39 research outputs found
Current status of herbal and their future perspectives
Traditional medicine is the synthesis of therapeutic experience of generations of practicing physicians of indigenous systems of medicine. Throughout the history of mankind, many infectious diseases have been treated with herbals. The traditional medicine is increasingly solicited through the tradipractitioners and herbalists in the treatment of infectious diseases. Among the remedies used, plant drugs constitute an important part. A number of scientific investigations have highlighted the importance and the contribution of many plant families i.e. Asteraceae, Liliaceae, Apocynaceae, Solanaceae, Caesalpinaceae, Rutaceae, Piperaceae, Sapotaceae used as medicinal plants. Medicinal plants play a vital role for the development of new drugs (export and import diverse parts or bioactive compounds in the current market). The bioactive extract should be standardized on the basis of active compound. The bioactive extract should undergo limited safety studies
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Touch, taste, & smell user interfaces: the future of multisensory HCI
The senses we call upon when interacting with technology are very restricted. We mostly rely on vision and audition, increasingly harnessing touch, whilst taste and smell remain largely underexploited. In spite of our current knowledge about sensory systems and sensory devices, the biggest stumbling block for progress concerns the need for a deeper understanding of people’s multisensory experiences in HCI. It is essential to determine what tactile, gustatory, and olfactory experiences we can design for, and how we can meaningfully stimulate such experiences when interacting with technology. Importantly, we need to determine the contribution of the different senses along with their interactions in order to design more effective and engaging digital multisensory experiences. Finally, it is vital to understand what the limitations are that come into play when users need to monitor more than one sense at a time. The aim of this workshop is to deepen and expand the discussion on touch, taste, and smell within the CHI community and promote the relevance of multisensory experience design and research in HCI
Effect of phospholipase A(2 )inhibitory peptide on inflammatory arthritis in a TNF transgenic mouse model: a time-course ultrastructural study
We evaluated the therapeutic effect of secretory phospholipase A(2 )(sPLA(2))-inhibitory peptide at a cellular level on joint erosion, cartilage destruction, and synovitis in the human tumor necrosis factor (TNF) transgenic mouse model of arthritis. Tg197 mice (N = 18) or wild-type (N = 10) mice at 4 weeks of age were given intraperitoneal doses (7.5 mg/kg) of a selective sPLA(2 )inhibitory peptide, P-NT.II, or a scrambled P-NT.II (negative control), three times a week for 4 weeks. Untreated Tg197 mice (N = 10) were included as controls. Pathogenesis was monitored weekly for 4 weeks by use of an arthritis score and histologic examinations. Histopathologic analysis revealed a significant reduction after P-NT.II treatment in synovitis, bone erosion, and cartilage destruction in particular. Conspicuous ultrastructural alterations seen in articular chondrocytes (vacuolated cytoplasm and loss of nuclei) and synoviocytes (disintegrating nuclei and vacuoles, synovial adhesions) of untreated or scrambled-P-NT.II-treated Tg197 mice were absent in the P-NT.II-treated Tg197 group. Histologic scoring and ultrastructural evidence suggest that the chondrocyte appears to be the target cell mainly protected by the peptide during arthritis progression in the TNF transgenic mouse model. This is the first time ultrastructural evaluation of this model has been presented. High levels of circulating sPLA(2 )detected in untreated Tg197 mice at age 8 weeks of age were reduced to basal levels by the peptide treatment. Attenuation of lipopolysaccharide- and TNF-induced release of prostaglandin E(2 )from cultured macrophage cells by P-NT.II suggests that the peptide may influence the prostaglandin-mediated inflammatory response in rheumatoid arthritis by limiting the bioavailability of arachidonic acid through sPLA(2 )inhibition
A study on the differential protein profiles in liver cells of heat stress rats with and without turpentine treatment
<p>Abstract</p> <p>Background</p> <p>Heat stress (HS) and related illnesses are a major concern in military, sports, and fire brigadiers. HS results in physiologic responses of increased temperature, heart rate and sweating. In heat stroke, inflammatory response plays an important role and it is evidenced that turpentine (T) induced circulating inflammatory cytokines reduced survival rate and duration at 42°C. Here we report the alteration in the protein expression in liver cells upon HS with and without T treatment using two dimensional gel electrophoresis (2-DE), tryptic in-gel digestion and MALDI-TOF-MS/MS approaches</p> <p>Results</p> <p>The effects of HS and T treatments alone and a combined treatments (T+HS) was performed in Wistar rat models. Proteomic analysis of liver in the HS and T+HS groups were analyzed compared to liver profiles of resting control and T treated groups. The study revealed a total of 25 and 29 differentially expressed proteins in the HS and T+HS groups respectively compared to resting control group. Fourteen proteins showed altered expression upon T treatment compared to resting control group. Proteins that are involved in metabolic and signal transduction pathways, defense, redox regulation, and cytoskeletal restructuring functions were identified. The altered expression of proteins reflected in 2D gels were corroborated by quantitative real time RT-PCR analysis of 8 protein coding genes representing metabolic and regulatory pathways for their expression and normalized with the house keeping gene β-actin</p> <p>Conclusion</p> <p>The present study has identified a number of differentially expressed proteins in the liver cells of rats subjected to T, HS and T+HS treatments. Most of these proteins are implicated in cell metabolism, as well as adaptive response to incurred oxidative stress and tissue damage due to T+HS and HS effects.</p
Cytoskeletal Rearrangements in Synovial Fibroblasts as a Novel Pathophysiological Determinant of Modeled Rheumatoid Arthritis
Rheumatoid arthritis is a chronic inflammatory disease with a high prevalence and substantial socioeconomic burden. Despite intense research efforts, its aetiology and pathogenesis remain poorly understood. To identify novel genes and/or cellular pathways involved in the pathogenesis of the disease, we utilized a well-recognized tumour necrosis factor-driven animal model of this disease and performed high-throughput expression profiling with subtractive cDNA libraries and oligonucleotide microarray hybridizations, coupled with independent statistical analysis. This twin approach was validated by a number of different methods in other animal models of arthritis as well as in human patient samples, thus creating a unique list of disease modifiers of potential therapeutic value. Importantly, and through the integration of genetic linkage analysis and Gene Ontology–assisted functional discovery, we identified the gelsolin-driven synovial fibroblast cytoskeletal rearrangements as a novel pathophysiological determinant of the disease