Steganography is one of the leading strategy that is employed to hide restricted content into a cover media so that the person unaware of the fact can’t predict that the cover media can acquire some ...secret information. The effectiveness of any steganographic approach is appraised on imperceptibility of the stego-media, payload of the cover media, integrity of the secret information, security, and computational complexity. The work presented in this paper focuses on these important concerns of secured data transmission. The proposed steganographic approach uses multimedia files including animated image sequences as cover media for concealing secret messages. The entire secret information to be embedded is converted to a code using Secure Hash Algorithm-1 (SHA-1) (National Institute of Standards, and Technology (US). Technology Administration. Secure hash standard, 1993) and shared with the secret message to validate the authenticity of the transmitted secret information. The whole secret message is converted to its ASCII to embed them by replacing the least significant digit (LSD) (Liu et al. In Proceedings of the 2012 IEEE International Conference on Communications (ICC), IEEE, 2012). The receiver validates the transmitted information with SHA-1 again generating a code, which validates with the existing code sent over from the transmitting end. The proposed algorithm is worked upon a variety of text messages with a large set of color animated image sequences as cover media and also has been tested carefully by different parametric measures. This algorithm gives robust outputs in terms of visual imperceptibility, safety, and embedding capability.
Ashwagandha (
) has gained worldwide popularity for a multitude of health benefits inclusive of cancer-preventive and curative effects. Despite numerous research data supporting the benefits of this ...wonder herb, the actual use of ashwagandha for cancer treatment in clinics is limited. The primary reason for this is the inconsistent therapeutic outcome due to highly variable composition and constitution of active ingredients in the plant extract impacting ashwagandha's pharmacology. We investigate here an engineered yield: an ashwagandha extract (Oncowithanib) that has a unique and fixed portion of active ingredients to achieve consistent and effective therapeutic activity. Using the MCF7 cell line, Oncowithanib was studied for its anti-neoplastic efficacy and drug targets associated with cell cycle regulation, translation machinery, and cell survival and apoptosis. Results demonstrate a dose-dependent decline in Oncowithanib-treated MCF7 cell viability and reduced colony-forming ability. Treated cells showed increased cell death as evidenced by enhancement of Caspase 3 enzyme activity and decreased expressions of cell proliferation markers such as Ki67 and Aurora Kinase A. Oncowithanib treatment was also found to be associated with expressional suppression of key cellular kinases such as RSK1, Akt1, and mTOR in MCF7 cells. Our findings indicate that Oncowithanib decreases MCF7 cell survival and propagation, and sheds light on common drug targets that might be good candidates for the development of cancer therapeutics. Further in-depth investigations are required to fully explore the potency and pharmacology of this novel extract. This study also highlights the importance of the standardization of herbal extracts to get consistent therapeutic activity for the disease indication.
Display omitted
Elevation of the level of intracellular reactive oxygen species (ROS) has immense implication in the biological system. On the one hand, ROS promote the signaling cascades for the ...maintenance of normal physiological functions, the phenomenon referred to as redox biology, and on the other hand increased ROS can cause damages to the cellular macromolecules as well as genetic material, the process known as oxidative stress. Oxidative stress acts as an etiological factor for wide varieties of pathologies, cancer being one of them. ROS is regarded as a “double-edged sword” with respect to oncogenesis. It can suppress as well as promote the malignant progression depending on the type of signaling pathway it uses. Moreover, the attribution of ROS in promoting phenotypic plasticity as well as acquisition of stemness during neoplasia has become a wide area of research. The current review discussed all the aspects of ROS in the perspective of tumor biology with special reference to epithelial-mesenchymal transition (EMT) and cancer stem cells.
Background. Ashwagandha extracts play a significant role in traditional Indian medicine to help treat a wide range of disorders from amnesia, erectile dysfunction, neurodegenerative and ...cardiovascular diseases, cancer, stress, anxiety, and many more. Ashwagandha root is enriched with bioactive plant metabolites of which withanolides are the most important ones. The concentration and constitution of withanolides primarily determine ashwagandha’s potency and pharmacology. Various factors modulate the withanolide constitution in the plant-derived extracts, rendering inconsistent therapeutic efficacy. Standardisation of the extraction protocol and a better understanding of the pharmacology mechanism of different extracts with varied withanolide constitutions is therefore critical for developing reliable, repeatable, and effective ashwagandha-based treatment. Objectives. Here, we work toward defining indication mechanisms for two varieties of ashwagandha extract—ASHWITH (ASH-Ext1) and Regenolide (ASH-Ext2)—with different proprietary withanolide proportions. Methods. ASH-Ext1 was studied for antioxidant signaling modulation using HEK293, HeLa, and A549 cells, and ASH-Ext2 was studied for subcellular drug targets associated with the reactivation and longevity of human hair follicles, using primary human hair follicle dermal papilla cells (HFDPCs). Results. Study findings support the antioxidant activity and Nrf2 signaling modulation by ASH-Ext1 in various cell models. Of note, ASH-Ext2 was found to increase β-catenin and telomerase reverse transcriptase (TERT) protein expression levels in HFDPCs. Conclusion. The results of drug target modulation show us that the withanolide constitution associated with different extraction protocols influences the pharmacological potential of the extract significantly and points to the value of standardisation not only of total withanolide content but also of internal withanolide proportions.
Display omitted
•Oxidative stress in association with hypoxia promotes EMT in OSF and OSCC.•Oxidative stress mediated EMT is associated with p-ERK up-regulation.•EMT in OSF promotes sub-epithelial ...fibrosis and in OSCC associates metastasis.•Acquisition of stemness in OSCC associated with EMT.•Hypoxia associated Shh/ Gli-1 signaling promotes disease pathophysiologies.
Oral sub-mucous fibrosis (OSF) is a pathophysiological state of oral cavity or oropharynx having a high chance of conversion to oral squamous cell carcinoma (OSCC). It involves fibrotic transformation of sub-epithelial matrix along with epithelial abnormalities. The present work aims to unveil the mechanistic domain regarding OSF to OSCC conversion exploring the scenario of hypoxia associated oxidative stress, epithelial-mesenchymal transition (EMT), metastasis and stemness acquisition. The study involves histopathological analysis of the diseased condition along with the exploration of oxidative stress status, assessment of mitochondrial condition, immunohistochemical analysis of HIF-1α, E-cadherin, vimentin, ERK, ALDH-1, CD133, Shh, Gli-1 and survivin expressions in the oral epithelial region together with the quantitative approach towards collagen deposition in the sub-epithelial matrix. Oxidative stress was found to be associated with type-II EMT in case of OSF attributing the development of sub-epithelial fibrosis and type-III EMT in case of OSCC favoring malignancy associated metastasis. Moreover, the acquisition of stemness during OSCC can also be correlated with EMT. Alteration of Shh and Gli-1 expression pattern revealed the mechanistic association of hypoxia with the phenotypic plasticity and disease manifestation in case of OSF as well as OSCC. Shh/ Gli-1 signaling can also be correlated with survivin mediated cytoprotective phenomenon under oxidative stress. Overall, the study established the correlative network of hypoxia associated oxidative stress, EMT and manifestation of oral pre-cancerous and cancerous condition in a holistic approach that may throw rays of hope in the therapeutic domain of the concerned diseases.
Display omitted
•Hematopoietic catastrophe during marrow aplasia associated with ROS generation.•Increased ROS and disruption of hematopoietic niche under aplastic stress.•Decline of stromal ...components and deregulation of Notch-1/ Jagged-1 signaling axis in aplastic marrow.•Altered DNA methylation and H-3 phosphorylation status associated with redox imbalance in aplastic marrow.
Aplastic anemia or bone marrow failure often develops as an effect of chemotherapeutic drug application for the treatment of various pathophysiological conditions including cancer. The long-term bone marrow injury affects the basic hematopoietic population including hematopoietic stem/progenitor cells (HSPCs). The present study aimed in unearthing the underlying mechanisms of chemotherapeutics mediated bone marrow aplasia with special focus on altered redox status and associated effects on hematopoietic microenvironment and epigenetic status of hematopoietic cells. The study involves the development of busulfan and cyclophosphamide mediated mouse model for aplastic anemia, characterization of the disease with blood and marrow analysis, cytochemical examinations of bone marrow, flowcytometric analysis of hematopoietic population and microenvironmental components, determination of ROS generation, apoptosis profiling, expressional studies of Notch-1 signaling cascade molecules, investigation of epigenetic modifications including global CpG methylation of DNA, phosphorylation of histone-3 with their effects on bone marrow kinetics and expressional analysis of the anti-oxidative molecules viz; SOD-2 and Sdf-1. Severe hematopoietic catastrophic condition was observed during aplastic anemia which involved peripheral blood pancytopenia, marrow hypocellularity and decreased hematopoietic stem/progenitor population. Generation of ROS was found to play a central role in the cellular devastation in aplastic marrow which on one hand can be correlated with the destruction of hematopoiesis supportive niche components and alteration of vital Notch-1 signaling and on other hand was found to be associated with the epigenetic chromatin modifications viz; global DNA CpG hypo-methylation, histone-3 phosphorylation promoting cellular apoptosis. Decline of anti-oxidant components viz; Sdf-1 and SOD-2 hinted towards the irreversible nature of the oxidative damage during marrow aplasia. Collectively, the findings hinted towards the mechanistic correlation among ROS generation, microenvironmental impairment and epigenetic alterations that led to hematopoietic catastrophe under aplastic stress. The findings may potentiate successful therapeutic strategy development for the dreadful condition concerned.
Aplastic anemia is the bone marrow failure condition characterized by the development of hypocellularity in both marrow and peripheral blood compartments. Anti-tumor chemotherapeutic agents often ...exert secondary effect on hematopoietic system leading to aplastic anemia by marrow failure. The precise mechanisms behind the marrow ablative effects of the drugs remain yet to be established. The present study holds a mechanistic approach to unveil the mystery. Aplastic anemia was generated in mice with the administration of busulfan and cyclophosphamide followed by the characterization of the disease with peripheral blood hemogram, histopathological and cytochemical examinations of bone marrow. To gain deep knowledge about the molecular mechanisms of the hematopoietic disruption, cytotoxicity assay, DNA damage measurement, apoptosis study, replicative senescence analysis, redox balance study, mitochondrial membrane potential change assessment, flowcytometric expressional analysis of p21, p53, ATM, Chk-2, Necdin, Gfi-1, c-myc, KU-80 and Sod-2 were done with marrow hematopoietic stem/ progenitor cells (HSPCs). Severe blood pancytopenia and marrow hypocellularity was found in aplastic mice. Proliferative hindrance and apoptosis of marrow cells were identified as the cause behind the hematopoietic catastrophe. The genotoxic effects of the drugs triggered chromatin damage and induced replicative senescence in aplastic HSPCs by upregulating p21 in a p53 independent manner. Moreover, accumulation of genomic insults also caused apoptotic elimination of marrow cells due to disruption of mitochondrial membrane potential by generating redox imbalance. The study established the underlying mechanisms behind hematopoietic disruption during drug induced marrow aplasia. Outcome of the study may be helpful in successful designing of therapeutic strategies for the disease concerned.
Myelodysplastic syndrome (MDS) is a poorly understood dreadful hematopoietic disorder that involves maturational defect and abnormalities in blood cell production leading to dysplastic changes and ...peripheral blood pancytopenia. The present work aims in establishing the mechanistic relationship of the expressional alterations of major tumor suppressor cascade, vital cell cycle inhibitors and hematopoietic microenvironmental components with the disease pathophysiologies. The study involves the development of N-N′ Ethylnitrosourea (ENU) induced mouse model of MDS, characterization of the disease with blood film and bone marrow smear studies, scanning electron microscopic observation, mitochondrial membrane potential determination, flowcytometric analysis of osteoblastic and vascular niche components along with the expressional study of cleaved caspase-3, PCNA, Chk-2, p53, Ndn, Gfi-1, Tie-2, Sdf-1, Gsk-3β, p18 and Myt-1 in the bone marrow compartment. Dysplastic features were found in peripheral blood of MDS mice which seemed to be the consequence of three marrow pathophysiological conditions viz; aberrant rise of cellular proliferation, increased apoptosis and crowding of abnormal blast population. Expressional decline of the p53 cascade involving Chk-2, p53, Ndn, Gfi-1 along with the downregulation of major cell cycle inhibitors seemed to be associated with the hyper-proliferative nature of bone marrow cells during MDS. Moreover the disruption of osteoblastic niche components added to the decreased hematopoietic quiescency. Increased marrow vascular niche components signified the pre-malignant state of MDS. Elevated cellular apoptosis and rise in the blast burden were also found to be associated with the p53 expression dependent collapsing of mitochondrial membrane potential and upregulation of Tie-2 respectively. The study established the mechanistic correlation between the alterations of the mentioned signaling components and hematopoietic anomalies during MDS which may be beneficial for the development of therapeutic strategies for the disease.
Display omitted
•Cellular hyper-proliferation in MDS marrow associated with p53 axis deregulation.•Aberrant cell division and decline of vital cell cycle inhibitors in MDS marrow.•p53 axis alteration related mitochondrial disruption and apoptosis in MDS marrow.•p53 decline, Tie-2 up-regulation and associated blast burden rise in MDS marrow.•MDS pathophysiologies associated with alteration of hematopoietic niche components.
A Review of Super plastic forming Chatterjee, Ritam; Mukhopadhyay, Jyoti
Materials today : proceedings,
2018, 2018-00-00, Letnik:
5, Številka:
2
Journal Article
Recenzirano
Super plasticity is the property exhibited by a few metals and alloys which involves, under tensile loading, very high elongation without necking until failure. This was first closely studied by Back ...ofen, Turner and Avery at MIT in 1964 1. Their pioneering work has since given rise to the multi-million dollar superplastic forming industry which has been highly successful in fabrication of complex shaped components mainly for the aerospace and automobile industries. The present paper reviews the developments related to superplastic forming that has taken place mainly over the past two decades. The process parameters, underlying mechanisms, constitutive equations and the process economics have been discussed in details. Furthermore, there is a brief discussion about quick-plastic forming which is an upcoming metal forming technique that promises to replace superplastic forming in the near future. This is largely due to the faster forming times associated with quick-plastic forming as compared to superplastic forming.
PDF
