Development of Advanced Hybrid, Nano-Sized, Brine Sludge Impregnated MWCNT Composite Material Useful for Broad Application Spectrum

A novel microwave irradiated process has been developed for the synthesis of advanced hybrid, nano-sized, functionalized, brine sludge impregnated MWCNT composite material useful for broad application spectrum. MWCNTs and brine sludge are mainly used as raw materials and are heated in flask using microwave synthesizer in the temperature range of 50-60 ºC for the duration of 20- 25 minutes. Brine sludge act as a novel agent wherein simultaneously and synergistically in-situ funtionization of MWCNTs takes place and therefore enabling synthesis of dark grey colored advanced hybrid, nano-sized, functionalized, brine sludge impregnated MWCNT composite material useful for broad application spectrum. The synthesized advance material has been characterized by various complementary techniques namely XRD, FTIR, FESEM and EDXA. FESEM study reveals the increase in the thickness of the MWCNT wall thereby confirms the brine sludge impregnation on MWCNT. The applications of synthesized material lie in the area such as radiation shielding materials, hybrid polymeric materials to advanced chemically designed composite (ACDC) materials useful for broad application spectrum

STUDY ON IMPLICATIONS OF COPY NUMBER VARIATIONS (CNVs) IN HUMAN POPULATION

Objective: To investigate the role and implications of copy number variations (CNVs) in different diseases found in the human population using various computational tools and databases.Methods: Five different diseases were taken into consideration namely Autism, Type-II Diabetes, Rheumatoid Arthritis, Breast Cancer, and Psoriasis. To validate the CNV's associated with various human diseases different tools and databases were used such as CNV annotator, DECIPHER, Database of Genomic Variants (DGV), CNVD, CNV Workshop, CNV Web store. Finally, the results were analysed to identify the extent of CNVs association in selected diseases.Results: Among all the selected diseases, the maximum numbers of CNV's were found in the case of breast cancer which in total 3851 at chromosome number one. Among all the selected diseases, minimum numbers of CNV's were found in the case of psoriasis, and a significant amount of CNVs are present in all the selected diseases.Conclusion: CNVs constitutes a substantial fraction of total genetic variability and it has the importance in modulating human diseases. This study has shown a significant presence of CNVs in all the selected diseases. Hence it can be concluded that CNVs can be major causing factors in many other life threatening diseases as well and a specific study designed to identify these variations can open a new dimension in the development of novel therapy for those diseases

Construction of genetic linkage map of the medicinal and ornamental plant Catharanthus roseus

An integrated genetic linkage map of the medicinal and ornamental plant Catharanthus roseus, based on different types of molecular and morphological markers was constructed, using a F2 population of 144 plants. The map defines 14 linkage groups (LGs) and consists of 131 marker loci, including 125 molecular DNA markers (76 RAPD, 3 RAPD combinations; 7 ISSR; 2 EST-SSR from Medicago truncatula and 37 other PCR based DNA markers), selected from a total of 472 primers or primer pairs, and six morphological markers (stem pigmentation, leaf lamina pigmentation and shape, leaf petiole and pod size, and petal colour). The total map length is 1131.9 cM (centiMorgans), giving an average map length and distance between two markers equal to 80.9 cM and 8.6 cM, respectively. The morphological markers/genes were found linked with nearest molecular or morphological markers at distances varying from 0.7 to 11.4 cM. Linkage was observed between the morphological markers concerned with lamina shape and petiole size of leaf on LG1 and leaf, stem and petiole pigmentation and pod size on LG8. This is the first genetic linkage map of C. roseus

Advances in Bamboo Composites for Structural Applications: A Review

The fastest-growing plant on earth is bamboo; it grows three times as quickly as most other species and is a renewable, adaptable resource with high strength and lightweight. Bamboos are a valuable alternative resource with high physical similarities with genuine hardwoods. Using these naturally available renewable bamboo resources provides a practical approach to an eco-friendly industry mainly based on green materials and sustainable technologies with minimum impact on nature. In this regard, developing advanced bamboo-based composites is an attractive step. The extensive use of bamboo composites is a result of their advantageous qualities, including dimensional stability, natural colour, exquisite texture, and ease of manufacturing. The bamboo-based composites have immense potential to perform as a wood substitute that can reduce timber import and meet future timber requirements that are presently fulfilled by cutting trees or importing timber. This chapter aims to exhibit these advanced bamboo composites as a competitive and sustainable substitution for conventional timber material for structural applications. The present chapter highlights the advanced bamboo composites as engineered materials utilised mainly for structural applications in housing sectors and construction industries in the form of standard regular shapes such as beams, planks, lumbers, truss elements etc. One of the sections would be dedicated to the future scope of these advanced bamboo composites and recommendations

A Glimpse into the Role and Mechanism of UL135 in HCMV Apoptosis

Human cytomegalovirus (HCMV) exists indefinitely in infected individuals through a latent infection that is poorly characterized in hematopoetic cells. We have previously demonstrated that the UL133-UL138 locus within the ULb' region encodes proteins that are integral membrane proteins that are co-localized to the Golgi and are involved in the regulation of viral replication. UL135 is of interest in that it is predicted to activate viral replication. Given preliminary results, exogenous expression of UL135 outside of the context of infection results in apoptosis in fibroblasts through caspase pathways. UL135 possesses five SH3 domain binding sites; we hypothesize that UL135 functions through its interaction with SH3 domain-containing proteins. To confirm the importance of the SH3 domain binding sites, I mutated three of the five SH3 domain binding sites both individually and collectively. Preliminary studies show that UL135 exhibits decreased ability to induce apoptosis when the SH3 domain binding sites are mutated, which suggests that UL135 is indeed acting to activate viral replication by suppressing UL138, a protein previously identified as necessary in establishing a latent infection. Future directions include repetition of these preliminary experiments in addition to creating viruses with these mutants in order to analyze their effect on latency during infection

Emerging Insights into the Metabolic Alterations in Aging Using Metabolomics

Metabolomics is the latest ‘omics’ technology and systems biology science that allows for comprehensive profiling of small-molecule metabolites in biological systems at a specific time and condition. Metabolites are cellular intermediate products of metabolic reactions, which reflect the ultimate response to genomic, transcriptomic, proteomic, or environmental changes in a biological system. Aging is a complex biological process that is characterized by a gradual and progressive decline in molecular, cellular, tissue, organ, and organismal functions, and it is influenced by a combination of genetic, environmental, diet, and lifestyle factors. The precise biological mechanisms of aging remain unknown. Metabolomics has emerged as a powerful tool to characterize the organism phenotypes, identify altered metabolites, pathways, novel biomarkers in aging and disease, and offers wide clinical applications. Here, I will provide a comprehensive overview of our current knowledge on metabolomics led studies in aging with particular emphasis on studies leading to biomarker discovery. Based on the data obtained from model organisms and humans, it is evident that metabolites associated with amino acids, lipids, carbohydrate, and redox metabolism may serve as biomarkers of aging and/or longevity. Current challenges and key questions that should be addressed in the future to advance our understanding of the biological mechanisms of aging are discussed

The Utility of Hemoglobin A1c in Detecting Prediabetes in Obese Youth

A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.Introduction. The incidence and prevalence of Type 2 diabetes mellitus has been steadily increasing over the past ten years, and is currently approximately 4.1 per 1000 12‐19 year olds in the US2. This increase has been linked to obesity and a sedentary lifestyle. Prediabetes, in the pediatric population is defined as having a fasting plasma glucose concentration ≥ 100 to 125 mg/dL or 2‐hour glucose concentration during an oral glucose tolerance test ≥ 140 mg/dL but <200 mg/dL. Aims. The goal of this study is to describe the sensitivity and specificity of hemoglobin A1c at various thresholds to identify prediabetes, as defined by impaired fasting glucose and/or impaired glucose tolerance; the population included in this study consist of obese youth referred to the Division of Endocrinology and Diabetes at Phoenix Children’s Hospital for weight‐related issues. We anticipate describing various levels of sensitivity and specificity of hemoglobin A1c in comparison with gold standard tests, such that it can be used to propel further studies to ultimately reduce the immense patient burden of fasting in the pediatric population. Methods. We conducted a retrospective cross‐sectional chart review and employed receiver operating characteristic (ROC) curve analysis of data including but not limited to hemoglobin A1c, fasting plasma glucose, and 2‐hr post‐prandial plasma glucose. The benefits of this study include the potential of reducing the patient burden of fasting prior to examination. This review will determine, if any, the potential value in being able to use hemoglobin A1c clinically to detect prediabetes in pediatric patients; determining this may provide critical information to improve the monitoring and screening of prediabetes. Conclusions. Compared to the gold standards of fasting plasma glucose and oral glucose tolerance tests, we found that hemoglobin A1c had a low sensitivity and specificity for identifying prediabetes.This item is part of the College of Medicine - Phoenix Scholarly Projects 2016 collection. For more information, contact the Phoenix Biomedical Campus Library at [email protected]

Natural and engineered strategies that modulate oxidative phosphorylation defects associated with mitochondrial DNA mutations

Oxidative phosphorylation (OXPHOS) dysfunction has been implicated in several human diseases. It is caused by the mutations that affect the function of electron transport chain enzyme complexes and/or ATP production. We have studied the potential consequences of the mtDNA mutations and mtDNA damage on OXPHOS function in a human colorectal cancer cell line, V425 and in a mouse model of mitochondrial myopathy. We found that the nonsense and nearly homoplasmic mutations in the catalytic subunits of the OXPHOS enzymes did not significantly alter the OXPHOS function in V425 cancer cells. However, the deleterious effects of the mutations on OXPHOS function were evident when the mitochondria from the V425 cells were transferred to an osteosarcoma nuclear background. We found that the V425 cancer cells had adapted to maintain an efficient OXPHOS function by upregulating the steady-state levels of several mitochondrial respiratory chain proteins and the transcriptional coactivator genes of the PGC-1 family that in turn regulate the expression of nuclear genes involved in mitochondrial biogenesis. We also studied the potential consequences of the mtDNA damage in the skeletal muscle of PstI-transgenic mice. We found that the mtDNA double-strand breaks induced by the expression of a restriction endonuclease in the skeletal muscle mitochondria were associated with the loss of functional mtDNA molecules leading to mtDNA depletion and the formation of large-scale mtDNA deletions. The molecular features of the deletions were similar to those found in humans with multiple mtDNA deletions suggesting that the double-strand breaks in mammalian mtDNA mediate the formation of large-scale deletions. We also devised a strategy to modulate mtDNA heteroplasmy. Since most human mitochondrial diseases are heteroplasmic and are manifested when the percentage of mutant mtDNA exceeds a critical threshold, a slight shift in the heteroplasmy could be useful in disease prevention. We showed that a mitochondrially-targeted restriction endonuclease has the ability to selectively degrade mtDNA haplotypes that harbor the restriction enzyme sites. The therapeutic potential of this approach applies to a subgroup of mitochondrial diseases where the pathogenic mtDNA mutation creates a novel restriction enzyme site which is absent from the wild-type mtDNA haplotype.</p

The Mitochondrial Basis of Aging and Age-Related Disorders

Aging is a natural phenomenon characterized by progressive decline in tissue and organ function leading to increased risk of disease and mortality. Among diverse factors that contribute to human aging, the mitochondrial dysfunction has emerged as one of the key hallmarks of aging process and is linked to the development of numerous age-related pathologies including metabolic syndrome, neurodegenerative disorders, cardiovascular diseases and cancer. Mitochondria are central in the regulation of energy and metabolic homeostasis, and harbor a complex quality control system that limits mitochondrial damage to ensure mitochondrial integrity and function. The intricate regulatory network that balances the generation of new and removal of damaged mitochondria forms the basis of aging and longevity. Here, I will review our current understanding on how mitochondrial functional decline contributes to aging, including the role of somatic mitochondrial DNA (mtDNA) mutations, reactive oxygen species (ROS), mitochondrial dynamics and quality control pathways. I will further discuss the emerging evidence on how dysregulated mitochondrial dynamics, mitochondrial biogenesis and turnover mechanisms contribute to the pathogenesis of age-related disorders. Strategies aimed to enhance mitochondrial function by targeting mitochondrial dynamics, quality control, and mitohormesis pathways might promote healthy aging, protect against age-related diseases, and mediate longevity