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Regulation of autonomic functions following two high frequency yogic breathing techniques
Joydeb Mondal,Ragavendrasamy Balakrishnan,Manjunath Nandi Krishnamurthy 셀메드 세포교정의약학회 2015 셀메드 (CellMed) Vol.5 No.1
Yoga is an ancient Indian system of life, encompassing various practices including practices for self-discipline and also for regulating the health states of the individual, being practiced for thousands of years. The present study aims at understanding the effect of two high frequency breathing practices over autonomic nervous system. Forty healthy male volunteers of age 21 ± 2 years with 9 ± 3 months of Yoga practice experience were recruited. The two high frequency Yoga breathing practices, kapalabhati (KB) and bhastrika (BH) were given as interventions randomly on either of the two days to minimise laboratory bias. They were assessed before and immediately after the interventions for heart rate, respiratory rate, heart rate variability (HRV), blood pressure and peripheral oxygen saturation. There was a significant increase in heart rate (p < 0.01; p < 0.001), systolic blood pressure (p < 0.01; p < 0.001), NN50 (p < 0.01; p < 0.001) component of HRV for both KB and BH groups respectively. There was a significant reduction in respiratory rate in both the groups (p < 0.001, and p < 0.05, BH and KB respectively) immediately following intervention. A significant increase in LF component of HRV and reduction in Diastolic blood pressure and high frequency (HF) component following KB was also observed (p < 0.05, for all comparisons). The Mean peripheral oxygen saturation remained unaltered in both the groups (p > 0.05). The results suggest that high frequency yoga breathing practices induce physiological arousal immediately as evidenced by increased blood pressure and heart rate. The sympathetic arousal was more following KB session as evidenced by an increased diastolic blood pressure, LF power and a decrease in HF power of HRV as compared to the BH session.
The Promise of Dried Fruits in Cancer Chemoprevention
Kundu, Joydeb Kumar,Chun, Kyung-Soo Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.8
Chemoprevention is an attempt to use nontoxic natural and synthetic substances or their mixtures to intervene the relatively early stages of carcinogenesis, before invasive characteristics are manifested. The consumption of fruits is well known to reduce the risk of human cancers. Although most fruits are available only on a seasonal basis, recent advances in food processing technologies have made it possible to extend the shelf life of fruits and fruit-products. Fruits can be preserved by applying different drying processes to reduce the moisture content. Different varieties of dried fruits are now sold in supermarkets, thereby making them readily accessible to consumers. Since oxidative stress and chronic inflammation play important roles in cancer development, dried fruits with antioxidative and anti-inflammatory properties hold promise for cancer chemoprevention. The antioxidant, anti-inflammatory and chemopreventive activities of dried fruits are largely attributed to their polyphenols and vitamins. Dried fruits contain adequate amounts of bioactive principles, such as anthocyanins, acetogenins, catechins, coumarins, phenolic acids, terpenes, xanthones, and others. Since numerous health beneficial phytochemicals in fruits are conserved even after processing, regular intake of dried fruits can help prevent cancer. This review addresses the chemopreventive potential of representative dried fruits and their active constituents.
Kundu, Joydeb Kumar,Surh, Young-Joon Elsevier 2005 Mutation research Vol.591 No.1-2
<P><B>Abstract</B></P><P>Center to the cancer biology is disrupted intracellular signaling network, which transmits improper signals resulting in abnormal cellular functioning. Therefore, modulation of inappropriate cell signaling cascades might be a rational approach in achieving chemoprevention. Inflammation has long been suspected to contribute to carcinogenesis. A new horizon in chemoprevention research is the recent discovery of molecular links between inflammation and cancer. Components of the cell signaling network, especially those converge on redox-sensitive transcription factor nuclear factor-κB involved in mediating inflammatory response, have been implicated in carcinogenesis. Intracellular signaling through another redox-sensitive transcription factor AP-1 and that transmitted via a more recently identified oncoprotein β-catenin are also considered to be crucial for inflammation-associated cancer. Epidemiological and experimental studies have revealed that a wide variety of phytochemicals present in our daily diet are potential chemopreventive agents that can alter or correct undesired cellular functions caused by abnormal pro-inflammatory signal transmission. Modulation of cellular signaling involved in chronic inflammatory response by anti-inflammatory phytochemicals may comprise a rational and pragmatic strategy in molecular target-based chemoprevention.</P>
서영준,Joydeb Kumar Kundu,Mei-Hua Li,나혜경,Young-Nam Cha 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.8
Nitrosative stress caused by reactive nitrogen species such as nitric oxide and peroxynitrite overproduced during inflammation leads to cell death and has been implicated in the pathogenesis of many human ailments. However, relatively mild nitrosative stress may fortify cellular defense capacities, rendering cells tolerant or adaptive to ongoing and subsequent cytotoxic challenges, a phenomenon known as ‘preconditioning’ or ‘hormesis’. One of the key components of cellular stress response is heme oxygenase-1 (HO-1), the rate limiting enzyme in the process of degrading potentially toxic free heme into biliverdin, free iron and carbon monoxide. HO-1 is upregulated by a wide array of stimuli and has antioxidant, anti-inflammatory and other cytoprotective functions. This review is intended to provide readers with a welldocumented account of the research done in the area of cellular adaptive survival response against nitrosative stress with special focus on the role of HO-1 upregulation, especially through activation of the transcription factor, Nrf2.
신준완,Kundu, Joydeb Kumar,Young-Joon Surh 한국식품영양과학회 2012 Journal of medicinal food Vol.15 No.3
The present study investigated the effect of phloretin [20,40,60-trihydroxy-3-(4-hydroxyphenyl)-propiophenone] on 12-O-tetradecanoylphorbol 13-acetate (TPA)–induced cyclooxygenase-2 (COX-2) expression and tumor promotion in mouse skin and explored the underlying molecular mechanisms. Topical application of phloretin significantly inhibited 7,12-dimethylbenz[a]anthracene-initiated and TPA-promoted mouse skin carcinogenesis. Pretreatment with phloretin on the dorsal skin of mice inhibited TPA-induced COX-2 expression in a dose-dependent manner. To elucidate the molecular mechanism underlying COX-2 inhibition by phloretin, we examined its effect on TPA-induced activation of nuclear factor-jB (NF-jB), a ubiquitous transcription factor responsible for TPA-induced COX-2 expression in mouse skin. Topically applied phloretin decreased the TPA-induced DNA binding of NF-jB. In addition, phloretin inhibited the phosphorylation as well as the catalytic activity of extracellular signal-regulated kinase (ERK), which was previously found to activate NF-jB and induce COX-2 expression in TPA-treated mouse skin. Taken together, the inhibitory effects of phloretin on TPA-induced NF-jB activation and COX-2 expression through the modulation of ERK signaling may partly account for its antitumor-promoting effect on mouse skin carcinogenesis.