Lagrangian treatment of magnetic dielectrics.
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Journal Article↗
Biomedical subjects
B Chen
Publications and source records attributed to B Chen.
Attenuation of fungal virulence by synthetic infectious hypovirus transcripts.
Noninfectious, cytoplasmically transmissible viral double-stranded RNAs of the genus Hypovirus cause reduced virulence (hypovirulence) in the chestnut blight fungus Cryphonectria parasitica, providing the basis for virus-mediated biological control of a fungal disease. Synthetic transcripts corresponding to a full-length hypovirus RNA coding strand are infectious when introduced into fungal spheroplasts by electroporation. Hypovirus infections were readily established in Cryphonectria parasitica and in related fungal species not previously reported to harbor viruses. These results demonstrate the use of a synthetic mycovirus transcript to expand fungal host range, thereby broadening the potential application of virus-mediated hypovirulence to control fungal pathogenesis.
Ascomycota↗
The second intron of the K-ras gene contains regulatory elements associated with mouse lung tumor susceptibility.
We have previously demonstrated the preferential activation of the K-ras gene from the susceptible A/J parent in lung tumors from F1 mouse hybrids. In the present study, the mechanism of this observation is further investigated. Higher levels of expression of A/J K-ras allele were detected in lung adenomas (30 of 30) from the C3A mouse. In addition, three K-ras alleles, designated as susceptible (Ks), intermediate (Ki), or resistant (Kr), were identified by sequence analysis of the second intron of the K-ras gene from 32 strains of mice. These K-ras alleles are associated with differences in mouse lung tumor susceptibility. All Kr alleles have a tandem 37-bp direct repeat (nt 282-355) in the second intron of the K-ras gene. Ks and Ki alleles have only one copy of the 37-bp sequence (nt 282-318). Ks strains have three base variations at nt 288, 296, and 494, and Ki strains have two base variations at nt 288 and 494 in the second intron of the K-ras gene. Differential protein-binding patterns were observed in gel-mobility-shift experiments between the duplicated 37-bp sequence of the Kr allele and the single 37-bp sequence of the Ks and Ki alleles. DNase I footprinting assay revealed protein binding sites in the second intron of the K-ras gene that correspond to the tandem repeat sequences. Our data suggest that higher expression of the A/J allele relative to C3H allele may be responsible for the allele-specific activation of the K-ras gene in lung tumors from F1 hybrid mice.
Adenoma↗
Scaling behavior of giant magnetotransport effects in Co/Cu superlattices.
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Journal Article↗
Si diffusion in GaAs and Si-induced interdiffusion in GaAs/AlAs superlattices.
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Journal Article↗
Differential expression of mast cell growth factor receptor (c-kit) by peritoneal connective tissue-type mast cells and tissue culture-derived mast cells.
The peritoneal cavity of the mouse is a major source of connective tissue-type mast cells (CTMCs). Flow cytometric analysis using biotinylated recombinant murine mast cell growth factor (rMuMGF) showed that 1 to 3% of the cells in the peritoneal cavity exhibited MGF receptor (MGFR) (or c-kit). CTMCs were the only cell types expressing MGFR in the peritoneal cavity, and every one of them expressed MGFR. More than half the peritoneal CTMCs retained the potential to proliferate in the presence of recombinant murine interleukin 3 (rMuIL-3), rMuIL-4, and rMuMGF and gave rise to pure, alcian blue-positive "mast cells," which actively expressed c-kit transcripts and MGFR. Flow cytometric analysis and receptor assay carried out at 4 degrees C showed that the number of MGFRs on culture-derived mast cells (CDMCs) was one-third that of peritoneal CTMCs (6 x 10(4) vs. 1.8 x 10(5) MGFR/cell). At 37 degrees C, the total number of membrane MGFRs detected in CDMC was two to three times more than that detected at 4 degrees C, indicating that nearly 70% of total MGFR in CDMCs, compared with only 40% in peritoneal CTMCs, existed as "cryptic sites" unable to interact with exogenous ligand at 4 degrees C. Thus, diminished expression of MGFR is one of the phenotypic characteristics associated with CDMCs.
Animals↗
Role of apoptosis in mediating phosphoramide mustard-induced rat embryo malformations in vitro.
Phosphoramide mustard, an active metabolite of the anticancer drug cyclophosphamide, causes malformations in rat embryos undergoing organogenesis in vitro. The purpose of the present study was to investigate the hypothesis that apoptosis plays an important role in mediating the teratogenicity of phosphoramide mustard. Apoptosis is a process of active or programmed cell death which is characterized by internucleosomal DNA fragmentation and de novo RNA and protein synthesis. Sulphated glycoprotein-2 (SGP-2) or clusterin is induced in some models of apoptosis and is one of the proteins likely to be involved in the maintenance of cell integrity. In the present study, day 10 rat embryos were cultured for 6, 12, 24, and 45 hr, with or without the addition of 10 microM phosphoramide mustard. After culture for 24 or 45 hr with exposure to 10 microM phosphoramide mustard, the embryos were both growth-retarded and malformed. Exposure to phosphoramide mustard for 6 or 12 hr did not significantly alter the relative amounts of either the mRNA or protein for SGP-2; this treatment also had no effect on DNA fragmentation in embryos or their yolk sacs. After 24 hr in culture, the relative amounts of SGP-2 protein, but not mRNA, were increased 2-fold in the yolk sacs of the phosphoramide mustard-exposed embryos, but not in the embryos themselves. At this time, DNA fragmentation was detected in phosphoramide mustard-exposed embryos, but not in their yolk sacs or in control embryos. After 45 hr in culture, SGP-2 protein and mRNA levels were increased 2-4-fold above the controls in the phosphoramide mustard-exposed embryos and their yolk sacs. Immunohistochemical analysis revealed that in control embryos cultured for 45 hr, the SGP-2 reaction product was localized in the heart, hindgut, and yolk sac. In contrast, in phosphoramide mustard-treated embryos cultured for 45 hr, SGP-2 immunostaining was found throughout the embryo, with a strong immunoreaction in the mesenchyme and ectoplacental cone. DNA fragmentation in the embryos exposed to phosphoramide mustard for 45 hr was more extensive than that found after 24 hr, but fragmentation was still not detected in the yolk sac. Thus exposure in vitro to a teratogenic concentration of phosphoramide mustard resulted in DNA fragmentation and an increased expression of SGP-2 in the embryo. These data suggest that apoptosis is involved in mediating the teratogenicity of phosphoramide mustard.
Abnormalities, Drug-Induced↗
12-O-tetradecanoyl-phorbol-13-acetate-induced rat embryo malformations in vitro are associated with an increased relative abundance of embryonic E-cadherin mRNA.
Epithelial-cadherin (E-cadherin) is a member of a family of Ca(2+)-dependent cell adhesion molecules which are localized in zonulae adherens and play an important role during development. E-cadherin is abundant in rat embryos and their yolk sacs during organogenesis. The phorbol ester, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), has been reported to disrupt the morphology and functional development of the rat embryonic visceral yolk sac. The present study investigated the possibility that the effect of TPA on yolk sac development may be due to the altered expression of E-cadherin. Rat embryos, with their yolk sacs intact, were cultured on day 10 of gestation for 1 hr. At this time the vehicle, dimethyl sulfoxide (DMSO), or TPA (at different concentrations) was added to the culture medium; the cultures were continued for up to 24 hr. Embryos and yolk sacs were collected separately at the end of each culture period. The relative abundances of E-cadherin mRNA and protein were analyzed with Northern and Western blot analyses. Despite the TPA-induced abnormalities in yolk sac development, the relative abundance of E-cadherin mRNA or protein in the yolk sac was not altered by TPA exposure. However, in embryos exposed to dysmorphogenic concentrations of TPA, the relative abundance of E-cadherin mRNA was significantly increased after 24 hr in culture, compared to either controls or embryos exposed to non-dysmorphogenic concentrations of TPA. The magnitude of the increase in embryonic E-cadherin mRNA appeared to correlate with the severity of the embryo malformations.(ABSTRACT TRUNCATED AT 250 WORDS)
Abnormalities, Drug-Induced↗
Decreased phosphorylation of four 20-kDa proteins precedes staurosporine-induced disruption of the actin/myosin cytoskeleton in rat astrocytes.
The changes in protein phosphorylation and cytoskeletal structure preceding the dramatic morphological changes in staurosporine-treated rat astrocytes were examined, and the dependence of these effects on protein kinase C (PKC) was studied. Fluorescence and photoelectron microscopy revealed that a 20-min exposure to the kinase inhibitor staurosporine at 100 nM substantially decreased the thickness and linear appearance of actin microfilament bundles (stress fibers) prior to major changes in cell shape, while 60 min of staurosporine depleted virtually all microfilament bundles and caused arborization and contraction of the cell body. The distribution of myosin light chain (MLC) labeling within the cytoplasm was also dramatically altered by staurosporine, progressing from a linear punctate pattern coincident with the linear pattern of filamentous actin to a diffuse pattern in cells in which microfilament dissolution was taking place. Two-dimensional gel analysis of astrocyte phosphoproteins demonstrated 50-80% reduction of 32P incorporation into four 20-kDa spots, one of which was recognized by an antibody to MLC, following a 15-min treatment with 100 nM staurosporine. Depletion of functinal PKC from astrocytes by a 24-h exposure to phorbol myristate acetate prior to staurosporine exposure did not reduce the extent of the cytoskeletal alterations or alter the decrease in protein phosphorylation. Two other protein kinase inhibitors which affect astrocyte morphology, H-7 and the MLC kinase inhibitor ML-9, were also observed to disrupt microfilament bundles with accompanying decreases in 32P incorporation into these same phosphoproteins, whereas the more selective PKC inhibitor Ro 31-8220 did not do either. The early onset of decreased phosphorylation of the 20-kDa proteins supports a direct relationship between the rapid dissociation of myosin light chain from actin microfilament bundles, the disruption of actin patterns, and the subsequent morphological alterations. These data also suggest that staurosporine and H-7 may exert their effects via a pathway involving inhibition of MLC kinase.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Cadmium-induced rat embryotoxicity in vitro is associated with an increased abundance of E-cadherin protein in the yolk sac.
Cadmium, a cytotoxic heavy metal, is embryotoxic. Cadmium interferes with the functions of other cations such as zinc and calcium. Cadherins, calcium-dependent cell adhesion molecules, are expressed and spatiotemporally regulated in embryos and their yolk sacs during organogenesis. Cadmium has been shown to disrupt calcium-dependent cell-cell interactions and to alter the distribution of epithelial or E-cadherin in cultured cells. The purpose of this study was to determine whether the embryotoxicity of cadmium is mediated through an effect on E-cadherin. Day 10 rat embryos were cultured for 1 hr without cadmium and then cultured for another 2, 6, or 20 hr in the presence or absence of 2.5 microM CdCl2. Embryos and yolk sacs were collected and analyzed separately. The growth of embryos and yolk sacs after exposure to cadmium for 2 or 6 hr was not different from that of controls. After 20 hr exposure to cadmium, embryos were growth retarded, with morphological scores 10-15% lower than those of controls; more dramatically, their yolk sacs were thickened and decreased in diameter to only half of that of control yolk sacs. Northern blot analysis revealed no significant differences in the relative amounts of E-cadherin mRNA between control and cadmium-treated embryos or their yolk sacs. There was also no alteration in the abundance of E-cadherin protein in cadmium-treated embryos at any of the times examined. There was a gradual decline in the relative amount of E-cadherin protein in control yolk sacs with time in culture; interestingly, cadmium treatment appeared to prevent this decline, resulting in significantly higher concentrations of E-cadherin protein in the cadmium-exposed yolk sacs after 6 hr (1.7-fold) or 20 hr (2.3-fold) of culture. The relative abundance of other structural proteins such as alpha- or beta-tubulin and actin was unchanged. Exposure of embryos for 20 hr to concentrations of cadmium varying from nonembryotoxic to embryotoxic resulted in concentration-dependent increases in E-cadherin protein in the yolk sac; E-cadherin was only increased in the yolk sac of growth-retarded embryos. Thus, an increase in yolk sac E-cadherin protein is associated with the induction of embryotoxicity by cadmium. To determine the ability of cadmium to interact directly with the cadherins, the binding of radioactive 109Cd to embryo and yolk sac proteins was assessed. 109Cd bound to an unidentified 87-kDa protein; binding to this protein was attenuated by 1 mM zinc, but not by 1 mM calcium.(ABSTRACT TRUNCATED AT 400 WORDS)
Actins↗
cDNA-derived hypovirus RNA in transformed chestnut blight fungus is spliced and trimmed of vector nucleotides.
Unencapsidated double-stranded viral RNAs belonging to the genus Hypovirus attenuate virulence of the chestnut blight fungus, Cryphonectria parasitica. A full-length cDNA clone of hypovirus CHV1-713 double-stranded RNA was recently shown to be infectious when introduced into the C. parasitica genome by DNA-mediated transformation. In this study, we show that the viral RNA derived from the chromosomally integrated cDNA copy is trimmed of extraneous vector nucleotide sequences. The cDNA-derived viral RNA was also found to contain a 73-bp deletion located within the 5'-noncoding leader sequence as a result of a pre-mRNA splicing event. Implications of these results are discussed in terms of hypovirus RNA replication and anticipated field studies involving engineered hypovirulent C. parasitica strains.
Base Sequence↗
Detection of human papillomavirus DNA in esophageal squamous cell carcinomas by the polymerase chain reaction using general consensus primers.
We studied 40 formalin-fixed, paraffin-embedded esophageal squamous cell carcinomas from a high risk region for this tumor for the presence of human papillomavirus (HPV) DNA by the polymerase chain reaction (PCR). We used two general consensus primers from a highly conserved E1 region of HPV types 6, 11, 16, and 18. Human papillomavirus DNA was detected in 60% (24 of 40) of the cases without relation to the tumor grade. Two lymph node metastases had the same HPV types as the primary tumor. Human papillomavirus types were determined in the 24 HPV-positive cases by Southern blot analysis of amplified DNA. Human papillomavirus type 6 was detected in 50% (12 of 24) of the cases, HPV type 16 in 8% (two of 24), and HPV types 6 and 16 in 17% (four of 24); in 25% (six of 24) of the cases the type was unknown. Human papillomavirus types 11 and 18 were not detected. Esophageal mucosa adjacent to the tumor was studied for morphological changes of HPV effect in 27 cases. Adjacent esophageal mucosa in 16 HPV-positive tumors showed statistically significant (P < .05) koilocytosis in six cases. Papillomatosis was the next most frequent finding in four cases. This study supports the role of HPV in the causation of esophageal squamous cell carcinomas, especially in high risk regions for this tumor.
Adult↗
Voltammetric determination of dopamine in the presence of ascorbic acid at over-oxidized polypyrrole-indigo carmine film-coated electrodes.
Over-oxidized polypyrrole films doped with indigo carmine (PPy-IC) offer substantial improvements in voltammetric sensitivity and selectivity towards dopamine. This polymer coating attenuates the voltammetric response of ascorbic acid while the oxidation peak current of dopamine is enhanced by over one order of magnitude compared with that at the bare electrode. The high sensitivity and selectivity for dopamine appears to be mainly due to the charge discrimination and the analyte accumulation. The detection limit is dependent on both film thickness and preconcentration time. At a 0.25 micron thick PPy-IC film-coated electrode, for a 2 min preconcentration time, the detection limit is 10(-8) mol l-1, over two orders of magnitude lower than at a bare glassy carbon electrode. The concomitant ascorbic acid shows no interference although its concentration is as high as 0.1 mmol l-1. The effects of various experimental parameters on the voltammetric response of dopamine were also investigated. The attractive permselective and preconcentrating properties of the PPy-IC films make them valuable for in vivo electrochemistry.
Ascorbic Acid↗
Allele-specific activation and expression of the K-ras gene in hybrid mouse lung tumors induced by chemical carcinogens.
A mouse hybrid, (C3H x A/J)F1 or C3A, was developed by crossing male A/J mice (high lung tumor susceptibility) with female C3H mice (low lung tumor susceptibility). The lung tumor responses of the C3A mice to dimethylnitrosamine (DMN) or benzo[a]pyrene (B[a]P) were found to be intermediate between those of the two parental strains. Mutational activation of the K-ras gene was found at a high frequency in both the B[a]P- and DMN-induced C3A lung tumors. To explore the genetic basis of the K-ras gene involvement in mouse lung tumor susceptibility, the parental origin of the K-ras oncogene in the chemically induced C3A lung tumors was determined. K-ras oncogenes were found on the allele inherited from the susceptible A/J parent in 14/16 of DMN-induced tumors and 15/17 of B[a]P-induced tumors from C3A mice. Furthermore, the K-ras mRNA transcribed from the A/J allele was 5-20 times more than C3H K-ras transcripts in 10/10 DMN-induced and 10/10 B[a]P-induced C3A lung tumors. These data suggest that an activated A/J K-ras allele could be more tumorigenic than an activated C3H allele due to the differential expression of the two alleles in lung cells.
Alleles↗
Isovector meson contribution in the relativistic Hartree-Fock approach for finite nuclei.
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Journal Article↗
Genetic study of indirect inguinal hernia.
We performed a genetic analysis of 280 families with congenital indirect inguinal hernia ascertained in Shandong province. The multifactorial threshold model and segregation analysis were applied to these families to investigate the mode of inheritance of congenital indirect inguinal hernia. Our results indicate that congenital indirect inguinal hernia is not compatible with a multifactorial threshold model, and the frequent vertical transmission and high segregation ratio suggest autosomal dominant inheritance with incomplete penetrance and sex influence. Through further pedigree analysis of the multiple case families with at least two closely related affected members, we noted preferential paternal transmission of the disease gene, which might suggest the role of genomic imprinting in the aetiology of this condition.
Chi-Square Distribution↗
A little emperor. One-child family.
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Asia↗
Experimental study on electrochemical treatment of cancer in mice.
Electrochemical treatment of cancers in mice resulted in at least partial regression or disappearance of transplanted SRS solid tumours and increased the survival time. Six days after treatment, lymphocyte infiltration in the tumour tissue was found. Seventy-one days after treatment, tumour cells were rarely found in the tissue. The application of direct current was found to facilitate the destruction of tumour cells in a shear stress field.
Animals↗