Simple and secured access to networked home appliances via internet using SSL, BioHashing and single Authentication Server

This thesis describes a web-based application that will enable users to access their networked home appliances over the Internet in an easy, secured, accessible and cost effective manner, using the user's iris image only for authentication. As Internet is increasingly gaining significance and popularity in our daily lives, various home networking technologies also started gaining importance from consumers, which helped in facilitating interoperability, sharing of services and exchange of information between different electronic devices at home. As a result, the demand to be able to access home appliances or security cameras over the Internet gradually grew. In this research, we propose an efficient, secured, low-cost and user-friendly method to access networked home appliances over the Internet, providing strong, well integrated, three levels of security to the whole application and user data. According to our design, the user's iris data after hashing (using BioHashing) is sent through a secure communication channel utilizing Secure Sockets Layer v-3.0. The deterministic feature sequence from the iris image is extracted using 1D log-Gabor filters and while performing BioHashing, the orthonormalization of the pseudorandom number is implemented employing Gram-Schmidt orthonormalization algorithm. In addition to this protected data transfer mechanism, we propose the design of an Authentication Server that can be shared among multiple homes, allowing numerous users to access their home appliances in a trouble-free and secured manner. It can also bring down the cost of commercial realization of this endeavor and increase its accessibility without compromising on system security. We demonstrate that the recognition efficiency of this system is computationally effective with equal error rate (EER) of 0% and 6.75% (average) in two separate conditions on CASIA 1 and CASIA 2 iris image datasets

Hydrologic modelling

Advances in computational tools and modeling techniques combined with enhanced process knowledge have, in recent decades, facilitated a rapid progress in hydrologic modeling. From the use of traditional lumped models, the hydrologic science has moved to the much more complex, fully distributed models that exude an enhanced knowledge of hydrologic processes. Despite this progress, uncertainties in hydrologic predictions remain. The Indian contribution to hydrologic science literature in the recent years has been significant, covering areas of surface water, groundwater, climate change impacts and quantification of uncertainties. Future scientific efforts in hydrologic science in India are expected to involve better, more robust observation techniques and datasets, deeper process-knowledge at a range of spatio-temporal scales, understanding links between hydrologic and other natural and human systems and integrated solutions using multidisciplinary approaches

IDO1 is an Integral Mediator of Inflammatory Neovascularization.

The immune tolerogenic effects of IDO1 (indoleamine 2,3-dioxygenase 1) have been well documented and genetic studies in mice have clearly established the significance of IDO1 in tumor promotion. Dichotomously, the primary inducer of IDO1, the inflammatory cytokine IFNγ (interferon-γ), is a key mediator of immune-based tumor suppression. One means by which IFNγ can exert an anti-cancer effect is by decreasing tumor neovascularization. We speculated that IDO1 might contribute to cancer promotion by countering this anti-neovascular effect of IFNγ, possibly through IDO1-potentiated elevation of the pro-tumorigenic inflammatory cytokine IL6 (interleukin-6). In this study, we investigated how genetic loss of IDO1 affects neovascularization in mouse models of oxygen-induced retinopathy and lung metastasis. Neovascularization in both models was significantly reduced in mice lacking IDO1, was similarly reduced with loss of IL6, and was restored in both cases by concomitant loss of IFNγ. Likewise, the lack of IDO1 or IL6 resulted in reduced metastatic tumor burden and increased survival, which the concomitant loss of IFNγ abrogated. This insight into IDO1\u27s involvement in pro-tumorigenic inflammatory neovascularization may have important ramifications for IDO1 inhibitor development, not only in cancer where clinical trials are currently ongoing, but in other disease indications associated with neovascularization as well

Indoleamine 2,3-Dioxygenase and Its Therapeutic Inhibition in Cancer

The tryptophan catabolic enzyme indoleamine 2,3-dioxygenase-1 (IDO1) has attracted enormous attention in driving cancer immunosuppression, neovascularization, and metastasis. IDO1 suppresses local CD8 + T effector cells and natural killer cells and induces CD4 + T regulatory cells (iTreg) and myeloid-derived suppressor cells (MDSC). The structurally distinct enzyme tryptophan dioxygenase (TDO) also has been implicated recently in immune escape and metastatic progression. Lastly, emerging evidence suggests that the IDO1-related enzyme IDO2 may support IDO1-mediated iTreg and contribute to B-cell inflammed states in certain cancers. IDO1 and TDO are upregulated widely in neoplastic cells but also variably in stromal, endothelial, and innate immune cells of the tumor microenviroment and in tumor-draining lymph nodes. Pharmacological and genetic proofs in preclinical models of cancer have validated IDO1 as a cancer therapeutic target. IDO1 inhibitors have limited activity on their own but greatly enhance “immunogenic” chemotherapy or immune checkpoint drugs. IDO/TDO function is rooted in inflammatory programming, thereby influencing tumor neovascularization, MDSC generation, and metastasis beyond effects on adaptive immune tolerance. Discovery and development of two small molecule enzyme inhibitors of IDO1 have advanced furthest to date in Phase II/III human trials (epacadostat and navoximod, respectively). Indoximod, a tryptophan mimetic compound with a different mechanism of action in the IDO pathway has also advanced in multiple Phase II trials. Second generation combined IDO/TDO inhibitors may broaden impact in cancer treatment, for example, in addressing IDO1 bypass (inherent resistance) or acquired resistance to IDO1 inhibitors. This review surveys knowledge about IDO1 function and how IDO1 inhibitors reprogram inflammation to heighten therapeutic responses in cancer

Indoleamine 2,3-Dioxygenase and Its Therapeutic Inhibition in Cancer

The tryptophan catabolic enzyme indoleamine 2,3-dioxygenase-1 (IDO1) has attracted enormous attention in driving cancer immunosuppression, neovascularization, and metastasis. IDO1 suppresses local CD8 + T effector cells and natural killer cells and induces CD4 + T regulatory cells (iTreg) and myeloid-derived suppressor cells (MDSC). The structurally distinct enzyme tryptophan dioxygenase (TDO) also has been implicated recently in immune escape and metastatic progression. Lastly, emerging evidence suggests that the IDO1-related enzyme IDO2 may support IDO1-mediated iTreg and contribute to B-cell inflammed states in certain cancers. IDO1 and TDO are upregulated widely in neoplastic cells but also variably in stromal, endothelial, and innate immune cells of the tumor microenviroment and in tumor-draining lymph nodes. Pharmacological and genetic proofs in preclinical models of cancer have validated IDO1 as a cancer therapeutic target. IDO1 inhibitors have limited activity on their own but greatly enhance “immunogenic” chemotherapy or immune checkpoint drugs. IDO/TDO function is rooted in inflammatory programming, thereby influencing tumor neovascularization, MDSC generation, and metastasis beyond effects on adaptive immune tolerance. Discovery and development of two small molecule enzyme inhibitors of IDO1 have advanced furthest to date in Phase II/III human trials (epacadostat and navoximod, respectively). Indoximod, a tryptophan mimetic compound with a different mechanism of action in the IDO pathway has also advanced in multiple Phase II trials. Second generation combined IDO/TDO inhibitors may broaden impact in cancer treatment, for example, in addressing IDO1 bypass (inherent resistance) or acquired resistance to IDO1 inhibitors. This review surveys knowledge about IDO1 function and how IDO1 inhibitors reprogram inflammation to heighten therapeutic responses in cancer

Ecological Advancements and Developments of Agroforestry

Agroforestry is a conventional method of land use that could help to address agricultural environmental issues. In order to take advantage of the ensuing ecological and economic interactions, agroforestry is the technique of consciously integrating woody vegetation (trees or shrubs) with crop and/or animal systems. According to recent studies, the global agri-food industry may reach more sustainable methods of producing food and fiber by adopting agroforestry techniques and principles more widely. This would benefit farmers economically and would benefit society as a whole in terms of the environment. Agroforestry promotes eco-intensification based on resource efficiency and offers a wide range of provisioning, regulating, cultural, supporting ecosystem services, and environmental advantages. In this review, we discussed agroforestry with its advantages and developments

A Rapid, Efficient and Green Method for Synthesis of 3,3'-Arylmethylene-bis-4-hydroxycoumarins without Use of any Solvent, Catalyst or Solid Surface

Abstract: A rapid, efficient and green methodology has been developed for the synthesis of 3,3'-arylmethylene-bis-4-hydroxycoumarins by microwave assisted condensation of aromatic aldehydes and 4-hydroxycoumarin without use of any solvent, catalyst or solid surface

IDO1 and Inflammatory Neovascularization: Bringing New Blood to Tumor-Promoting Inflammation

In parallel with the genetic and epigenetic changes that accumulate in tumor cells, chronic tumor-promoting inflammation establishes a local microenvironment that fosters the development of malignancy. While knowledge of the specific factors that distinguish tumor-promoting from non-tumor-promoting inflammation remains inchoate, nevertheless, as highlighted in this series on the \u27Hallmarks of Cancer\u27, it is clear that tumor-promoting inflammation is essential to neoplasia and metastatic progression making identification of specific factors critical. Studies of immunometabolism and inflamometabolism have revealed a role for the tryptophan catabolizing enzyme IDO1 as a core element in tumor-promoting inflammation. At one level, IDO1 expression promotes immune tolerance to tumor antigens, thereby helping tumors evade adaptive immune control. Additionally, recent findings indicate that IDO1 also promotes tumor neovascularization by subverting local innate immunity. This newly recognized function for IDO1 is mediated by a unique myeloid cell population termed IDVCs (IDO1-dependent vascularizing cells). Initially identified in metastatic lesions, IDVCs may exert broader effects on pathologic neovascularization in various disease settings. Mechanistically, induction of IDO1 expression in IDVCs by the inflammatory cytokine IFNγ blocks the antagonistic effect of IFNγ on neovascularization by stimulating the expression of IL6, a powerful pro-angiogenic cytokine. By contributing to vascular access, this newly ascribed function for IDO1 aligns with its involvement in other cancer hallmark functionalities, (tumor-promoting inflammation, immune escape, altered cellular metabolism, metastasis), which may stem from an underlying role in normal physiological functions such as wound healing and pregnancy. Understanding the nuances of how IDO1 involvement in these cancer hallmark functionalities varies between different tumor settings will be crucial to the future development of successful IDO1-directed therapies