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Retinoblastoma is a rare pediatric tumor of the retina, caused by the homozygous loss of the Retinoblastoma 1 (RB1) tumor suppressor gene. Previous microarray studies have identified changes in the expression profiles of coding genes; however, our understanding of how non-coding genes change in this tumor is absent. This is an important area of research, as in many adult malignancies, non-coding genes including LNC-RNAs are used as biomarkers to predict outcome and/or relapse. To establish a complete and in-depth RNA profile, of both coding and non-coding genes, in Retinoblastoma tumors, we conducted RNA-seq from a cohort of tumors and normal retina controls. This analysis identified widespread transcriptional changes in the levels of both coding and non-coding genes. Unexpectedly, we also found rare RNA fusion products resulting from genomic alterations, specific to Retinoblastoma tumor samples. We then determined whether these gene expression changes, of both coding and non-coding genes, were also found in a completely independent Retinoblastoma cohort. Using our dataset, we then profiled the potential effects of deregulated LNC-RNAs on the expression of neighboring genes, the entire genome, and on mRNAs that contain a putative area of homology. This analysis showed that most deregulated LNC-RNAs do not act locally to change the transcriptional environment, but potentially function to modulate genes at distant sites. From this analysis, we selected a strongly down-regulated LNC-RNA in Retinoblastoma, DRAIC, and found that restoring DRAIC RNA levels significantly slowed the growth of the Y79 Retinoblastoma cell line. Collectively, our work has generated the first non-coding RNA profile of Retinoblastoma tumors and has found that these tumors show widespread transcriptional deregulation.

Swetha Rajasekaran et al. integrate transcriptional, proteomic, and metabolomic data to explore how cells adapt to inactivation of RB1, a hallmark of cancer. Combined with their genetic analyses in a Drosophila model, the authors identify key metabolic pathways that may be involved in the growth of RB1-depleted cancer cells.

AIM: To access the association of forty-eight single nucleotide polymorphisms (SNPs) identified from Caucasian population with steroid-induced ocular hypertension (OHT) in India population. METHODS: Fifty-four triamcinolone-acetonide (TA) and forty-seven dexamethasone (Dex) administered subjects were enrolled in the study after a written consent. Intraocular pressure (IOP) values were recorded for a period of 6-month post steroid injections and patients were grouped as steroid-responders (SR: IOP≥21 mm Hg) and non-responders (NR: IOP≤20 mm Hg). Genomic DNA was isolated from peripheral venous blood. Forty-eight SNPs identified in TA treated Caucasian patients by genome wide association study (GWAS) were genotyped using iPLEXTM MassARRAY among TA as well as Dex administered Indian patients. Genotyping data of 48 general subjects from a previous study were considered as reference controls for statistical analysis. Genotypic frequencies were calculated and P-value, Chi-square and odds ratio at 95% confidence-interval of group A (steroid treated vs controls), group B (SR vs NR), group C (phenotype correlation: influence of time, severity and gender on IOP rise), were calculated. P30 mm Hg) and immediate (

Inhibition of the interaction between p53 and HDM2 is an effective therapeutic strategy in cancers that harbor a wild-type p53 protein such as retinoblastoma (RB). Nanoparticle-based delivery of therapeutic molecules has been shown to be advantageous in localized delivery, including to the eye, by overcoming ocular barriers. In this study, we utilized biocompatible gold nanoparticles (GNPs) to deliver anti-HDM2 peptide to RB cells. Characterization studies suggested that GNP-HDM2 was stable in biologically relevant solvents and had optimal cellular internalization capability, the primary requirement of any therapeutic molecule. GNP-HDM2 treatment in RB cells in vitro suggested that they function by arresting RB cells at the G2M phase of the cell cycle and initiating apoptosis. Analysis of molecular changes in GNP-HDM2-treated cells by qRT-PCR and western blotting revealed that the p53 protein was upregulated; however, transactivation of its downstream targets was minimal, except for the PUMA-BCl2 and Bax axis. Global gene expression and in silico bioinformatic analysis of GNP-HDM2-treated cells suggested that upregulation of p53 might presumptively mediate apoptosis through the induction of p53-inducible miRNAs.

Certain contaminants are termed as emerging (Contaminants of Emerging Concern, CEC) since all aspects of these pollutants are not known and their regulation is not ununiform across the nations. The CECs include many classes of compounds that are used in various industries, plant protection chemicals, personal care products and medicines. They accumulate in waterbodies, soils, organisms including humans. They cause deleterious effects on plant animal and human health. Therefore, alternative greener synthesis of these chemicals, sustainable economic methods of waste disposal, scaling up and circular methods using sludge for removing the contaminants are innovative methods that are pursued. There are several improvements in chemical waste treatments using electro-oxidation coupled with solar energy, high performing recycled granular activated charcoal derived from biomass are few advances in the field. Similarly, use of enzymes from microbes for waste removals is a widely used technique for bioremediation. The organisms are genetically engineered to remove hazardous chemicals, dyes, and metals. Novel technologies for mining economically the precious and rare earth elements from e-waste can improve circular economy. However, there is additional need for participation of various nations in working towards greener Earth. There should be pollution awareness in local communities that can work along with Government legislations. [ABSTRACT FROM AUTHOR]

Background & Method: The aim of the study is to establish association between age, sex BMI and flat foot. The parents or the caregivers of the subjects under study were explained the purpose of study and written consent was obtained from the parents or the caregivers. A plastic platform with a plane paper which is immobilized with the help of clips is kept on smooth surface. The child is seated in front of the platform and the foot to be studied is equally impregnated with stamp ink with the help of roller and requested child to put this foot on to the platform but opposite foot out of platform now child is asked to stand up and perform a small flexion of the ipsilateral knee and then go back to initial position removing the foot from the platform. Result: Observation shows that correlation between BMI and plantar arch index PI is significant for both the sides with correlation value 0.31 for right side and 0.49 for left side and p<0.05 for both the side. Conclusion: Foot print of both the foot of every subjects were taken by using Staheli's plantar arch index method and PI values were calculated. The study concluded that incidence of flat foot deformity is higher in the boy than girls and incidence of flat foot decreases with increase in age. From the present study it is also concluded that higher PI are expected in lower age group. [ABSTRACT FROM AUTHOR]

Retinoblastoma is a rare pediatric tumor of the retina, caused by the homozygous loss of the Retinoblastoma 1 (RB1) tumor suppressor gene. Previous microarray studies have identified changes in the expression profiles of coding genes; however, our understanding of how non-coding genes change in this tumor is absent. This is an important area of research, as in many adult malignancies, non-coding genes including LNC-RNAs are used as biomarkers to predict outcome and/or relapse. To establish a complete and in-depth RNA profile, of both coding and non-coding genes, in Retinoblastoma tumors, we conducted RNA-seq from a cohort of tumors and normal retina controls. This analysis identified widespread transcriptional changes in the levels of both coding and non-coding genes. Unexpectedly, we also found rare RNA fusion products resulting from genomic alterations, specific to Retinoblastoma tumor samples. We then determined whether these gene expression changes, of both coding and non-coding genes, were also found in a completely independent Retinoblastoma cohort. Using our dataset, we then profiled the potential effects of deregulated LNC-RNAs on the expression of neighboring genes, the entire genome, and on mRNAs that contain a putative area of homology. This analysis showed that most deregulated LNC-RNAs do not act locally to change the transcriptional environment, but potentially function to modulate genes at distant sites. From this analysis, we selected a strongly down-regulated LNC-RNA in Retinoblastoma, DRAIC, and found that restoring DRAIC RNA levels significantly slowed the growth of the Y79 Retinoblastoma cell line. Collectively, our work has generated the first non-coding RNA profile of Retinoblastoma tumors and has found that these tumors show widespread transcriptional deregulation.