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Biomedical subjects

J Feng

Publications and source records attributed to J Feng.

At least 181 records · Page 10Linked to original sources
PubMed1998

[Application of multi-tumor markers in ovarian carcinoma].

OBJECTIVE: To improve the specificity and sensitivity of diagnosis and to strengthen postoperative monitoring for patients with ovarian cancer. METHODS: Sera obtained from patients-ovarian epithelial carcinoma (67 cases), benign ovarian tumor (33 cases) and from donor (38 cases) as control. Serologic examination of 5 tumor markers--SA, LSA, CA125, CP2, and 6B11Ab2 was performed. RESULTS: The sensitivity and specificity in diagnosis of ovarian cancer were 83.6% and 85.9% respectively for CA125 alone (> 35 kU/L) whereas 86.6% and 94.4% respectively for multi-tumor markers combined in which 3 or more indices showed positive. In addition, serial measurements of multi-tumor markers have been done for 1 year after operation in 24 cases of ovarian epithelial carcinoma. The correlations between the levels of multi-tumor markers either and the results of second look operation or and clinical manifestation of recurrence were analyzed. CONCLUSION: Multi-tumor markers examination could improve the diagnosis of ovarian cancer and early detection of recurrence.

Biomarkers, Tumor↗
PubMed1998

[A clinical report of high-dose epirubicin combined with cyclophosphamide and fluorouracil for advanced breast cancer].

OBJECTIVE: To evaluate safety and efficacy of high-dose epirubicin combined with cyclophosphamide and fluorouracil for advanced breast cancer. METHODS: Thirty two cases with stage III and IV breast cancer were treated with epirubicin (EPI) 90-110 mg/m2, cyclophosphamide (CTX) 600 mg/m2 and 5-fluorouracil (5-Fu) 900 mg/m2 every 21 days. The therapeutic effect was compared with that in patients treated with low-dose EPI(50 mg/m2). RESULTS: The response rate (RR) in patients treated with high-dose EPI was 71.9% (CR = 4, PR = 19) which was significantly better than that in the low-dose EPI-treated patients (CR = 2, PR = 5). The therapeutic effect was slightly better in patients initially diagnosed than in patients in recurrence (RR: 80% vs 68.2%) the median remission and surriving peroid was 7.4 months and 12.5 months, respectively. The major side effect was leukopenia. Mild to moderate GI tract side effects were obsevved. There was no significant cardiotoxicity. CONCLUSION: High-dose EPI combined with CTX, 5-Fu is a safe and effective regimen for patients with advanced breast cancer worthy of further clinical trial.

Adenocarcinoma↗
PubMed1998

Protective effects of taurine against reperfusion-induced arrhythmias in isolated ischemic rat heart.

The protective effect of taurine (CAS 107-35-7) against reperfusion-induced arrhythmias has been investigated in isolated perfused rat heart (Langendorff method). Partial ischemia was induced by occlusion of left descending artery for 15 min, followed by 10 min reperfusion. Left ventricular pressure and epicardial ECG were continuously monitored before and during ischemia and reperfusion. A control group was submitted to partial ischemia without taurine treatment. Three groups were submitted to partial ischemia, under taurine (10 mmol/l) treatment in the Krebs-Henseleit perfusing buffer during ischemia only (group 1), at reperfusion (group 2) and throughout the experimental period (group 3). Malondialdehyde levels were measured as an index of lipid peroxidation and heart muscle damage. The incidence of irreversible ventricular fibrillation was significantly diminished from 83% (control group) to 36% in group 1, 42% in group 2 and 16% in group 3. The incidence of premature ventricular beats and ventricular tachycardia at reperfusion as well as malondialdehyde levels were significantly decreased under taurine treatment. The results indicate that taurine protects ischemic heart against reperfusion-induced arrhythmias, via both its properties as membrane stabilizer and oxygen free radical scavenger.

Animals↗
PubMed1997

Jak1 plays an essential role for receptor phosphorylation and Stat activation in response to granulocyte colony-stimulating factor.

The proliferation and differentiation of neutrophils is regulated by granulocyte-specific colony-stimulating factor (G-CSF). G-CSF uses a receptor of the cytokine receptor superfamily and, in common with all members of the family, induces the tyrosine phosphorylation and activation of members of the Janus protein tyrosine kinase (Jak) family. In both myeloid cells and a human fibrosarcoma cell line expressing the G-CSF receptor, G-CSF induces the tyrosine phosphorylation and activation of Jak1, Jak2, and Tyk2. In addition, G-CSF induces the tyrosine phosphorylation of the receptor and members of the signal transducers and activators of transcription (Stat) family, including Stat3, as well as Stat1 and Stat5, depending on the cells involved. Using mutant cell lines lacking various Jaks, we show here that Jak1 is critical for G-CSF-mediated Stat activation, whereas Jak2 or Tyk2 are either not required or play redundant or ancillary roles. In the absence of Jak1, G-CSF induces activation of Jak2 and Tyk2, but fails to induce receptor tyrosine phosphorylation and induces dramatically reduced levels of Stat activation. A kinase-inactive Jak2, when overexpressed in cells lacking endogenous Jak2, can suppress Jak1 activation, receptor phosphorylation, and Stat activation, suggesting competition in the receptor complex either for Jak1 binding or substrates. Because the requirement for Jak1 is very similar to that previously shown for interleukin-6 signaling, the data support the concept that the G-CSF receptor and gp130 are both structurally and functionally similar.

Animals↗
PubMed1997

Interaction of smooth muscle myosin phosphatase with phospholipids.

The 130 kDa myosin-binding subunit (MBS) of smooth muscle myosin phosphatase was detected in cytoskeletal, cytosolic, and membrane fractions of T24 cells. Also, MBS was distributed between cytoplasm and plasmalemma in mitotic REF52 cells. These observations prompted this study of the interaction(s) of phospholipids with myosin phosphatase. Using a sedimentation assay, gizzard myosin phosphatase bound to vesicles of acidic phospholipids, i.e. phosphatidylserine (PS), phosphatidylinositol, and phosphatidic acid (PA). Neutral phospholipids did not bind. Binding of PS to myosin phosphatase also was demonstrated by electrophoresis under nondenaturing conditions. Preferential binding of PA, compared to that of the other acidic phospholipids, was indicated. Interaction of acidic phospholipids with myosin phosphatase inhibited phosphatase activity toward phosphorylated myosin. The extent of PS binding with myosin phosphatase decreased on increasing ionic strength and Mg2+ concentration. MBS (M130/M133) and M20 were phosphorylated by protein kinase A to 3 and 1 mol of P/(mol of subunit), respectively. Phosphorylation of the holoenzyme decreased phospholipid binding with recovery of phosphatase activity. Using limited proteolysis of the holoenzyme and various mutants, it was shown that phospholipid binding was associated with the C-terminal part of MBS, Ser 667-Ile 1004, and M20. The phosphorylation site involved in regulation of phospholipid binding is within the C-terminal MBS sequence. These results suggest that myosin phosphatase may interact with membranes and that phosphorylation by protein kinase A could modify this interaction. This mechanism could be important in localization of myosin phosphatase and in targeting substrates at different loci.

Animals↗
PubMed1997

Elucidation of the sequence and the genomic organization of the human dentin matrix acidic phosphoprotein 1 (DMP1) gene: exclusion of the locus from a causative role in the pathogenesis of dentinogenesis imperfecta type II.

The dentin matrix acidic phosphoprotein 1 (DMP1) gene has been mapped to human chromosome 4q21 and shown to exhibit no recombination with the autosomal dominant disorder of dentin formation, dentinogenesis imperfecta type II. In the current study, sequencing of DMP1 cDNA and genomic clones has indicated that the human gene contains an open reading frame of 1539 bp, which predicts a highly acidic, serine-rich protein of 513 amino acids. Comparison of the human DMP1-coding sequence with that of the rat, mouse, and cow indicated that the predicted protein contains a conserved hydrophobic signal peptide sequence and an Arg-Gly-Asp cell attachment sequence. The gene is encoded by six exons, the splicing phase of which is type 0, the first exon containing solely 5' untranslated sequence. Sequencing of each of the coding exons in individuals affected by dentinogenesis imperfecta type II failed to reveal any disease-specific mutations, suggesting that mutations in DMP1 are not causative of this condition at least in the two families examined in this study.

Amino Acid Sequence↗
PubMed1997

Time-dependent alteration of epidermal growth factor receptor in rat stomach by ethanol feeding.

This study investigated the time-dependent effects of ethanol (EtOH) feeding on epidermal growth factor binding and epidermal growth factor-mediated functions in the stomach. Adult male rats were fed either an isocaloric control or EtOH-containing liquid diet (36% total calories as EtOH) for 2, 4 and 6 weeks. At the end of each feeding period, animals were sacrificed and the stomach was dissected for the sample preparation. EtOH caused a time-dependent alteration (r = 0.89) of the 125I-epidermal growth factor binding to the gastric mucosal membrane (% control: week 2, 114%; week 4, 64%* and week 6, 45%*, n = 5, *P < 0.05). Protein kinase analysis also showed that EtOH caused a time-dependent decrease of epidermal growth factor-stimulated autophosphorylation of epidermal growth factor receptor protein (180 kDa) during three feeding periods. Western blot analysis, using anti-tyrosine phosphorylated epidermal growth factor receptor (active form) antibody, revealed a major immunoreactive protein band (180 kDa) in all samples pre-incubated with 1 microM epidermal growth factor. Consistent with data from kinase analysis, treatment of EtOH decreased the immunoreactivity of the active form of epidermal growth factor receptor (180 kDa) in the stomach. In conclusion, EtOH feeding caused a time-dependent alteration of epidermal growth factor receptor in the stomach, which may be one of the mechanisms underlying the gastric pathology associated with alcohol abuse.

Animals↗
PubMed1997

Dentin phosphoprotein and dentin sialoprotein are cleavage products expressed from a single transcript coded by a gene on human chromosome 4. Dentin phosphoprotein DNA sequence determination.

Dentin is the major mineralized extracellular matrix of the tooth. The organic components of dentin consist of type I collagen (90%) with 10% noncollagenous proteins, which are also components of bone. Two dentin proteins, dentin sialoprotein and dentin phosphoprotein, have been shown to be tooth-specific being expressed mostly by odontoblast cells. In this study, we screened a mouse molar tooth library for dentin sialoprotein and dentin phosphoprotein cDNA clones. Analysis of the clones resulted in characterization of a 4420-nucleotide cDNA that contained a 940-amino acid open reading frame. The signal peptide and NH2-terminal sequence was 75% homologous to the cDNA sequence of rat dentin sialoprotein. The continued open reading frame, however, contained a RGD sequence followed by a region of repeated aspartic acid and serine residues. This portion of the protein codes for amino acid sequence consistent with that of dentin phosphoprotein. The noncoding region contains three potential polyadenylation signals, two of which were shown to be utilized. Northern blot analysis indicated the presence of two major transcripts of 4.4 and 2.2 kilobases in odontoblasts. Chromosomal mapping localized the gene to human chromosome 4. These data suggest that the previously identified dentin extracellular matrix proteins, dentin sialoprotein and dentin phosphoprotein, are expressed as a single cDNA transcript coding for a protein that is specifically cleaved into two smaller polypeptides with unique physical-chemical characteristics. Therefore, we propose that the gene be named dentin sialophosphoprotein. The location of the human dentin sialophosphoprotein gene on chromosome 4 suggests that this gene may be a strong candidate gene for the genetic disease dentinogenesis imperfecta type II.

Amino Acid Sequence↗
PubMed1997

Effect of atmosphere on phase transformation in plasma-sprayed hydroxyapatite coatings during heat treatment.

The purpose of this study was to evaluate the effect of atmosphere on the phase transformation in hydroxyapatite (HA) coatings during heat treatment by varying the atmosphere in the furnace pipe. Heat treatment always increased the crystallinity of HA coatings regardless of the kind of atmosphere. Water molecules in atmosphere further promoted HA recrystallization during heat treatment. In a dry atmosphere, tricalcium phosphate (TCP) and tetracalcium phosphate (TTCP) were more stable than HA, so heat treatment could not convert them into HA. However, in a humid atmosphere, heat treatment would transform TCP and TTCP into HA by hydrolytic reactions.

Atmosphere↗
PubMed1997

Effect of water vapor pressure and temperature on the amorphous-to-crystalline HA conversion during heat treatment of HA coatings.

X-ray diffraction was used to characterize the increment of crystallinity of HA coatings after heat treatment. Coatings were heated over the temperature (T) interval of 300 degrees-460 degrees C with a partial water vapor pressure of 0.01 MPa and 0.001 MPa. Heat treatment also was done in air, as a contrast. It was found that the ratio (n) of the increment of crystallinity to the crystallinity of the as-received HA coatings was more significant for the coatings heated in atmosphere with water vapor than for those heated in air. This ratio also increased with water vapor pressure. The logarithm of the ratio increased linearly with 1/T, indicating that the ratio is exponential to T. The reason might be that recrystallization of the amorphous phase is a diffusion controlled process; the nucleation rate and growth velocity of the crystallites are in proportion to the diffusion coefficient, which is exponential to the temperature (T). Incorporation of water vapor in the atmosphere during heat treatment may decrease the activation energy for diffusion, which helps raise the diffusion coefficient of the atoms. Thus recrystallization of the amorphous phase can be accelerated.

Biocompatible Materials↗
PubMed1997

Investigation on arteriosclerosis among population in a rare earth area in south China.

An ophthalmofunduscope was used to investigate arteriosclerosis among villagers aged 20-40 yr old in two rare earth areas in Ganzhou, Jiangxi Province. It was noted that the occurrence of arteriosclerosis of the fundus aculi was significantly high (P < 0.05-0.01), the detection of serum cholesterol (CHO) was remarkably increased (P < 0.01), and the level of IgM was also elevated. However, high-density lipoprotein (HDL) remained at a low level. The effect of taking rare earth elements (REE) could be direct or indirect, thus causing an increase in cholesterol and interfering with the synthesis of high-density lipoprotein. Furthermore, rare earth could also cause immunogenic damage to the vascular wall. All of these could facilitate the formation of arteriosclerosis.

Adult↗
PubMed1997

Bioelectrical activity of the central nervous system among populations in a rare earth element area.

Auditory brainstem electric response (ABR) and somatosensory evoked potential (SEP) of 21 subjects (41 ears) among villagers in a rare earth element (REE) area in Gan County, Jiangxi, China, were studied. No difference in ABR between the subjects from the REE area and the control group was noted. However, the conduction detected by SEP from the median nerve to the thalamus (P15) was shortened (P < 0.05), especially to the first-grade primary somatosensory responsive region (S1) (P < 0.01) and the amplitude of S1 decreased (P < 0.05), indicating that REE was difficult to accumulate in the brainstem, but it was susceptible to cerebral cortex, thus causing sub-clinical damage. This condition was confirmed in the animal experiment. It was suggested that the toxicity through long-term intake of small doses of REE might not be negligible, and the hazard of REE environments should be investigated.

Acetylcholinesterase↗
PubMed1997

Effects of tetramethylpyrazine on the release of PGI2 and TXA2 in the hypoxic isolated rat heart.

We examined the effect on 6-Keto-PGF1a and TXB2 (the stable metabolites of PGI2 and TXA2) outflow of pretreatment with tetramethylpyrazine in the hypoxic isolated rat heart. In control hearts, 6-Keto-PGF1a was increased from 185 +/- 46 pg/ml of baseline value to 335 +/- 76 pg/ml after 2 min of hypoxia and TXB2 increased from 136 +/- 28 pg/ml of baseline value to 230 +/- 43 pg/ml at 20 min of hypoxia and 252 +/- 32 pg/ml after 5 min of reoxygenation. Pretreatment with tetramethylpyrazine increased the 6-Keto-PGF1a concentration to 266 +/- 51 pg/ml (143% of control heart), 471 +/- 89 pg/ml (150% of control heart) and 332 +/- 47 pg/ml (195% of control heart) at 15 min of normoxia, 2 min of hypoxia and 5 min of reoxygenation, respectively (p < 0.05 vs control). On the other hand, tetramethylpyrazine diminished the release of TXB2 to 78 +/- 21 pg/ml (174% of control heart), 160 +/- 30 pg/ml (144% of control heart), and 196 +/- 23 pg/ml (128% of control heart) at 15 min of normoxia, 20 min of hypoxia and 5 min of reoxygenation, respectively (p < 0.05 vs control). These data show that pretreatment with tetramethylpyrazine enhances PGI2 outflow and attenuates release of TXA2 in the rat heart during normoxia, hypoxia and reoxygenation.

6-Ketoprostaglandin F1 alpha↗
PubMed1997

A JAK1/JAK2 chimera can sustain alpha and gamma interferon responses.

Cell lines that are mutated in interferon (IFN) responses have been critical in establishing an essential role for the JAK family of nonreceptor tyrosine kinases in interferon signalling. Mutant gamma1A cells have previously been shown to be complemented by overexpression of JAK2. Here, it is shown that these cells carry a defect in, and can also be complemented by, the beta-subunit of the IFN-gamma receptor, consistent with the hypothesis that the mutation in these cells affects JAK2-receptor association. In contrast, mutant gamma2A cells lack detectable JAK2 mRNA and protein. By using gamma2A cells, the role of various domains and conserved tyrosine residues of JAK2 in IFN-gamma signalling was examined. Individual mutation of six conserved tyrosine residues, mutation of a potential phosphatase binding site, or mutation of the arginine residue in the proposed SH2-like domain had no apparent effect on signalling in response to IFN-gamma. Results with deletion mutants, however, indicated that association of JAK2 with the IFN-gammaR2 subunit requires the amino-terminal region but not the pseudokinase domain. Consistent with this, in chimeras with JAK1, the JAK2 amino-terminal region was required for receptor association and STAT1 activation. Conversely, a JAK1-JAK2 chimera with the amino-terminal domains of JAK1 linked to the pseudokinase and kinase domains of JAK2 is capable of reconstituting JAK-STAT signalling in response to IFN-alpha and -gamma in mutant U4C cells lacking JAK1. The specificity of the JAKs may therefore lie mainly in their structural interaction with different receptor and signalling proteins rather than in the substrate specificity of their kinase domains.

Amino Acid Sequence↗
PubMed1997

Activation of Jak2 catalytic activity requires phosphorylation of Y1007 in the kinase activation loop.

The Janus protein tyrosine kinases (Jaks) play critical roles in transducing growth and differentiation signals emanating from ligand-activated cytokine receptor complexes. The activation of the Jaks is hypothesized to occur as a consequence of auto- or transphosphorylation on tyrosine residues associated with ligand-induced aggregation of the receptor chains and the associated Jaks. In many kinases, regulation of catalytic activity by phosphorylation occurs on residues within the activation loop of the kinase domain. Within the Jak2 kinase domain, there is a region that has considerable sequence homology to the regulatory region of the insulin receptor and contains two tyrosines, Y1007 and Y1008, that are potential regulatory sites. In the studies presented here, we demonstrate that among a variety of sites, Y1007 and Y1008 are sites of trans- or autophosphorylation in vivo and in in vitro kinase reactions. Mutation of Y1007, or both Y1007 and Y1008, to phenylalanine essentially eliminated kinase activity, whereas mutation of Y1008 to phenylalanine had no detectable effect on kinase activity. The mutants were also examined for the ability to reconstitute erythropoietin signaling in gamma2 cells, which lack Jak2. Consistent with the kinase activity, mutation of Y1007 to phenylalanine eliminated the ability to restore signaling. Moreover, phosphorylation of a kinase-inactive mutant (K882E) was not detected, indicating that Jak2 activation during receptor aggregation is dependent on Jak2 and not another receptor-associated kinase. The results demonstrate the critical role of phosphorylation of Y1007 in Jak2 regulation and function.

Amino Acid Sequence↗