Biomedical subjects

B Madhukar

Publications and source records attributed to B Madhukar.

5 recordsLinked to original sources

PubMed1997

Considerations on genetic and environmental factors that contribute to resistance or sensitivity of mammals including humans to toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds. Part 1: Genetic factors affecting the toxicity of TCDD.

The marked species differences in short-term toxicity (30-day LD50) of ca. 10,000 (LD50: guinea pigs ca. 1 microgram/kg body wt and Han/Wistar Kuopio rats more than 9600 micrograms/kg body wt) of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is one of the central issues of the controversies that have developed on the validity of risk assessment strategies for TCDD and related compounds. One of the most challenging issues that toxicologists face today is the identification of genes that contribute to or are responsible for increased resistance or sensitivity to TCDD and related compounds. It is assumed that most, if not all, toxic effects of TCDD are mediated more or less through the binding affinity to the Ah receptor. This hypothesis was extended and tries to explain the differences in sensitivity/resistance of animals including humans to TCDD by their total fat (lipid) content. In this respect the gene or genes which is or are responsible for obesity of mammals including humans are of great interest. An obvious linear positive logarithmic relationship between the oral 30-day LD50 (microgram/kg) of TCDD in different species and strains of mammals and their total body fat content (TBF%) was found: log LD50 = 5.30 x log (TBF)-3.22, or LD50 = 0.000603 x (TBF)5.30. By means of this regression the toxicity of TCDD in mammals including humans of different age and/or body weight can be predicted if their total body fat content is known. Examples of single-gene and polygenic disease models in different mammals, such as nonobese diabetic, diabetic, viable yellow, obese, and fat mice, as well as transgenic mice, and other suitable animal models, such as fatty Zucker rats, Han/Wistar (Kuopio) rats, and minipigs, are discussed, and predicted LD50 values of TCDD in these animals and humans are presented.

Animals↗

PubMed1993

ECG data compression by modeling.

The paper presents a novel algorithm for data compression of single lead electrocardiogram (ECG) data. The method is based on parametric modeling of the discrete cosine transformed ECG signal. Improved high frequency reconstruction is achieved by separately modeling the low and the high frequency regions of the transformed signal. Differential pulse code modulation is applied on the model parameters to obtain a further increase in the compression. Compression ratios up to 1:40 were achieved without significant distortion.

Algorithms↗

PubMed1993

Expression of protein kinase C isozymes in rat glial cell line.

To study the presence and distribution of various isozymes of PKC in glial cells, immunofluorescent studies were performed on a cortical glial cell line cultured derived from rat cerebral cortex and analyzed by a highly sensitive automated laser cytometric device, ACAS-570 (Adherent Cell Analysis and Sorting). The antibodies tested were against alpha, beta, gamma and epsilon isozymes of PKC, and the catalytic domain (cd), i.e. antibody against the cd to all isozymes of PKC. The data indicate that rat cortical glial cell line expresses at least three isozymes of PKC, epsilon, beta, and alpha, the degree of intensity of immunofluorescence being epsilon > beta > alpha. The immunofluorescence for PKC-cd was the most intense.

Animals↗

PubMed1992

Expression of protein kinase C in postischemic brain: an in situ hybridization study.

Cerebral ischemia leads to a number of biochemical and molecular changes which include increase in intracellular calcium, arachidonic acid, and diacylglycerol, all of which are capable of activating protein kinase C (PKC). To investigate how the expression of PKC is affected in postischemic brain, ischemia was produced in gerbils by bilateral common carotid artery occlusion for 10 min followed by reperfusion for 15 min, 6 h, and 24 h. The brains of postischemic and normal control animals were removed, forebrains dissected, fresh frozen, and processed for in situ hybridization. The mRNA expression of PKC was analyzed by using oligonucleotide probes based on the sequences of PKC alpha and epsilon isozymes in this preliminary study. There was no change observed in the expression of PKC alpha in any region of the brain in any of the postischemic groups examined. There was, however, a qualitative increase in the transcription for PKC epsilon in two out of three brains of 15 min postischemic group which continued through 24 h of reperfusion. Since the protein itself was not examined, it can not be said how these observations regarding transcription relate to the synthesis of the protein and whether there are any changes in the subcellular distribution of PKC following ischemia. However, since there was no decrease in transcription demonstrated in our study, it appears that the reported decrease in PKC activity following ischemia is not due to decreased mRNA expression.

Animals↗

PubMed1992

ECG data compression by modeling.

This paper presents a novel algorithm for data compression of single lead Electrocardiogram (ECG) data. The method is based on Parametric modeling of the Discrete Cosine Transformed ECG signal. Improved high frequency reconstruction is achieved by separately modeling the low and the high frequency regions of the transformed signal. Differential Pulse Code Modulation is applied on the model parameters to obtain a further increase in the compression. Compression ratios up to 1:40 were achieved without significant distortion.

Algorithms↗