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Biomedical subjects

Yan Xu

Publications and source records attributed to Yan Xu.

At least 127 records · Page 7Linked to original sources
PubMed2005

[Clinical observation of Stark cesarean section as secondary abdominal surgery].

OBJECTIVE: To analyze secondary abdominal surgery after Stark cesarean section. METHODS: A retrospective analysis of the secondary operation after cesarean section was performed. Group A was Stark cesarean section (n = 89), group B was the longitudinal incision cesarean section (n = 212), and group C was Pfannenstiel incision cesarean section (n = 52). Stark cesarean section was compared with Pfannenstiel incision cesarean section and the longitudinal incision cesarean section in abdominal wall scar healing, adhesion of rectus muscles, peritoneum, omentum, and healing or adhesion of visceral peritoneum. RESULTS: The rate of good abdominal incision healing and slender scar was 86.5% (77/89) in group A, 29.3% (62/212) in group B, and 75.0% (39/52) in group C, respectively. The rate of adhesion of rectus muscles was 25.8% (23/89) in group A, 53.8% (114/212) in group B, and 13.5% (12/89) in group C, respectively. The rate of adhesion of omentum was 13.5% (12/89) in group A, 56.1% (119/212) in group B, and 25.0% (13/52) in group C, respectively. The rate of peritoneal adhesion was 15.7% (14/89) in group A, 46.2% (98/212) in group B, and 11.5% (6/52) in group C, respectively. Only one case in group C the peritoneum was not healed. The rate of adhesion of visceral peritoneum was 15.7% (14/89) in group A, 55.2% (117/212) in group B, and 13.5% (7/52) in group C, respectively. Abdominal wall scar healing, adhesion of rectus muscles, omentum, peritoneum, and visceral peritoneum in group A were all better than group B. The difference was statistically significant (P < 0.05). There were no differences between group A and group C (P > 0.05). CONCLUSIONS: The study shows that the Stark cesarean section is better than the longitudinal incision cesarean section in healing of abdominal wall scar, adhesion of rectus muscles, omentum, peritoneum, and visceral peritoneum, but compared with Pfannenstiel incision cesarean section, there is no difference statistically. However, the advantages of the Stark cesarean section lie in short surgical time, few injury, little bleeding, quick recovery, and short hospital stay time, thus it should be further popularized.

Abdomen↗
PubMed2005

[Protective effects of the granule of Sambucus chinensis lindl on acute hepatic injury].

OBJECTIVE: To investigate the protective effects of the granule of Sambucus chinensis Lindl on acute hepatic injury. METHODS: The acute liver-injury model induced by CCl4 or D-GalN or ConA was established in mice or rats. RESULTS: The granule of Sambucus chinensis Lindl showed significantly protective effects on mice acute hepatic injury induced by CCl4 ,and the effects were concern of antagonizing lipoperoxidation and improving energy of Ca2+ -ATPase of theca mitochondria and microsome. It showed significantly protective effects on mice or rats acute hepatic injury induced by D-GalN or Con A, too. CONCLUSION: The granule of Sambucus chinensis Lindl showed significantly protective effects against many kinds of chemical and immunological liver injuries.

Animals↗
PubMed2005

[Comparison of the effectiveness of chemotherapy and autologous hematopoietic stem cell transplantation as postremission treatment for adult acute lymphoblastic leukemia patients].

OBJECTIVE: To evaluate the effectiveness of chemotherapy (CT) and autologous hematopoietic stem cell transplantation (ASCT) as post-remission treatment for adult acute lymphoblastic leukemia (AL) patients. METHODS: Seventy-four ALL patients achieved first complete remission (CR(1)) with induction therapy, and then received early-stage sequential intensive consolidation chemotherapy. After that, 40 patients received chemotherapy (CT group) and 34 received ASCT (ASCT group) as post-remission treatment. The median follow-up was 20.5 months. The rates of leukemia free survival (LFS), overall survival (OS) and relapse were compared between the two groups. RESULTS: (1) The median LFS and OS were 14.0 and 20.6 months respectively for CT group and both were more than 53.5 months for ASCT groups. (2) Relapse occurred in 28 patients (70%) in CT group in a median time of 8.5 months (range, 1-72 months) and 20 of them (71.43%) relapsed within 1 year. Eleven patients (32.35%) relapsed in ASCT group, in a median time of 6 (2-30) months after transplantation. (3) There was no statistic difference in LFS, OS and relapse rate at 1 year between CT and ASCT groups (P > 0.05), whereas both LFS and OS at 3 and 5 years for ASCT group were significantly better than those for CT group (P < 0.05). Relapse rate for ASCT group was lower than that for CT group. (4) Higher LFS and OS and lower relapse rate were found for those who received monoclonal antibody purged autografts followed by immunotherapy and (or) maintenance therapy after ASCT (P < 0.05). CONCLUSIONS: Early sequential intensive consolidation chemotherapy followed by auto-HSCT could significantly reduce late relapse rate for adult ALL patients, and those received ex vivo purged autografts and immunotherapy and (or) maintenance therapy after ASCT have lower late relapse rate and superior survival.

Adolescent↗
PubMed2004

The perlecan heparan sulfate proteoglycan mediates cellular uptake of HIV-1 Tat through a pathway responsible for biological activity.

Cell surface heparan sulfate proteoglycans (HSPGs) mediate internalization of HIV-1 Tat. Herein, we report that human WiDr cells, which express perlecan but no other HSPGs, can internalize 125I-labeled Tat with minimal lysosomal degradation. Pre-treatment of cells with heparitinase almost completely abolished 125I-Tat surface binding, while the use of an HIV-1 long terminal repeat (LTR) promoter-reporter construct demonstrated that transactivation was potently blocked by pretreatment of cells with heparitinase, indicating an essential role for perlecan in the biologic effects of Tat. We conclude that the perlecan mediates Tat uptake and is required for HIV-1 LTR-directed transactivation in this human cell type.

Cell Line↗
PubMed2004

Homology modeling and molecular dynamics simulations of transmembrane domain structure of human neuronal nicotinic acetylcholine receptor.

A three-dimensional model of the transmembrane domain of a neuronal-type nicotinic acetylcholine receptor (nAChR), (alpha4)2(beta2)3, was constructed from a homology structure of the muscle-type nAChR recently determined by cryo-electron microscopy. The neuronal channel model was embedded in a fully hydrated DMPC lipid bilayer, and molecular-dynamics simulations were performed for 5 ns. A comparative analysis of the neuronal- versus muscle-type nAChR models revealed many conserved pore-lining residues, but an important difference was found near the periplasmic mouth of the pore. A flickering salt-bridge of alpha4-E266 with its adjacent beta2-K260 was observed in the neuronal-type channel during the course of the molecular-dynamics simulations. The narrowest region, with a pore radius of approximately 2 A formed by the salt-bridges, does not seem to be the restriction site for a continuous water passage. Instead, two hydrophobic rings, formed by alpha4-V259, alpha4-L263, and the homologous residues in the beta2-subunits, act as the gates for water flow, even though the region has a slightly larger pore radius. The model offers new insight into the water transport across the (alpha4)2(beta2)3 nAChR channel, and may lead to a better understanding of the structures, dynamics, and functions of this family of ion channels.

Amino Acid Sequence↗
PubMed2004

An effective chromatographic separation of chicken red blood cell coproporphyrinogen oxidase and uroporphyrinogen decarboxylase, two enzymes in heme biosynthesis.

Of the heme biosynthetic pathway enzymes, coproporphyrinogen oxidase is one of the least understood. Substrate recognition studies [Prepr. Biochem. Biotech.1997, 27, 47, J. Org. Chem.1999, 64, 464] have been done using chicken blood hemolysates (CBH) as the source of this enzyme. However, the enzyme uroporphyrinogen decarboxylase is also present in these preparations and separation of these two enzymes from CBH had not yet been achieved. Thus, a substrate ligand column was developed by covalently linking coproporphyrin-III to a sepharose resin following a similar procedure previously used for the purification of uroporphyrinogen decarboxylase [Int. J. Biochem.1992, 24, 105]. The ligand-resin chromatography step rapidly separates coproporphyrinogen oxidase from uroporphyrinogen decarboxylase as well as the majority of the hemoglobin.

Animals↗
PubMed2004

Activin type II receptor restoration in ACVR2-deficient colon cancer cells induces transforming growth factor-beta response pathway genes.

The activin type II receptor (ACVR2) gene is a putative tumor suppressor gene that is frequently mutated in microsatellite-unstable colon cancers (MSI-H colon cancers). ACVR2 is a member of the transforming growth factor (TGF)-beta type II receptor (TGFBR2) family and controls cell growth and differentiation. SMAD proteins are major intracellular effectors shared by ACVR2 and TGFBR2 signaling; however, additional shared effector mechanisms remain to be explored. To discover novel mechanisms transmitting the ACVR2 signal, we restored ACVR2 function by transfecting wild-type ACVR2 (wt-ACVR2) into a MSI-H colon cancer cell line carrying an ACVR2 frameshift mutation. The effect of ACVR2 restoration on cell growth, SMAD phosphorylation, and global molecular phenotype was then evaluated. Decreased cell growth was observed in wt-ACVR2 transfectants relative to ACVR2-deficient vector-transfected controls. Western blotting revealed higher expression of phosphorylated SMAD2 in wt-ACVR2 transfectants versus controls, suggesting cells deficient in ACVR2 had impaired SMAD signaling. Microarray-based differential expression analysis revealed substantial ACVR2-induced overexpression of genes implicated in the control of cell growth and tumorigenesis, including the activator protein (AP)-1 complex genes JUND, JUN, and FOSB, as well as the small GTPase signal transduction family members, RHOB, ARHE, and ARHGDIA. Overexpression of these genes is shared with TGFBR2 activation. This observed similarity between the activin and TGF-beta signaling systems suggests that activin may serve as an alternative activator of TGF-beta effectors, including SMADs, and that frameshift mutation of ACVR2 may contribute to MSI-H colon tumorigenesis via disruption of alternate TGF-beta effector pathways.

Activin Receptors, Type II↗
PubMed2004

Foxa2 is required for transition to air breathing at birth.

Toward the end of gestation in mammals, the fetal lung undergoes a process of differentiation that is required for transition to air breathing at birth. Respiratory epithelial cells synthesize the surfactant proteins and lipids that together form the pulmonary surfactant complex necessary for lung function. Failure of this process causes respiratory distress syndrome, a leading cause of perinatal death and morbidity in newborn infants. Here we demonstrate that expression of the forkhead gene Foxa2 in respiratory epithelial cells of the peripheral lung controls pulmonary maturation at birth. Newborn mice lacking Foxa2 expression in the lung develop severe pulmonary disease on the first day of life, with all of the morphological, molecular, and biochemical features of respiratory distress syndrome in preterm infants, including atelectasis, hyaline membranes, and the lack of pulmonary surfactant lipids and proteins. RNA microarray analysis at embryonic day 18.5 demonstrated that Foxa2-regulated expression of a group of genes mediating surfactant protein and lipid synthesis, host defense, and antioxidant production. Foxa2 regulates a complex pulmonary program of epithelial cell maturation required for transition to air breathing at birth.

Animals↗
PubMed2004

Rapid analysis of docetaxel in human plasma by tandem mass spectrometry with on-line sample extraction.

A simple, rapid, and sensitive analytical method for the measurement of docetaxel in human plasma was developed and validated. The method is based on positive electrospray ionization tandem mass spectrometry (ESI+-MS-MS) with on-line sample extraction. It uses paclitaxel as internal standard for calibration. The on-line sample extraction minimizes sample handling and is readily adopted for automation. Quantitation of plasma docetaxel was done by the multiple reaction monitoring (MRM) mode. The method had a linear calibration range of 1.00-3000 ng/mL with a correlation coefficient >0.9999. The limit of quantitation (LOQ) for docetaxel in plasma was 1.00 ng/mL. The on-line extraction recovery of docetaxel was between 86.1-94.7%, with %CV < or = 6.1%. This method has high accuracy (90.1-96.3%), and excellent intra-assay (0.6-3.8%) and inter-assay (2.0-5.7%) precision. Its applicability to clinical samples was demonstrated by measuring patient plasma samples after treatment of weekly docetaxel at 25 mg/m2 as 60-min infusion.

Calibration↗
PubMed2004

Binding of distamycin A to UV-damaged DNA.

We have found that distamycin A can bind to DNA duplexes containing the (6-4) photoproduct, one of the major UV lesions in DNA, despite the changes, caused by photoproduct formation, in both the chemical structure of the base moiety and the local tertiary structure of the helix. A 20-mer duplex containing the target site, AATT.AATT, was designed, and then one of the TT sequences was changed to the (6-4) photoproduct. Distamycin binding to the photoproduct-containing duplex was detected by CD spectroscopy, whereas specific binding did not occur when the TT site was changed to a cyclobutane pyrimidine dimer, another type of UV lesion. Distamycin binding was analyzed in detail using 14-mer duplexes. Curve fitting of the CD titration data and induced CD difference spectra revealed that the binding stoichiometry changed from 1:1 to 2:1 with photoproduct formation. Melting curves of the drug-DNA complexes also supported this stoichiometry.

Chemical Phenomena↗
PubMed2004

Esophagin and proliferating cell nuclear antigen (PCNA) are biomarkers of human esophageal neoplastic progression.

PCNA and esophagin have been implicated in the multistep process of carcinogenesis, but simultaneous characterization of these proteins in the early stages of esophageal neoplastic progression has yet to be undertaken. In morphologically normal esophageal epithelium, esophagin stains the granular layer cells, principally in their cell membrane portions. PCNA, in contrast, stains the nuclei of cells in the parabasal and basal layers. We examined 201 regions from 47 patients that represented different stages of esophageal neoplasia, comprising 34 areas of normal mucosa, 18 of dysplasia in squamous epithelium (DYS/SC), 39 squamous cell carcinoma (SCCA), 29 areas of Barrett's esophagus, 48 of Barrett's dysplasia (DYS/BAR) and 33 areas of adenocarcinoma (AC). The immunostaining patterns of esophagin and PCNA were evaluated and graded for level of expression. There was loss of esophagin expression in the high- and low-grade dysplasias compared to normal epithelia. In the squamous dysplasias, there was more intense staining (of esophagin) in the atypical nuclei and superficial squamous epithelial cells than in the basal cells. PCNA staining was increased in intensity in the high-grade dysplasias relative to normal basal layer cells. Combined analysis of esophagin and PCNA appears to reveal an inverse relationship between proliferation and differentiation during esophageal neoplastic progression. Moreover, this combined staining approach also offers promise for detecting esophageal cancer in early, precancerous stages.

Barrett Esophagus↗
PubMed2004

Helicase-dependent isothermal DNA amplification.

Polymerase chain reaction is the most widely used method for in vitro DNA amplification. However, it requires thermocycling to separate two DNA strands. In vivo, DNA is replicated by DNA polymerases with various accessory proteins, including a DNA helicase that acts to separate duplex DNA. We have devised a new in vitro isothermal DNA amplification method by mimicking this in vivo mechanism. Helicase-dependent amplification (HDA) utilizes a DNA helicase to generate single-stranded templates for primer hybridization and subsequent primer extension by a DNA polymerase. HDA does not require thermocycling. In addition, it offers several advantages over other isothermal DNA amplification methods by having a simple reaction scheme and being a true isothermal reaction that can be performed at one temperature for the entire process. These properties offer a great potential for the development of simple portable DNA diagnostic devices to be used in the field and at the point-of-care.

Animals↗
PubMed2004

(P)-helicene displays chiral selection in binding to Z-DNA.

Enantiomeric helicenes of (P)-A and (M)-A were synthesized. The binding of the helicenes to B- and Z-DNA was studied quantitatively by CD, equilibrium dialysis, and fluorescence spectroscopy. Enantiomeric (P)-A not only bound selectively to Z-DNA but also effectively converted the B-DNA conformation to Z-DNA. The enantioselectivity of the helicenes offers a new route for the rational design of inhibitors of biological functions that may depend on Z-DNA.

Base Sequence↗
PubMed2004

Highly efficient photochemical 2'-deoxyribonolactone formation at the diagonal loop of a 5-iodouracil-containing antiparallel G-quartet.

To explore the structure-dependent hydrogen abstraction in antiparallel and parallel G-quartet DNA structures, the photochemical reactivity of 5-iodouracil ((I)U)-containing human telomeric DNA 22-mers was investigated under the 302 nm UV irradiation conditions. We discovered that only antiparallel ODN 4, in which the second T residue in the diagonal loop of the antiparallel G-quartet is substituted with (I)U, was rapidly consumed as compared with parallel ODN 4 and the other (I)U-containing 22-mers under the irradiation conditions. Product analysis of the photolyzate of antiparallel ODN 4 indicated that a 2'-deoxyribonolactone residue was effectively produced at the 5' side of the (I)U residue in the diagonal loop. Photochemical 2'-deoxyribonolactone formation was also found in the (I)U-containing diagonal loop of antiparallel G-quartets d(GGGGTTT(I)UGGGG)(2) and d(GGGGTT(I)UTGGGG)(2), whereas the reaction did not occur at other DNA structures, including the single-stranded form, the loop region of the hairpin, and linear four-stranded G-quartets. The results clearly indicate that this type of 2'-deoxyribonolactone formation efficiently occurrs only in the diagonal loop of the antiparallel G-quartet. Furthermore, we found that 2'-deoxyribonolactone was formed at the (I)U-containing G-rich sequence of the IgG switch regions and the 5' termini of the Rb gene, suggesting the formation of an antiparallel G-quartet with a diagonal loop in these sequences. These results suggest that the present photochemical method can be used as a specific probe for the antiparallel G-quartet with the diagonal loop.

Chromatography, High Pressure Liquid↗
PubMed2004

HIV-1-mediated apoptosis of neuronal cells: Proximal molecular mechanisms of HIV-1-induced encephalopathy.

The induction of neuronal cell death in vivo has been recognized as a prominent feature of HIV type I (HIV-1) infection leading to HIV-1-induced encephalopathy. Viral and host cell products, released from HIV-1-infected cells, have been implicated as inducers of neuronal cell apoptosis. It is unclear which is more important in this process. Neuronal cells were treated with media bearing HIV-1 virions derived from infected T cells and macrophage or the same set of media depleted of virions. T cell media bearing virus induced high levels of apoptosis, whereas that depleted of virions did not. In contrast, neurons treated with media from infected macrophages induced cell death whether virions were present or depleted by ultracentrifugation. The former initiated a repeatedly and significantly higher degree of apoptosis. These data suggest that exposure of neurons to viral products is critical for the induction of apoptosis, in addition to putative host factors released from virally infected cells. Protein-array analyses identified host cell factors up-regulated from infected macrophages, versus their uninfected counterparts, and these host cell factors may be prime candidates for contributing to neuronal apoptosis. Gene-array analyses also identified mRNAs up-regulated in human neurons after treatment with purified HIV-1 gp120 envelope protein or virus-containing media from HIV-1-infected macrophages. These analyses suggest molecular mechanisms for the induction of apoptosis relating to the exposure of viral and host cell factors and rationally designed approaches toward neuroprotection.

AIDS Dementia Complex↗
PubMed2004

Measurement of the anticancer agent gemcitabine and its deaminated metabolite at low concentrations in human plasma by liquid chromatography-mass spectrometry.

A liquid chromatography/mass spectrometry (LC-MS) method has been developed and validated for the determination of the anticancer agent gemcitabine (dFdC) and its metabolite 2',2'-difluoro-2'-deoxyuridine (dFdU) in human plasma. An Oasis((R)) HLB solid phase extraction cartridge was used for plasma sample preparation. Separation of the analytes was achieved with a YMC ODS-AQ (5 microm, 120 A, 2.0 mm x 150 mm) column. The initial composition of the mobile phase was 2% methanol/98% 5mM ammonium acetate at pH 6.8 (v/v), and the flow rate was 0.2 ml/min. An isocratic gradient was used for 3min, followed by a linear gradient over 4 min to 30% methanol/70% 5mM ammonium acetate at pH 6.8. The gradient returned to the initial conditions over 2 min and remained there for 6 min. The retention times of dFdC, dFdU, and the internal standard 5'-deoxy-5-fluorouridine (5'-DFUR) were 11.46, 12.63, and 13.58 min. The mass spectrometer was operated under negative electrospray ionization conditions. Single-ion-monitoring (SIM) mode was used for analyte quantitation at m/z 262 for [dFdC-H](-), m/z 263 for [dFdU-H](-), and m/z 245 for [5'-DFUR-H](-). The average recoveries for dFdC, dFdU, and 5'-DFUR were 88.4, 84.6, and 99.3%, respectively. The linear calibration ranges were 5-1000 ng/ml for dFdC, and 5-5000 ng/ml for dFdU. The intra- and inter-assay precisions (%CV) were </=3 and </=7% at three concentration levels (50.0, 500, and 5000 ng/ml). The limits of quantitation (defined as 10 times of signal-to-noise ratio) were 3.16 ng/ml for dFdC, and 1.35 ng/ml for dFdU with 50-microl sample injections. This method has been used for measuring plasma concentrations of dFdC and dFdU in samples from adult cancer patients in a Phase I trial of weekly dFdC given as 150 (or lower) mg/(m(2) 24-h) infusion. The average plasma dFdC concentrations at 22- and 23-h into the infusion were 18.3 and 16.8 ng/ml at 150 and 100mg/m(2), respectively; the values for dFdU averaged 2950 and 1372 ng/ml.

Adult↗
PubMed2004

Identification of genes uniquely involved in frequent microsatellite instability colon carcinogenesis by expression profiling combined with epigenetic scanning.

Gene silencing through CpG island hypermethylation has been associated with genesis or progression of frequent microsatellite instability (MSI-H) cancers. To identify novel methylation sites unique to MSI-H colon cancers in an unbiased fashion, we conducted a global expression profiling-based methylation target search. We identified 81 genes selectively down-regulated in MSI-H cancers using cDNA microarray analysis of 41 primary colon cancers. Forty six of these 81 genes contained CpG islands overlapping their 5'untranslated regions. Initial screening of six genes in 57 primary colon cancers detected the following gene with MSI-H cancer-specific hypermethylation: RAB32, a ras family member and A-kinase-anchoring protein, was methylated in 14 of 25 (56%) MSI-H cancers but in none of 32 non-MSI-H cancers or 23 normal colonic specimens. RAB32 hypermethylation correlated with RAB32 mRNA down-regulation and with hMLH1 hypermethylation. In addition, the protein-tyrosine phosphatase receptor type O gene, PTPRO, was frequently methylated in right-sided tumors. This methylation screening strategy should identify additional genes inactivated by epigenetic silencing in colorectal and other cancers.

Adaptor Proteins, Signal Transducing↗