Visceral fat index/percentage body fat ratio is independently associated with proximal aortic dilatation in a middle-aged and aged Chinese population in Liujiang of Guangxi.

BACKGROUND AND AIMS: Increased volume of visceral adipose tissue is associated with worsening of cardiovascular disease risk factors that contribute to aortic dilatation. We investigated the effects of visceral fat index (VFI) and VFI/percentage body fat (PBF) ratio on proximal aortic size and proximal aortic dilatation (PAD), to assess whether excess visceral fat deposition is an independent risk factor for PAD. METHODS: 738 participants aged 35 years or more were included in this cross-sectional survey. The sizes of aortic valve annulus (AVA), sinuses of Valsalva (SV), sinotubular junction (STJ), and ascending aorta (AscAo) were measured by transthoracic ultrasound. Multivariate linear regression, binary logistic regression, Bayesian linear regression, and receiver operating characteristic curves were performed to clarify the effects of VFI and VFI/PBF ratio on PAD. RESULTS: There were 78 participants (10.6%) with PAD. VFI and VFI/PBF ratio in the population with PAD was significantly increased, compared to the population without PAD (p < 0.001). However, PBF was not significantly different between the two populations. VFI/PBF ratio was positively associated with sizes of AVA, SV, STJ, and AscAo (p < 0.05), and was independently related to PAD (p < 0.05). A 1-SD increment in VFI/PBF ratio was associated with 13.35-fold increased risk of PAD (odds ratio: 13.35, p < 0.05). CONCLUSIONS: VFI/PBF ratio is independently associated with PAD. An increased proportion of visceral fat may contribute to PAD. VFI/PBF ratio calculation may be used for the preliminary identification of individuals at high risk of PAD in the Chinese population.

Preoperative transcatheter arterial chemotherapy may suppress oxidative stress in hepatocellular carcinoma cells and reduce the risk of short-term relapse.

In this study, we aim to investigate oxidative stress in hepatocellular carcinoma (HCC) tissues in patients receiving preoperative transcatheter arterial chemotherapy (TAC) and its association with prognosis. A total of 89 HCC patients enrolled in this study, 39 received preoperative TAC 1 week before surgery (pTAC group) and 50 did not (non-pTAC group). All patients underwent hepatectomy and postoperative TAC and were followed up to 400 weeks. Samples of liver tissue without HCC and hepatitis (n = 15) served as normal controls. Cellular levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), TP53, and p21waf1/cip1 were measured in both cancer and surrounding tissues using an immunohistochemistry assay. Taken together, our data suggested that preoperative TAC might postpone postoperative HCC relapse within 1 year via suppression of tumor cells by induction of high levels of oxidative stress.

Genome-wide and differential proteomic analysis of hepatitis B virus and aflatoxin B1 related hepatocellular carcinoma in Guangxi, China.

Both hepatitis B virus (HBV) and aflatoxin B1 (AFB1) exposure can cause liver damage as well as increase the probability of hepatocellular carcinoma (HCC). To investigate the underlying genetic changes that may influence development of HCC associated with HBV infection and AFB1 exposure, HCC patients were subdivided into 4 groups depending upon HBV and AFB1 exposure status: (HBV(+)/AFB1(+), HBV(+)/AFB1(-), HBV(-)/AFB1(+), HBV(-)/AFB1(-)). Genetic abnormalities and protein expression profiles were analyzed by array-based comparative genomic hybridization and isobaric tagging for quantitation. A total of 573 chromosomal aberrations (CNAs) including 184 increased and 389 decreased were detected in our study population. Twenty-five recurrently altered regions (RARs; chromosomal alterations observed in ≥10 patients) in chromosomes were identified. Loss of 4q13.3-q35.2, 13q12.1-q21.2 and gain of 7q11.2-q35 were observed with a higher frequency in the HBV(+)/AFB1(+), HBV(+)/AFB1(-) and HBV(-)/AFB1(+) groups compared to the HBV(-)/AFB(-) group. Loss of 8p12-p23.2 was associated with high TNM stage tumors (P = 0.038) and was an unfavorable prognostic factor for tumor-free survival (P =0.045). A total of 133 differentially expressed proteins were identified in iTRAQ proteomics analysis, 69 (51.8%) of which mapped within identified RARs. The most common biological processes affected by HBV and AFB1 status in HCC tumorigenesis were detoxification and drug metabolism pathways, antigen processing and anti-apoptosis pathways. Expression of AKR1B10 was increased significantly in the HBV(+)/AFB1(+) and HBV(-)/AFB1(+) groups. A significant correlation between the expression of AKR1B10 mRNA and protein levels as well as AKR1B10 copy number was observered, which suggest that AKR1B10 may play a role in AFB1-related hepatocarcinogenesis. In summary, a number of genetic and gene expression alterations were found to be associated with HBV and AFB1- related HCC. The possible synergistic effects of HBV and AFB1 in hepatocarcinogenesis warrant further investigations.

Gradient vector flow with mean shift for skin lesion segmentation.

Image segmentation is an important task in the analysis of dermoscopy images since the extraction of skin lesion borders provides important cues for accurate diagnosis. In recent years, gradient vector flow based algorithms have demonstrated their merits in image segmentation. However, due to the compromise of internal and external energy forces within the partial differential equation these methods commonly lead to under- or over-segmentation problems. In this paper, we introduce a new mean shift based gradient vector flow (GVF) algorithm that drives the internal/external energies towards the correct direction. The proposed segmentation method incorporates a mean shift operation within the standard GVF cost function. Theoretical analysis proves that the proposed algorithm converges rapidly, while experimental results on a large set of diverse dermoscopy images demonstrate that the presented method accurately determines skin lesion borders in dermoscopy images.

[Association between myocardial calpain activation and apoptosis in lipopolysaccharide-induced septic mouse model].

OBJECTIVE: in septic mice, myocardial calpain was activated and induced caspase-3 activation, the association between calpain activation and apoptosis was explored in this experiment. METHODS: in in vivo model, adult C57 mice were injected with lipopolysaccharide (LPS, 4 mg/kg, i.p.) to induce sepsis. Myocardial calpain and caspase-3 activities, protein levels of calpain-1, calpain-2, calpastatin, Bcl-2 and Bid were detected by Western blot analysis and myocardial apoptosis was detected by TUNEL, myocardiac function was evaluated by Langendorff system. In in vitro model, adult rat cardiomyocytes were incubated with LPS (1 microg/ml) or co-incubated with calpain inhibitor-III (10 micromol/L), calpain activity, caspase-3 activity, protein levels of Bcl-2 and Bid, and cardiomyocyte apoptosis were detected. RESULTS: in septic mice, myocardial calpain and caspase-3 activity were increased up to 2.7- and 1.8-folds, respectively. Both calpain inhibitor-III and PD150606 significantly attenuated the increase of caspase-3 activity. Myocardial protein levels of calpain-1, calpain-2, calpastatin, Bcl-2 and Bid were similar between control and septic mice, and no cleavage of both Bcl-2 and Bid was found in septic mice. Calpain inhibitor-III significantly improved myocardial function in septic mice. In in vitro model, calpain and caspase-3 activities were increased after 4 h LPS treatment, co-treatment with calpain inhibitor-III prevented caspase-3 activity increase, protein Bcl-2 and Bid were similar between normal cardiomyocytes and LPS-treated cardiomyocytes. Cardiomyocyte apoptosis was similar in in vivo and in vitro septic models. CONCLUSION: myocardial calpain activity is increased in LPS induced septic mice, subsequent caspase-3 activation may contribute to myocardial dysfunction in septic mice without aggravating myocardial apoptosis and Bcl-2 and Bid are not involved on calpain induced caspase-3 activation in our model.

Skin lesion segmentation using an improved snake model.

Accurate identification of lesion borders is an important task in the analysis of dermoscopy images since the extraction of skin lesion borders provides important cues for accurate diagnosis. Snakes have been used for segmenting a variety of medical imagery including dermoscopy, however, due to the compromise of internal and external energy forces they can lead to under- or over-segmentation problems. In this paper, we introduce a mean shift based gradient vector flow (GVF) snake algorithm that drives the internal/external energies towards the correct direction. The proposed segmentation method incorporates a mean shift operation within the standard GVF cost function. Experimental results on a large set of diverse dermoscopy images demonstrate that the presented method accurately determines skin lesion borders in dermoscopy images.

An improved gradient vector flow algorithm for optic disc segmentation.

The optic disc provides important cues for accurate diagnosis of various retinopathic diseases. Accurate segmentation of the optic disc is therefore an important step in the analysis of retinal images. Gradient vector flow (GVF) based segmentation algorithms have been used successfully on a variety of medical imagery, however, due to the compromise of internal and external energy forces, it can lead to less accurate segmentation in certain cases. In this paper, we show, that through incorporation of a mean shift term into the GVF framework, improved segmentation accuracy can be achieved. Experimental results on a large dataset of retinal images demonstrate that the presented method reliably detects the border of the optic disc.

[Cardiomyocyte apoptosis and death receptor pathway in a rat model of coronary microembolization].

OBJECTIVE: To investigate the dynamic changes of cardiomyocyte apoptosis and the role of death receptor apoptotic pathway in a rat model of coronary microembolization (CME). METHODS: Adult rats were randomized to coronary microembolization (CME group, n = 63) or sham-operated group (S group, n = 55). CME model was established by aortic injection of 0.1 ml microspheres (42 microm, 3 x 10(4)/ml) into the left ventricle when the ascending aorta was temporarily clamped.S group received 0.1 ml saline injection and survived rats were randomly examined at 0, 3, 6, 12 and 24 hour post CME (n = 10 each). Heart function was evaluated by echocardiography. Myocardium sample was stained with hematoxylin-eosin and hematoxylin-basic fuchsin-picric acid to detect infarct areas. Cardiomyocyte apoptosis was detected with TUNEL staining. The expression of caspase-3 and caspase-8 was measured by Western blot analysis. RESULTS: Compared with S group, the left ventricular ejection fraction was significantly decreased and left ventricular end-diastolic diameter was significantly increased in CME group (all P < 0.05) except 0 hour CME group. The infarct sizes were similar in 3 hour, 6 hour, 12 hour, and 24 hour CME groups (P > 0.05). The apoptosis index (AI) in CME group were significantly higher at each time point compared to S group (P < 0.05) except 0 hour CME group and peaked at 6 hours. Apoptotic cardiomyocytes were found mainly in the myocardial microinfarcted area and border zones. The relative expression of caspase-3 and caspase-8 in CME group were both significantly increased at 3 hours and peaked at 6 hour post CME (P < 0.05). CONCLUSION: Cardiomyocytes apoptosis was significantly increased after coronary microembolization via activating death receptor apoptotic pathway in this coronary microembolization model.

Enhanced prothrombin formation and platelet activation in Chinese patients after transcatheter closure of atrial septal defect.

BACKGROUND: The objective of this study was to investigate changes in coagulation activation and platelet activation after transcatheter closure of atrial septal defect (ASD) by determining the levels of specific markers over time to provide insight into preventing postprocedural embolism. HYPOTHESIS: We hypothesis that the activation status of coagulation and the platelet would be changed after the closure of ASD. METHODS: Forty consecutive patients who underwent transcatheter closure of ASD with the Lifetech ASD occluder (Lifetech Scientific, Shenzhen, China) were included in this prospective study. The serum level of prothrombin fragment 1 + 2 (F1 + 2) and expressions of P-selectin (CD62P) and platelet glycoprotein IIb/IIIa receptor (CD41a) on the surface of platelets were evaluated at baseline and at 1 day, 1 month, and 3 months after the closure. RESULTS: The median F1 + 2 level was 0.96 nmol/L. This increased to a maximal value of 1.43 nmol/L at 1 day after closure, but gradually returned to the baseline level at 1 month after closure and remained there at 3 months after closure (medians were 0.98 nmol/L and 1.08 nmol/L, respectively). Platelet surface expression of CD62P and CD41a decreased at 1 day, 1 month, and 3 months after closure. For CD62P, average expressions were 8.21% +/- 2.11%, 6.28% +/- 1.72%, 5.29% +/- 1.52%, and 4.41% +/- 1.11%, respectively, for baseline and 1 day, 1 month, and 3 months after closure. For CD41a, average expressions were 79.37% +/- 14.14%, 71.98% +/- 13.77, 56.69% +/- 13.05%, and 54.88% +/- 11.62%, respectively. CONCLUSIONS: Transcatheter closure of ASD with the Lifetech ASD occluder was associated with significantly increased coagulation activation and decreased platelet activation. No evidence supporting the use of aspirin to prevent thrombus formation after closure was found.

[Myocardial inflammation and injury induced by coronary microembolization in rats: role of ERK1/2 signaling pathway].

OBJECTIVE: To determine the role of extracellular signal-regulated kinases1/2 (ERK1/2) signaling pathway in regulating myocardial inflammation and cardiac function in a rat model of coronary microembolization (CME). METHODS: The Sprague-Dawley rats were randomly divided into three groups: sham-operated group (n = 15), coronary microembolization group (n = 15) and PD98059 group (n = 15). CME model was established by injection of 42 microm microspheres 0.1 ml (3 x 10(4)/ml, 3000)into left ventricle while occluding the ascending aorta. At 30 minutes pre-operation, rats of PD98059 group were injected with PD98059 IV, a specific ERK1/2 inhibitor. Western blot and immunochemical analysis were used to determine the activation and distribution of ERK1/2. Echocardiography was employed to evaluate cardiac functions. The hematoxylin-eosin staining was used to assay myocardial inflammation. Expression of TNF-alpha and MIF mRNA was determined by RT-PCR analysis and activity of NF-kappaB assessed by electrophoretic mobility shift assay. RESULTS: In comparison with sham-operated group, CME increased phosphorylation of ERK1/2 (0.92 +/- 0.10 vs 0.61 +/- 0.04), local myocardial inflammatory cells (455 +/- 16 vs 47 +/- 7), expression of TNF-alpha mRNA (0.94 +/- 0.04 vs 0.60 +/- 0.09) and MIF mRNA(1.30 +/- 0.44 vs 0.63 +/- 0.25) and activity of NF-kappaB (541 +/- 25 vs 311 +/- 65) in myocardium(all P < 0.05). All of these dramatically induced cardiac dysfunction [LVEF (73 +/- 3)% vs (83 +/- 4)%, P < 0.05]. To compare with CME group, treatment of specific ERK1/2 inhibitor PD98059 blocked the activation of ERK1/2 (0.48 +/- 0.11 vs 0.92 +/- 0.10, P < 0.05), decreased inflammatory cells (401 +/- 12 vs 455 +/- 16, P < 0.05), decreased expression of TNF-alpha mRNA (0.42 +/- 0.06 vs 0.94 +/- 0.04, P < 0.05) and suppressed activity of NF-kappaB (105 +/- 14 vs 541 +/- 25, P < 0.05). Most importantly, PD98059 treatment ameliorated cardiac functions dramatically [LVEF (76 +/- 4)% vs (73 +/- 3)%, P < 0.05]. However there was no significant change in the expression of MIF mRNA (1.17 +/- 0.37 vs 1.30 +/- 0.44, P > 0.05). CONCLUSION: The present study demonstrates a novel role of ERK1/2 signaling pathway in promoting myocardial inflammation in CME. And ERK1/2 may be a novel drug target for CME therapy.

[Association between aldehyde dehydrogenase-2/cytochrome P450 2E1 genetic polymorphism and habit of alcohol drinking and the susceptibility of hepatocellular carcinoma].

OBJECTIVE: To study the relationship between aldehyde dehydrogenase-2 (ALDH2) and cytochrome P450 2E1 (CYP2E1) gene polymorphism and alcohol drinking habit with the susceptibility of hepatocellular carcinoma( HCC). METHODS: 300 cases of HCC and 292 controls were genotyped for the ALDH2 and CYP2E1 polymorphisms by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: The frequencies of ALDH2 and CYP2E1 variant genotypes in cases and controls were 50.3%, 48.0% and 32.3%, 32.9%, respectively. There was no significant difference of ALDH2 and CYP2E1 genotypes distribution between cases and controls (P > 0.05). The risk for liver cancer was 3.334 times higher in alcoholics ( > or =3 times drinking per week) with ALDH2 * 2 genotype than that that in cases carrying ALDH2 * 1 genotype while drinking less than 3 times per week (95% CI = 1.746 - 6.406) , and the risk for liver cancer was 1.803 times higher in alcoholics ( > or =3 times drinking per week) with CYP2E1c2 genotype than that in cases carrying CYP2E1cl genotype while drinking less than 3 times per week (95% CI = 0.974 - 3.336). Haplotype of the two genotypes increased liver cancer risk to 1.200 folds (95% CI = 0.730 - 1.972), and interaction between drinking and genotypes increases risk of liver cancer to 1.816 folds (95% CI = 0.985 - 3.348). CONCLUSION: ALDH2 or CYP2E1 genotypes alone render no significant risk for HCC, while frequent alcoholic consumption together with ALDH2 or CYP2E1 variant genotypes are associated with risk of hepatocarcinogenesis, suggesting a gene-environment interaction in increasing risk for HCC among Guangxi residents.

GATA4 mutations in Chinese patients with congenital cardiac septal defects.

The object of the study was to elucidate the mutations of the GATA4 gene in Han ancestry patients with congenital cardiac septal defects. Fifty Han ancestry patients with sporadic and familial cardiac septal defects and 200 normal subjects of the same ethnical background were studied. A total of six exons and the intron-exon boundaries of GATA4 were amplified by polymerase chain reaction (PCR). The PCR products were purified and directly sequenced with an ABI PRISM 3730 Automatic DNA sequencer. Two novel heterozygous mutations were discovered in the GATA4 gene in five children with cardiac septal defects (10%, 5/50), His28Tyr in exon 2 and His436Tyr in exon 7, respectively, which were neither found in the control population nor reported in the SNP database at the website http://www.ncbi.nlm.nih.gov/SNP. In addition, we did not identify any mutations in GATA4 in three familial atrial septal defects and two familial ventricular septal defects. Our finding suggests that the mutations in the transcription factor GATA4 might be related to congenital cardiac septal defects in Han ancestry patients.

[Association between GATA-4 mutations and congenital cardiac septal defects in Han Chinese patients].

OBJECTIVE: To elucidate the association between GATA-4 gene mutations and congenital cardiac septal defects in Han Chinese patients. METHODS: Fifty Han Chinese patients with congenital cardiac septal defects and 100 normal subjects with the same ethnical background were studied. Total six exons and the intron-exon boundaries of GATA-4 were amplified by the polymerase chain reaction. The polymerase chain reaction products were purified and directly sequenced with automatic sequencer. RESULTS: Two novel heterozygous mutations were discovered in the GATA-4 gene of patients with congenital cardiac septal defects, His28Tyr in exon 2 and His436Tyr in exon 7 respectively, which were absent in the control population and not reported in the SNP database (http://www.ncbi.nlm.nih.gov/SNP). CONCLUSION: Our finding suggests that the mutations in the transcription factor GATA-4 may be related to congenital cardiac septal defects in Han Chinese patients.

[Preliminary functional analysis of a novel mutation in GATA-4 gene in Chinese patients with congenital cardiac septal defects].

OBJECTIVE: To perform the functional analysis of a novel H436Y mutation of GATA-4 gene identified in Han Chinese patients with congenital cardiac septal defects. METHODS: Using bioinformatics to predict if the H436Y mutation in the GATA-4 gene affects its protein function. H436Y mutation in the GATA-4 gene was generated by Quick Change Lightning site-directed mutagenesis kit and verified by DNA sequencing. GATA-4-wt or GATA-4-mut DNA was cotransfected into Hela cells with DNA for the luciferase reporter gene atrial natriuretic factor (ANF), and luciferase activity was measured by an LKB luminometer 48 h after transient transfection. RESULTS: Alignment of the GATA-4 amino acid sequence indicated that the histidine residue at position 436 was conserved, and H436Y mutation in the GATA-4 gene is expected to affect its protein function. The H436Y mutation significantly reduced the transcriptional activation of downstream reporter ANF when compared to wild-type GATA-4 (P<0.01). CONCLUSION: The mutation c.1306C-->T of the GATA-4 gene impaired the activation of the downstream target, suggesting that the H436Y mutation in the C-terminal region of the GATA-4 gene might prevent its biological function.

[Effects of Astragalus injection in reversing left ventricular hypertrophy induced by renal hypertension in rats].

OBJECTIVE: To explore whether the Astragalus injection (AI) has effect for reversing left ventricular hypertrophy and myocardial fibrosis induced by renal vascular hypertension in rats. METHODS: Thirty male SD rats were randomized equally into three groups: the AI group, the control group and the sham-operated group. All rats, except those in the sham-operated group, were established into the hypertension models by two kidney one clip (2K1C) operation. Blood pressure was measured before operation and every 4 weeks after operation. AI intervention was given to rats in the AI group starting from the 4th week of experiment at dose of 8 g/kg by peritoneal injecting once a day for 8 weeks, while for rats in the other 2 groups, equal volume of normal saline was given instead. All rats were sacrificed 12 weeks after operation by cervical breaking. And indexes including left ventricular mass index (LVMI), left ventricular wall thickness (LVWT), inter-ventricular septal thickness (IVST), left ventricular diameter (LVD), cardiomyocytes diameter (CCD), collagen volume fraction (CVF), and peri-vascular volume collagen area (PVCA) in rats were measured. RESULTS: Blood pressure was not different in the three groups before operation (P>0.05), whereas it rose in the control group and the AI group 4, 8 and 12 weeks after operation correspondingly, showing no difference between the two groups, but significantly higher than that in the sham-operated group (P<0.05). The related indexes in the sham-operated group, control group and AI group were: LVMI, 2.71 +/- 0.24, 3.42 +/- 0.26, 3.13 +/- 0.23, respectively; LVWT (mm), 2.25 +/- 0.42, 4.26 +/- 0.48, 3.28 +/- 0.36; IVST (mm), 2.13 +/- 0.38, 3.98 +/- 0.32, 3.02 +/- 0.28; and LVD (mm), 3.76 +/- 0.29, 2.18 +/- 0.27, 2.82 +/- 0.20 respectively. Comparisons showed that LVMI, LVWT and IVST were significantly higher, but LVD was significantly lower in the control group than those in the sham-operated group (P<0.05); LVMI, LVWT and IVST were significantly lower but LVD was significantly higher in the AI group than those in the control group (P<0.05). CCD, CVF and PVCA in the three groups (in the fore-mentioned order) were: CCD (microm), 14.54 +/- 2.25, 19.56 +/- 2.53, 16.58 +/- 2.46; CVF(%), 3.83 +/- 1.40, 11.21 +/- 2.96, 7.83 +/- 1.67; PVCA (%), 15.71 +/- 3.85, 30.58 +/- 6.25, 21.76 +/- 4.36, respectively. These indexes showed that CCD, CVF, PVCA in the control group were significantly higher than those in the sham-operated group (P<0.05); and those were significantly lower in the AI group than in the control group (P<0.05). CONCLUSION: AI intervention can reverse the left ventricular hypertrophy and myocardial fibrosis induced by renal vascular hypertension in rats.

Hepatitis B virus infection contributes to oxidative stress in a population exposed to aflatoxin B1 and high-risk for hepatocellular carcinoma.

Biomarkers of hepatitis B virus (HBV) infection, aflatoxin B1 (AFB1) exposure and oxidative stress were detected in 71 hepatocellular carcinoma (HCC) patients and 694 controls from southern China. Plasma level of AFB1-albumin-adducts (AAA) and protein carbonyl content (PCC) were significantly higher in the 71 HCC cases than in any age/gender matched HBV sero-status groups (p<0.001). HCC patients positive for the p53-249 G-T mutation had a marginally higher level of PCC than those negative for the mutation (p=0.077). HBV infection had a prominent influence on the association between AFB1 exposure and oxidative stress biomarkers in the controls. Our study indicates a significant contribution from HBV infection to oxidative stress in a population with AFB1 exposure which might substantially increase risk for HCC in this region.

Combination of cardiac pacing and epinephrine does not always improve outcome of cardiopulmonary resuscitation.

We hypothesized that the combination of cardiac pacing and epinephrine would yield a better efficacy for cardiopulmonary resuscitation (CPR) and the combination of 2 therapies at different opportunity would achieve the same results of CPR. Cardiac arrest was induced by clamping the tracheal tubes in 60 Sprague-Dawley rats. At 10 minutes of asphyxia, the animals were prospectively randomized into 5 groups (n = 12/group), and received saline (Sal-gro, 1 mL, intravenous [i.v.]), epinephrine (Epi-gro, 0.4 mg/kg, i.v.), pacing (Pac-gro, transesophageal cardiac pacing combined with saline 1 mL, i.v.), pacing + epinephrine group 1 (PE-gro1, transesophageal cardiac pacing combined with epinephrine 0.4 mg/kg, i.v.), or pacing + epinephrine group 2 (PE-gro2, transesophageal cardiac pacing combined with epinephrine 0.4 mg/kg, i.v., 4 minutes after the transesophageal cardiac pacing initiating and failing to resuscitate the animals), followed by initiation of CPR. Restoration of spontaneous circulation in Sal-gro was lower than in Epi-gro, Pac-gro, PE-gro1, and PE-gro2 (16.67% vs 66.67%, 66.67%, 100%, and 100%; P < .05 or P < .001, respectively). The proportions of withdrawing ventilator and 2-hour survival proportions in Pac-gro and PE-gro2 were higher than in Epi-gro and PE-gro1 (8/8, 10/12 vs 1/8, 2/12, respectively, P < .01, and 7/8, 8/12 vs 1/8, 2/12, respectively, P < .05 or P < .01). Mean survival time in Pac-gro and PE-gro2 were longer than in Epi-gro and PE-gro1 (P < .05 or P < .01). Therefore, the combination of 2 therapies does not always improve outcome of CPR. It is obvious that the combination of transesophageal cardiac pacing with delayed administration of epinephrine yields a better outcome compared to the combination of 2 therapies at the same time during CPR in a rat asphyxia cardiac arrest model.

Evaluation of oxidative stress in a group of adolescents exposed to a high level of aflatoxin B1--a multi-center and multi-biomarker study.

The association between aflatoxin B1 (AFB1) exposure and oxidative stress was extensively examined in 84 adolescents from an area at high risk for hepatocellular carcinoma in China. Plasma level of aflatoxin B1-albumin adducts (AAAs) was associated with AFB1 excretion in urine (r = 0.394, P < 0.001). Urinary AFB1 was also associated with both the urinary excretion of 8-hydroxydeoxyguanosine (8-OHdG) (r > or = 0.479, P < 0.001) and 8-OHdG and hOGG1 levels in peripheral leukocytes (r > or = 0.308, P < or = 0.005). Similarly, AAA was significantly associated with both the urinary excretion of 8-OHdG (r > or = 0.259, P < or = 0.018) and the 8-OHdG and hOGG1 levels in peripheral leukocytes (r > or = 0.313, P < or = 0.004). In addition, urinary 8-OHdG was correlated with both the level of DNA 8-OHdG (r > or = 0.24, P < or = 0.05) and the expression of hOGG1 in peripheral leukocytes (r > or = 0.429, P < 0.001). Protein carbonyl content (PCC) level was significantly associated with not only the level of DNA 8-OHdG (r > or = 0.366, P < 0.001) and the urinary 8-OHdG (r > or = 0.258, P < or = 0.018) but also the expression of hOGG1 in peripheral leukocytes (r = 0.485, P < 0.001). A significant but weak association was found between high-performance liquid chromatograph-electrochemical detection (HPLC-ECD) and enzyme-linked immunosorbent assay (ELISA) for urinary 8-OHdG (r = 0.334, P = 0.002) and between HPLC-ECD and flow cytometry assays for 8-OHdG in leucocytes (r = 0.395, P < 0.001). Significant associations were observed between AAA and PCC and liver function indices (alanine aminotransferase and aspartate aminotransferase). These findings suggest significant contribution from AFB1 exposure to oxidative stress and subsequent repair among adolescents that may impose substantial risk for hepatocarcinogenesis in adulthood in this region.

[Effect of mesenchymal stem cells transplantation on heart function after acute myocardial infarction].

OBJECTIVE: To investigate whether mesenchymal stem cells (MSCs) transplantation after acute myocardial infarction (AMI) can improve heart function and decrease infarct size in rabbits and their correlation. METHODS: Twenty-four rabbits were randomly divided into AMI group and MSCs group, each n=12. Exogenous MSCs labeled with bromodeoxyuridine (BrdU) were injected into the border and central area of the ischemic myocardium. Heart function was assessed with echocardiography before transplantation of MSCs and in 6th week after the transplantation. Surviving MSCs in infarcted myocardium were identified by immunohistochemistry. Infarct size was measured histologically. Correlation of heart function and infarct size were analysed. RESULTS: Immunohistochemical stain revealed that BrdU-positive cells were seen in the infarcted myocardium in MSCs group but not in AMI group. Transplantation of MSCs was associated with a significant diminution of left ventricular end-diastolic dimension (LVEDD), and left ventricular end-systolic dimension (LVESD, both P<0.05), and left ventricular ejection fraction (LVEF) and fractional shortening (DeltaFS%)increased (both P<0.05) as compared with AMI group. Infarct size as measured histologically was significant smaller in MSCs group than AMI group (P<0.05). There were negative correlations between LVEF and infarct size in two groups (both P<0.01). CONCLUSION: Exogenous MSCs transplantation can improve heart function by decreasing infarct size and therefore it might be beneficial in the treatment of AMI.