The SARS epidemic in China and laboratory function.
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China↗
Biomedical subjects
Hui Zhao
Publications and source records attributed to Hui Zhao.
Early down-regulation of Bcl-xL expression during megakaryocytic differentiation of thrombopoietin-induced CD34+ bone marrow cells in essential thrombocythemia.
BACKGROUND AND OBJECTIVES: Essential thrombocythemia (ET) is a chronic myeloproliferative disorder with abnormal megakaryocyte/platelet production. Recent studies have found that Bcl-xL, as a member of the bcl-2 family of proteins that inhibit apoptosis, is essential in megakaryocytic differentiation. In this study the expression of Bcl-xL was evaluated during megakaryocytic differentiation in ET patients. DESIGN AND METHODS: To study the role of Bcl-xL in megakaryocyte differentiation, we evaluated the effect of small interfering RNA (siRNA) on the expression of Bcl-xL. CD34+ cells from patients with ET, chronic myeloid leukemia (CML), polycythemia vera (PV) and normal individuals were cultured in serum-free medium supplemented with thrombopoietin (TPO). Immunocytochemical staining and flow cytometric analysis were used to evaluate the Bcl-xL expression during megakaryocytic differentiation of CD34+ cells. RESULTS: When exposured to si-Bcl-xL, the percentage of K562 cells induced into megakaryocytes in 72 hours was lower than the corresponding percentage of control cells. CD41a+ cells from the three groups of patients and the control group were cultured. At day 10, the percentage of Bcl-xL- cells in CD41a+ cells from ET patients was 61.0+/-28.1%, which was significantly higher than that from patients with CML (2.5+/-20.9%), PV (33.6+/-10.0%) or control subjects (15.1+/-13.0%).] INTERPRETATION AND CONCLUSIONS: These results demonstrate that Bcl-xL is down-regulated early during in vitro differentiation of megakaryocytes from ET patients; this might reflect an early entry of megakaryocytes into a degenerating mature stage.
Adult↗
[Investigation of cross-infection of Pseudomonas aeruginosa in an intensive care unit].
OBJECTIVE: To investigate the factors responsible for Pseudomonas aeruginosa nosocomial cross-infection in the intensive care unit (ICU) and provide effective measure for the prevention and management. METHODS: The homology of 7 Pseudomonas aeruginosa strains isolated from the patients in the ICU and the environment was examined by biological, serological, drug-resistance and plasmid analysis. RESULTS: The results of serological and plasmid analyses had good consistency, which demonstrated that the 7 Pseudomonas aeruginosa strains originated from solution in the oxygen humidifier, with uniform serological and plasmid type, and belonged to the same clone with cross-infection by contact between the patients or nursing staff and the objects in the ICU. CONCLUSION: Serological and plasmid analyses are more practical for identifying the sources of Pseudomonas aeruginosa cross-infection, which can be prevented by strict disinfection of the instrument and supervision of the nursing staff in the ICU.
Cross Infection↗
[The difference in distribution of HCV genotypes between patients infected with HCV by transfusion and non-transfusion routes].
OBJECTIVE: To investigate the HCV genotypes distribution in northern and southern cities in China and the difference between patients infected with HCV by transfusion and non-transfusion routes. METHODS: The HCV genotypes of the patients with chronic hepatitis C from 9 cities belonging to different regions were genotyped by the PCR products of 5 prime untranslated region NTR digested with restriction endonucleases, and the HCV genotypes distribution among different cities or between the patients infected with HCV through transfusion and other routes was analyzed. RESULTS: The HCV genotypes of 214 in 219 cases were determined; 197 patients were infected with monogenotype HCV. The major epidemic genotypes of HCV isolates in China were 1b (76.64%) and 2a (18.22%), but 5.14% of patients were infected with HCV belonging to genotype 3b and this was the first report that there is genotype 4a in China. The HCV genotype distribution was not different in northern and southern areas, but was significantly different between patients infected with HCV through transfusion and non-transfusion routes (P=0.036). In patients infected trough transfusion, the rates of monogenotype HCV infection and genotype 1b were 93.88% and 76.87%, respectively, which were higher than those (86.57% and 58.21%) in the patients infected with HCV through non-transfusion routes. The rate of patient infected with mixed genotype HCV strains in non-transfusion group was 13.43%, which was higher than that (6.12%) of patients in transfusion group. CONCLUSION: The HCV genotype distribution in northern and southern regions were similar, but was significantly different between the patients infected through transfusion and other routes.
5' Untranslated Regions↗
[Short-term effects of chemotherapy with combination of hydroxycamptothecine and oxaliplatin in the treatment of advanced digestive tract cancers].
OBJECTIVE: To evaluate the short-term therapeutic effects and side effects of combined hydroxycamptothecine and oxaliplatin in the treatment of advanced digestive tract cancers. METHODS: Thirty patients suffering from advanced digestive tract tumors including gastric cancer 8, colorectal cancer 20, cholecystic cancer 1 and malignant fibroadenoma 1 were studied. They were treated with hydroxycamptothecine plus oxaliplatin for 2 cycles with interval of 21 days. RESULTS: The complete response, partial response, stable disease and progressive disease rates were 3.3% (1/30), 36.7% (11/30), 53.3% (15/30) and 6.7% (3/30) respectively with an overall response rate (CR + PR) of 40.0% (12/30). In the whole 77 cycles, leukocytopenia was observed in 34 cycles (44.2%) and 19 cycles (55.9%) at grades III and IV. Diarrhea developed in 42 cycles (54.5%) and 20 cycles (47.6%) grades III and IV. The other side effects were fever, alopecia, nausea and vomiting, constipation, hepatic and renal function abnormity and neuritis. CONCLUSION: Satisfactory response rate is obtainable in advanced colorectal cancer as treated by hydroxycamptothecine plus oxaliplatin. The toxicity consists of severe leukocytopenia and diarrhea.
Adenocarcinoma↗
Maternally inherited aminoglycoside-induced and nonsyndromic deafness is associated with the novel C1494T mutation in the mitochondrial 12S rRNA gene in a large Chinese family.
We report here the characterization of a large Chinese family with maternally transmitted aminoglycoside-induced and nonsyndromic deafness. In the absence of aminoglycosides, some matrilineal relatives in this family exhibited late-onset/progressive deafness, with a wide range of severity and age at onset. Notably, the average age at onset of deafness has changed from 55 years (generation II) to 10 years (generation IV). Clinical data reveal that the administration of aminoglycosides can induce or worsen deafness in matrilineal relatives. The age at the time of drug administration appears to be correlated with the severity of hearing loss experienced by affected individuals. Sequence analysis of mitochondrial DNA in this pedigree identified a homoplasmic C-to-T transition at position 1494 (C1494T) in the 12S rRNA gene. The C1494T mutation is expected to form a novel U1494-1555A base pair, which is in the same position as the C1494-1555G pair created by the deafness-associated A1555G mutation, at the highly conserved A site of 12S rRNA. Exposure to a high concentration of paromomycin or neomycin caused a variable but significant average increase in doubling time in lymphoblastoid cell lines derived from four symptomatic and two asymptomatic individuals in this family carrying the C1494T mutation when compared to four control cell lines. Furthermore, a significant decrease in the rate of total oxygen consumption was observed in the mutant cell lines. Thus, our data strongly support the idea that the A site of mitochondrial 12S rRNA is the primary target for aminoglycoside-induced deafness. These results also strongly suggest that the nuclear background plays a role in the aminoglycoside ototoxicity and in the development of the deafness phenotype associated with the C1494T mutation in the mitochondrial 12S rRNA gene.
Adult↗
Prenatal diagnosis and in utero treatment of torsades de pointes associated with congenital long QT syndrome.
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Adult↗
Novel carbonyl allylation mediated by SnCl2/TiCl3 in water.
[reaction: see text] Under the Lewis acid catalysis offered by TiCl(3), SnCl(2) can efficiently mediate the aqueous Barbier reactions between aldehydes and allyl chloride or bromide.
Journal Article↗
Xenopus X-box binding protein 1, a leucine zipper transcription factor, is involved in the BMP signaling pathway.
We describe a novel basic leucine zipper transcription factor, XXBP-1, which interacts with BMP-4 in a positive feedback loop. It is a maternal factor and is zygotically expressed in the dorsal blastopore lip and ventral ectoderm with the exception of the prospective neural plate during gastrulation. Overexpression of XXBP-1 leads to ventralization of early embryos as described for BMP-4, and inhibits neuralization of dissociated ectoderm. Consistent with mediating BMP signaling, we show that the ectopic expression of XXBP-1 recovers the expression of epidermal keratin and reverses the dorsalization imposed by truncated BMP receptor type I, indicating that it may act downstream of the BMP receptor. Its effects can be partially mimicked by a fusion construct containing the VP16 activator domain and the XXBP-1 DNA-binding domain. In contrast, fusing the DNA-binding domain to the even-skipped repressor domain leads to upregulation of the neural markers NCAM and nrp-1 in animal cap assay. Taken together, the results suggest a role for XXBP-1 in the control of neural differentiation, possibly as an activator.
Amino Acid Sequence↗
A novel, solventless reductive coupling of carbonyl compounds by alkali metals, catalysed by bromobenzene.
Catalysed by bromobenzene, alkali metals including Li, Na, and K can mediate the reductive coupling of carbonyl compounds under mild, solventless conditions to furnish the corresponding pinacol products.
Journal Article↗
Anoxia and reoxygenation of human endothelial cells decrease ceramide glucosyltransferase expression and activates caspases.
Endothelial oxidative stress induces cellular activation and sometimes death. Endothelial death can occur via necrosis or apoptosis. Understanding the mechanisms involved in cellular activation and death may lead to therapeutics designed to increase death or preserve cellular function. In the present study, brief periods of anoxia (3 h) followed by varying lengths of reoxygenation (0-5 h) lead to a time-dependent increase in human umbilical vein endothelial cell (HUVEC) caspase activity. Furthermore, ROCK-1 cleavage, which is dependent on caspase-3 activity, was also increased in cells undergoing oxidative stress compared with normoxic cells. Microarray data demonstrated that glucosylceramide synthase (GCS; glucosylceramide transferase), but not acid sphingomyelinase, was modulated by anoxia and reoxygenation. We confirmed that GCS mRNA and protein expression were significantly decreased in a time-dependent fashion following oxidative stress by real-time polymerase chain reaction and Western blot, respectively. Treatment of normoxic cells with the GCS-specific inhibitor, D,L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), increased caspase activity to the same degree as cells undergoing oxidative stress. Fumonisin B1, the N-acyl-sphinganine dehydrogenase (e.g., ceramide synthase) inhibitor significantly attenuated caspase activity in HUVECs undergoing oxidative stress. These data suggest that alterations in GCS expression following brief periods of oxidative stress in human endothelial cells lead to increased caspase activity.
Animals↗
A candidate metastasis-associated DNA marker for ductal mammary carcinoma.
BACKGROUND: Molecular genetic markers to identify the 13% lymph node-negative mammary carcinomas that are prone to develop metastases would clearly be of considerable value in indicating those cases in need of early aggressive therapy. METHODS: Representational difference analysis was used in an attempt to identify genetic alterations related to breast cancer metastasis by comparing genomic DNA from microdissected normal cells and from metastatic cells of ductal breast carcinoma patients. RESULTS: Representational difference analysis products yielded 10 unique metastasis-associated DNA sequences (MADS), i.e. products apparently lost in metastatic cell DNA. Of these sequences, MADS-IX was found to be lost in the transition from primary to metastasis in two out of five ductal breast carcinoma cases. This sequence was localized on chromosome 10q21 by radiation hybrid mapping and fluorescence in situ hybridization. The PTEN gene, which is also located on chromosome 10q, was detected to be present by PCR in all five cases. On the contrary, a breast carcinoma cell line, HCC-1937, which has homozygous loss of a region encompassing the PTEN gene, showed the presence of MADS-IX. PCR screening of three additional breast carcinoma cell lines with known losses in specific chromosomal regions also showed the presence of MADS-IX. CONCLUSION: These data suggest that MADS-IX possibly is part of a novel candidate metastasis-associated gene located close to the PTEN gene on chromosome 10q. The first set of PCR screening in five patient samples indicates that it could be used as a molecular marker for ductal mammary metastasis.
Breast Neoplasms↗
Role for the alternative complement pathway in ischemia/reperfusion injury.
The terminal complement components play an important role in mediating tissue injury after ischemia and reperfusion (I/R) injury in rats and mice. However, the specific complement pathways involved in I/R injury are unknown. The role of the alternative pathway in I/R injury may be particularly important, as it amplifies complement activation and deposition. In this study, the role of the alternative pathway in I/R injury was evaluated using factor D-deficient (-/-) and heterozygote (+/-) mice. Gastrointestinal ischemia (GI) was induced by clamping the mesenteric artery for 20 minutes and then reperfused for 3 hours. Sham-operated control mice (+/- versus -/-) had similar baseline intestinal lactate dehydrogenase activity (P = ns). Intestinal lactate dehydrogenase activity was greater in -/- mice compared to +/- mice after GI/R (P = 0.02) thus demonstrating protection in the -/- mice. Intestinal myeloperoxidase activity in +/- mice was significantly greater than -/- mice after GI/R (P < 0.001). Pulmonary myeloperoxidase activity after GI/R was significantly higher in +/- than -/- mice (P = 0.03). Addition of human factor D to -/- animals restored GI/R injury and was prevented by a functionally inhibitory antibody against human factor D. These data suggest that the alternative complement pathway plays an important role in local and remote tissue injury after GI/R. Inhibition of factor D may represent an effective therapeutic approach for GI/R injury.
Animals↗
Microsatellite dinucleotide (T-G) repeat: a candidate DNA marker for breast metastasis.
A dinucleotide (T-G) repeat sequence was isolated by comparing DNA from metastatic lymph node and matched normal breast samples from a ductal mammary carcinoma patient using representational difference analysis (RDA) method. Our present study used this metastasis associated DNA sequence (MADS) as a diagnostic probe to screen five patient samples by slot blot method. A new approach to isolate single cells by microdissection, namely single cell microdissection (SCM) was developed to obtain homogeneous population of tumor cells (approximately 1000) from matched primary tumors and corresponding positive lymph nodes of five patients. We isolated DNA from these homogeneous tumor cells and used for the RDA and DNA slot blot experiments. The screening of patient samples showed loss of this MADS in the transition from primary to metastasis in four out of five cases (80%) suggesting its possible role in breast metastasis.
Biomarkers, Tumor↗
A genome sequence of novel SARS-CoV isolates: the genotype, GD-Ins29, leads to a hypothesis of viral transmission in South China.
We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.
Base Sequence↗
Hepatitis C virus-related adult chronic idiopathic thrombocytopenic purpura: experience from a single Chinese center.
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Adolescent↗
Dual phosphorylation controls Cdc25 phosphatases and mitotic entry.
Negative regulation of the Cdc25C protein phosphatase by phosphorylation on Ser 216, the 14-3-3-binding site, is an important regulatory mechanism used by cells to block mitotic entry under normal conditions and after DNA damage. During mitosis, Cdc25C is not phosphorylated on Ser 216 and ionizing radiation (IR) does not induce either phosphorylation of Ser 216, or binding to 14-3-3. Here, we show that Cdc25C is phosphorylated on Ser 214 during mitosis, which in turn prevents phosphorylation of Ser 216. Mutation of Ser 214 to Ala reconstitutes Ser 216 phosphorylation and 14-3-3 binding during mitosis. Introduction of exogenous Cdc25C(S214A) into HeLa cells depleted of endogenous Cdc25C results in a substantial delay to mitotic entry. This effect was fully reversed in a S214A/S216A double-mutant, implying that the inhibitory effect of S214A mutant was entirely dependent on Ser 216 phosphorylation. A similar regulatory mechanism may also apply to another mitotic phosphatase, Cdc25B, as well as mitotic phosphatases of other species, including Xenopus laevis. We propose that this pathway ensures that Cdc2 remains active once mitosis is initiated and is a key control mechanism for maintaining the proper order of cell-cycle transitions.
14-3-3 Proteins↗
The in vitro reconstitution of nucleosome and its binding patterns with HMG1/2 and HMG14/17 proteins.
Using atomic force microscopy (AFM), the dynamic process of the in vitro nucleosome reconstitution followed by slow dilution from high salt to low salt was visualized. Data showed that the histone octamers were dissociated from DNA at 1M NaCl. When the salt concentration was slowly reduced to 650 mM and 300 mM, the core histones bound to the naked DNA gradually. Once the salt concentration was reduced to 50 mM the classic "beads-on-a-string" structure was clearly visualized. Furthermore, using the technique of the in vitro reconstitution of nucleosome, the mono- and di- nucleosomes were assembled in vitro with both HS2core (-10681 to -10970 bp) and NCR2 (-372 to -194 bp) DNA sequences in the 5 flanking sequence of human b-globin gene. Data revealed that HMG 1/2 and HMG14/17 proteins binding to both DNA sequences are changeable following the assembly and disassembly of nucleosomes. We suggest that the changeable binding patterns of HMG 14/17 and HMG1/2 proteins with these regulatory elements may be critical in the process of nucleosome assembly, recruitment of chromatin-modifying activities, and the regulation of human b-globin gene expression.
Animals↗