Translating the Potential of Stem Cells for Diabetes Mellitus: Challenges and Opportunities.

BACKGROUND: Diabetes mellitus, the widely prevalent disease of pancreas, is a metabolic disorder caused by autoimmune destruction of ß cells or insulin insufficiency or insulin resistance. Replacement of damaged ß cells by cell therapy can mitigate the condition and re-establish normal metabolic control. This has opened up new horizons for research, such as stem cells, cellular reprogramming and ß cell regeneration. OBJECTIVE: The goal of the study was to summarize the available literature on the use of stem cells for the regeneration of pancreatic ß cells and treatment of diabetes mellitus. RESULTS AND CONCLUSION: Stem cells are exceptional having the potential to self renew and differentiate in many lineages. Stem cells hold tremendous potential to regenerate ß cells and treat diabetes mellitus but many milestones on the way are yet to be achieved. But researchers do believe that stem cells and regenerative medicines will be widely used in clinical practices and possibly new effective methodology would be designed for even cure, mitigate and reduce the social burden of diabetes mellitus.

Genetic characterization and disease mechanism of retinitis pigmentosa; current scenario.

Retinitis pigmentosa is a group of genetically transmitted disorders affecting 1 in 3000-8000 individual people worldwide ultimately affecting the quality of life. Retinitis pigmentosa is characterized as a heterogeneous genetic disorder which leads by progressive devolution of the retina leading to a progressive visual loss. It can occur in syndromic (with Usher syndrome and Bardet-Biedl syndrome) as well as non-syndromic nature. The mode of inheritance can be X-linked, autosomal dominant or autosomal recessive manner. To date 58 genes have been reported to associate with retinitis pigmentosa most of them are either expressed in photoreceptors or the retinal pigment epithelium. This review focuses on the disease mechanisms and genetics of retinitis pigmentosa. As retinitis pigmentosa is tremendously heterogeneous disorder expressing a multiplicity of mutations; different variations in the same gene might induce different disorders. In recent years, latest technologies including whole-exome sequencing contributing effectively to uncover the hidden genesis of retinitis pigmentosa by reporting new genetic mutations. In future, these advancements will help in better understanding the genotype-phenotype correlations of disease and likely to develop new therapies.

Eukaryotic translation initiation factors and cancer.

Recent technological advancements have shown tremendous mechanistic accomplishments in our understanding of the mechanism of messenger RNA translation in eukaryotic cells. Eukaryotic messenger RNA translation is very complex process that includes four phases (initiation, elongation, termination, and ribosome recycling) and diverse mechanisms involving protein and non-protein molecules. Translation regulation is principally achieved during initiation step of translation, which is organized by multiple eukaryotic translation initiation factors. Eukaryotic translation initiation factor proteins help in stabilizing the formation of the functional ribosome around the start codon and provide regulatory mechanisms in translation initiation. Dysregulated messenger RNA translation is a common feature of tumorigenesis. Various oncogenic and tumor suppressive genes affect/are affected by the translation machinery, making the components of the translation apparatus promising therapeutic targets for the novel anticancer drug. This review provides details on the role of eukaryotic translation initiation factors in messenger RNA translation initiation, their contribution to onset and progression of tumor, and how dysregulated eukaryotic translation initiation factors can be used as a target to treat carcinogenesis.