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Biomedical subjects

J Basak

Publications and source records attributed to J Basak.

16 recordsLinked to original sources
PubMed2001

Learning Hough transform: a neural network model.

A single-layered Hough transform network is proposed that accepts image coordinates of each object pixel as input and produces a set of outputs that indicate the belongingness of the pixel to a particular structure (e.g., a straight line). The network is able to learn adaptively the parametric forms of the linear segments present in the image. It is designed for learning and identification not only of linear segments in two-dimensional images but also the planes and hyperplanes in the higher-dimensional spaces. It provides an efficient representation of visual information embedded in the connection weights. The network not only reduces the large space requirement, as in the case of classical Hough transform, but also represents the parameters with high precision.

Algorithms↗
PubMed1999

Blind separation of a mixture of uniformly distributed source signals: A novel approach.

A new, efficient algorithm for blind separation of uniformly distributed sources is proposed. The mixing matrix is assumed to be orthogonal by prewhitening the observed signals. The learning rule adaptively estimates the mixing matrix by conceptually rotating a unit hypercube so that all output signal components are contained within or on the hypercube. Under some ideal constraints, it has been theoretically shown that the algorithm is very similar to an ideal O(1/T2) convergent algorithm, which is much faster than the existing O(1/T) convergent algorithms. The algorithm has been generalized to take care of the noisy signals by adaptively dilating the hypercube in conjunction with its rotation.

Algorithms↗
PubMed1997

Beta-carotene inhibits rat liver chromosomal aberrations and DNA chain break after a single injection of diethylnitrosamine.

Beta-carotene (BC) has recently been found to possess potent anti-tumour activity in chemically induced rat liver carcinogenesis. In the present study, attempts have been made to understand the basic cytogenetic and molecular mechanism of the anti-tumour effect of BC by monitoring its effect on rat liver chromosomal aberrations (CAs) and DNA chain breaks during the early preneoplastic stage of diethylnitrosamine (DEN)-induced hepatocarcinogenesis in male rats. DNA chain breaks, however, can be detected with great sensitivity by exposing crude cell lysates to alkaline solutions and monitoring the rate of strand unwinding so that one strand break per chromosome can easily be detected. Supplementary BC, in basal diet (120 mg kg[-1]), was given to rats 15 days before carcinogenic threat with DEN. Under these experimental conditions, BC was found to afford a unique protection against DEN-induced CAs 96 h after DEN injection. Long-term treatment with BC also triggered a protective effect on induction of CAs 15, 30 or 45 days after DEN treatment, which was maximal on structural aberrations followed by numerical and physiological types. BC treatment for 15 days before DEN injection was found to offer a significant (P < 0.001) protection in the generation of single-strand breaks compared with DEN control. Thus, BC ranks as a potential chemopreventive agent for the future so far as chemical rat liver carcinogenesis is concerned.

Animal Nutritional Physiological Phenomena↗
PubMed1996

Characterization of the adaptive response to ionizing radiation induced by low doses of X-rays to Vibrio cholerae cells.

Pretreatment with sublethal doses of X-rays induced an adaptive response in Vibrio cholerae cells as indicated by their greater resistance to the subsequent challenging doses of X-irradiation. The adaptive response was maximum following a pre-exposure dose of 1.7 Gy X-rays and an optimum incubation period of 40 min at 37 degrees C. Pre-exposure to a sublethal dose of 1.7 Gy X-rays made the Vibrio cholerae cells 3.38-fold more resistant to the subsequent challenge by X-rays. Pretreatment with a sublethal dose of hydrogen peroxide offered a similar degree of protection to the bacterial cells against subsequent treatment with challenging doses of X-ray radiation. However, exposure of Vibrio cholerae cells to mild heat (42 degrees C for 10 min) before X-ray irradiation decreased their survival following X-irradiation.

Adaptation, Physiological↗
PubMed1996

On the nature of the adaptive response induced by mitomycin C in Vibrio cholerae OGAWA 154 cells.

The induction of an adaptive response in Vibrio cholerae OGAWA 154 cells was obtained using an alkylating agent, mitomycin C, as both stimulating and challenging agent. Cross-adaptive response was observed in V. cholerae cells when pretreated with a sublethal dose of another alkylating agent, N-methyl-N'nitro-N-nitrosoguanidine, followed by challenging treatment with mitomycin C. The dose of mitomycin C for 50% survival (D50) became almost double for mitomycin C pretreated cells and 1.5 times for N-methyl-N-'nitro-N-nitrosoguanidine pretreated cells, compared to nonpretreated cells. It was also shown that pretreatment with a sublethal dose of oxidative DNA damaging agents, viz, hydrogen peroxide or nitrofurantoin, did not show any cross-adaptive response against subsequent challenge by mitomycin C.

Acclimatization↗
PubMed1996

Estimation of single-strand breaks induced in the dried film of DNA by high energy alpha particle from a cyclotron.

DNA extracted and purified from Vibrio cholerae OGAWA 154 cells and prepared in the form of a dry thin film was exposed in air to a beam of alpha particles obtained from a Variable Energy Cyclotron. The number of single-strand breaks per DNA unit exhibited a linear dose-effect relationship indicating the occurrence of single-hit kinetics. The efficiency and yield of alpha-induced single-strand breaks were approximately 72 eV/break and 1.39 respectively.

Alpha Particles↗
PubMed1995

Inter-strand cross-linking of Vibrio cholerae DNA induced by furazolidone: a quantitative assay by four simple methods.

Four simple methods, i.e., (i) UV absorption spectrophotometry, (ii) hydroxyapatite chromatography, (iii) fluorescence analysis of ethidium bromide bound to DNA and (iv) assay of S1 endonuclease action, were used in parallel for the estimation of furazolidone-induced inter-strand cross-links in Vibrio cholerae DNA. The data produced by the four methods were in reasonable agreement with each other and provided similar linear dose-response relations, the correlation (between dose and response) coefficient being in any case numerically greater than 0.98. When the data obtained by four independent methods were plotted in a single graph, the resulting dose-response relation could be described by the equation log NR = 1.41 - 0.54 log D, where NR is the % non-reversible DNA remaining in the cells treated by furazolidone at dose D micrograms/ml x h. The correlation coefficient in this plot was -0.98 and significant to a level better than 0.1%. This study thus brings out that any one of these four methods can be used with reasonable confidence for the diagnosis and assay of inter-strand cross-links in DNA.

Chromatography, Liquid↗
PubMed1994

Induction of adaptive response by nitrofurantoin against oxidative DNA damage in some bacterial cells.

Pretreatment with a sublethal dose of nitrofurantoin did not give any protection to Vibrio cholerae OGAWA 154 (wild-type) cells against subsequent treatment with challenging doses of MNNG and vice versa. However, pretreatment with a sublethal dose of nitrofurantoin offered significant protection to the bacterial cells against subsequent treatment with challenging doses of H2O2 and vice versa. Further, sublethal doses of nitrofurantoin or H2O2 produced almost the same degree of protection against challenges by H2O2 or nitrofurantoin. Both the alkylating agent MNNG and the oxidative agent H2O2 induced adaptive responses in Vibrio cholerae OGAWA 154 cells against subsequent challenge by the respective agents. The experiments presented in this communication revealed that nitrofurantoin produced an adaptive response in bacterial cells against oxidative and not alkylating DNA damage.

Adaptation, Physiological↗
PubMed1992

Adaptive response of Vibrio cholerae and Escherichia coli to nitrofurantoin.

Pretreatment with sublethal doses of nitrofurantoin induced adaptive response in both Vibrio cholerae and Escherichia coli cells as indicated by their greater resistance to the subsequent challenging doses of the same drug. Adaptive response was maximum corresponding to pretreatment drug concentrations of 0.40 microgram/ml and 0.015 microgram/ml respectively for V. cholerae OGAWA 154 (wild type) and E. coli K-12 AB 2463 (recA-) cells. Adaptive response was inhibited by chloramphenicol (100 micrograms/ml) indicating the need of concomitant protein synthesis. Induction of adaptive response in recA deficient E. coli cells indicated that it was different from the conventional "SOS" response. Melting temperature of DNA of V. cholerae cells subjected to adaptive (0.4 microgram/ml for 1 hr) and challenging (120 micrograms/ml for 1 hr) doses of nitrofurantoin (76 degrees C) was closer to that of native DNA (75 degrees C) vis-a-vis DNA isolated from nonadapted and drug treated cells (77.5 degrees C). Also, DNA isolated from V. cholerae cells subjected to adaptive and challenging doses of the drug revealed the presence of fewer interstrand cross-links (16% reversible DNA) vis-a-vis DNA from nonadapted but drug treated cells (55% reversible DNA). Photomicrographic studies revealed that V. cholerae cells that were nonadapted but drug treated grew into long filamentous forms (4.25 +/- 2.97 micron) whereas those subjected to both adaptive and challenge doses of the drug exhibited much less filamentation (2.08 +/- 0.84 micron) vis-a-vis native cells (1.42 +/- 0.5 micron). Similar results on DNA melting temperature, cross-links in DNA, and filamentation of cells were obtained for E. coli AB 2463 (recA-) cells subjected to adaptive and challenging treatments with nitrofurantoin. Almost equal degree of resistance against nitrofurantoin could be induced in both V. cholerae OGAWA 154 (wild type) and E. coli strain PJ3 (AB 1157 ada-) when these cells were pretreated with nontoxic doses of hydrogen peroxide or nitrofurantoin. Evidence obtained in this work on the nature of the nitrofuratoin induced adaptive response with particular references to the oxidative and/or alkylating DNA damages were discussed. Nitrofuratoin induced adaptive response appeared similar to that elicited by furazolidone in V. cholerae cells and appeared to be directed towards oxidative and not alkylating adaptive repair pathway.

Adaptation, Physiological↗
PubMed1990

DNA damage and prophage induction and toxicity of nitrofurantoin in Escherichia coli and Vibrio cholerae cells.

Repair-deficient and repair-proficient strains of E. coli K12 were sensitive to nitrofurantoin treatment to varying degrees with the double mutant strain (uvrA 6, recA 13) being most sensitive. Ultraviolet absorption data and thermal chromatography through a hydroxyapatite column revealed that nitrofurantoin treatment of V. cholerae strain OGAWA 154 produced a maximal amount of 55% reversibly bihelical DNA at a nitrofurantoin dose of 120 micrograms/ml/h, which indicated the formation of inter-strand cross-links in DNA. Nitrofurantoin also produced prophage-lambda induction in E. coli K12 strain GY 5027: envA, uvrB, ampA 1, strA (lambda), in a dose-dependent manner, the maximum induction being highly significant (P less than 0.001). Previously published mutation data coupled with the prophage induction data presented here suggest that the genotoxic properties of nitrofurantoin are mediated through the SOS pathway.

Bacteriophage lambda↗
PubMed1990

DNA damage and cell killing by nitrofurantoin in relation to its carcinogenic potential.

Nitrofurantoin inhibited growth and produced loss of viability of Vibrio cholerae cells in a dose-dependent manner, the 10% (D10) and 37% (D37) survival doses being 18.0 and 5.5 micrograms/ml x hr. respectively. The drug also caused filamentation of the cells in a very significant manner. Ultraviolet absorption data and thermal chromatography through hydroxyapatite column revealed that nitrofurantoin treatment of Vibrio cholerae cells produced a maximum amount of 55% of DNA reversibly bihelical due to the formation of inter-strand cross-links. Helix-coil transition studies carried out by viscometric and also, spectrophotometric methods revealed that the nitrofurantoin-induced cross-links in Vibrio cholerae DNA, imparted to this DNA greater thermal stability than that of native DNA. The quantitative aspect and also the mode of nitrofurantoin action on DNA of Vibrio cholerae and Escherichia coli cells vis-à-vis the carcinogenic potential of the drug were discussed.

Carcinogens↗
PubMed1989

Furazolidone-induced interstrand cross-links in Vibrio cholerae DNA. Study of conformational change by circular dichroism.

Vibrio cholerae DNA bearing furazolidone-induced interstand cross-links show a change in the characteristic circular dichroism spectra of the DNA itself in dilute buffer. The change in c.d. spectra was characterized by a shift of the positive band around 272 nm to lower wavelength and a loss of ellipticity of the negative band around 242 nm, and is similar to that exhibited by mitomycin linked Vibrio cholerae DNA under identical conditions and is suggestive of a conformational change of DNA bearing such cross-links. Both furazolidone-induced and mitomycin-induced cross-linking of Vibrio cholerae DNA inhibited the salt-induced conformation change, i.e. increase in winding angle of DNA, the percentage inhibition being greater for mitomycin-linked DNA.

Buffers↗
PubMed1987

DNA damage by 5-nitro-2-furylacrylic acid, a nitrofuran derivative.

5-Nitro-2-furylacrylic acid (5-NFA) caused dose dependent inhibition of growth of Escherichia coli K-12 strain AB 2480 (uvr-, rec-), the 37% (D37) and 10% (D10) survival doses being 1.0 microgram/ml.h and 1.75 micrograms/ml.h, respectively. Although much higher doses of drug were required to achieve comparable inhibition of growth of E. coli strain 1157 (repair proficient), significant filamentation of these cells was produced by treatment with 1.0 microgram/ml 5-NFA for 4 hr. Ultraviolet absorption data and thermal chromatography through hydroxyapatite (HAP) column revealed that 5-NFA treatment of E. coli strain AB 2480 produced more than 80% of DNA reversibly bihelical due to the formation of interstrand cross-links and the initial part of the reaction obeyed a first order relation. 5-NFA also produced dose-dependent increase of prophage induction in E. coli strain GY 5027: envA, uvrB, ampA1, strA (lambda). The implications of the action of 5-NFA on DNA in relation to the induction of 'SOS' functions and carcinogenesis were discussed.

Acrylates↗
PubMed1983

DNA damage, prophage induction and mutation by furazolidone.

Ultraviolet absorption data and thermal chromatography through hydroxyapatite (HAP) column revealed that furazolidone treatment of Vibrio cholerae cells produced more than 80% of DNA reversibly bihelical due to the formation of interstrand cross-links and the reaction obeyed a first order relation. Sensitivities of the Escherichia coli strains to the lethal action of the drug were in the order: AB 2480(uvr- rec-) greater than AB 2463(rec-) greater than AB 1886(uvr-) greater than AB 1157(repair proficient) or AB 4401(wild type). Furazolidone was 'Rec test' positive, produced dose-dependent prophage induction in E. coli cells and also dose-dependent streptomycin-resistance forward mutation in V. cholerae cells. The quantitative aspect and also the mode of furazolidone action on DNA were discussed.

DNA Repair↗
PubMedDate not supplied

The effect of three different ranitidine dosage regimens on reducing gastric acidity and volume in ambulatory surgical patients.

STUDY OBJECTIVE: To evaluate three different preoperative oral dosing regimens of ranitidine in ambulatory patients who had significant risk of aspiration pneumonitis (gastric pH < or = 2.5 or volume > or = 25 ml at intubation or extubation). DESIGN: Double-blind, placebo-controlled, randomized trial. SETTING: St. Francis Hospital of Buffalo, New York. PATIENTS: Two hundred seventy-one ambulatory patients about to undergo a surgical procedure under general anesthesia, of whom 241 (89%) completed the trial and were considered evaluable. INTERVENTIONS: Patients were randomly assigned to receive one of four regimens administered orally before surgery: placebo at bedtime the night before and in the morning on the day of surgery; ranitidine 150 mg at bedtime and in the morning; ranitidine 150 mg at bedtime and placebo in the morning; or ranitidine 300 mg at bedtime and placebo in the morning. MEASUREMENTS AND MAIN RESULTS: Patients who received ranitidine 150 mg twice/day, ranitidine 150 mg at bedtime, or ranitidine 300 mg at bedtime had a significantly (p < 0.05) lower frequency of a gastric pH 2.5 or below at intubation or extubation than those taking placebo twice/day (3%, 45%, and 31%, respectively, vs 86%). In addition, gastric volume at intubation or extubation was 25 ml or above in significantly fewer patients receiving ranitidine 150 mg at bedtime than placebo (37% vs 13%, p < 0.05). Overall, the number of patients with risk factors for aspiration pneumonitis was significantly lower with ranitidine 150 mg twice/day (20%), ranitidine 150 mg at bedtime (48%), and ranitidine 300 mg at bedtime (35%) than placebo (86%) (p < 0.001), and significantly lower with ranitidine 150 mg twice/day than ranitidine 150 mg at bedtime (p < 0.05). CONCLUSIONS: Ranitidine 150 mg twice/day preoperatively reduced to the greatest degree the percentage of patients who developed significant risk factors for aspiration pneumonitis after surgery under general anesthesia.

Ambulatory Surgical Procedures↗