Search

This work accounts for the green synthesis of iron oxide nanoparticles using Moringa oleifera leaf extract as a stabilizing and reducing agent. The preliminary confirmation of synthesized Fe3O4NPs was done by UV–visible spectroscopy in the wavelength range of 190–900 nm. The crystalline nature of Fe3O4 NPs was established via X-ray diffraction analysis. FT-IR studies reveal the bioactive phytochemicals present in the Moringa leaf extract based Fe3O4 NPs. A DLS particle size analyser was used to determine the size of green synthesized Fe3O4 NPs and its spherical morphology was determined by using SEM and TEM techniques. The growth of Brassica oleracea var. italica seedlings was measured by analysing biophysical and biochemical parameters in two concentrations of Fe3O4 NPs i.e. 15 mg/L and 30 mg/L alone and in combination with cadmium. Treatments were designated as control C, NP1, NP2, Cd+NP1, Cd+NP2, and Cd. Fe3O4 NPs treated broccoli seedlings showed noteworthy improvement in shoot length, root length, plant biomass, total chlorophyll content, carotenoid content, total soluble sugars, protein content, and nitrate reductase activity, while decline in electrolyte leakage, lipid peroxidation, proline content, superoxide dismutase activity and catalase activity was reported as compared to control. Exposure of iron oxide nano-treatments was found efficacious in reducing cadmium accumulation at a concentration of 30 mg/L. The seedlings exposed to NP2 (30 mg/L) concentration of green synthesized nano iron oxide increased nutrient uptake and thus stimulating plant growth, and also improved morphological and physiological characteristics of Brassica oleracea seedlings. Therefore, the present study reported that bio-based iron oxide nanoparticles were significantly useful for plant growth, by enhancing the plant defense mechanism in response to cadmium induced toxicity.

Novel coronavirus disease 2019 (COVID-19) is the biggest threat to human being globally. The first case was identified in a patient with flu symptoms along with severe acute respiratory syndrome in Wuhan, China in December 2019 and now it has spread in more than 200 countries. COVID-19 is more lethal in the elderly and people with an underlying condition such as asthma, cancer, diabetes. Here we performed bioinformatic analysis to investigate the interaction of S2 subunit protein of SARS-nCoV-2 of novel coronavirus with tumor suppressor proteins p53 and BRCA-1/2. In this short communication we report the interaction between S2 subunit proteins with tumor suppressor proteins for the first time. This preliminary result will open up a new direction to investigate the effect of a novel coronavirus in cancer patients.

Ubiquilin (UBQLN) proteins are adaptors thought to link ubiquitinated proteins to the proteasome. However, our lab has recently reported a previously unappreciated role for loss of UBQLN in lung cancer progression. In fact, UBQLN genes are lost in over 50% of lung cancer samples examined. However, a reason for the loss of UBQLN has not been proposed, nor has a selective pressure that could lead to deletion of UBQLN been reported. Diesel Exhaust Particles (DEP) are a major concern in the large cities of developing nations and DEP exposed populations are at an increased risk of developing a number of illnesses, including lung cancer. A connection between DEP and UBQLN has never been examined. In the present study, we determined the effect of DEP on lung cell lines and were interested to determine if UBQLN proteins could potentially play a protective role following treatment with DEP. Interestingly, we found that DEP treated cells have increased expression of UBQLN proteins. In fact, over-expression of UBQLN was capable of protecting cells from DEP toxicity. To investigate the mechanism by which DEP leads to increased UBQLN protein levels, we identified and interrogated microRNAs that were predicted to regulate UBQLN mRNA. We found that DEP decreases the oncogenic microRNA, MIR155. Further, we showed that MIR155 regulates the mRNA of UBQLN1 and UBQLN2 in cells, such that increased MIR155 expression increased cell invasion, migration, wound formation and clonogenicity in UBQLN-loss dependent manner. This is the first report of an environmental carcinogen regulating expression of UBQLN proteins. We show that exposure of cells to DEP causes an increase in UBQLN levels and that MIR155 regulates mRNA of UBQLN. Thus, we propose that DEP-induced repression of MIR155 leads to increased UBQLN levels, which in turn may be a selective pressure on lung cells to lose UBQLN1.

A pair of Down syndrome (DS) human iPSCs (hiPSCs) and isogenic euploid hiPSCs generated by using an integration-free Sendai viral vector system showed trisomy 21 (47; XY) and typical (46; XY) karyotype respectively. Pluripotency of both hiPSC lines was confirmed by pluripotency marker expression and three germ layer differentiation potentials.

Human mouse chimeric models are valuable tools to develop in-vivo disease models. However, in-vivo detection of human cells limits their analysis. To facilitate in-vivo modeling of Down syndrome (DS), we generated a stable AAVS1-EGFP isogenic pair of DS human iPSCs by zinc finger mediated genetic engineering of the AAVS1 locus. These lines overcome the limitation of reporter human iPSCs generated using random integration, which may not express reporter gene in all tissues due to heterochromatin-induced gene silencing. These reporter cell lines provide a valuable tool to facilitate in-vivo tracking of the graft cell integration, differentiation, and distinction from host cells.

Human-induced pluripotent stem cells (hiPSCs) clones NSi001-A, NSi001-B, and NSi001-C were generated from a female individual of Indian origin having Robertsonian translocation down syndrome (DS) by reprogramming peripheral blood mononuclear cells (PBMCs) using integration-free Sendai viral vectors. The established hiPSCs clones had karyotype similar to the patient sample with Robertsonian translocation [46, XX rob (14;21)], normal ES-like morphology, expression of pluripotency markers, and potential for three germ layer differentiation, i.e., ectoderm, mesoderm, and endoderm.