Interpretative study of Vedanta philosophy of Brahmasūtra of Bādarāyaṇa.

Chiefly on spiritual life and ethics in Hinduism, as reflected in the works of Rāmadāsa, 1608-1681, Marathi saint.

"In the present work at attempt has been made to point out that according to Dharmakīrti continued significance and relevance of Buddha's philosophy could be legitimately hoped to be brought out with reference to paradigmaticity of emprical [i.e., empirical] world, the problem of pain and auffering [i.e., suffering] coming to human lot and doctrine of Anattā."--Page 4.

Rett syndrome (RTT) is an X‐linked dominant neurodevelopmental disorder affecting almost exclusively girls. Although mutations in methyl‐CpG‐binding protein (MeCP2) are known to be associated with RTT, gene expression patterns are not significantly altered in MeCP2‐deficient cells. A recent study1 identified MeCP2‐mediated histone modification and formation of a higher‐order chromatin loop structure specifically associated with silent chromatin at the Dlx5–Dlx6 locus in normal cells, and its absence thereof in RTT patients. This altered expression of Dlx5 through loss of silent chromatin loop (...) formation provides a molecular mechanism underlying RTT and proposes a novel role for MeCP2 in chromatin organization and imprinting. © 2005 Wiley Periodicals, Inc. BioEssays 27:676–680, 2005. © 2005 Wiley Periodicals, Inc. (shrink)

Silencing of tumor suppressor genes (TSGs), by DNA methylation, is well known in adult cancers. However, based on the “stem cell” theory of tumorigenesis, the early epigenetic events arising in malignant precursors remain unknown. A recent report1 demonstrates that, while pluripotent embryonic stem cells lack DNA methylation and possess a “bivalent” pattern of activating and repressive histone marks in numerous TSGs, analogous multipotent malignant cells derived from germ cell tumors (embryonic carcinoma cells) gain additional silencing modifications to those same genes. (...) These results suggest a possible mechanism by which aberrant differentiation, mediated by histone and DNA methylation, instigates tumor progression. BioEssays 29:842–845, 2007. © 2007 Wiley Periodicals, Inc. (shrink)