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Biomedical subjects

Jian Yu

Publications and source records attributed to Jian Yu.

At least 19 recordsLinked to original sources
PubMed2007

Genome evolution and functional divergence in Yersinia.

The steadily increasing number of prokaryotic genomes has accelerated the study of genome evolution; in particular, the availability of sets of genomes from closely related bacteria has made exploration of questions surrounding the evolution of pathogenesis tractable. Here we present the results of a detailed comparison of the genomes of Yersinia pseudotuberculosis IP32593 and three strains of Yersinia pestis (CO92, KIM10, and 91001). There appear to be between 241 and 275 multigene families in these organisms. There are 2,568 genes that are identical in the three Y. pestis strains, but differ from the Y. pseudotuberculosis strain. The changes found in some of these families, such as the kinases, proteases, and transporters, are illustrative of how the evolutionary jump from the free-living enteropathogen Y. pseudotuberculosis to the obligate host-borne blood pathogen Y. pestis was achieved. We discuss the composition of some of the most important families and discuss the observed divergence between Y. pseudotuberculosis and Y. pestis homologs.

Base Sequence↗
PubMed2007

The DNA methylation profile within the 5'-regulatory region of DRD2 in discordant sib pairs with schizophrenia.

Studies of discordance in monozygotic twins have demonstrated that environmental effects play an important role in the pathogenesis of schizophrenia. DNA microarray analysis has revealed upregulation of the DRD2 gene in peripheral blood lymphocytes of schizophrenic patients. We hypothesized that this expression alteration could involve the DNA (CpG) methylation status that is implicated to the transcription status of the gene and in this study we used bisulfited sequence analysis to determine the DNA methylation status of a typical CpGs island within the 5'-regulatory region of DRD2 in peripheral blood lymphocytes from 48 discordant sib pairs suffering from schizophrenia. We found that the methylated cytosines occurred mainly in three clusters. No statistically significant difference in frequency of site-specific cytosine methylation modification of DRD2 between patients and normal controls was found nor did we find any significant association between sex, age on admission or age at onset of schizophrenia and methylated cytosines of DRD2. Our study did not support the hypothesis that site-specific cytosine methylation of DRD2 plays a role in the psychopathology of schizophrenia.

5' Flanking Region↗
PubMed2006

Long-term persistence of robust antibody and cytotoxic T cell responses in recovered patients infected with SARS coronavirus.

Most of the individuals infected with SARS coronavirus (SARS-CoV) spontaneously recovered without clinical intervention. However, the immunological correlates associated with patients' recovery are currently unknown. In this report, we have sequentially monitored 30 recovered patients over a two-year period to characterize temporal changes in SARS-CoV-specific antibody responses as well as cytotoxic T cell (CTL) responses. We have found persistence of robust antibody and CTL responses in all of the study subjects throughout the study period, with a moderate decline one year after the onset of symptoms. We have also identified two potential major CTL epitopes in N proteins based on ELISPOT analysis of pooled peptides. However, despite the potent immune responses and clinical recovery, peripheral lymphocyte counts in the recovered patients have not yet been restored to normal levels. In summary, our study has, for the first time, characterized the temporal and dynamic changes of humoral and CTL responses in the natural history of SARS-recovered individuals, and strongly supports the notion that high and sustainable levels of immune responses correlate strongly with the disease outcome. Our findings have direct implications for future design and development of effective therapeutic agents and vaccines against SARS-CoV infection.

Adult↗
PubMed2006

p53 independent induction of PUMA mediates intestinal apoptosis in response to ischaemia-reperfusion.

BACKGROUND: The small intestine is highly sensitive to ischaemia-reperfusion (I/R) induced injury which is associated with high morbidity and mortality. Apoptosis, or programmed cell death, is a major mode of cell death occurring during I/R induced injury. However, the mechanisms by which I/R cause apoptosis in the small intestine are poorly understood. p53 upregulated modulator of apoptosis (PUMA) is a p53 downstream target and a member of the BH3-only group of Bcl-2 family proteins. It has been shown that PUMA plays an essential role in apoptosis induced by a variety of stimuli in different tissues through a mitochondrial pathway. AIMS: The role of PUMA in I/R induced injury and apoptosis in the small intestine was investigated. The mechanisms by which PUMA is regulated in I/R induced intestinal apoptosis were also studied. METHODS: Ischaemia was induced by superior mesenteric artery occlusion in the mouse small intestine. Induction of PUMA in response to ischaemia alone, or ischaemia followed by reperfusion (I/R), was examined. I/R induced intestinal apoptosis and injury were compared between PUMA knockout and wild-type mice. The mechanisms of I/R induced and PUMA mediated apoptosis were investigated through analysis of caspase activation, cytosolic release of mitochondrial cytochrome c and alterations of the proapoptotic Bcl-2 family proteins Bax and Bak. To determine whether PUMA is induced by reactive oxygen species and/or reactive nitrogen species generated by I/R, superoxide dismutase (SOD) and N-nitro-l-arginine methyl ester (L-NAME) were used to treat animals before I/R. To determine whether p53 is involved in regulating PUMA during I/R induced apoptosis, PUMA induction and apoptosis in response to I/R were examined in p53 knockout mice. RESULTS: PUMA was markedly induced following I/R in the mucosa of the mouse small intestine. I/R induced intestinal apoptosis was significantly attenuated in PUMA knockout mice compared with that in wild-type mice. I/R induced caspase 3 activation, cytochrome c release, Bax mitochondrial translocation and Bak multimerisation were also inhibited in PUMA knockout mice. SOD or L-NAME significantly blunted I/R induced PUMA expression and apoptosis. Furthermore, I/R induced PUMA expression and apoptosis in the small intestine were not affected in the p53 knockout mice. CONCLUSIONS: Our data demonstrated that PUMA is activated by oxidative stress in response to I/R to promote p53 independent apoptosis in the small intestine through the mitochondrial pathway. Inhibition of PUMA is potentially useful for protecting against I/R induced intestinal injury and apoptosis.

Animals↗
PubMed2006

Up-regulation of DLK1 as an imprinted gene could contribute to human hepatocellular carcinoma.

Dysregulation of a genomic imprinting gene can contribute to carcinogenesis. Here, delta-like 1 homolog (Drosophila) (DLK1), a paternally expressed gene, was found to be significantly up-regulated in 60 (73.2%) of a total of 82 hepatocellular carcinoma (HCC) specimens using reverse transcription-polymerase chain reaction. In addition, immunohistochemistry staining was performed in another 88 HCC specimens, of which 50 (56.8%) cancerous tissues were considered as positive. The expression of DLK1 was obviously induced in HCC cells, Bel-7402 and MHCC-H, by a demethylation agent, 5-aza-2'-deoxycytidine. Furthermore, both demethylation of the DLK1 promoter (-565 to -362) and hypermethylation of the imprinting control domain in the region upstream of maternally expressed gene 3 were identified in a few HCC specimens. This implies that deregulation of genomic DNA methylation of the imprinted domain could be attributed to the up-regulation of DLK1 in HCC, although the undoubtedly complex mechanisms involved in the epigenetic event should be further investigated in HCC. Surprisingly, the expression of DLK1 in HCC was confirmed to be monoallelic specific, not biallelic, in three HCC specimens with a single nucleotide polymorphism as at T852C (rs2295660). Importantly, the exogenous DLK1 can significantly promote the cell proliferation of SMMC-7721 cells, a HCC cell line, whereas the suppression of endogenetic DLK1 through RNA interference can markedly inhibit cell growth, colony formation and tumorigenicity of HepG2, Hep3B and HuH-7 cells. These data suggest that DLK1 as an imprinted gene could be significantly up-regulated in HCC due to certain epigenetic events and contribute to the oncogenesis of this tumor.

Animals↗
PubMed2006

Overexpression of proline oxidase induces proline-dependent and mitochondria-mediated apoptosis.

Proline oxidase (POX), a mitochondrial inner-membrane protein, catalyzes the rate-limiting oxidation of proline to pyrroline- 5-carboxylate (P5C). Previously we showed that overexpression of POX is associated with generation of reactive oxygen species (ROS) and apoptosis in POX-inducible colorectal cancer cells, DLD-1.POX. We also showed expression of mitochondrial MnSOD partially blunts POX-induced ROS generation and apoptosis. To further investigate the molecular basis of POX-induced apoptosis, we utilized the DLD-1.POX cells to show that cells overproducing POX exhibit an L-proline-dependent apoptotic response. The apoptotic effect is specific for L-proline, detectable at 0.2 mM, maximal at 1 mM, and occurs during 48-72 h following the addition of L-proline to cells with maximally induced POX. The apoptotic response is mitochondria-mediated with release of cytochrome c, activation of caspase-9, chromatin condensation/DNA fragmentation, and cell shrinkage. We conclude that in the presence of proline, high POX activity is sufficient to induce mitochondria-mediated apoptosis.

Apoptosis↗
PubMed2006

Adsorption behavior of bisphenol A on sediments in Xiangjiang River, Central-south China.

The overall objective of this study was to investigate adsorption behavior of bisphenol A (BPA) on sediments through batch adsorption experiments. The sediment samples were collected from Xiangjiang River (Changsha, Central-south China). Data obtained from adsorption experiments show that the rapid adsorption plays the main role rather than slow adsorption in adsorption process of BPA on sediments. Freundlich model can describe the adsorption behavior of BPA on sediments very well. The calculated K(f) (mg(1-n)l(n)g(-1)) ranged from 0.0072 to 0.0178 (n ranged from 0.6944 to 0.8106). Through analyzing the data of adsorption experiments and properties of sediments, we consider that black carbon (e.g. soot- and charcoal-like material, collectively termed black carbon or BC) and hole-filling domain of the organic matters in sediment are responsible for the observed nonlinear adsorption and desorption hysteresis. The calculated hysteresis coefficient H ranged from 0.6718 to 1.0928. Negative and low molar formation enthalpy (DeltaH(0)= -5.735 kJmol(-1)) indicates that adsorption process of BPA on sediments is an exothermic reaction, attributed to the physical adsorption which is dominated by dispersive force and driven by enthalpy thoroughly. In this study, the amount of adsorbed BPA on sediment was found to decrease as sediment concentration increased, whereas it increased with an increase of ironic concentration. In acidic surroundings, the amount of adsorbed BPA on the sediment was found to decrease as pH value increased, whereas it varied indistinctively in alkaline surroundings.

Adsorption↗
PubMed2006

PUMA sensitizes lung cancer cells to chemotherapeutic agents and irradiation.

PURPOSE: Lung cancer, the leading cause of cancer mortality worldwide, is often diagnosed at late stages and responds poorly to conventional therapies, including chemotherapy and irradiation. A great majority of lung tumors are defective in the p53 pathway, which plays an important role in regulating apoptotic response to anticancer agents. PUMA was recently identified as an essential mediator of DNA damage-induced and p53-dependent apoptosis. In this study, we investigated whether the regulation of PUMA by anticancer agents is abrogated in lung cancer cells and whether PUMA expression suppresses growth of lung cancer cells and/or sensitizes lung cancer cells to chemotherapeutic agents and irradiation through induction of apoptosis. EXPERIMENTAL DESIGNS: The expression of PUMA was examined in lung cancer cells with different p53 status treated with chemotherapeutic agents. An adenovirus expressing PUMA (Ad-PUMA), alone or in combination with chemotherapeutic agents or gamma-irradiation, was used to treat lung cancer cells. The growth inhibitory and apoptotic effects of PUMA in vitro and in vivo were examined. The mechanisms of PUMA-mediated growth suppression and apoptosis were investigated through analysis of caspase activation and release of mitochondrial apoptogenic proteins. The cytotoxicities of PUMA on cancer and normal/nontransformed cells were compared. The efficacy of PUMA and p53 in suppressing the growth of lung cancer cells was also compared. RESULTS: We showed that the induction of PUMA by chemotherapeutic agents is abolished in p53-deficient lung cancer cells. PUMA expression resulted in potent growth suppression of lung cancer cells and suppressed xenograft tumor growth in vivo through induction of apoptosis. Low dose of Ad-PUMA significantly sensitized lung cancer cells to chemotherapeutic agents and gamma-irradiation through induction of apoptosis. The effects of PUMA are mediated by enhanced caspase activation and release of cytochrome c and apoptosis-inducing factor into the cytosol. Furthermore, PUMA seems to be selectively toxic to cancer cells and more efficient than p53 in suppressing lung cancer cell growth. CONCLUSIONS: Our findings indicate that PUMA is an important modulator of therapeutic responses of lung cancer cells and is potentially useful as a sensitizer in lung cancer therapy.

Animals↗
PubMed2006

PUMA Dissociates Bax and Bcl-X(L) to induce apoptosis in colon cancer cells.

PUMA is a BH3-only Bcl-2 family protein that plays an essential role in DNA damage-induced apoptosis. PUMA interacts with anti-apoptotic Bcl-2 and Bcl-X(L) and is dependent on Bax to induce apoptosis. In this study, we investigated how the interactions of PUMA with the antiapoptotic proteins coordinate with Bax to initiate apoptosis in HCT116 colon cancer cells. We found that Bcl-X(L) was most effective among several antiapoptotic proteins in suppressing PUMA-induced apoptosis and PUMA-dependent apoptosis induced by the DNA-damaging agent adriamycin. Mutant Bcl-X(L) that cannot interact with Bax was unable to protect cells from PUMA-mediated apoptosis. Knockdown of Bcl-X(L) by RNA interference significantly enhanced PUMA-mediated apoptosis in HCT116 cells but not in PUMA-knockout cells. Furthermore, Bax was found to be dissociated preferentially from Bcl-X(L) in HCT116 cells but not in the PUMA-knockout cells, in response to PUMA induction and adriamycin treatment. PUMA inhibited the association of Bax and Bcl-X(L) in vitro by directly binding to Bcl-X(L) through its BH3 domain. Finally, we found that wild-type Bax, but not mutant Bax deficient in either multimerization or mitochondrial localization, was able to restore PUMA-induced apoptosis in the BAX-knockout cells. Together, these results indicate that PUMA initiates apoptosis in part by dissociating Bax and Bcl-X(L), thereby promoting Bax multimerization and mitochondrial translocation.

Amino Acid Sequence↗
PubMed2006

Administration of PUMA adenovirus increases the sensitivity of esophageal cancer cells to anticancer drugs.

Esophageal cancer is one of the most lethal human tumors, characterized by relative chemoresistance and poor prognosis. Researchers have been seeking for multimodality to improve its outcome of therapy. PUMA (p53 upregulated modulator of apoptosis) is a potent proapoptotic molecule that is rapidly induced in cells following DNA damage and is required for p53-induced apoptosis. We evaluated the therapeutic potential of PUMA adenovirus against esophageal cancer cell lines (KYSE-150, KYSE-410, KYSE-510 and YES-2). Infection with Ad-PUMA (PUMA Adenovirus) resulted in the more powerful cytotoxicity in these cell lines compared with Ad-p53. Furthermore, we assessed the efficacy of a combined treatment with Ad-PUMA and anticancer drug (cisplatin, paclitaxel, 5-fluorouracil, respectively) for these cells and found PUMA significantly increased the chemosensitivity of esophageal cancer cells, which may result from more abundant apoptosis induction. Interestingly, Ad-PUMA was found to be more efficient than Ad-p53 in inhibiting cell growth and enhancing the chemosensitivity of esophageal cancer cell lines irrespective of the p53 status. These results suggest that Ad-PUMA is a potent cytotoxic agent and could be a promising alternative in the cancer gene therapy in combination with chemotherapeutic agents.

Antineoplastic Agents↗
PubMed2006

Antibody responses against SARS coronavirus are correlated with disease outcome of infected individuals.

Most of the SARS-CoV-infected patients spontaneously recovered without clinical intervention while a small percentage succumbed to the disease. Here, we characterized temporal changes in N protein-specific and S glycoprotein-specific neutralizing antibody (Nab) responses in infected patients who have either recovered from or succumbed to SARS-CoV infection. Recovered patients were found to have higher and sustainable levels of both N protein-specific and S glycoprotein-specific Nab responses, suggesting that antibody responses likely play an important role in determining the ultimate disease outcome of SARS-CoV-infected patients.

Antibodies, Viral↗
PubMed2006

Complete genomic sequences for hepatitis C virus subtypes 6e and 6g isolated from Chinese patients with injection drug use and HIV-1 co-infection.

In one of our recent studies, two HCV genotype 6 variants were identified in patients from Hong Kong and Guangxi in southern China, with injection drug use and HIV-1 co-infection. We report the complete genomic sequences for these two variants: GX004 and HK6554. Their entire genome lengths were 9,468 and 9,462 nt; the 5' UTRs were 338 nt followed by single ORFs of 9,069 nt; the 3' UTRs were 61 and 55 nt including 29 and 23 nt poly(U) tracks. Phylogenetic analysis using a maximum likelihood method showed that HK6554 was classified into subtype 6g and GX004 represented the first complete genome sequence for subtype 6e. Further analysis with reference sequences in three different genomic regions revealed that GX004 closely clustered with a group of subtype 6e variants, which were previously exclusively found in Vietnam and recently increasingly identified in injection drug users from the Guangxi province in southern China that borders Vietnam. This suggests that subtype 6e could become epidemic in southern China by network transmission among injection drug users.

China↗
PubMed2006

Proteomic examination of Ralstonia eutropha in cellular responses to formic acid.

In this study, Ralstonia eutropha was used to elucidate protein changes in response to formic acid. Sixty-three differentially expressed proteins in relation to formic acid in R. eutropha were found with 1-D PAGE and nano-LC-MS/MS. Among the proteins with decreased expression, four were involved in the shikimate pathway and three proteins in the pyrimidine biosynthesis pathway. With the increased expression of proteins, a dramatic change occurred in the induction of ion transporters in relation to maintenance of the acid-base balance. A detoxification process of formic acid in the bacteria might be related to a membrane enzyme, formate hydrogenylase. Three proteins in polyhydroxyalkanoate synthesis were enhanced and five proteins in glutathione biosynthesis increased in response to formic acid. Three enzymes in mevalonate biosynthesis and heat shock proteins were also elevated in the cells. Therefore, formic acid might have an inhibitory effect on aromatic amino acid production and pyrimidine biosynthesis in R. eutropha. R. eutropha cells seemed to attempt to overcome the effects of formic acid by increasing ion transporters and proteins that metabolized formic acid.

Bacterial Proteins↗
PubMed2006

Influence of bactibilia after preoperative biliary stenting on postoperative infectious complications.

The aim of this study was to correlate the bactibilia found after preoperative biliary stenting with that of the bacteriology of postoperative infectious complications in patients with obstructive jaundice. One hundred thirty-eight patients (83% malignant and 17% benign etiologies) with obstructive jaundice had both their bile and all postoperative infectious complications cultured. Eighty-six (62%) had preoperative biliary stents (stent group) and 52 (38%) did not (no-stent group). There were no differences for age, sex, incidence of malignancy, type of operation, estimated blood loss, transfusion requirements, hospital length of stay, morbidity, or mortality rates between the two groups. Of 31 infectious complications, 23 were in the stent group and eight were in the no-stent group (P > 0.05), but only 13 (42%) infectious complications had bacteria that were also cultured from the bile. Only wound infection (P = 0.03) and bacteremia (P = 0.04) were more likely to occur in stented patients. Taken together, these data show that preoperative biliary stenting increases the incidence of bactibilia, bacteremia, and wound infection rates but does not increase morbidity, mortality, or hospital length of stay. Jaundiced patients can undergo preoperative biliary stenting while maintaining an acceptable postoperative morbidity rate.

Anastomosis, Roux-en-Y↗
PubMed2006

A margin-negative R0 resection accomplished with minimal postoperative complications is the surgeon's contribution to long-term survival in pancreatic cancer.

Pancreatic cancer has a poor prognosis with complete surgical resection being the only therapy to offer a realistic chance for long-term survival. The aim of this study is to identify surgery-related variables that influence long-term survival. Between 1990 and 2002, 226 consecutive patients (mean age of 64+/-11 years) had resection for pancreatic adenocarcinoma. Prognostic variables in these patients were analyzed using univariate and multivariate analysis. Two hundred four patients (90%) had pancreaticoduodenectomy, 13 patients (6%) had distal pancreatectomy, and 9 patients (4%) had a TP. Stage I disease was present in 50 (22%), stage II disease in 170 (75%), and stage III disease in 6 (3%). R0 resections were achieved in 70%. Operative morbidity was 36% and 30-day mortality was 6%. Actual 1-year, 3-year, and 5-year survival rates were 49% (n=111), 14% (n=31), and 4% (n=9). Using multivariate analysis: tumor size, tumor differentiation, obtaining an R0 resection, and lack of postoperative complications were variables associated with long-term survival. Long-term survival in patients with pancreatic cancer after resection remains poor. Achieving a margin negative resection (R0) with no postoperative complications are prognostic variables that can be affected by the surgeon.

Adenocarcinoma↗
PubMed2006

Mechanical properties and biocompatibility of soluble eggshell membrane protein/poly(vinyl alcohol) blend films.

Poly(vinyl alcohol) (PVA) has been blended with soluble eggshell membrane protein (SEP) to improve the mechanical properties of SEP film that is brittle. Tensile strength and elongation-at-break increase with increasing amount of PVA. When the SEP/PVA proportion is 1:1, a strong and flexible film is obtained, having a tensile strength of 22.7 MPa and elongation-at-break of 106%. Although scanning electron microscopy observation of the freeze-fractured cross-section shows microphase separation, interaction between SEP and PVA exists, as revealed by FT-IR. NIH3T3 cell culture demonstrates that SEP/PVA blend films with up to 50% of PVA show biocompatibility comparable to pure SEP film.

3T3 Cells↗
PubMed2006

[Depth profiles of high-density polyethylenes filled with different inorganic fillers during natural photo-oxidation by infrared microscopy].

The natural photo-oxidation degradation of HDPE filled with different inorganic fillers was carried out, and the depth profiles of the standard samples were characterized by infrared microscopy (IM) and scanning electron spectroscopy (SEM). The results show that HDPE filled with different inorganic fillers show different depth profiles. For HDPE and CaCO3-filled HDPE, there are no cracks on the cross sections, and the carbonyl indexes remain nearly zero from the surface to the interior. For HDPE filled with black mica, mica, kaolin and diatomite, there are more or less parallel, comb-like cracks on the cross sections, and the carbonyl indexes show decreasing trends from the surface to the interior. Furthermore, the transition points in CI curves are basically consistent with the formation of cracks in these samples. The UV absorbances of these inorganic fillers demonstrate the relationship between the photo-oxidation of HDPE and the relative absorbances of inorganic fillers. This implies that the UV absorbance of the inorganic filler may be responsible for the occurrence of cracks and oxidation in the standard samples.

English Abstract↗