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PurposeStandard balanced SSFP (bSSFP) cine MRI often suffers from blood outflow artifacts. We propose a method that spatially encodes these outflowing spins to reduce their effects in the intended slice.MethodsBloch simulations were performed to characterize through-plane flow and to investigate how the use of phase encoding along the slice select's direction ("slice encoding") could alleviate its issues. Phantom scans and in vivo cines were acquired on a 3T system, comparing the standard 2D acquisition to the proposed slice-encoding method. Nineteen healthy volunteers were recruited for short-axis and horizontal long-axis oriented scans. An expert radiologist evaluated each slice-encoded/standard cine pairs in a rank comparison test and graded their quality on a 1-5 scale. The grades were used for a nonparametric paired evaluation for independent samples with a null hypothesis that there was no statistical difference between the two quality-grade distributions for α = 0.05 significance.ResultsBloch simulation results demonstrated this technique's feasibility, showing a fully resolved slice profile given a sufficient number of slice encodes. These results were confirmed with the phantom experiments. Each in vivo slice-encoded cine had a higher quality than its corresponding standard acquisition. The nonparametric paired evaluation came to 0.01 significance, encouraging us to reject the null hypothesis and conclude that slice-encoding effectively works in reducing outflow effects.ConclusionThe slice-encoding balanced SSFP technique is helpful in mitigating outflow effects and is achievable within a single breath hold, being a useful alternative for cases in which the flow artifacts are significant.

A hallmark of working memory (WM) is its limited capacity. While visual and verbal domains of WM are able to store multiple items, the capacity of parametric vibrotactile WM (vtWM) has not yet been established for supra-threshold, one-dimensional sensory vibrotactile frequencies. The present study extends the standard delayed match-to-sample vibrotactile discrimination task to determine the capacity of the vtWM and its cognitive mechanism. Here, by presenting subjects with 2 to 6 vibratory frequencies sequentially in each trial, the present study demonstrates that it is possible to retain about only two vibrotactile frequencies information in vtWM. The results also showed that the capacity of vtWM does not depend on whether sequentially presented vibrotactile frequencies are delivered to the same or to different fingers. At the same time, the rate of correct report depends on sequence length and when in the sequence the stimuli are presented, suggesting the dynamic updating of vtWM similar to that of visual WM., Author(s): Chundi Wang [sup.1] [sup.2] [sup.3] , Hu Deng [sup.2] , Yu Dong [sup.3] , Xuemin Zhang [sup.4] , Da-Hui Wang [sup.3] [sup.5] Author Affiliations: (1) grid.64939.31, 0000 0000 9999 [...]

Abstract Background Obesity increases the risk of many diseases. However, there has been little literature about the epidemiology of obesity classified by body mass index (BMI) or waist (abdominal obesity) among urban Chinese adults. This study is to fill the gap by assessing the prevalence of obesity and associated risk factors among urban Chinese adults. Methods A representative sample of 25,196 urban adults aged 18 to 74 years in Northeast China was selected and measurements of height, weight and waist circumference (WC) were taken from 2009–2010. Definitions of overweight and obesity by the World Health Organization (WHO) were used. Results The overall prevalence rates of general obesity and overweight classified by BMI were 15.0% (15.7% for men and 14.3% for women, ppp Conclusions Obesity and overweight have become epidemic in urban populations in China; associations of risk factors with obesity differ between men and women.

Abstract Background Expression of WRAP53 protein has oncogenic properties and it is up regulated in several types of tumors. Methods We examined expression of WRAP53 protein in rectal cancers and analyzed its relationship to the response to preoperative radiotherapy and patient survival. The WRAP53 protein was examined by immunohistochemistry in normal mucosa, primary tumors and lymph node metastases from 143 rectal cancer patients participated in a Swedish clinical trial of preoperative radiotherapy. Results Frequency of WRAP53 protein expression was increased in primary rectal cancer compared to the normal mucosa (p Conclusion WRAP53 may be a new biomarker used to predict prognosis and to select suitable patients for preoperative radiotherapy.

Abstract Background The relationship between pet exposure and the respiratory disease in childhood has been a controversial topic, much is still unknown about the nature of the associations between pet exposure and children’s respiratory health stratified by gender and allergic predisposition. The objective of the present study was to assess the relationship between pet exposure and respiratory symptoms in Chinese children, and to investigate the modified effects of gender and allergic predisposition on such relationship. Methods 31,049 children were selected from 25 districts of 7 cities in Northeast China in 2009. Information on respiratory health and exposure to home environmental factors was obtained via a standard questionnaire designed by the American Thoracic Society. Results Children with an allergic predisposition were found to have more frequent exposure to pets than those without an allergic predisposition (18.5% vs. 15.4%). In children without an allergic predisposition, pet exposure was associated with increased susceptibility to respiratory symptoms/diseases, with girls being more susceptible than boys. No association was found between pet exposure and respiratory symptoms/diseases in boys with an allergic predisposition. In girls with an allergic predisposition, association was found between doctor-diagnosed asthma and pet exposure of their mother during pregnancy (adjusted odds ratio (ORs) = 2.03; 95% confidence interval (CI): 1.01-4.33), and their current pet exposure (ORs = 1.37; 95%CI: 1.00-1.88). Conclusions Pet exposure in children without an allergic predisposition was associated with increased susceptibility to respiratory disease, with girls being more susceptible than boys.

Abstract Background The purpose of the study is to determine whether exposure to malnutrition during early life is associated with increased risk of stomach cancer in later life. Methods The design protocol included analyzing the trend of gastric cancer mortality and nutrition and evaluating the association between nutrient deficiency in early life and the risk of gastric cancer by hierarchical age–period–birth cohort (APC) analysis using general log-linear Poisson models and to compare the difference between birth cohorts who were exposed to the 1959–1961 Chinese famine and those who were not exposed to the famine. Data on stomach cancer mortality from 1970 to 2009 and the dietary patterns from 1955 to 1985 which included the 1959–1961 Chinese famine period in the Zhaoyuan County population were obtained. The nutrition information was collected 15 years prior to the mortality data as based on the latest reference of disease incubation. Results APC analysis revealed that severe nutrition deficiency during early life may increase the risk of stomach cancer. Compared with the 1960–1964 birth cohort, the risk for stomach cancer in all birth cohorts from 1900 to 1959 significantly increased; compared with the 1970–1974 cohort, the risk for stomach cancer in the 1975–1979 cohort significantly increased, whereas the others had a steadily decreased risk; compared with 85–89 age group in the 2005–2009 death survey, the ORs decreased with younger age and reached significant levels for the 50–54 age group after adjusting the confounding factors. The 1930 to 1964 group (exposed to famine) had a higher mortality rate than the 1965 to 1999 group (not exposed to famine). For males, the relative risk (RR) was 2.39 and the 95% confidence interval (CI) was 1.51 to 3.77. For females, RR was 1.64 and 95% CI was 1.02 to 2.62. Conclusion The results of the present study suggested that prolonged malnutrition during early life may increase the risk of stomach cancer mortality in later life.

Abstract Background Catalase is an important antioxidant enzyme that regulates the level of intracellular hydrogen peroxide and hydroxyl radicals. The effects of catalase deficiency on albuminuria and progressive glomerulosclerosis have not yet been fully elucidated. The adriamycin (ADR) nephropathy model is considered to be an experimental model of focal segmental glomerulosclerosis. A functional catalase deficiency was hypothesized to exacerbate albuminuria and the progression of glomerulosclerosis in this model. Methods ADR was intravenously administered to both homozygous acatalasemic mutant mice (C3H/AnLCsbCsb) and control wild-type mice (C3H/AnLCsaCsa). The functional and morphological alterations of the kidneys, including albuminuria, renal function, podocytic, glomerular and tubulointerstitial injuries, and the activities of catalase were then compared between the two groups up to 8 weeks after disease induction. Moreover, the presence of a mutation of the toll-like receptor 4 (tlr4) gene, which was previously reported in the C3H/HeJ strain, was investigated in both groups. Results The ADR-treated mice developed significant albuminuria and glomerulosclerosis, and the degree of these conditions in the ADR-treated acatalasemic mice was higher than that in the wild-type mice. ADR induced progressive renal fibrosis, renal atrophy and lipid peroxide accumulation only in the acatalasemic mice. In addition, the level of catalase activity was significantly lower in the kidneys of the acatalasemic mice than in the wild-type mice during the experimental period. The catalase activity increased after ADR injection in wild-type mice, but the acatalasemic mice did not have the ability to increase their catalase activity under oxidative stress. The C3H/AnL strain was found to be negative for the tlr4 gene mutation. Conclusions These data indicate that catalase deficiency plays an important role in the progression of renal injury in the ADR nephropathy model.

Abstract Background Targeting the ubiquitin-proteasome pathway is a promising approach for anticancer strategies. Recently, we found Bik accumulation in cancer cell lines after they were treated with bortezomib. However, recent evidence indicates that proteasome inhibitors may also induce the accumulation of anti-apoptotic Bcl-2 family members. The current study was designed to analyze the levels of several anti-apoptotic members of Bcl-2 family in different human cancer cell lines after they were treated with proteasome inhibitors. Methods Different human cancer cell lines were treated with proteasome inhibitors. Western blot were used to investigate the expression of Mcl-1 and activation of mitochondrial apoptotic signaling. Cell viability was investigated using SRB assay, and induction of apoptosis was measured using flow cytometry. Results We found elevated Mcl-1 level in human colon cancer cell lines DLD1, LOVO, SW620, and HCT116; human ovarian cancer cell line SKOV3; and human lung cancer cell line H1299, but not in human breast cancer cell line MCF7 after they were treated with bortezomib. This dramatic Mcl-1 accumulation was also observed when cells were treated with other two proteasome inhibitors, MG132 and calpain inhibitor I (ALLN). Moreover, our results showed Mcl-1 accumulation was caused by stabilization of the protein against degradation. Reducing Mcl-1 accumulation by Mcl-1 siRNA reduced Mcl-1 accumulation and enhanced proteasome inhibitor-induced cell death and apoptosis, as evidenced by the increased cleavage of caspase-9, caspase-3, and poly (ADP-ribose) polymerase. Conclusions Our results showed that it was not only Bik but also Mcl-1 accumulation during the treatment of proteasome inhibitors, and combining proteasome inhibitors with Mcl-1 siRNA would enhance the ultimate anticancer effect suggesting this combination might be a more effective strategy for cancer therapy.

Abstract Background MicroRNAs (miRNAs) are a class of non-coding regulatory RNAs of ~22 nucleotides in length. miRNAs regulate gene expression post-transcriptionally, primarily by associating with the 3' untranslated region (UTR) of their regulatory target mRNAs. Recent work has begun to reveal roles for miRNAs in a wide range of biological processes, including cell proliferation, differentiation and apoptosis. Many miRNAs are expressed in cardiac and skeletal muscle, and dysregulated miRNA expression has been correlated with muscle-related disorders. We have previously reported that the expression of muscle-specific miR-1 and miR-133 is induced during skeletal muscle differentiation and miR-1 and miR-133 play central regulatory roles in myoblast proliferation and differentiation in vitro. Methods In this study, we measured the expression of miRNAs in the skeletal muscle of mdx mice, an animal model for human muscular dystrophy. We also generated transgenic mice to overexpress miR-133a in skeletal muscle. Results We examined the expression of miRNAs in the skeletal muscle of mdx mice. We found that the expression of muscle miRNAs, including miR-1a, miR-133a and miR-206, was up-regulated in the skeletal muscle of mdx mice. In order to further investigate the function of miR-133a in skeletal muscle in vivo, we have created several independent transgenic founder lines. Surprisingly, skeletal muscle development and function appear to be unaffected in miR-133a transgenic mice. Conclusions Our results indicate that miR-133a is dispensable for the normal development and function of skeletal muscle.

Abstract Background Unisexual vertebrates have been demonstrated to reproduce by gynogenesis, hybridogenesis, parthenogenesis, or kleptogenesis, however, it is uncertain how the reproduction mode contributes to the clonal diversity. Recently, polyploid gibel carp has been revealed to possess coexisting dual modes of unisexual gynogenesis and sexual reproduction and to have numerous various clones. Using sexual reproduction mating between clone D female and clone A male and subsequent 7 generation multiplying of unisexual gynogenesis, we have created a novel clone strain with more than several hundred millions of individuals. Here, we attempt to identify genetic background of the novel clone and to explore the significant implication for clonal diversity contribution. Methods Several nuclear genome markers and one cytoplasmic marker, the mitochondrial genome sequence, were used to identify the genetic organization of the randomly sampled individuals from different generations of the novel clone. Results Chromosome number, Cot-1 repetitive DNA banded karyotype, microsatellite patterns, AFLP profiles and transferrin alleles uniformly indicated that nuclear genome of the novel clone is identical to that of clone A, and significantly different from that of clone D. However, the cytoplasmic marker, its complete mtDNA genome sequence, is same to that of clone D, and different from that of clone A. Conclusions The present data indicate that the novel clone is a nucleo-cytoplasmic hybrid between the known clones A and D, because it originates from the offspring of gonochoristic sexual reproduction mating between clone D female and clone A male, and contains an entire nuclear genome from the paternal clone A and a mtDNA genome (cytoplasm) from the maternal clone D. It is suggested to arise via androgenesis by a mechanism of ploidy doubling of clone A sperm in clone D ooplasm through inhibiting the first mitotic division. Significantly, the selected nucleo-cytoplasmic hybrid female still maintains its gynogenetic ability. Based on the present and previous findings, we discuss the association of rapid genetic changes and high genetic diversity with various ploidy levels and multiple reproduction modes in several unisexual and sexual complexes of vertebrates and even other invertebrates.

Abstract Background Catalase is preferentially expressed in bronchiolar and alveolar epithelial cells, and acts as an endogenous antioxidant enzyme in normal lungs. We thus postulated epithelial damage would be associated with a functional deficiency of catalase during the development of lung fibrosis. Methods The present study evaluates the expression of catalase mRNA and protein in human interstitial pneumonias and in mouse bleomycin-induced lung injury. We examined the degree of bleomycin-induced inflammation and fibrosis in the mice with lowered catalase activity. Results In humans, catalase was decreased at the levels of activity, protein content and mRNA expression in fibrotic lungs (n = 12) compared to control lungs (n = 10). Immunohistochemistry revealed a decrease in catalase in bronchiolar epithelium and abnormal re-epithelialization in fibrotic areas. In C57BL/6J mice, catalase activity was suppressed along with downregulation of catalase mRNA in whole lung homogenates after bleomycin administration. In acatalasemic mice, neutrophilic inflammation was prolonged until 14 days, and there was a higher degree of lung fibrosis in association with a higher level of transforming growth factor-β expression and total collagen content following bleomycin treatment compared to wild-type mice. Conclusions Taken together, these findings demonstrate diminished catalase expression and activity in human pulmonary fibrosis and suggest the protective role of catalase against bleomycin-induced inflammation and subsequent fibrosis.