Academic literature on the topic 'Krittibas'

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Journal articles on the topic "Krittibas"

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Chakravarty, Saumitra. "Defeating Patriarchy on Its Own Terms: The Paradox of Female Chastity in Krittivasa’s Ramayana." Journal of Asian Research 3, no. 2 (March 19, 2019): 70. http://dx.doi.org/10.22158/jar.v3n2p70.

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<em>This essay attempts to analyze the role of women in the Bengali Ramayana of Krittivasa, a regional version of the original Sanskrit epic composed by Valmiki. It does so from the perspective of the strict code of female chastity enshrined in a patriarchal society and enforced upon its women by their male guardians within and beyond the home. While on the one hand, it is an instrument of female subjugation, this essay make an attempt to analyze how the strict observance of this code by the women in the epic, makes it a weapon of female empowerment across the different strata of society through which the text operates. The powerful spiritual energy generated in the process by these women can threaten even the most powerful of patriarchs including the epic hero Rama himself.</em>
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Jamnongsong, Supawan, Patipark Kueanjinda, Piyathida Tawornparcha, Kulthida Vaeteewoottacharn, Seiji Okada, Siwanon Jirawatnotai, Ananya Pongpaibul, Krittiya Korphaisarn, and Somponnat Sampattavanich. "Abstract 6588: Systems biology-based drug repositioning and biomarker discovery for Thai liver fluke-associated cholangiocarcinoma." Cancer Research 83, no. 7_Supplement (April 4, 2023): 6588. http://dx.doi.org/10.1158/1538-7445.am2023-6588.

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Abstract Our group has recently reported the successful use of comprehensive drug response and pan-omic profiling for identifying repurposable drug shortlists in Asian cholangiocarcinoma. We also developed the CCA45 gene-expression signature that could accurately predict the prognosis of CCA patients, especially those with Asian ethnic backgrounds. To further explore therapeutic candidates and potential resistance mechanisms, we have established CCA1 cell lines resistant to their subgroup-specific drug candidates: MEK and SRC inhibitors. Reverse-phase protein arrays (RPPA)-based proteomic profiling revealed upregulation of cell cycle, apoptosis, MAPK, and mTOR-related proteins in both MEKi- and SRCi-resistant cells. Src pathway activity was found to be more significantly reduced in SRCi-resistant cells. We identified CDK4/6 inhibitors as the second-line therapeutic candidates for MEK inhibitor-resistant cells by systematic drug screening. SRCi-resistant cells unexpectedly developed cross-resistance to MEK inhibitors and showed sensitivity to only a few CDK4/6 inhibitors. These data are beneficial for the clinical translation of our proposed drug candidates for Asian CCA, preparing the alternate regimens after drug resistance. We also adopted the DSP-based spatial transcriptomic platform to compare the tumor microenvironment between chemotherapy-sensitive and chemotherapy-resistant CCA patients. While the CTA panel showed consistent patterns of normalized gene expression to those of the WTA panel, the CTA panel can only measure 17 of the 45 genes required for our CCA45 signature. Out of these 17 genes, ITGB4, FGFR3, VEGFC, NOTCH1, and RRAD showed significant gene expression changes with reducing tumor percentage. The microenvironment of gemcitabine/cisplatin responder (R) non-responder (NR) exhibited negative regulation of ERK1/2 and MAPK, high WNT pathway activity, and high tumor-infiltrating lymphocyte (TIL). In contrast, the microenvironment of the non-responder (NR) subgroup showed high neutrophil-related activity, high NFκB, high Treg, and the exhausted immune phenotype. Overall, our study contributes toward realizing the precision medicine concept for CCA patients. Citation Format: Supawan Jamnongsong, Patipark Kueanjinda, Piyathida Tawornparcha, Kulthida Vaeteewoottacharn, Seiji Okada, Siwanon Jirawatnotai, Ananya Pongpaibul, Krittiya Korphaisarn, Somponnat Sampattavanich. Systems biology-based drug repositioning and biomarker discovery for Thai liver fluke-associated cholangiocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6588.
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Tanjak, Pariyada, Amphun Chaiboonchoe, Tharathorn Suwatthanarak, Onchira Acharayothin, Kullanist Thanormjit, Jantappapa Chanthercrob, Thanawat Suwatthanarak, et al. "Abstract 2242: KRAS mutations suppress the tumor immune microenvironment in colorectal cancer." Cancer Research 83, no. 7_Supplement (April 4, 2023): 2242. http://dx.doi.org/10.1158/1538-7445.am2023-2242.

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Abstract Background: KRAS mutations (KRASmut) drive tumorigenesis through various signaling pathways that are associated with worse survival in colorectal cancer patients (CRC). Immune evasion is a hallmark of KRAS-driven cancer, but the role of KRASmut in the regulation of the immune response is unclear, particularly in the tumor microenvironment (TME), which often assists cancer cells to thrive and successfully escape immune surveillance. Here, we explore the immunobiological impacts of KRASmut in CRC patients. Methods: A total of 97 fresh frozen tumor samples were collected from each CRC patient with stage I-IV who underwent surgical treatment at the Department of Surgery, Faculty of Medicine Siriraj Hospital between October 2010 and March 2011. First, all patients were identified KRAS mutational status and compared overall survival (OS) with wild-type KRAS (KRASwt). Next, we analyzed the gene expression profiling of KRASmut which was performed using the Nanostring platform. Finally, we performed the biological network analysis focusing on immunological pathways associated with KRASmut using the Ingenuity Pathway Analysis (IPA). Results: We observed KRASmut in 41.24% (n=40) of the total cases. Mutations occurred primarily in exon 2 (total n=36; codon 12, n=28; codon 13, n=8) and rarely in exon 3 (n=4). Patients with KRASmut CRC in exon 2 and exon 3, showed significantly worse OS compared to KRASwt (HR 1.77, 95% CI 1.07-2.93; P&lt;0.05). Comparing gene expression profiles between KRASmut and KRASwt, found that the survival outcome of patients with KRASmut was correlated with immunosuppressive TME by activation of genes encoded in TGFβ signaling pathway. In addition to activating TGFβ pathway, the gene expression profile of KRASmut also interrupted gene encoded pro-inflammatory cytokines, including TNFRSF12, IRF6, CCR2, CCL8, CCL11, CXCR3 and CXCL10. IPA analysis revealed that differentially expressed genes of KRASmut were significantly enriched in regulation of epithelial mesenchymal transition (EMT) and macrophage-stimulating protein receptor d'origine nantais (MSP-RON) signaling pathways (P value&lt;0.001), which are strongly associated with maintaining the stability of the TME and contributing to immune escape in the immune TME. Conclusions: Our results suggested that KRASmut activated TGFβ and interrupted pro-inflammatory cytokine to suppress tumor immune microenvironment in CRC. Future studies and clinical trials in patients with CRC with KRASmut should take these transcriptional profiles into account. Citation Format: Pariyada Tanjak, Amphun Chaiboonchoe, Tharathorn Suwatthanarak, Onchira Acharayothin, Kullanist Thanormjit, Jantappapa Chanthercrob, Thanawat Suwatthanarak, Bundit Wannasuphaphol, Kemmapon Chumchuen, Bhoom Suktitipat, Somponnat Sampattavanich, Krittiya Korphaisarn, Ananya Pongpaibul, Naravat Poungvarin, Harald Grove, Woramin Riansuwan, Atthaphorn Trakarnsanga, Asada Methasate, Manop Pithukpakorn, Vitoon Chinswangwatanakul. KRAS mutations suppress the tumor immune microenvironment in colorectal cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2242.
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Benjamin, Esther, Gaurav Joshi, Bharathi Rajamani, Krittika Nandy, Shaji Velayudhan, and Poonkuzhali Balasubramanian. "Abstract 3153: Imatinib mesylate treatment improves reprogramming efficiency, and morphology of chronic myeloid leukemia derived induced pluripotent stem cells." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3153. http://dx.doi.org/10.1158/1538-7445.am2022-3153.

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Abstract Chronic myeloid leukemia (CML) is a hematopoietic stem cell disorder characterized by the BCR-ABL1 fusion gene with constitutively active tyrosine kinase activity. Although the tyrosine kinase inhibitors (TKI) have revolutionized the treatment for CML, withdrawal of TKI therapy in patients on deep molecular response causes disease relapse, primarily due to the persistence of leukemic stem cells (LSCs) that are insensitive to TKI. As LSCs are a rare population of cells, it is challenging to understand the molecular basis of the disease relapse to tailor strategies to eliminate them selectively. Induced pluripotent stem cells (iPSCs) derived from primary CML are increasingly used for disease modeling and high through drug screening. Cryopreserved CD34+ from three chronic phase CML patients (n=3) and CD34+ cells from a normal donor after mobilization were expanded in SFEM II supplemented with CD34+ Expansion Supplement (10X) including UM729 for 3-days and were nucleofected with episomal reprogramming plasmids as described previously (Manian et al., 2018). The nucleofection efficiency was 15% in the expanded CD34+ CML and normal cells. While the normal CD34+ cells formed iPSCs with the characteristic flat morphology between 20-24 days, the CML CD34+ cells formed several dome-shaped colonies after 30 days. Two normal CD34+ iPSC colonies continued to maintain their morphology for 12 passages. All the CML iPSC colonies (n=11) expressed the same type of BCR-ABL1 transcript as the CD34+ cells and did not carry any mutations in the BCR-ABL1 kinase domain. However, only three of the 11 CML-iPSC colonies could be maintained without significant differentiation after five passages. They lacked typical iPSC morphology and appeared as small cell aggregates or dome-shaped colonies. To understand whether this atypical morphology of the CML iPSC colonies was due to the expression of the BCR-ABL fusion protein within the cells, the medium was supplemented with 10μM imatinib. There was an increase in cell proliferation rate and gain of typical iPSCs morphology similar to normal iPSCs within two days after adding IM. Withdrawal of IM from the IM-treated CML iPSC resulted in a dome-shaped morphology, reduced proliferation rate, and reduction in TRA1-60 expression after 96 hrs. The CML iPSC cultured in the presence of IM showed significant downregulation of phospho-CRKL, a BCR-ABL1 downstream signaling protein, compared to the colonies cultured in the absence of IM. These results suggest that suppression of BCR-ABL1 by treatment with IM produced stable CML iPSC-like phenotype while IM withdrawal resulted in dome-shaped colonies and pushed the cells towards differentiation. This proof-of-concept study identified a unique CML LSCs mimetic model. It would serve as an excellent platform for screening small molecules to eliminate LSCs as it thrives on TKI therapy. Citation Format: Esther Benjamin, Gaurav Joshi, Bharathi Rajamani, Krittika Nandy, Shaji Velayudhan, Poonkuzhali Balasubramanian. Imatinib mesylate treatment improves reprogramming efficiency, and morphology of chronic myeloid leukemia derived induced pluripotent stem cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3153.
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Karmakar, Bikas. "Decoding the Impact of the Srirama Panchali on Baranagar Temples Facades: The Driving Force behind Terracotta Artisans’ Narrativization of Ramayana Events." Rupkatha Journal on Interdisciplinary Studies in Humanities 13, no. 4 (December 11, 2021). http://dx.doi.org/10.21659/rupkatha.v13n4.39.

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Valmiki Ramayana is one of the most popular, universally read, and widely circulated literary works. The poets of different languages in India ornamented Valmiki’s Sanskrit Ramayana with the vibrancy of their own indigenous languages and cultures. A significant number of such versions trace their roots to Bengal. The epic was first translated into the Bengali language by the great poet Krittibas Ojha. Its influences and popularity have been such as to justify it being called the Bible of the people of Bengal. Its intense undiminished popularity among the populace has also left an indelible impression on the artisans of Bengal and their creations in different eras. The study primarily aims to investigate the Ramayana narratives that have been found on the facades of the temples of Baranagar in Murshidabad, West Bengal, India. The intention is to trace the impact of Krittibas’s Srirama Panchali on the portrayals of the Ramayana episodes. The formal method of Art History has been employed to provide an in-depth description of the formal elements that have been incorporated by the artisans. Besides, a detailed critical inspection of the concerned portrayals has been complemented with literary references to get a lucid understanding of the intended issues.
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"First person – Krittika Sudhakar." Biology Open 11, no. 7 (July 15, 2022). http://dx.doi.org/10.1242/bio.059500.

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ABSTRACT First Person is a series of interviews with the first authors of a selection of papers published in Biology Open, helping early-career researchers promote themselves alongside their papers. Krittika Sudhakar is first author on ‘ Alterations in lifespan and sleep:wake duration under selective monochromes of visible light in Drosophila melanogaster’, published in BiO. Krittika conducted the research described in this article while a PhD student (DST-INSPIRE-senior research fellow) in Dr. Pankaj Yadav's lab at SASTRA University, Tirumalaisamudram, India. She is now a Postdoctoral Fellow in the lab of Dr. Adelheid Lempradl at the Van Andel Institute, Michigan, USA, investigating Deciphering the short and long-term effects of nutrition influences Drosophila physiology, aging and metabolism.
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"First person – Sudhakar Krittika." Biology Open 8, no. 6 (June 6, 2019): bio044966. http://dx.doi.org/10.1242/bio.044966.

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Dissertations / Theses on the topic "Krittibas"

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Dutta, Mitali. "Madhab Kandalee o Krittibaser Ramayan tulanamulak parjalachana মাধব কন্দলী ও কৃত্তিবাসের রামায়ণ তুলনামূলক পর্যালোচনা." Thesis, University of North Bengal, 1994. http://hdl.handle.net/123456789/1767.

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Tongkoom, Krittiya [Verfasser], and Georg [Akademischer Betreuer] Cadisch. "Reconciling indigenous and scientific ecosystem and soil fertility indicators in swidden systems of Northern Thailand / Krittiya Tongkoom ; Betreuer: Georg Cadisch." Hohenheim : Kommunikations-, Informations- und Medienzentrum der Universität Hohenheim, 2021. http://d-nb.info/1238686990/34.

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Books on the topic "Krittibas"

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Division, India Ministry of Information and Broadcasting Publications. Ramayana, Mahabharata and Bhagavata writers: Kamban, Pampa, Nannaya-Tikkana, Madhava Kandali Ekanath, Krittivasa, Sarala Dasa, Potana, Tunchattu Eluttacchan, Tulasi Das, Premananda, Bopadeva. New Delhi: Publications Division, Ministry of Information and Broadcasting, Govt. of India, 2013.

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Krittibas sankalan. Calcutta: Papyrus, 1986.

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Mazumdar, Jashojit Sarma. Devi Durga in Krittivas' Ramayan. Independently Published, 2020.

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Krittivyas birachita sachitra saptakanda Ramayanam. Calcutta: Dey's publishing, 1986.

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Trivedi, Prash. The 27 CELESTIAL PORTALS. Lotus Press, 2005.

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Book chapters on the topic "Krittibas"

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Vanita, Ruth. "Krittivasa Ramayana: The Birth of Bhagiratha (Bengali)." In Same-Sex Love in India, 100–102. New York: Palgrave Macmillan US, 2000. http://dx.doi.org/10.1007/978-1-349-62183-5_12.

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Vanita, Ruth. "Krittivasa Ramayana: The Birth of Bhagiratha (Bengali)." In Same-Sex Love in India, 100–102. New York: Palgrave Macmillan US, 2000. http://dx.doi.org/10.1007/978-1-137-05480-7_12.

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