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Articles by Y Gao
Total Records ( 8 ) for Y Gao
  Y Gao , A Raine , P. H Venables , M. E Dawson and S. A. Mednick
  Objective

Amygdala dysfunction is theorized to give rise to poor fear conditioning, which in turn predisposes to crime, but it is not known whether poor conditioning precedes criminal offending. This study prospectively assessed whether poor fear conditioning early in life predisposes to adult crime in a large cohort.

Method

Electrodermal fear conditioning was assessed in a cohort of 1,795 children at age 3, and registration for criminal offending was ascertained at age 23. In a case-control design, 137 cohort members with a criminal record were matched on gender, ethnicity, and social adversity with 274 noncriminal comparison members. Statistical analyses compared childhood fear conditioning for the two groups.

Results

Criminal offenders showed significantly reduced electrodermal fear conditioning at age 3 compared to matched comparison subjects.

Conclusions

Poor fear conditioning at age 3 predisposes to crime at age 23. Poor fear conditioning early in life implicates amygdala and ventral prefrontal cortex dysfunction and a lack of fear of socializing punishments in children who grow up to become criminals. These findings are consistent with a neurodevelopmental contribution to crime causation.

  Z Cao , Y Gao and G. Tao
 

A 56-yr-old woman with chronic hepatitis B and decompensated hepatic cirrhosis was treated with liver transplantation. At the beginning of the neohepatic phase, her arterial blood pressure remained at 60/40 mm Hg for approximately 40 min and did not respond to vasoconstrictive drugs. Her other clinical and laboratory values remained normal, apart from a high cardiac output and low systemic vascular resistance. This patient was diagnosed with vasoplegic syndrome and was treated with IV infusion of methylene blue (0.5 mg/kg) and norepinephrine. This report has potential significance to treatment in patients who undergo orthotopic liver transplantation.

  Y Gao , Y He , J Ding , K Wu , B Hu , Y Liu , Y Wu , B Guo , Y Shen , D Landi , S Landi , Y Zhou and H. Liu
 

Hepatocellular carcinoma (HCC) is the fifth most common malignancy caused by environmental and genetic factors. MicroRNAs (miRNAs) are a class of short non-coding RNAs with posttranscriptional regulatory functions. They participate in diverse biological pathways and function as gene regulators. Genetic polymorphisms in 3' untranslated regions (3' UTRs) targeted by miRNAs alter the strength of miRNA binding, with consequences on regulation of target genes thereby affecting the individual's cancer risk. We have previously predicted polymorphisms falling in miRNA-binding regions of cancer genes. We selected an insertion/deletion (Indel) polymorphism (rs3783553) in the 3' UTR of interleukin (IL)-1 (IL1A) for a case–control study in a Chinese population. With samples from 403 HCC patients and 434 healthy control individuals, strong evidence of association was observed for the variant homozygote. This association was validated in a second independent case–control study with 1074 HCC patients and 1239 healthy control individuals (odds ratio = 0.62; 95% confidence interval = 0.49–0.78). We further show that the ‘TTCA’ insertion allele for rs3783553 disrupts a binding site for miR-122 and miR-378, thereby increasing transcription of IL-1 in vitro and in vivo. These findings suggest that functional polymorphism rs3783553 in IL1A could contribute to HCC susceptibility. Considering IL-1 affects not only various phases of the malignant process, such as carcinogenesis, tumor growth and invasiveness, but also patterns of interactions between malignant cells and the host's immune system, our results indicated that IL-1 may be a promising target for immunotherapy, early diagnosis and intervention of HCC.

  L Wang , J Zheng , Y Du , Y Huang , J Li , B Liu , C. j Liu , Y Zhu , Y Gao , Q Xu , W Kong and X. Wang
 

Rational: Vascular smooth muscle cells (VSMCs) switching from a contractile/differentiated to a synthetic/dedifferentiated phenotype has an essential role in atherosclerosis, postangioplastic restenosis and hypertension. However, how normal VSMCs maintain the differentiated state is less understood.

Objective: We aimed to indentify the effect of cartilage oligomeric matrix protein (COMP), a normal vascular extracellular matrix, on modulation of VSMCs phenotype.

Methods and Results: We demonstrated that COMP was associated positively with the expression of VSMC differentiation marker genes during phenotype transition. Knockdown of COMP by small interfering (si)RNA favored dedifferentiation. Conversely, adenoviral overexpression of COMP markedly suppressed platelet-derived growth factor-BB-elicited VSMC dedifferentiation, characterized by altered VSMC morphology, actin fiber organization, focal adhesion assembly, and the expression of phenotype-dependent markers. Whereas 7 integrin coimmunoprecipitated with COMP in normal rat VSMCs and vessels, neutralizing antibody or siRNA against 7 integrin inhibited VSMC adhesion to COMP, which indicated that 7β1 integrin is a potential receptor for COMP. As well, blocking or interference by siRNA of 7 integrin completely abolished the effect of COMP on conserving the contractile phenotype. In accordance, ectopic adenoviral overexpression of COMP greatly retarded VSMC phenotype switching, rescued contractility of carotid artery ring, and inhibited neointima formation in balloon-injured rats.

Conclusions: Our data suggest that COMP is essential for maintaining a VSMC contractile phenotype and the protective effects of COMP are mainly mediated through interaction with 7β1 integrin. Investigations to identify the factors affecting the expression and integrity of COMP may provide a novel therapeutic target for vascular disorders.

  J. B Li , Y Gao , J Aach , K Zhang , G. V Kryukov , B Xie , A Ahlford , J. K Yoon , A. M Rosenbaum , A. W Zaranek , E LeProust , S. R Sunyaev and G. M. Church
 

Utilizing the full power of next-generation sequencing often requires the ability to perform large-scale multiplex enrichment of many specific genomic loci in multiple samples. Several technologies have been recently developed but await substantial improvements. We report the 10,000-fold improvement of a previously developed padlock-based approach, and apply the assay to identifying genetic variations in hypermutable CpG regions across human chromosome 21. From ~3 million reads derived from a single Illumina Genome Analyzer lane, ~94% (~50,500) target sites can be observed with at least one read. The uniformity of coverage was also greatly improved; up to 93% and 57% of all targets fell within a 100- and 10-fold coverage range, respectively. Alleles at >400,000 target base positions were determined across six subjects and examined for single nucleotide polymorphisms (SNPs), and the concordance with independently obtained genotypes was 98.4%–100%. We detected >500 SNPs not currently in dbSNP, 362 of which were in targeted CpG locations. Transitions in CpG sites were at least 13.7 times more abundant than non-CpG transitions. Fractions of polymorphic CpG sites are lower in CpG-rich regions and show higher correlation with human–chimpanzee divergence within CpG versus non-CpG sites. This is consistent with the hypothesis that methylation rate heterogeneity along chromosomes contributes to mutation rate variation in humans. Our success suggests that targeted CpG resequencing is an efficient way to identify common and rare genetic variations. In addition, the significantly improved padlock capture technology can be readily applied to other projects that require multiplex sample preparation.

  E. Y. Y Chan , Y Gao and S. M. Griffiths
  Background

Over the last 100 years, China has experienced the world's three most fatal earthquakes. The Sichuan Earthquake in May 2008 once again reminded us of the huge human toll geological disaster can lead to.

Methods

In order to learn lessons about the impact of earthquakes on health in China during the past century, we conducted a bilingual literature search of the publicly available health-related disaster databases published between 1906 and 2007.

Results

Our search found that research was limited and there were major gaps in the published literature about the impact on health in the post-earthquake period. However, the experiences recorded were similar to those of other parts of the world. The available studies provide useful information about preparedness and rapid early response. Gaps identified included care of chronic disease.

Conclusion

Our literature review highlights the paucity of literature on the impact on health post-earthquake in China between 1906 and 2007. Disaster mitigation policies need to reflect the needs not only of the disaster-related impacts on health but also of the ongoing health needs of the chronically ill and to establish safeguards for the well-being of the vulnerable populations.

  C. M Balut , Y Gao , S. A Murray , P. H Thibodeau and D. C. Devor
 

The number of intermediate-conductance, Ca2+-activated K+ channels (KCa3.1) present at the plasma membrane is deterministic in any physiological response. However, the mechanisms by which KCa3.1 channels are removed from the plasma membrane and targeted for degradation are poorly understood. Recently, we demonstrated that KCa3.1 is rapidly internalized from the plasma membrane, having a short half-life in both human embryonic kidney cells (HEK293) and human microvascular endothelial cells (HMEC-1). In this study, we investigate the molecular mechanisms controlling the degradation of KCa3.1 heterologously expressed in HEK and HMEC-1 cells. Using immunofluorescence and electron microscopy, as well as quantitative biochemical analysis, we demonstrate that membrane KCa3.1 is targeted to the lysosomes for degradation. Furthermore, we demonstrate that either overexpressing a dominant negative Rab7 or short interfering RNA-mediated knockdown of Rab7 results in a significant inhibition of channel degradation rate. Coimmunoprecipitation confirmed a close association between Rab7 and KCa3.1. On the basis of these findings, we assessed the role of the ESCRT machinery in the degradation of heterologously expressed KCa3.1, including TSG101 [endosomal sorting complex required for transport (ESCRT)-I] and CHMP4 (ESCRT-III) as well as VPS4, a protein involved in the disassembly of the ESCRT machinery. We demonstrate that TSG101 is closely associated with KCa3.1 via coimmunoprecipitation and that a dominant negative TSG101 inhibits KCa3.1 degradation. In addition, both dominant negative CHMP4 and VPS4 significantly decrease the rate of membrane KCa3.1 degradation, compared with wild-type controls. These results are the first to demonstrate that plasma membrane-associated KCa3.1 is targeted for lysosomal degradation via a Rab7 and ESCRT-dependent pathway.

 
 
 
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