents with ADHD. METHODS: Brain images using technetium-99m ethyl cysteinate dimmer ((99m)Tc-ECD) single photon emission computed tomography (SPECT) were done in 10 drug-naïve adolescents with ADHD without DCD and 5 adolescents with ADHD comorbid DCD. The baseline rCBF and changes of rCBF after 10 mg MPH challenge between two groups were compared using statistical parametric mapping (SPM99) analysis. RESULTS: Lower rCBF of bilateral frontal lobe, inferior parental lobe, and increased rCBF of right posterior cingulate gyrus, anterior lobe of cerebellum were found in ADHD comorbid DCD group compared to ADHD without DCD group. Decreased rCBF in the right occipital, inferior temporal lobe was found in ADHD comorbid DCD group after MPH while ADHD alone group revealed increased rCBF in bilateral occipital lobe. CONCLUSIONS: The results help us understand the pathophysiology of DCD in ADHD adolescents. The different rCBF response to MPH provides a clue for future intervention of DCD in ADHD adolescents.

Vibrio parahaemolyticus is a marine foodborne pathogenic bacterium commonly found in seawater or seafood. This bacterium often encounters low salinity stress when the contaminated seafood is washed with fresh water during food processing. This study was conducted to investigate the response of exponential- and stationary-phase cells of V. parahaemolyticus ST550 to lethal or sublethal low salinity. Tolerance to lethal low salinity (0.25% NaCl) was enhanced in V. parahaemolyticus cells in the exponential phase by previous adaptation in sublethal low salinity (0.6% NaCl). Low salinity-adapted cells in the exponential phase were also cross-protected against the challenge of lethal low pH, indifferent to heat, and sensitized to bile, acetic acid, and lactic acid stress. The adapted cells in the stationary phase were significantly protected against heat treatment at 44°C for 10 and 15 min, sensitized to bile and acetic acid treatment, and indifferent to low pH and lactic acid.

OBJECTIVESThe aim of this study was to assess the standard uptake value in clinical stage I non-small cell lung cancer (NSCLC) and its correlation with pathological status and prognosis.METHODSWe retrospectively reviewed 674 patients diagnosed with NSCLC between January 2002 and June 2005. Patients with clinical stage I diseases undergone a preoperative positron emission tomography-computed tomography scan followed by anatomic resection. We reviewed the clinical features of 152 patients with an average follow-up of 87 months.RESULTSWe analysed the clinical features of 108 patients with stage I NSCLC and 44 patients with non-stage I NSCLC. There were no statistical differences in age, histological type, location or tumour differentiation between the two groups. In the Stage I group, the patients had lower maximum standard uptake value (SUVmax; 3.80 ± 3.17 vs 5.73 ± 3.65, P = 0.001), lower carcinoembryonic antigen (CEA) levels (2.86 ± 4.80 vs 9.11 ± 17.21 ng/ml, P = 0.027) and smaller tumour size (2.39 ± 0.98 vs 3.73 ± 2.04 cm, P < 0.001). The patients with higher SUVmax had a more advanced pathological stage, poorer tumour differentiation and larger tumour size. A higher SUVmax was an independent factor predicting an advanced pathological stage (SUVmax ≥3.3, odds ratio 3.246). The median survival of patients with SUVmax ≥3.3 and SUVmax <3.3 were 64.32 and 53.08 months, respectively (P = 0.654).CONCLUSIONSHigher preoperative 18-fluorodeoxyglucose uptake by a tumour was significantly associated with an advanced pathological stage but not correlated with a poorer prognosis. An aggressive preoperative work-up for occult N2 disease should be emphasized, avoiding inappropriate thoracotomy.

INTRODUCTION: Serotonin transporter (SERT) has been associated with many psychiatric diseases. This study investigated the biodistribution of a serotonin transporter imaging agent, N,N-dimethyl-2-(2-amino-4-(18)F-fluorophenylthio)benzylamine (4-[(18)F]-ADAM), in nonhuman primate brain using positron emission tomography (PET). METHODS: Six and four Macaca cyclopis monkeys were used to determine the transit time (i.e., time necessary to reach biodistribution equilibrium) and the reproducibility of 4-[(18)F]-ADAM biodistribution in the brain, respectively. The sensitivity and specificity of 4-[(18)F]-ADAM binding to SERT were evaluated in one monkey challenged with different doses of fluoxetine and one monkey treated with 3,4-methylendioxymethamphetamine (MDMA). Dynamic PET imaging was performed for 3 h after 4-[(18)F]-ADAM intravenous bolus injection. The specific uptake ratios (SURs) in the midbrain (MB), thalamus (TH), striatum (ST) and frontal cortex (FC) were calculated. RESULTS: The distribution of 4-[(18)F]-ADAM reached equilibrium 120-150 min after injection. The mean SURs were 2.49±0.13 in MB, 1.59±0.17 in TH, 1.35±0.06 in ST and 0.34±0.03 in FC, and the minimum variability was shown 120-150 min after 4-[(18)F]-ADAM injection. Using SURs and intraclass coefficient of correlation, the test/retest variability was under 8% and above 0.8, respectively, in SERT-rich areas. Challenge with fluoxetin (0.75-2 mg) dose-dependently inhibited the SURs in various brain regions. 4-[(18)F]-ADAM binding was markedly reduced in the brain of an MDMA-treated monkey compared to that in brains of normal controls. CONCLUSION: 4-[(18)F]-ADAM appears to be a highly selective radioligand for imaging SERT in monkey brain.

BACKGROUND: The aim of this study is to compare the results between surgery alone, preoperative radiotherapy (RT), or preoperative concurrent chemoradiotherapy (CCRT) followed by surgery in the treatment of locally advanced rectal cancer in Asian patients. METHODS: This study included 151 consecutive patients with clinical T3, T4 or node-positive rectal cancer from Jan. 2005 to Dec. 2007. Eighty-six patients underwent total mesorectal excision (TME) alone, 28 patients received preoperative RT (25 Gy in 5 fractions) followed by TME in 1 week, and 37 patients received preoperative CCRT (50.4 Gy in 28 fractions) followed by TME in 4-6 weeks. RESULTS: The 3-year loco-regional recurrence (LRR), distant metastasis, overall and disease-free survival rates are comparable among Surgery, RT and CCRT groups. By multivariate analysis, pT4, distal margin <2 cm, the ratio of positive lymph nodes to totally dissected lymph nodes ≥0.2, and non-R0 resection were significant factors for LRR. In subgroup analysis, TME alone produced comparable LRR to RT or CCRT (3.3 vs.. 4.8%) for favorable patients (0-1 risk factors). For unfavorable patients (2 or more risk factors), the LRR rose to 37% in patients receiving surgery alone as compared with 15% in the RT or CCRT patients. CONCLUSIONS: Preoperative RT or CCRT followed by TME produced good local control in favorable and unfavorable patients with locally advanced rectal cancer. If preoperative RT or CCRT is not given, TME alone has a high incidence of local recurrence in unfavorable patients with 2 or more risk factors.

Flavonoids have been demonstrated to exert health benefits in humans. We investigated whether the flavonoid baicalein would inhibit the adhesion, migration, invasion, and growth of human hepatoma cell lines, and we also investigated its mechanism of action. The separate effects of baicalein and baicalin on the viability of HA22T/VGH and SK-Hep1 cells were investigated for 24h. To evaluate their invasive properties, cells were incubated on matrigel-coated transwell membranes in the presence or absence of baicalein. We examined the effect of baicalein on the adhesion of cells, on the activation of matrix metalloproteinases (MMPs), protein kinase C (PKC), and p38 mitogen-activated protein kinase (MAPK), and on tumor growth in vivo. We observed that baicalein suppresses hepatoma cell growth by 55%, baicalein-treated cells showed lower levels of migration than untreated cells, and cell invasion was significantly reduced to 28%. Incubation of hepatoma cells with baicalein also significantly inhibited cell adhesion to matrigel, collagen I, and gelatin-coated substrate. Baicalein also decreased the gelatinolytic activities of the matrix metalloproteinases MMP-2, MMP-9, and uPA, decreased p50 and p65 nuclear translocation, and decreased phosphorylated I-kappa-B (IKB)-β. In addition, baicalein reduced the phosphorylation levels of PKCα and p38 proteins, which regulate invasion in poorly differentiated hepatoma cells. Finally, when SK-Hep1 cells were grown as xenografts in nude mice, intraperitoneal (i.p.) injection of baicalein induced a significant dose-dependent decrease in tumor growth. These results demonstrate the anticancer properties of baicalein, which include the inhibition of adhesion, invasion, migration, and proliferation of human hepatoma cells in vivo.

The type 1 fimbriae of uropathogenic Escherichia coli (UPEC) have been described as important for the establishment of bladder infections and urinary tract infections (UTI). Urinary prostaglandin (PG) levels and cyclooxygenase (COX)-2 expression in urine particulates may increase with infectious and inflammatory processes, including UTIs. We investigated the mechanisms underlying the modulation of COX-2 expression through the invasion of type 1 fimbriated UPEC strain J96 (J96-1) in human bladder 5637 cells. Bladder 5637 cells infected with J96-1 induced increases in the expression of COX-2 and secretion of PGE(2). By using specific inhibitors and short hairpin RNA (shRNA), we have demonstrated that the activation of extracellular signal-related kinase (ERK), c-Jun-NH(2)-terminal kinase (JNK) and p38 MAPK pathways is critical for J96-1-induced COX-2 expression. Luciferase reporters and chromatin immunoprecipitation assays suggest that J96-1 invasion increases NF-κB- and AP-1-DNA-binding activities in 5637 cells. Inhibition of NF-κB and AP-1 activations blocked the J96-1-induced COX-2 promoter activity and expression. The effect of J96-1 on 5637 cell signalling and COX-2 expression is mediated by Toll-like receptor (TLR)-4. In summary, our findings provide the molecular pathways underlying type 1 fimbriated J96-dependent COX-2 expression in 5637 cells, providing insight into the function of UPEC invasion in bladder epithelial cells.