This study was conducted to identify the Colletotrichum species causing anthracnose disease of strawberry in Balgladesh and to evaluate in vitro activity of commercial fungicides it. Based on morphological and cultural characteristics, all 22 isolates were identified as Colletotrichum gloeosporioides. They developed white or glittery colonies with grey to dark grey reverse colony colors and they produced cylindrical conidia. The efficacy of five commercial fungicides, Bavistin DF, Dithane M-45, Sulcox 50 WP, Corzim 50 WP and Rovral 50 WP, were tested against the fungus. Bavistin inhibited radial growth completely and was followed in efficacy by Dithane M-45. In Bavistin DF treated media, the fungus did not produce conidia. The percent inhibition of radial growth of the fungus was increased with the increasing concentrations of fungicide.
Aminoimidazole Carboxamide ; Bangladesh ; Benzimidazoles ; Carbamates ; Colletotrichum ; Cultural Characteristics ; Fragaria ; Fungi ; Humans ; Hydantoins ; Maneb ; Spores, Fungal ; Zineb

OBJECTIVE1-Bromo-3-chloro-5,5-dimethylhydantoin (BCDMH) is a solid oxidizing biocide for water disinfection. The objective of this study was to investigate the toxic effect of BCDMH on zebrafish.

METHODSThe developmental toxicity of BCDMH on zebrafish embryos and the dose-effect relationship was determined. The effect of BCDMH exposure on histopathology and tissue antioxidant activity of adult zebrafish were observed over time.

RESULTSExposure to 4 mg/L BCDMH post-fertilization was sufficient to induce a number of developmental malformations, such as edema, axial malformations, and reductions in heart rate and hatching rate. The no observable effects concentration of BCDMH on zebrafish embryo was 0.5 mg/L. After 96 h exposure, the 50% lethal concentration (95% confidence interval (CI)) of BCDMH on zebrafish embryo was 8.10 mg/L (6.15-11.16 mg/L). The 50% inhibitory concentration (95% CI) of BCDMH on hatching rate was 7.37 mg/L (6.33-8.35 mg/L). Histopathology showed two types of responses induced by BCDMH, defensive and compensatory. The extreme responses were marked hyperplasia of the gill epithelium with lamellar fusion and epidermal peeling. The histopathologic changes in the gills after 10 days exposure were accompanied by significantly higher catalase activity and lipid peroxidation.

CONCLUSIONThese results have important implications for studies on the toxicity and use of BCDMH and its analogs.

Animals ; Antioxidants ; metabolism ; Disinfectants ; toxicity ; Dose-Response Relationship, Drug ; Embryo, Nonmammalian ; drug effects ; Hydantoins ; toxicity ; Time Factors ; Water ; chemistry ; Water Pollutants, Chemical ; toxicity ; Zebrafish

Hydantoin-utility-enzyme is widely used in enzymic production of various amino acids. One of its component, carbamoylase, is responsible for the conversion of N-carbamylamino acids to corresponding amino acids, which is crucial for the stereoselectivity and rate limiting. To improve the production of the enzyme, an L-N-carbamoylase gene from Arthrobacter BT801, a hydantoinase producting strain being able to convert 5-benzylhydantoin to phenylalanine, was cloned into E. coli. The gene was highly expressed in E. coli M15 under control of T5 promoter. A protein band about 44kD was detected by SDS-PAGE in the recombinant cell lysate. The objective product, which is principally in soluble form, represented 40% of total cell protein. The N-carbamoylase specific activity of the recombinant M15/pQE60- hyuC is 53 times higher than that of Arthrobacter BT801. The total biotransformation activity increased 8.1 times when. M15/pQE60-hyuC was added into the Arthrobacter BT801 reaction system. The successful expression of the enzyme is significant for the application of the hydantoinase producing strain or the enzyme thereof.
Amidohydrolases ; genetics ; metabolism ; Arthrobacter ; enzymology ; genetics ; Electrophoresis, Polyacrylamide Gel ; Escherichia coli ; genetics ; metabolism ; Genetic Vectors ; genetics ; Hydantoins ; metabolism ; Models, Genetic ; Phenylalanine ; metabolism ; Plasmids ; genetics ; Polymerase Chain Reaction

Amiodarone ; therapeutic use ; Anti-Arrhythmia Agents ; classification ; therapeutic use ; Arrhythmias, Cardiac ; drug therapy ; Child ; Clinical Trials as Topic ; Humans ; Hydantoins ; Imidazoles ; therapeutic use ; Imidazolidines ; Phenethylamines ; therapeutic use ; Piperazines ; therapeutic use ; Sulfonamides ; therapeutic use

Due to the complicated pathogenesis of cardiac arrhythmia, the safe and effective therapeutic strategies for cardiac arrhythmia remain an urgent medical problems in the recent years. In this paper, we introduced the research practice of anti-arrhythmic agents targeting on potassium ion channel. The research progress of anti-arrhythmic agents in up-to-date literatures were also reviewed and prospected.
Amiodarone ; analogs & derivatives ; chemistry ; pharmacology ; therapeutic use ; Animals ; Anti-Arrhythmia Agents ; chemistry ; pharmacology ; therapeutic use ; Arrhythmias, Cardiac ; drug therapy ; physiopathology ; Humans ; Hydantoins ; Imidazolidines ; chemistry ; pharmacology ; therapeutic use ; Molecular Structure ; Piperazines ; chemistry ; pharmacology ; therapeutic use ; Potassium Channel Blockers ; pharmacology ; therapeutic use ; Potassium Channels ; drug effects

OBJECTIVETo evaluate the antiandrogenic effect of heterocyclic fungicide dimethachlon and its mechanism.

METHODSA combination of in vivo and in vitro assays was selected. Hershberger assay was used to determine the antiandrogenic potential of dimethachlon in vivo. Six-week-old castrated male SD rats were administrated once daily for 7 days with testosterone propionate (TP, 100 micro g/d, sc) plus gavage doses of dimethachlon (50, 100 or 200 mg x kg(-1) x d(-1)), or procymidone (150 or 300 mg x kg(-1) x d(-1), positive control), or iprodione (100 mg x kg(-1) x d(-1), positive control), or flutamide (50 mg x kg(-1) x d(-1), positive control). Transcriptional activation assay in vitro was employed to determine the mechanism of antiandrogenic activity of dimethachlon. Human hepatoma liver cells HepG2 were transiently cotransfected with human androgen receptor (AR) expression plasmid and AR-dependent luciferase report plasmid. Transfected cells were exposed to various concentrations of dimethachlon or flutamide with or without dihydrotestosterone to induce the expression of luciferase gene.

RESULTSIn Hershberger assay, dimethachlon, as well as other known antiandrogens, caused decrease in weight of androgen dependent organs or tissues. In 200 mg/kg group, the weight of seminal vesicle, ventral prostate, dorsolateral prostate, Cowper's gland, and levator ani plus bulbocavernosus muscles decreased by 57.8%, 44.8%, 43.9%, 30.1%, and 34.1% respectively, but did not decrease in the vehicle control group. The order of their antiandrogenic potencies was: flutamide > procymidone > dimethachlon > iprodione. In transcriptional activation assay, dimethachlon could inhibit dihydrotestosterone-dependent AR activity in transfected HepG2 cells in dose-effect relationship. The inhibiting potency of dimethachlon was about 1/100 of that of flutamide.

CONCLUSIONDimethachlon has antiandrogenic effect, and acts as an AR antagonist. Its antiandrogenic potency is lower than flutamide and procymidone, but higher than iprodione.

Aminoimidazole Carboxamide ; analogs & derivatives ; pharmacology ; toxicity ; Androgen Antagonists ; pharmacology ; toxicity ; Androgens ; blood ; metabolism ; Animals ; Body Weight ; drug effects ; Bridged Bicyclo Compounds ; pharmacology ; toxicity ; Cell Line, Tumor ; Chlorobenzenes ; pharmacology ; toxicity ; Dose-Response Relationship, Drug ; Flutamide ; pharmacology ; toxicity ; Fungicides, Industrial ; pharmacology ; toxicity ; Humans ; Hydantoins ; Luciferases ; genetics ; metabolism ; Male ; Pesticides ; pharmacology ; toxicity ; Plasmids ; genetics ; Rats ; Rats, Sprague-Dawley ; Receptors, Androgen ; drug effects ; genetics ; metabolism ; Succinimides ; pharmacology ; toxicity ; Transfection

No abstract available.
Phenytoin* ; Rhabdomyolysis*

No abstract available.
Phenytoin* ; Rhabdomyolysis*

No abstract available.
Phenytoin* ; Stevens-Johnson Syndrome*

It is important to predict time to reach therapeutic concentration in phenytoin toxicity. In tradition, frequent drug monitoring is inevitable until the therapeutic serum level is reached. A method of estimating Vmax and Vd of phenytoin with application to estimating time to reach therapeutic concentration of phenytoin is described. We evaluated the usefulness of that method in twelve patients with phenytoin toxicity whose initial levels ranging from 27.7 to 74.0 ug/ml. We compaired the observed time defined as the time of returning from the initial toxic level to the optimum therapeutic level by serial measurement of serum concentration with the calculated time by using the modified Michaelis-Menten equation (Km x In (C1/C2) +Cl-C2=Vmax/vd x T). We determined individual patient's Vmax (maximal metabolic rate of concentration), Vd(volume of distribution of concentration), and Km(constants of Michaelis-Menten equation) for phenytoin, using data obtained from two consecutive serum concentration and known value of Km in Korean. And then, we calculated the decline time of phenytoin. The calculated decline time did not differ significantly from observed decline time (P=0.830). It is possible to predict the time to the therapeutic range and to reduce the unnecessarily frequent drug monitoring.
Drug Monitoring ; Humans ; Phenytoin*