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X Chen

Publications and source records attributed to X Chen.

At least 721 records · Page 40Linked to original sources
PubMed1999

Tandem application of flow cytometry and polymerase chain reaction for comprehensive detection of minimal residual disease in childhood acute lymphoblastic leukemia.

Children with acute lymphoblastic leukemia (ALL) with > or = 0.01% leukemic cells in the bone marrow after remission induction are at a greater risk of relapse. The most promising methods of detecting minimal residual disease (MRD) are flow cytometric identification of leukemia-associated immunophenotypes and polymerase chain reaction (PCR) amplification of antigen-receptor genes. However, neither assay can be applied to all patients. Moreover, both assays carry the risk of false-negative findings due to clonal evolution. The simultaneous use of both assays might resolve these problems, but the correlation between the methods is unknown. We studied serial dilutions of normal and leukemic cells by flow cytometry and PCR amplification of IgH genes and found the two methods highly sensitive (one leukemic cell among 10(4) or more normal cells), accurate (r2 was 0.999 for flow cytometry and 0.960 for PCR by regression analysis) and concordant (r2 = 0.962). We then examined 62 bone marrow samples collected from children with ALL in clinical remission. In 12 samples, both techniques detected MRD levels > or = 1 in 10(4). The percentages of leukemic cells measured by the two methods correlated well (r2 = 0.978). Of the remaining 50 samples, 48 had MRD levels < 1 in 10(4). In only two samples results were discordant: 2 in 10(4) and 5 in 10(4) leukemic cells by PCR but < 1 in 10(4) by flow cytometry. We conclude that immunologic and molecular techniques can be used in tandem for universal monitoring of MRD in childhood ALL.

Child↗
PubMed1999

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1-independent DSB repair pathway.

BACKGROUND: DMC1, the meiosis-specific eukaryotic homologue of bacterial recA, is required for completion of meiotic recombination and cell cycle progression past prophase. In a dmc1 mutant, double strand break recombination intermediates accumulate and cells arrest in prophase. We isolated genes which, when present at high copy numbers, suppress the meiotic arrest phenotype conferred by dmc1 mutations. RESULTS: Among the genes isolated were two which suppress arrest by altering the recombination process. REC114 suppresses formation of double strand break (DSB) recombination intermediates. The low viability of spores produced by dmc1 mutants carrying high copy numbers of REC114 is rescued when reductional segregation is bypassed by mutation of spo13. High copy numbers of RAD54 suppress dmc1 arrest, promote DSB repair, and allow formation of viable spores following reductional segregation. Analysis of the combined effects of a null mutation in RED1, a gene required for meiotic chromosome structure, with null mutations in RAD54 and DMC1 shows that RAD54, while not normally important for repair of DSBs during meiosis, is required for efficient repair of breaks by the intersister recombination pathway that operates in red1 dmc1 double mutants. CONCLUSIONS: Over-expression of REC114 suppresses meiotic arrest by preventing formation of DSBs. High copy numbers of RAD54 activate a DMC1-independent mechanism that promotes repair of DSBs by homology-mediated recombination. The ability of RAD54 to promote DMC1-independent recombination is proposed to involve suppression of a constraint that normally promotes recombination between homologous chromatids rather than sisters.

Cell Cycle Proteins↗
PubMed1999

Filamentous growth of Candida albicans in response to physical environmental cues and its regulation by the unique CZF1 gene.

Hyphal growth in the opportunistic fungal pathogen Candida albicans is believed to contribute to the virulence of the organism by promoting penetration of fungal cells into host tissue. In this study, stimulation of hyphal growth by a feature of the physical environment was demonstrated. Specifically, growth of cells embedded within a matrix promoted the formation of hyphae. The CZF1 gene, encoding a putative transcription factor, was shown to be involved in the regulation of hyphal growth under certain conditions, including embedded conditions. Ectopic expression of CZF1 in embedded cells promoted the rapid formation of hyphae. Elimination of CZF1 and CPH1, encoding a homologue of the Saccharomyces cerevisiae Ste12p transcription factor, led to a pronounced defect in filamentous growth of embedded cells. Elimination of CZF1 alone led to a moderate defect in hyphal growth under some conditions, including embedded conditions. Hyphal morphogenesis in response to matrix embedding may occur in the opportunistic pathogen, C. albicans, to promote invasion of fungal cells into host tissue.

Candida albicans↗
PubMed1999

The gene encoding tobacco gibberellin 3beta-hydroxylase is expressed at the site of GA action during stem elongation and flower organ development.

Gibberellin 3beta-hydroxylase catalyzes the final step in the biosynthetic pathway leading to the plant hormone gibberellin (GA) and, therefore, the in vivo localization of this enzyme should give a direct indication of the site of synthesis of bioactive GAs in plants. We have isolated a cDNA clone, Nty (Nicotiana tabacum GA 3beta-hydroxylase), which encodes a putative GA 3beta-hydroxylase, by RT-PCR using RNA from tobacco shoot apices. Functional analysis, using an NTY protein expressed in Escherichia coli, revealed that Nty encoded an active GA 3beta-hydroxylase. A high expression level of Nty was observed in shoot apices, flowers, roots, young internodes but not in leaves or seeds. We performed more detailed expression analyses using in situ hybridization and histochemical analyses of the GUS activity in transgenic tobacco plants carrying an Nty promoter:GUS fusion gene. These studies revealed that expression of Nty was restricted to specific regions, including actively dividing and elongating cells in the various organs; rib meristem and elongation zones of shoot apices, tapetum and pollen grains in developing anthers and root tips, which are consistent with the sites of GA action. It is proposed that GA actions depend on the modulation of endogenous bioactive GA levels through the regulation of GA 3beta-hydroxylase expression in situ.

Amino Acid Sequence↗
PubMed1999

Simvastatin inhibits cardiac hypertrophy and angiotensin-converting enzyme activity in rats with aortic stenosis.

1. In the present study, we tested the hypothesis that long-term administration of the hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor simvastatin may regress hypertrophy and the possible effect of simvastatin on angiotensin-converting enzyme (ACE) activity in rats with pressure-overload cardiac hypertrophy. 2. Pressure-overload left ventricular hypertrophy (LVH) of rats was induced by part coarctation of the abdominal aorta; a sham-operated group served as the control. Six weeks after operation, animals were divided into three groups and an 8 week treatment period was insitgated as follows: (i) the simvastatin treatment group received simvastatin at 3.6 mg/kg per day, p.o.; (ii) the ACE inhibitor group received captopril at 50 mg/kg per day, p.o.; and (iii) the LVH control group received no drug treatment. 3. At the end of the treatment period, left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) were monitored in vivo. Diastolic pressure-volume relationships were evaluated in a Langendorff preparation with a balloon-in-left ventricle (LV) heart. Myocyte cell width was measured. Angiotensin-converting enzyme activity and angiotensin (Ang)II and hydroxyproline contents of the LV were determined. 4. At the end of the experiments, LVH was established in the LVH control group by increases in LV weight, LV weight/body-weight ratio, LV weight/right ventricle weight ratio, LV myocyte cell width, LVSP and LVEDP by 40, 26, 19, 61, 56 and 59%, respectively (all P < 0.01), compared with the sham-operated group. In the simvastatin-treated and ACE inhibitor groups all these parameters were significantly reduced compared with sham-operated controls. In the LVH control group, ACE activity and AngII and hydroxyproline contents of LV tissue increased by 180, 123 and 70, respectively (all P < 0.01), compared with the sham-operated group. Compared with the LVH group, in the simvastatin-treated and ACE inhibitor groups ACE activity was reduced by 36 (P < 0.05) and 48% (P < 0.01), respectively, AngII content was reduced by 11 (P < 0.05) and 43% (P < 0.01), respectively, and hydroxyproline content was reduced by 23 (P < 0.01) and 10% (P < 0.05), respectively. 5. For the first time, the results of the present study demonstrate that simvastatin significantly reduces LVH, cardiac tissue ACE activity and improves LV performance in pressure-overloaded rats. Because, compared with captopril, simvastatin is more potent in its reduction of LVH and less potent in its inhibition of ACE activity, the mechanism of its antihypertrophic action, in addition to ACE inhibition, may involve inhibition of the mevalonic acid pathway, the main target of action of statins. Thus, HMG-CoA reductase inhibitors may be beneficial for the clinical treatment of cardiac hypertrophy.

Angiotensin II↗
PubMed1999

Calcium influx through NMDA receptors, chronic receptor inhibition by ethanol and 2-amino-5-phosponopentanoic acid, and receptor protein expression.

Chronic treatment of neurons with either ethanol or competitive and noncompetitive antagonists of NMDA receptors leads to enhanced expression of NMDA receptor density and function in neurons. The signal transduction pathways for such receptor up-regulation are not known. The focus of the present study was on the role of Ca2+ entry into neurons, either through receptor or voltage-gated channels, in the expression of the NMDA receptor subunit NR1 and the 71-kDa glutamate-binding protein (GBP) of a glutamate/NMDA receptor-like complex. Chronic inhibition of NMDA receptors in cortical neurons in primary cultures by either 100 mM ethanol or 100 microM 2-amino-5-phosphonopentanoic acid (2-AP5) increased the expression of NR1 and GBP. The effect of 2-AP5 on the expression of the two proteins was not additive with that of ethanol when neuronal cultures were treated with both agents at the same time. However, the effects of ethanol on NR1 and GBP expression were blocked by the simultaneous treatment with NMDA (50 microM). Activation or inhibition of other glutamate ionotropic receptors had no effect on the expression of NR1 and GBP. The inhibition of L- or N-type voltage-sensitive Ca2+ channels and voltage-gated Na+ channels also had little effect on the expression of either protein; neither did exposure of neurons to elevated extracellular Ca2+ concentrations (3 or 5 mM). On the other hand, treatment of neurons for 48 h with the intracellular Ca2+ chelator BAPTA-AM as well as partial chelation of extracellular Ca2+ with EGTA caused an up-regulation in NR1 and GBP expression. The enhanced expression of NR1 in neurons treated for 48 h with either ethanol or EGTA was correlated with increases in the activity of NMDA receptors demonstrated as a doubling of the NMDA-stimulated rise in intracellular free Ca2+ concentration. The effects of chronic administration of EGTA on both NR1 expression as well as NMDA receptor function were probably related to an acute inhibition by EGTA of NMDA-induced Ca2+ influx into neurons. It appears that the expression of both the NR1 subunit of NMDA receptors and the GBP of a receptor-like complex is regulated by intracellular Ca2+, especially that entering through NMDA receptor ion channels.

2-Amino-5-phosphonovalerate↗
PubMed1999

Molecular mechanism(s) of action of isoproterenol on the expression of the angiotensinogen gene in opossum kidney proximal tubular cells.

BACKGROUND: beta-adrenoceptors are present in the renal proximal tubules. We have previously reported that isoproterenol stimulates the accumulation of intracellular cAMP and the expression of the angiotensinogen (ANG) gene in opossum kidney (OK) proximal tubular cells via the beta 1-adrenoceptor. We hypothesized that the molecular mechanism(s) of action of isoproterenol on the expression of the ANG gene is mediated via the interaction of the phosphorylated cAMP-responsive element binding protein (CREB) and the cAMP-responsive element (CRE; that is, ANG N-806/-779) in the 5'-flanking region of the rat ANG gene. METHODS: The fusion genes containing the putative ANG-CRE of the rat ANG gene inserted upstream of the rat ANG basal promoter (ANG N-53/+18) fused to a human growth hormone (hGH) gene as reporter were stably cotransfected, with or without the plasmid containing the cDNA for 43 kDa CREB, into the OK cells. The effect of various agonists and antagonists of adrenoceptors on the expression of the fusion genes was evaluated by the amount of immunoreactive hGH secreted into the culture medium. The interactions of OK cellular nuclear protein(s) with the ANG N-806/779 were determined by gel mobility shift assays and by Southwestern and Western blot analysis. RESULTS: The addition of isoproterenol, forskolin, or 8-Bromo-cAMP (8-Br-cAMP) stimulated the expression of pOGH (ANG N-806/-779/-53/+18) by 135, 150, and 160%, respectively, but not mutants of the ANG N-806/-779. The stimulatory effect of isoproterenol was blocked in the presence of propranolol, Rp-cAMP, and atenolol, but not by the presence of stauro-sporine, U73122, and ICI 118,551. Transient transfection of the plasmid containing the cDNA for the catalytic subunit of protein kinase A further enhanced the stimulatory effect of 43 kDa CREB on the expression of the fusion gene. The gel mobility shift assays revealed the the nuclear protein(s) of OK cells binds to the radioactive-labeled ANG N-806/-779. The binding of the labeled ANG N-806/-779 to the OK cell nuclear protein(s) was displaced by unlabeled ANG N-806/-779, but not by the CRE of the somatostatin gene, the CRE of the tyrosine amino-transferase gene, or the mutants of the ANG N-806/-779. Southwestern blot analysis revealed that the labeled ANG N-806/-779 binds to two nuclear species of 43 and 35 kDa proteins. Western blot analysis, however, revealed that rabbit polyclonal antibodies against the 43 kDa CREB interacted with only the 43 kDa molecular species but not with the 35 kDa species. CONCLUSION: These studies demonstrate that the stimulatory effect of isoproterenol on the expression of the ANG gene may be mediated, at least in part, via the interaction of the phosphorylated CREB and the CRE in the 5'-flanking region of the rat ANG gene. The novel 35 kDa nuclear protein that is immunologically different from the 43 kDa CREB may also play a role in the expression of the ANG gene.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Integrin alphavbeta3-RGDS interaction mediates fibrin-induced morphological changes of glomerular endothelial cells.

BACKGROUND: In our previous studies, we found that intraglomerular deposition of fibrin and its metabolites was related to glomerular sclerosis and reduced renal function. It has been reported that both overlying and underlying fibrin may induce specific morphological changes of cultured endothelial cells from large blood vessels. The dependency of these morphological changes on the integrin alphavbeta3-arginyl-glycyl-aspartyl-serine (RGDS) interaction is still controversial. We hypothesized that glomerular endothelial cells (GECs) stimulated by fibrin might undergo morphological changes through an integrin alphavbeta3-RGDS interaction. Methods. In vitro studies were performed to examine the growing status of GECs stimulated by overlying and underlying fibrin gels in the presence or absence of the following: 50 microg/ml anti-alphavbeta3 integrin monoclonal antibody 23C6 or nonimmune mouse IgG, 1 mg/ml synthetic RGDS or arginyl-glycyl-glycyl-serine (RGGS) peptide, 10 mg/ml sodium heparin, 100 microg/ml cycloheximide, and 10 microM actinomycin D. Fast protein liquid chromatography (FPLC)-purified fibrinogen and the third to fifth passages of human GECs were also used in this study. RESULTS: GECs developed capillary tube structure after 60 hours of culturing on fibrin gels, and GECs cultured on gelatin-coated plates displayed a monolayer of cobblestone-like cells in the presence or absence of 23C6 and synthetic RGDS peptide. Fibrin-induced capillary tube formation was promoted by 23C6 and inhibited by RGDS peptide, cycloheximide, and actinomycin D. Disorganization of the GEC monolayer was induced by overlying fibrin, but was not induced by overlying agarose gels and glass cover slips or culturing in fibrinogen, 0.05 NIH U/ml thrombin, fibrin supernatants, as well as in fibrin degradation products. Disorganization of GEC monolayer can be induced by both des-AA-fibrin and des-AABB-fibrin and was unaffected by heparin. Furthermore, both 23C6 and synthetic RGDS peptide prevented disorganization of GECs induced by overlying fibrin, whereas nonimmune mouse IgG, synthetic RGGS peptide, cycloheximide, and actinomycin D had no similar effect. CONCLUSIONS: GECs cultured on fibrin gels may develop capillary structure spontaneously, and GECs covered by fibrin gels may undergo disorganization. Our data suggest that these GEC morphological changes are mediated by an integrin alphavbeta3-RGDS interaction.

Antibodies, Monoclonal↗
PubMed1999

Effect of smoking and histological gastritis severity on the rate of H. pylori eradication with omeprazole, amoxicillin, and clarithromycin.

BACKGROUND: The combination of omeprazole, amoxicillin, and clarithromycin is a common regimen against Helicobacter pylori. Several recent studies have shown that smoking, high intragastric acidity, and the degree of histological gastritis are associated with H. pylori eradication failure. MATERIALS AND METHODS: One hundred and thirty-seven H. pylori-positive patients were treated with a 1-week regimen composed of omeprazole, 20 mg once daily; amoxicillin, 500 mg; and clarithromycin, 200 mg thrice daily. Success of the treatment was evaluated by histology and the 13C-urea breath test at least 4 weeks after completion of therapy. Data about age, gender, alcohol intake, smoking habits, and previous proton pump inhibitor intake were collected in patient interviews. We evaluated fasting gastric pH and the degree of histological gastritis before eradication of H. pylori. RESULTS: The overall eradication of H. pylori at 4 weeks was successful in 98 of 137 patients (72%). On the multivariate analysis, a low grade of inflammation in the antrum (p </=.01; 95% confidence interval [CI], 2.34-16.75), low grade of activity in the fundus (p </=.05; 95% CI, 1.31-9.65), and smoking (p </=.05; 95% CI, 1.27-6.82) were the significant independent factors predicting treatment failure. CONCLUSIONS: These findings indicate that H. pylori eradication therapy with omeprazole, amoxicillin, and clarithromycin is less effective in patients who smoke and more effective in patients with high scores of antral inflammation and fundal activity at baseline biopsy.

Adult↗
PubMed1999

Physical map of the region surrounding the ataxia-telangiectasia gene on human chromosome 11q22-23.

Ataxia telangiectasia (A-T) is an autosomal recessive disease affecting multiple systems, including the development of the cerebellum and thymus. This results in a progressive cerebellar ataxia with onset between 1-3 years, telangiectasia occurs within the subsequent 3-5 years. We localized the A-T gene by linkage analysis to chromosome 11q22-23, between the markers D11S384, and D11S535, and constructed a series of contigs using three BACs and twelve cosmids, spanning a region of approximately 400 kb. We developed a set of sequence-tagged site (STS) markers from the ends of the BACs and cosmids. The A-T gene was isolated from within this region. It is now possible to precisely orient specific BACs, cosmids, and STSs with respect to the exons of the A-T gene (ATM). We anticipate that this information will be useful for further studies of functional domains and regulatory elements within the ATM gene, as well as for other genes in this region. In addition, these clones can be used for FISH studies of deletions, translocations and for loss of heterozygosity in various tumors.

Ataxia Telangiectasia↗
PubMed1999

Endocytosis deficiency of epidermal growth factor (EGF) receptor-ErbB2 heterodimers in response to EGF stimulation.

Epidermal growth factor (EGF) stimulates the homodimerization of EGF receptor (EGFR) and the heterodimerization of EGFR and ErbB2. The EGFR homodimers are quickly endocytosed after EGF stimulation as a means of down-regulation. However, the results from experiments on the ability of ErbB2 to undergo ligand-induced endocytosis are very controversial. It is unclear how the EGFR-ErbB2 heterodimers might behave. In this research, we showed by subcellular fractionation, immunoprecipitation, Western blotting, indirect immunofluorescence, and microinjection that, in the four breast cancer cell lines MDA453, SKBR3, BT474, and BT20, the EGFR-ErbB2 heterodimerization levels were positively correlated with the ratio of ErbB2/EGFR expression levels. ErbB2 was not endocytosed in response to EGF stimulation. Moreover, in MDA453, SKBR3, and BT474 cells, which have very high levels of EGFR-ErbB2 heterodimerization, EGF-induced EGFR endocytosis was greatly inhibited compared with that in BT20 cells, which have a very low level of EGFR-ErbB2 heterodimerization. Microinjection of an ErbB2 expression plasmid into BT20 cells significantly inhibited EGF-stimulated EGFR endocytosis. Coexpression of ErbB2 with EGFR in 293T cells also significantly inhibited EGF-stimulated EGFR endocytosis. EGF did not stimulate the endocytosis of ectopically expressed ErbB2 in BT20 and 293T cells. These results indicate that ErbB2 and the EGFR-ErbB2 heterodimers are impaired in EGF-induced endocytosis. Moreover, when expressed in BT20 cells by microinjection, a chimeric receptor composed of the ErbB2 extracellular domain and the EGFR intracellular domain underwent normal endocytosis in response to EGF, and this chimera did not block EGF-induced EGFR endocytosis. Thus, the endocytosis deficiency of ErbB2 is due to the sequence of its intracellular domain.

Breast Neoplasms↗
PubMed1999

An esophagogastroduodenal anastomosis model for esophageal adenocarcinogenesis in rats and enhancement by iron overload.

The aim of this study is to establish a good animal model for esophageal adenocarcinoma (EAC) and to test the hypothesis that iron over-nutrition enhances EAC formation. With rats, esophagogastroduodenal anastomosis (EGDA) was accomplished by anastomosing the duodenum to the gastroesophageal junction. Iron supplementation was given by i.p. injection of iron dextran (4 mg Fe/kg/week). This model mimics the development of human EAC by introducing mixed reflux of gastric and duodenal contents. At 40 weeks after surgery, the body weight, food intake, hemoglobin, total serum iron, transferrin saturation, serum albumin, and plasma levels of alpha-tocopherol, gamma-tocopherol and retinol of the EGDA rats were not significantly different from those of the non-operated controls. The animals generally had only mild esophagitis, except that the area surrounding the anastomosis opening had more severe esophagitis. Columnar-lined esophagus (CLE), CLE with dysplasia, and EAC were diagnosed in 53.5, 34.9 and 25.6%, respectively, of the 43 rats. Intraperitoneal iron supplementation significantly enhanced esophageal lesions with CLE, CLE with dysplasia, and EAC to 78.0, 53. 7 and 53.7%, respectively, of the 41 rats. All the tumors were well-differentiated mucinous adenocarcinomas at the squamocolumnar junction area, where most iron deposition was observed. EGDA avoids nutritional problems seen in other animal models for EAC. We believe that direct anastomosis of squamous epithelium to columnar epithelium and mixed reflux of gastric and duodenal contents lead to the formation of CLE and EAC. With this model, we demonstrated that iron supplementation significantly enhanced EAC formation, suggesting that iron over-nutrition could also be a risk factor for human EAC.

Adenocarcinoma, Mucinous↗
PubMed1999

Attitudes toward anti-tobacco policy among California youth: associations with smoking status, psychosocial variables and advocacy actions.

To prevent smoking and exposure to environmental tobacco smoke, California has implemented anti-tobacco policies, including laws restricting youth access to tobacco, and smoking bans in workplaces, schools, restaurants and bars. Although studies have examined adults' attitudes toward anti-tobacco policies, little is known about adolescents' awareness of and support for these policies. This study examined attitudes toward anti-tobacco policies in a sample of 6887 10th grade California adolescents. Awareness of anti-tobacco policies was highest among current smokers and lowest among susceptible never-smokers. Support for anti-tobacco policies was highest among non-susceptible never-smokers and lowest among current smokers. Policy awareness and support were significantly associated with psychosocial tobacco-related variables (e.g. perceived consequences of smoking, friends' smoking, perceived access to cigarettes, prevalence estimates of smoking among peers, cigarette offers and cigarette refusal self-efficacy). Policy awareness and support were associated with the probability of performing advocacy actions against tobacco use. Although these results cannot prove a causal association, they suggest that adolescents' attitudes toward anti-tobacco policies may play a role in their decisions about smoking. Tobacco control and education programs should include information about existing anti-tobacco policies, and should educate youth about the importance and benefits of anti-tobacco policies.

Adolescent↗
PubMed1999

The effect of sennosides on bacterial translocation and survival in a model of acute hemorrhagic pancreatitis.

Bacterial translocation leading to subsequent infectious complications is a significant determinant of outcome in acute hemorrhagic pancreatitis (AHP). The colonic ileus and impaired intestinal barrier function that often accompany AHP may predispose to translocation. Sennoside is a naturally occurring cathartic and choleretic agent that stimulates intestinal mucous secretion and has potent promotility effects. The impact of sennoside-induced intestinal motility and secretory function on bacterial translocation and survival was studied in a rat model of AHP. Severe acute pancreatitis was induced in rats by the intraductal infusion of 2% sodium deoxycholate (DCA, 0.4 ml/kg). A group of sham-operated rats (group A) received intraductal saline, whereas experimental animals were subsequently administered distilled water (group B) or sennoside solution (group C) by gavage every 8 h. After 48 h, intestinal transit of fluorescein isothiocyanate-labeled dextran, serum endotoxin, and amylase levels, and bacterial translocation to mesenteric lymph nodes (MLNs) and pancreatic tissue were determined. The pancreas and intestine were sampled for histologic study. All group A animals survived and did not develop pancreatitis or endotoxemia, whereas groups B and C all demonstrated severe hemorrhagic pancreatitis with evidence of necrosis. Mortality at 48 h was 55% in group B versus 12.5% in group C. Inhibition of intestinal motility was noted in 40% versus 20%, and endotoxin levels were 61.36+/-28.26 pg/L versus 5.41+/-3.58 pg/L in group B versus group C rats, respectively (p<0.001). Pancreatic tissue and MLN cultures were positive in 100% of group B survivors versus 14% of group C survivors (p<0.05). Histologic examination of the intestine in group C animals showed increased mucous secretion, proliferation of goblet cells, and evidence of rapid turnover/renewal of enterocytes. Treatment with the cathartic agent, sennoside, reduced translocation of endotoxin and bacteria, restored intestinal motility, increased mucous secretion, and reduced mortality in a model of acute hemorrhagic pancreatitis in the rat. Other cathartics may have similar properties and may be useful in preventing infectious complications in acute pancreatitis.

Acute Disease↗
PubMed1999

New thermal wave aspects on burn evaluation of skin subjected to instantaneous heating.

Comparative studies on the well-known Pennes' equation and the newly developed thermal wave model of bioheat transfer (TWMBT) were performed to investigate the wave like behaviors of bioheat transfer occurred in thermal injury of biological bodies. The one-dimensional TWMBT in a finite medium was solved using separation of variables and the analytical solution showed distinctive wave behaviors of bioheat transfer in skin subjected to instantaneous heating. The finite difference method was used to simulate and study practical problems involved in burn injuries in which skin was stratified as three layers with various thermal physical properties. Deviations between the TWMBT and the traditional Pennes' equation imply that, for high flux heating with extremely short duration (i.e., flash fire), the TWMBT which accounts for finite thermal wave propagation may provide realistic predictions on burn evaluation. A general heat flux criterion has been established to determine when the thermal wave propagation dominates the principal heat transfer process and the TWMBT can be used for tissue temperature prediction and burn evaluation. A preliminary interpretation on the mechanisms of the wave like behaviors of heat transfer in living tissues was conducted. The application of thermal wave theory can also be possibly extended to other medical problems which involve instantaneous heating or cooling.

Body Temperature↗
PubMed1999

Typhoon hazards in the Shanghai area.

There are three major typhoon hazards that apply to the Shanghai area. First, galeforce winds can damage buildings and service facilities. The most severe damage from this occurs only when a typhoon strikes Shanghai directly. Second, both the urban and rural sections of Shanghai are liable to flooding during typhoon seasons. These floods occur when typhoon-induced storm surges coincide with high spring tides and meet with high discharges from the river network as a result of the typhoon downpours. Third, typhoon-induced torrential rain has caused waterlog hazards, particularly in the most densely populated parts of Shanghai. The waterlog hazard has been exacerbated by land subsidence and poor management of pumping systems. In order to prevent disasters happening and reduce the scale of damage, the government has issued construction guidelines and invested in flood defences. Further measures are to be brought in including engineering projects, educational programmes and insurance policies.

China↗
PubMed1999

PCR-based genotyping of epidemic and preepidemic Trichoderma isolates associated with green mold of Agaricus bisporus.

We used randomly amplified polymorphic DNA (RAPD)-PCR to estimate genetic variation among isolates of Trichoderma associated with green mold on the cultivated mushroom Agaricus bisporus. Of 83 isolates examined, 66 were sampled during the recent green mold epidemic, while the remaining 17 isolates were collected just prior to the epidemic and date back to the 1950s. Trichoderma harzianum biotype 4 was identified by RAPD analysis as the cause of almost 90% of the epidemic-related episodes of green mold occurring in the major commercial mushroom-growing region in North America. Biotype 4 was more closely allied to T. harzianum biotype 2, the predominant pathogenic genotype in Europe, than to the less pathogenic biotype 1 and Trichoderma atroviride (formerly T. harzianum biotype 3). No variation in the RAPD patterns was observed among the isolates within biotype 2 or 4, suggesting that the two pathogenic biotypes were populations containing single clones. Considerable genetic variation, however, was noted among isolates of biotype 1 and T. atroviride from Europe. Biotype 4 was not represented by the preepidemic isolates of Trichoderma as determined by RAPD markers and PCR amplification of an arbitrary DNA sequence unique to the genomes of biotypes 2 and 4. Our findings suggest that the onset of the green mold epidemic in North America resulted from the recent introduction of a highly virulent genotype of the pathogen into cultivated mushrooms.

Agaricus↗