Biomedical subjects
Publications and source records attributed to Y Fan.
The FEM analysis of Casson fluid flow in flow chamber under all wall conditions was made in this paper, and the result was compared with that of Newton and that of Casson fluid flow with plane hypothesis.
A high performance liquid chromatographic pre-column derivatization method with fluorescence detection for the analysis of glutamine (Gln) in rat intestinal mucosa is presented. Gln was derivatized with o-phthalaldehyde and 3-mercaptopropionic acid under an alkaline condition and separated by reversed-phase liquid chromatography on a Lichrosorb RP18 column (150 mm x 4.6 mm i.d., 5 microm). The mobile phase was consisted of 50 mmol/L phosphate buffer (pH 7.0)-acetonitrile (94:6, V/V) with a flow rate of 2.0 mL/min. The excited and emitted wavelength were selected at 230 nm and 389 nm respectively. The volume ratio of samples and derivatization reagent solution was 4:1 (V/V). The detection limit of Gln was 25 micromol/L (S/N= 3.5) and the regression equation was A = 16.9405C + 179.9339, r = 0.9996 at the linear range of 50-3200 micromol/L. The day-to-day deviation was 6.97% (n = 3) and the retention time of Gln was 3.158 min. This method is rapid, simple and highly sensitive, and has been applied to the determination of Gln in intestinal mucosa.
A set of resonance Raman spectrometer with excitation lines continuously tunable in 220-970nm, which is a first set in China, has been assembled. The factors influenced on the signal noise ratio (SNR) of spectra were analyzed in detail. The methods to improve the SNR were suggested and the parameters of the spectrometer were optimized. A satisfied Raman spectra can be obtained.
OBJECTIVE: Magnetic resonance spectroscopy (MRS) has the potential to noninvasively delineate early biochemical changes in denervated muscle. In this study, we examine metabolic changes in denervated rat facial muscles using quantitative invitro 1H and 31P MRS. METHODS: Forty male Wistar rats were subjected to transection of the facial nerve trunk on the left and sham exposure on the right, and allowed to recover. The animals were then reoperated at 1, 2, 4, or 8 weeks after the initial procedure. EMG of the facial muscles and facial nerve conduction studies were performed at both time points, and facial muscles were harvested from normal and control sides at the second procedure. Perchloric acid extracts of facial muscles were then prepared for analysis using MRS. RESULTS: The results showed a progressive time-dependent decrease in Cr, PCr, Pi, ATP, and ADP all on the transected side. CONCLUSION: This study is an important step in the development of clinically relevant noninvasive methods of assessing and quantifying degeneration in nerve-muscle systems.
OBJECTIVE: To investigate the prevalence of fragile X syndrome in the Chinese. METHODS: Fragile X syndrome was screened from 172,600 people living in Tongling city, Anhui province. Suspected patients were tested by PCR and Southern Blotting. RESULTS: Seven of 88 mental handicap children were found with fra (X), including 3 female and 4 male patients. Six patients, 3 normal transmitting males and 5 carriers were found in detailed search in these 6 fra (X) families. Genetic linkage analyses of 2 of the families were reported here. CONCLUSION: The prevalence of fragile X syndrome in the Chinese is not apparently different from the previous reports on the Caucasian population.
Human thrombopoietin (hTPO), a ligand for the protooncogene c-mpl, is the major humoral regulator of megakaryocytopoiesis and platelet production affecting the proliferation and maturation of committed cells. Recently the hTPO gene and cDNA were cloned from human genome and cDNA libraries. In this report, hTPO cDNA was synthesized by RT-PCR from a Chinese human fetal liver. The sequence of this cDNA showed a high homology with hTPO cDNA in the Genebank database (accession no. L36052) except that base substitution occurred at four sites (497, 595, 767, and 795 bp), which led to the change of three amino acid residues in the predicted protein.
OBJECTIVE: To investigate the relationship between fetal intrauterine growth retardation and anticardiolipin antibodies. METHODS: Serum anticardiolipin antibodies were detected with ELISA method in 5,330 cases of normal gravidas. Meanwhile, the observation of immunocomplex depositions in placentas in cases of positive anticardiolipin antibodies (ACA) were observed by immunofluorescence examination. RESULTS: The positive ACA rate in normal gravidas was 2.70%. The incidence of intrauterine growth retardation (IUGR) was 15.28% in cases of positive ACA, whereas was 1.77% in cases of negative ACA. There were significant differences between two groups (P < 0.001). Among children born in mothers with positive ACA, there were 5 cases of positive ACA. Immunocomplex depositions (Immunoglobulins & Complements) were all found in placenta of IUGR. CONCLUSIONS: ACA could be one of causes of IUGR. Determination of serum ACA would offer a new clue to diagnosis and treatment of IUGR.
The form of macro-particle is a close successive region in two-valued micro-particle image, and the detection of microparticles is actually that of close successive regions. Accordign to this theory, this paper present a new technique for micro-particles detecting based on an artificial neuron network modeled on the diffusing behaviour of real visual system, which has fluid properties. The results of simulation on computer shew that this method is very effect.
OBJECTIVE: To investigate the allelic heterogeneity of the ATP7B gene in Chinese patients with Wilson's disease (WD). METHODS: Exons of the ATP7B gene from 141 WD patients' DNA were amplified with polymerase chain reaction (PCR) 887-890. Mutations were then screened by single strand conformation polymorphism (SSCP) analysis and further identified by sequencing. RESULTS: The molecular structure of exon 7 of the ATP7B gene from 141 WD patients was analyzed. The same band shift in electrophoretic pattern of 4 cerebral type patients was identified with SSCP and subsequently sequenced. The results showed missense mutation at the second base of the codon as Ser 662 Cys, which is caused by a C to G transversion. CONCLUSIONS: Mutations of the ATP7B gene were investigated for the first time in China and a novel missense mutation was identified in four cases.
OBJECTIVE: To investigate the allelic heterogeneity of ATP 7 B gene in Chinese patients. METHODS: Exons of ATP7B gene from patient's DNA were amplified with PCR technique. Mutations were screened by single strand conformation polymorphism (SSCP) analysis and further confirmed by sequencing. RESULTS: The molecular structure of exon 7 of the ATP7B gene from 141 WD patients was preliminarily analyzed. A similar band shift of 4 encephalopathy type patients was identified with SSCP and sequencing. There was a missense mutation, Ser 662 Cys, which was caused by a C to G transversion at the second base of the codon. CONCLUSIONS: The mutations of Chinese ATP7B gene were investigated for the first time in China and a novel missense mutation was identified.
DPC4, a candidate tumor suppressor gene, was identified recently at chromosome 18q21.1. Frequent homozygous deletion or mutations of the gene were observed in pancreatic carcinomas. To investigate the role of this gene in head and neck squamous cell carcinomas (HNSCCs), we examined 16 HNSCC cell lines from 11 patients and 20 primary HNSCCs for alterations of the gene by sequencing all 11 exons of the gene. Fourteen cell lines from 10 patients showed monomers at marker D18s46 (l8q21.1). Full-length cDNA was detectable in all cell lines by reverse transcription-PCR. A nonsense mutation was identified at codon 526 (GAA to TAA, glutamine to termination) in two cell lines (UMSCC22A and UMSCC22B) derived from the primary tumor and lymph node metastasis of the same patient. Loss of heterozygosity was found in 7 of 15 (47%) informative primary tumors at D18s46, whereas only one polymorphism was observed in both tumor and normal tissues from the same patient (at codon 525; ATT to GTT, isoleucine to valine). Our data indicate that although DPC4 is altered infrequently in HNSCC, it may play some role in the tumorigenesis of a small subset of HNSCCs.
Tropomodulin is a newly characterized pointed end capping protein for actin filaments. It binds specifically to the N terminus of tropomyosin and blocks the elongation and depolymerization of tropomyosin-coated actin filaments. A 1.9-kb human tropomodulin cDNA clone was used to map its gene by fluorescence in situ hybridization. The tropomodulin gene was assigned to human chromosome 9q22.2-q22.3, a region that is also known to contain several other genes and disease loci and is proximal to the loci for gelsolin and alpha-fodrin. The gene for tropomodulin is expressed in major human tissues at different levels in the following order: heart and skeletal muscle much greater than that in brain, lung, and pancreas, which is greater than that in placenta, liver, and kidney. Human tropomodulin and a 64-kDa autoantigen in Graves disease (1D) are related: tropomodulin has 42 and 41% identity with the Graves protein in the N-terminal (69 residue) and C-terminal (194 residue) regions, respectively. The insertion of several homologous repeats in the midsection of the Graves protein, together with the extension of a proline-rich C terminus, accounts for the differences in length between the Graves protein (572 residues) and tropomodulin (359 residues). The significant sequence identity indicates that these two genes are evolved from a common ancestral gene.
Myoblast transplantation has been proposed as a potential therapy for Duchenne muscular dystrophy (DMD). A Y-chromosome-specific probe was used to track the fate of donor male myoblasts injected into dystrophic muscles of female mdx mice (which are an animal model for DMD). In situ analysis with the Y-probe showed extremely poor survival of isolated normal male (C57B1/10Sn) donor myoblasts after injection into injured or uninjured muscles of dystrophic (mdx) and normal (C57B1/10Sn) female host mice. A decrease in the numbers of donor (male) myoblasts was seen from 2 days and was marked by 7 days after injection: few or no donor myoblasts were detected in host muscles examined at 3-12 months. There was limited movement of the injected donor myoblasts and fusion into host myofibers was rare. The results of this study strongly suggest that the failure of clinical trials of myoblast transplantation in boys with DMD may have been due to rapid and massive death of the donor myoblasts soon after myoblast injection.
Therapeutic successes following treatment of murine tumors with tumor necrosis factor-alpha (TNF) have not been easily applied to clinical oncology because the concentrations of TNF required in humans induces systemic toxicity. This has led us to identify mediators which could sensitize tumors to the effects of TNF, permitting administration of lower doses and possible realization of the therapeutic potential of this cytokine. Our study reports the ability of a novel cytokine, endothelial-monocyte-activating polypeptide II (EMAP II), to sensitize initially resistant murine and human tumors to TNF-induced regression employing a murine model. Recombinant (r) EMAP II was purified from Escherichia coli transformed with a plasmid expressing mature EMAP II. The B16 melanoma, raised in C57BL/6 mice, or a human fibrosarcoma (HT-1080), grown in immunocompromised mice, was injected intratumorally with either vehicle or rEMAP II/heat-treated EMAP II (50-100 micrograms) followed by systemic TNF/heat-treated TNF (5 micrograms) and assessed for tumor volume, hemorrhage, and histologic appearance. Both the B16 melanoma and the HT-1080 human fibrosarcoma underwent thrombohemorrhagic and acute inflammatory changes concomitant with regression or significantly slowed growth after administration of intratumor EMAP II followed by systemic TNF. Omission or inactivation of either cytokine abrogated this effect. These results demonstrate that local treatment of certain tumors with EMAP II results in enhanced susceptibility to TNF-mediated induction of thrombohemorrhage and regression.
We describe the occurrence of acquired Pelger-Huet anomaly (APHA) in 23 patients treated with paclitaxel (13) or docetaxel (10). A consistent peak of Pelger-Huet cells (PHC) within a range of 3-9 d after treatment with taxoids was noted. The APHA generally disappeared by day 21 after treatment. Peak PHC values for the first course were significantly different in paclitaxel versus docetaxel versus control groups (P < 0.0001) with the maximum PHC counts being significantly higher for docetaxel compared with paclitaxel (P < 0.001) and for paclitaxel compared with controls (P = 0.007). We conclude that taxoid therapy produces transient APHA which peaks between days 3 and 9 and is more pronounced with docetaxel than with paclitaxel.
Exposure of mammalian cells to UV irradiation induces rapid and transient expression of early growth response-1 gene (Egr-1) encoding a transcription factor that plays a role in cell survival. These signals from the irradiated cell surface are likely to involve more than one pathway, and we show here that an essential pathway involves activation of several growth factor receptors by reactive oxygen intermediates (ROI). UVC irradiation causes the tyrosine phosphorylation of EGF receptor (EGFR) in mouse NIH 3T3 fibroblasts and HC11 mouse mammary cells. EGFR activation by irradiation of cells is abrogated by suramin, by antioxidants, and by the presence of a dominant negative EGFR. UV induces the formation of complexes between activated EGFR and SOS, Grb2, PLC gamma, and SHC that can be precipitated with antibodies to EGFR. The activation of EGFR by UV is mimicked by H2O2, suggesting that ROI may function upstream of EGFR activation. Our observations support the hypothesis that ROI and growth factor receptors operate in the early steps of the UV signal that lead to the enhanced expression and activity of Egr-1.
Irradiated female mice were reconstituted with male hematopoietic stem cells (HSCs) retrovirally marked with human adenine deaminase (hADA) complimentary DNA. HSCs were incubated with interleukin-6 and stem cell factor before coculture with GP+E86-producing cells. Bone marrow HSCs were infused intravenously to irradiated mice and spleen colony-forming units (CFU-S) were evaluated for hADA marked clones by Southern blot analysis. 45 of 54 CFU-S were marked by the hADA gene sequence with multiple copies integrated per genome. Oligoclonal hematopoiesis evolved over time with 1-2 clones demonstrated 5-11 months after reconstitution. Comparable results were obtained with embryonic fetal liver HSCs. Incubation of bone marrow HSCs with adherent stromal cells rather than growth factors produced less efficient gene transfer, and polyclonal hematopoiesis was not observed. Donor origin was established by the Y chromosome probe. These results support the clonal succession model of hematopoiesis.
Comprehensive cost-benefit evaluation for the improvement of rural water supply was conducted according to the national standard methods for analysis of water quality. Results showed total bacteria count and coliform group count in the water declined by 51% after the improvement, and synthetic index of water quality declined to 19% of that before the Improvement. Environmental epidemiological studies showed yearly incidence of hepatitis A, typhoid fever, diarrhea and enteritis decreased by 2.20/1,000, 0.39/1,000, 2.70/1,000 and 14.30/1,000, respectively, as compared with those before the improvement, and with the manpower capital method, economic loss caused by the above-mentioned diseases lowered by 37,238 yuan, economic benefit gained by saving labor-time for water-taking reached 198,644 yuan, and family income increased 164,188 yuan per year. It suggests the above indicators all can be used in comprehensive cost-benefit evaluation of the improvement of rural water supply.