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Biomedical subjects

J N Chen

Publications and source records attributed to J N Chen.

At least 37 records · Page 2Linked to original sources
PubMed2001

Heterogeneous catalytic ozonation of 2-chlorophenol aqueous solution with alumina as a catalyst.

Heterogenous catalytic ozonation of 2-chlorophenol (2-CP) in the presence of gamma-alumina as a solid catalyst has been investigated in this research. It showed that the rate for degradation of TOC could increase from 21% to 43%. The pseudo-first reaction constants of 2-CP could increase from 0.8688 min-1 to 0.1270, increasing by approximately 40%. At the same time, the consumption of ozone was only half that of ozone alone. This research also explored the effects of the catalyst dosage, pH values and removal kinetics of 2-CP. In addition, three consecutive running with the same catalyst revealed insignificant reduction of the activity. Furthermore, the elimination of toxicity was evaluated by Microtox analysis. The detoxification was more stable and with good results.

Aluminum Oxide↗
PubMed2001

Improving the numerical stability of the MAGIC model.

MAGIC is one of the most widely used models for forecasting long-term acidification. The model's code, however, has been experiencing numerical instability, though this might not be widely known to the public users. The major instability comes from the analytical solution to two cubic equations for calculating SO4(2-) concentration and the exchangeable fraction of Al on the soils. The mathematical algorithm for calculating the concentration of SO4(2-) from a quadratic equation is also found unstable. This paper is aimed at improving the instability above through proved numerical algorithms.

Adsorption↗
PubMed2001

[Investigation of genotyping HLA DRB1 gene using oligoneucleotide arrays].

We have developed a method performed on an oligoneucleotide array for genotyping HLA DRB1. The routine method Phenol-chloroform was used to extract genome DNA of standard samples. A pair of sense and antisense primers were designed according to the sequence of DRB1 exon2, then the primers and the Cy5-dCTP were used in the following PCR, thus the PCR products were labelled with Cy5. Many genotyping probes which were immobilized on the DNA Microarray made by APS-PDC method were designed. The labelled PCR products were hybridized with them, the signals were sanned by sanner and analyzed by Imagene software. We have genotyped 33 standard samples which have 12 DRB1 subtypes. The experimental results showed that the arrays we made and the method we used are accurate and sensitive. This proved that the DNA Microarray technique is good for DRB1 genotyping. Compared with PCR-SSP and PCR-SSO methods, the genotyping chip method is more intuitionistic and has the advantage of integration.

Genotype↗
PubMed2000

Genetics of heart development.

The genes that drive heart-cell differentiation in vertebrates and Drosophila are similar, even though the Drosophila 'heart' is a simple tube and the vertebrate heart is a multichambered physiologically complex organ. Mutational analysis in mice and, as particular focus of this review, in zebrafish, reveals the additional genes brought into play to fashion these evolutionarily 'new' organotypic components.

Animals↗
PubMed2000

[The relationship between the change of mitochondria and the fertility in CMS line of sorghum after heat shock].

The mitochondria of anther in pollen mother cell stage of cytoplasmic male sterility (CMS) line 3197A in sorghum were extracted after heat shock. The number of the mitochondria was measured by flow cytometer and some isoenzymes were analyzed by PAGE combined with stain for enzyme activity. The result of mitochondria quantity measurement shows that the number of the mitochondria in CMS line 3197A increased greatly up to 4.5 folds after heat shock. The analysis of isoenzymes also demonstrates that the type of isoenzyme in CMS line is in consistent with maintainer line. The study denoted the change of the quantity of mitochondria after heat shock and the relationship between this change and the fertility in sorghum.

Edible Grain↗
PubMed1999

Oxidation of dichlorvos with hydrogen peroxide using ferrous ion as catalyst.

This study examines how Fenton's reagent (Fe2+ and H2O2) decomposed dichlorvos insecticide. Results showed that dichlorvos decomposed in a two-stage reaction. The first stage is a Fe2+/H2O2 reaction in which dichlorvos swiftly decomposed. In the second stage, dichlorvos decomposed somewhat less rapidly, and it is a Fe3+/H2O2 reaction. The detection of ferrous ions also supports the theory of the two-stage reaction for the dichlorvos oxidation with Fenton's reagent. The dissolved oxygen of the solution decreased rapidly in the first stage reaction, but it slowly increased in the second stage with a zero-order kinetics. The Fenton system decomposed dichlorvos most rapidly when the initial pH in the solution is 3-4. In addition, increasing the concentration of hydrogen peroxide or ferrous ions can enhance the decomposition of dichlorvos. Consequently, the relationship of rate constant (kobs), [H2O2] and [Fe2+] at initial pH 3 is determined as kobs = 2.67 x 10(4)[H2O2]0.7[Fe2+]1.2.

Biodegradation, Environmental↗
PubMed1999

Effects of keratinocyte growth factor in the squamous epithelium of the upper aerodigestive tract of normal and irradiated mice.

PURPOSE: To investigate the effects of keratinocyte growth factor (KGF) on the structure of the stratified squamous epithelium of the tongue, buccal mucosa and oesophagus of normal and irradiated mice. MATERIALS AND METHODS: Female BDF1 mice were exposed to total body irradiation from a caesium source. The irradiated mice and normal, unirradiated mice were injected with 5 mg/kg per day KGF or vehicle. Thickness and proliferation in the epithelium were measured. RESULTS: KGF caused epithelial thickening of the non-keratinized layers in oral epithelium in normal mice. It increased the number of nucleated layers and influenced differentiation of post-mitotic cells in the upper layers by increasing the size and number of keratohyalin granules, and the number of desmosomes. Single and fractionated doses of radiation caused inhibition of proliferation as detected by markedly reduced BrdU incorporation following exposure, followed by epithelial atrophy. KGF treatment of mice reversed the inhibition of proliferation and atrophy that occurred in control irradiated mice. CONCLUSION: These data show that KGF reverses epithelial atrophy in mouse oral cavity caused by irradiation and suggest that KGF may be useful for the treatment of mucositis of the upper aerodigestive tract of patients treated with aggressive regimens of radiation therapy.

Animals↗
PubMed1999

[Experimental study on stimulation of guided bone regeneration by acid fibroblast growth factor].

OBJECTIVE: To investigate the effect of acid fibroblast growth factor (aFGF) on guided bone regeneration (GBR), to study whether aFGF can promote the repairing ability of GBR in bone defect. METHODS: 10 mm long segmental defects were created in the diaphyses of both radii in 16 New Zealand rabbits. The defect was bridged with a silicon tube. Human recombinant aFGF was instilled into the tube on the experimental side, while the contralateral tube was instilled with saline as control group. The radiographic, gross and histologic examination of the samples were analyzed at 2, 4, 6 and 8 weeks after operation. RESULTS: On the experimental side, there was new bone formation in the bone medullary cavity, the endosteum and the section surface of the cortex at 2 weeks. At 4 weeks, at the center of the blood clot in the tube there was new bone formation and bone defect was completely healed at 8 weeks. On the control side, new bone formation was less in every period compared with that of the experimental side. At 8 weeks, there was only partial healing of the bone defect. CONCLUSION: It can be concluded that aFGF can promote new bone formation and facilitate GBR in bone defect.

Animals↗
PubMed1998

Differential rescue of visceral and cardiac defects in Drosophila by vertebrate tinman-related genes.

tinman, a mesodermal NK2-type homeobox gene, is absolutely required for the subdivision of the early Drosophila mesoderm and for the formation of the heart as well as the visceral muscle primordia. Several vertebrate relatives of tinman, many of which are predominately expressed in the very early cardiac progenitors (and pharyngeal endoderm), also seem to promote heart development. Here, we show that most of these vertebrate tinman-related genes can readily substitute for Drosophila tinman function in promoting visceral mesoderm-specific marker gene expression, but much less in promoting cardiac-specific gene expression indicative of heart development. In addition, another mesodermal NK2-type gene from Drosophila, bagpipe, which is normally only needed for visceral mesoderm but not heart development, cannot substitute for tinman at all. These data indicate that the functional equivalence of the tinman-related subclass of NK2-type genes (in activating markers of visceral mesoderm development in Drosophila) is specific to this subclass and distinct from other homeobox genes. Despite the apparent overall conservation of heart development between vertebrates and invertebrates, the differential rescue of visceral mesoderm versus heart development suggests that some of the molecular mechanisms of organ formation may have diverged during evolution.

Animals↗
PubMed1998

Keratinocyte growth factor protects mice from chemotherapy and radiation-induced gastrointestinal injury and mortality.

Keratinocyte growth factor (KGF) stimulates the proliferation and differentiation of epithelial cells including those of the gastrointestinal tract. Although chemotherapeutics and radiation exposure kill rapidly proliferating tumor cells, rapidly dividing normal cells of the host's gastrointestinal tract are also frequently damaged, leading to the clinical condition broadly termed "mucositis." In this report, recombinant human KGF used as a pretreatment in several mouse models of chemotherapy and/or radiation-induced gastrointestinal injury significantly improved mouse survival. Using multiple-dose 5-fluorouracil, methotrexate, and radiation in combination and total body radiation alone models, KGF increased survival by 55% or greater. In the models that used chemotherapy with or without radiation, KGF significantly ameliorated weight loss after injury and accelerated weight gain during recovery. The basis of these systemic benefits appears to be due in part to the trophic effects of the growth factor on the intestinal epithelium because KGF pretreatment caused an increase in measures of mucosal thickness (villus height and crypt depth) that persisted during the course of 5-fluorouracil chemotherapy. Treatment with KGF also afforded a 3.5-fold improvement in crypt survival in the small intestine, suggesting that KGF also has a direct effect on the crypt stem cells. These data indicate that KGF may be therapeutically useful to lessen the intestinal side effects of current cancer therapy regimens.

Animals↗
PubMed1998

Regulation in the heart field of zebrafish.

In many vertebrates, removal of early embryonic heart precursors can be repaired, leaving the heart and embryo without visible deficit. One possibility is that this 'regulation' involves a cell fate switch whereby cells, perhaps in regions surrounding normal progenitors, are redirected to the heart cell fate. However, the lineage and spatial relationships between cells that are normal heart progenitors and those that can assume that role after injury are not known, nor are their molecular distinctions. We have adapted a laser-activated technique to label single or small patches of cells in the lateral plate mesoderm of the zebrafish and to track their subsequent lineage. We find that the heart precursor cells are clustered in a region adjacent to the prechordal plate, just anterior to the notochord tip. Complete unilateral ablation of all heart precursors with a laser does not disrupt heart development, if performed before the 18-somite stage. By combining extirpation of the heart precursors with cell labeling, we find that cells anterior to the normal cardiogenic compartments constitute the source of regulatory cells that compensate for the loss of the progenitors. One of the earliest embryonic markers of the premyocardial cells is the divergent homeodomain gene, Nkx2.5. Interestingly, normal cardiogenic progenitors derive from only the anterior half of the Nkx2.5-expressing region in the lateral plate mesoderm. The posterior half, adjacent to the notochord, does not include cardiac progenitors and the posterior Nkx2.5-expressing cells do not contribute to the heart, even after ablation of the normal cardiogenic region. The cells that can acquire a cardiac cell fate after injury to the normal progenitors also reside near the prechordal plate, but anterior to the Nkx2.5-expressing domain. Normally they give rise to head mesenchyme. They share with cardiac progenitors early expression of GATA 4. The location of the different elements of the cardiac field, and their response to injury, suggests that the prechordal plate supports and/or the notochord suppresses the cardiac fate.

Animals↗
PubMed1998

Sensorineural hearing loss in MELAS syndrome--case report.

A mitochondrial tRNA mutation at nucleotide 3,243 is known to be found in most patients with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes). We report a 30 year-old female patient of MELAS, diagnosed 5 years ago, who presented herself to our ENT outpatient department because of her bilateral tinnitus and progressive hearing impairment since 4 years ago. Two sequential pure tone audiograms showed bilateral symmetrical progressive sensorineural hearing loss, especially in the high frequency area in 1993 and 1996. The pure tone average was R-45 dB, L-47 dB in 1993 and R-62 dB, L-67 dB in 1996. Hearing loss is an important feature in MELAS syndrome and reported to be seen in about 30% of patients. It is often the first clinical symptom, too. In any case, mitochondrial cytopathies need to be considered by the otologist in forming a diagnosis of sensorineural hearing loss (SNHL), particularly in cases, which present adult-onset progressive hearing loss and neurologic symptoms before 50 years of age.

Adult↗
PubMed1997

Left-right pattern of cardiac BMP4 may drive asymmetry of the heart in zebrafish.

The first evident break in left-right symmetry of the primitive zebrafish heart tube is the shift in pattern of BMP4 expression from radially symmetric to left-predominant. The midline heart tube then 'jogs' to the left and subsequently loops to the right. We examined 279 mutations, affecting more than 200 genes, and found 21 mutations that perturb this process. Some cause BMP4 to remain radially symmetric. Others randomize the asymmetric BMP4 pattern. Retention of BMP4 symmetry is associated with failure to jog: right-predominance of the BMP4 pattern is associated with reversal of the direction of jogging and looping. Raising BMP4 diffusely throughout the heart, via sonic hedgehog injection, or the blocking of its action by injection of a dominant negative BMP4 receptor, prevent directional jogging or looping. The genes crucial to directing cardiac asymmetry include a subset of those needed for patterning the dorsoventral axis and for notochord and ventral spinal cord development. Thus, the pattern of cardiac BMP4 appears to be in the pathway by which the heart interprets lateralizing signals from the midline.

Animals↗
PubMed1996

Zebrafish tinman homolog demarcates the heart field and initiates myocardial differentiation.

The fashioning of a vertebrate organ requires integration of decisions of cell fate by individual cells with those that regulate organotypic form. Logical candidates for this role, in an organ such as the heart, are genes that initiate the differentiation process leading to heart muscle and those that define the earliest embryonic heart field, but for neither class are genes defined. We cloned zebrafish Nkx2.5, a homolog of the tinman homeodomain gene needed for visceral and cardiac mesoderm formation in Drosophila. In the zebrafish, its expression is associated with cardiac precursor cells throughout development, even in the early gastrula, where the level of zebrafish Nkx2.5 is in a gradient which spatially matches the regional propensity of ventral-marginal cells to become heart. Overexpression of Nkx2.5 causes formation of disproportionally larger hearts in otherwise apparently normal embryos. Transplanted cell expressing high levels of Nkx2.5 express cardiac genes even in ectopic locales. Fibroblasts transfected with myc-tagged Nkx2.5 express cardiac genes. These effects require the homeodomain. Thus, Nkx2.5 appears to mark the earliest embryonic heart field and to be capable of initiating the cardiogenic differentiation program. Because ectopic cells or transfected fibroblasts do not beat, Nkx2.5 is likely to be but one step in the determination of cardiac myocyte cell fate. Its overexpression increases heart size, perhaps by bringing cells on the edge of the field to a threshold level for initiation of cardiac differentiation.

Amino Acid Sequence↗
PubMed1996

Mutations affecting the formation and function of the cardiovascular system in the zebrafish embryo.

As part of a large-scale mutagenesis screen of the zebrafish genome, we have identified 58 mutations that affect the formation and function of the cardiovascular system. The cardiovascular system is particularly amenable for screening in the transparent zebrafish embryo because the heart and blood vessels are prominent and their function easily examined. We have classified the mutations affecting the heart into those that affect primarily either morphogenesis or function. Nine mutations clearly disrupt the formation of the heart. cloche deletes the endocardium. In cloche mutants, the myocardial layer forms in the absence of the endocardium but is dysmorphic and exhibits a weak contractility. Two loci, miles apart and bonnie and clyde, play a critical role in the fusion of the bilateral tubular primordia. Three mutations lead to an abnormally large heart and one to the formation of a diminutive, dysmorphic heart. We have found no mutation that deletes the myocardial cells altogether, but one, pandora, appears to eliminate the ventricle selectively. Seven mutations interfere with vascular integrity, as indicated by hemorrhage at particular sites. In terms of cardiac function, one large group exhibits a weak beat. In this group, five loci affect both chambers and seven a specific chamber (the atrium or ventricle). For example, the weak atrium mutation exhibits an atrium that becomes silent but has a normally beating ventricle. Seven mutations affect the rhythm of the heart causing, for example, a slow rate, a fibrillating pattern or an apparent block to conduction. In several other mutants, regurgitation of blood flow from ventricle to atrium is the most prominent abnormality, due either to the absence of valves or to poor coordination between the chambers with regard to the timing of contraction. The mutations identified in this screen point to discrete and critical steps in the formation and function of the heart and vasculature.

Animals↗
PubMed1996

Mutations affecting the cardiovascular system and other internal organs in zebrafish.

In a screen for early developmental mutants of the zebrafish, we have identified mutations specifically affecting the internal organs. We identified 53 mutations affecting the cardiovascular system. Nine of them affect specific landmarks of heart morphogenesis. Mutations in four genes cause a failure in the fusion of the bilateral heart primordia, resulting in cardia bifida. In lonely atrium, no heart venticle is visible and the atrium is directly fused to the outflow tract. In the overlooped mutant, the relative position of the two heart chambers is distorted. The heart is enormously enlarged in the santa mutant. In two mutants, scotch tape and superglue, the cardiac jelly between the two layers of the heart is significantly reduced. We also identified a number of mutations affecting the function of the heart. The mutations affecting heart function can be subdivided into two groups, one affecting heart contraction and another affecting the rhythm of the heart beat. Among the contractility group of mutants are 5 with no heart beat at all and 15 with a reduced heart beat of one or both chambers. 6 mutations are in the rhythmicity group and specifically affect the beating pattern of the heart. Mutations in two genes, bypass and kurzschluss, cause specific defects in the circulatory system. In addition to the heart mutants, we identified 23 mutations affecting the integrity of the liver, the intestine or the kidney. In this report, we demonstrate that it is feasible to screen for genes specific for the patterning or function of certain internal organs in the zebrafish. The mutations presented here could serve as an entry point to the establishment of a genetic hierarchy underlying organogenesis.

Animals↗