Since the Human Genome Project was successfully completed, humanity has entered a post-genome era, and the second-generation sequencing technology has gradually progressed and become more accurate. Meanwhile, circRNAs plays a crucial role in the regulation of diseases and potential clinical applications has gradually attracted the attention of physicians. However, the mechanisms of circRNAs regulation at the cellular and molecular level of diabetic foot ulcer (DFU) is still not well-understood. With the deepening of research, there have been many recent studies conducted to explore the effect of circRNAs on DFU. In this mini-review, we discuss the potential role of circRNAs as therapeutic targets and diagnostic markers for DFU in order to gain a better understanding of the molecular mechanisms that underlie the development of DFU and to establish a theoretical basis for accurate treatment and effective prevention.

Chordomas are primary low-grade bone tumors derived from the embryonic notochord that make up less than 5% of all osseous malignancies and commonly affect the spine at its vertebral body and at its two ends i.e., skull base and the sacrum. Although histologically defined to be low-grade, chordoma is locally destructive, metastatic, and has a serious recurrence rate, which all contribute to the dismal median survival rate of six years. Its locally destructive nature places the adjacent vital neurovascular structures at risk, making an en-bloc resection a challenge. This tumor is also known to show high resistance to currently available chemoradiotherapy, although the benefit of proton beam therapy for skull base chordoma has been demonstrated. There is an additional need to focus our attention on investigating the molecular biology of this chemoradiotherapy-resistant tumor to develop a more targeted therapy, which has additional diagnostic and prognostic values. In this paper, we discuss the therapeutic, diagnostic, and prognostic role of microRNAs (miRNAs) in chordomas.

Glaucoma is a leading cause of irreversible blindness worldwide. Primary open-angle glaucoma (POAG), the most common type, is a complex inherited disorder that is characterized by progressive retinal ganglion cell death, optic nerve head excavation, and visual field loss. The discovery of a large, and growing, number of genetic and chromosomal loci has been shown to contribute to POAG risk, which carry implications for disease pathogenesis. Differential gene expression analyses in glaucoma-affected tissues as well as animal models of POAG are enhancing our mechanistic understanding in this common, blinding disorder. In this review we summarize recent developments in POAG genetics and molecular genetics research.

Global re-emergence of Chikungunya virus (CHIKV) has renewed the interest in its cellular pathogenesis. We subjected CHIKV-infected Human Embryo Kidney cells (HEK293), a widely used cell-based system for CHIKV infection studies, to a high throughput expression proteomics analysis by Liquid Chromatography-tandem mass spectrometry. A total of 1047 differentially expressed proteins were identified in infected cells, consistently in three biological replicates. Proteins involved in transcription, translation, apoptosis and stress response were the major ones among the 209 proteins that had significant up-regulation. In the set of 45 down-regulated proteins, those involved in carbohydrate and lipid metabolism predominated. A STRING network analysis revealed tight interaction of proteins within the apoptosis, stress response and protein synthesis pathways. We short-listed a common set of 30 proteins that can be implicated in cellular pathology of CHIKV infection by comparing our results and results of earlier CHIKV proteomics studies. Modulation of eight proteins selected from this set was re-confirmed at transcript level. One among them, Nucleophosmin, a nuclear chaperone, showed temporal modulation and cytoplasmic aggregation upon CHIKV infection in double immunofluorescence staining and confocal microscopy. The short-listed cellular proteins will be potential candidates for targeted study of the molecular interactions of CHIKV with host cells.
UNASSIGNED: Chikungunya remained as a neglected tropical disease till its re-emergence in 2005 in the La RéUnion islands and subsequently, in India and many parts of South East Asia. These and the epidemics that followed in subsequent years ran an explosive course leading to extreme morbidity and attributed mortality to this originally benign virus infection. Apart from classical symptoms of acute fever and debilitating polyarthralgia lasting for several weeks, a number of complications were documented. These included aphthous-like ulcers and vesiculo-bullous eruptions on the skin, hepatic involvement, central nervous system complications such as encephalopathy and encephalitis, and transplacental transmission. The disease has recently spread to the Americas with its initial documentation in the Caribbean islands. The Asian genotype of this positive-stranded RNA virus of the Alphavirus genus has been attributed in these outbreaks. However, the disease ran a similar course as the one caused by the East, Central and South African (ECSA) genotype in the other parts of the world. Studies have documented a number of mutations in the re-emerging strains of the virus that enhances mosquito adaptability and modulates virus infectivity. This might support the occurrence of fiery outbreaks in the absence of herd immunity in affected population. Several research groups work to understand the pathogenesis of chikungunya and the mechanisms of complications using cellular and animal models. A few proteomics approaches have been employed earlier to understand the protein level changes in the infected cells. Our present study, which couples a high throughput proteomic analysis and a comparative review of these earlier studies, identifies a few critical molecules as hypothetical candidates that might be important in this infection and for future study.