Chromobacterium violaceum is a gram-negative bacterium, which has been used widely in microbiology labs involved in quorum sensing (QS) research. Among the QS-regulated traits of this bacterium, violacein production has received the maximum attention. Violacein production in this organism, however is not under sole control of QS machinery, and other QS-regulated traits of this bacterium also need to be investigated in better detail. Though not often involved in human infections, this bacterium is being viewed as an emerging pathogen. This review attempts to highlight the recent research advances on C. violaceum, with respect to violacein biosynthesis, development of various applications of this bacterium and its bioactive metabolite violacein, and its pathogenicity.

Background/Aims: Hepatocellular carcinoma (HCC) is the most common liver cancer with high mortality rate in patients suffering from liver diseases. The drug of choice used in advanced-stage of HCC is sorafenib. However, adaptive resistance has been observed in HCC patients undergoing long-term sorafenib treatment, lowering its effectiveness. Hence, it is important to overcome drug resistance to improve overall management of HCC. Here, we have identified a candidate biomarker for sorafenib resistance in a HCC model cell line, HepG2. Methods: Initially, comparative proteomic profiling of parental HepG2 [HepG2 (P)] and sorafenib-resistant HepG2 [HepG2 (R)] cells was performed via MALDI (matrix-assisted laser desorption/ionization) which revealed the deregulation of vimentin in HepG2 (R) cells. Gene and protein level expression of vimentin was also observed through quantitative real-time polymerase chain reaction (qRT PCR) and fluorescence-activated cell sorting (FACS), respectively. Furthermore, withaferin A was used to study regulation of vimentin expression and its significance in sorafenib resistance. Results: Both gene and protein level of vimentin expression was found to be downregulated in HepG2 (R) in comparison to HepG2 (P). Interestingly, the study demonstrated that withaferin A further lowered the expression of vimentin in HepG2 (R) cells in a dose-dependent manner. Also, inhibition of vimentin lowered ABCG2 expression and decreased cell viability in parental as well as sorafenib resistant HepG2 cells. Conclusions Hence, our study for the first time highlighted the probable therapeutic potential of vimentin in sorafenib resistant HepG2, a HCC model cell line.

Introduction: Resistant starch has elicited new possibilities around the globe due to its plausible health benefits and functional properties. This research aimed to evaluate the effect of processing on the resistant starch content in selected Indian rice varieties and its effect on postprandial blood glucose levels. Methods: Two Indian rice varieties (Sona Masuri and Mogra) were evaluated for resistant starch in raw form, after boiling, steaming, and refrigeration. Thereafter, the increment in resistance starch content by different processing methods was validated by oral glucose tolerance test (OGTT) on ten healthy participants. Results: Among the two rice varieties, raw Sona Masuri had a higher resistance starch content (10.86%). After processing, resistant starch was observed to be high in steamed Mogra variety (3.52%). In the boiling process, Sona Masuri developed a higher resistant starch content (2.44%) as compared to Mogra variety (1.05%). The assessment done after refrigeration revealed a slight increase in resistant starch content in both rice varieties. Mogra variety had higher resistant starch (3.68%) than the other rice variety (2.56%) after refrigeration. Validation of increase in resistant starch content and its effect on blood glucose responses done through OGTT revealed that Mogra rice (test food) did not cause a swift spike in blood glucose level compared to glucose (reference food). Differences in blood glucose responses by test and reference food at 0, 30, 60, 90, and 120 minutes were statistically significant. Conclusion: Steamed and refrigerated Mogra rice did not cause significant increase in blood glucose.