A Secure Image Encryption Algorithm Based on Hill Cipher System

We present a technique of image encryption based on Hill cipher system that provides better security than existing approach of Bibhudendra Acharya et al. by rendering the image content completely scrambled using multiple self-invertible keys, block shuffling and a new developed pel transformation. The Hill cipher algorithm is one of the symmetric key algorithms having several advantages in encryption. However, the inverse of the matrix used for encrypting the plain text in this algorithm may not always exist. Moreover this algorithm is susceptible to known plain text attack. Our proposed algorithm is aimed at better encryption of all types of images even ones with uniform background and makes the image encryption scheme more secure

A cross sectional study of knowledge, attitude and practices of medical students regarding COVID-19 in Northern India

Background: Practicing preventive measures essential to control the spread of infection and possessing the required knowledge, attitude and practices (KAP) towards COVID-19 could possibly affect the behavior and perception of medical students towards the disease which must be observed and studied. Studies have been conducted to assess medical students’ willingness to volunteer in the ongoing COVID-19 pandemic, but not many have focused on their level of pandemic preparedness and eligibility to volunteer. Our study explored the knowledge, attitude and practices of medical students, and also helps to develop effective action plans regarding the reopening of medical colleges in India. Material and methods: This cross-sectional observational study was done in a tertiary care center in North India on Medical and Dental undergraduate students spanning across all professional years after they gave a written informed consent. A self-designed questionnaire was established based on published literature. The study questionnaire consisted of four sections - socio-demographics of students, knowledge, attitudes/beliefs and practice-based statements about COVID-19. Results: 238 students participated in this study and for majority (79.4%) of students the major source of information for gaining knowledge towards COVID-19 was social media. All students were aware that COVID-19 spreads through droplet infection, 94.1% responded that people with chronic illnesses were at high-risk of infection and 91.2% and 88.2% reported that fever and dry cough were the main symptoms of COVID-19 respectively. The majority of students disagreed that they would avoid isolation (n=147), and the students also disagreed on aspect of keeping the report confidential if a near one is affected (n=140). Though there were no statistically significant differences (p<0.05) in the level of knowledge, attitude and practices found between students studying in different professional years. Conclusion: To conclude, the results of our study showed that major source of information for gaining knowledge for COVID-19, was through social media. The students demonstrated a satisfactory level of knowledge, attitude and practices for the prevention of COVID-19

The Structural Features of Trask That Mediate Its Anti-Adhesive Functions

Trask/CDCP1 is a transmembrane protein with a large extracellular and small intracellular domains. The intracellular domain (ICD) undergoes tyrosine phosphorylation by Src kinases during anchorage loss and, when phosphorylated, Trask functions to inhibit cell adhesion. The extracellular domain (ECD) undergoes proteolytic cleavage by serine proteases, although the functional significance of this remains unknown. There is conflicting evidence regarding whether it functions to signal the phosphorylation of the ICD. To better define the structural determinants that mediate the anti-adhesive functions of Trask, we generated a series of deletion mutants of Trask and expressed them in tet-inducible cell models to define the structural elements involved in cell adhesion signaling. We find that the ECD is dispensable for the phosphorylation of the ICD or for the inhibition of cell adhesion. The anti-adhesive functions of Trask are entirely embodied within its ICD and are specifically due to tyrosine phosphorylation of the ICD as this function is completely lost in a phosphorylation-defective tyrosine-phenylalanine mutant. Both full length and cleaved ECDs are fully capable of phosphorylation and undergo phosphorylation during anchorage loss and cleavage is not an upstream signal for ICD phosphorylation. These data establish that the anti-adhesive functions of Trask are mediated entirely through its tyrosine phosphorylation. It remains to be defined what role, if any, the Trask ECD plays in its adhesion functions

Protein synthesis inhibition by didemnin B: Mechanistic insights.

Didemnin B is an inhibitor of eukaryotic protein synthesis and displays potent anti-viral, antineoplastic and immunosuppressive properties. We have established a structure-activity relationship for the inhibition of protein synthesis by didemnin B in vitro. The SAR data obtained indicate that the native conformation of didemnin B is critically important for activity. The relative order of potency of didemnin analogs for protein synthesis inhibition in vitro correlates well with that in intact cells; thus, the inferences drawn regarding SAR for translation inhibition in vitro should also hold true in cells. Previous mechanistic studies had shown that didenmin B specifically inhibits translation elongation by preventing the eEF-2-mediated translocation step and that this inhibitory activity is mediated by eEF-1alpha in vitro . We have examined this mechanism in greater detail. We have shown that didemnin B binds to the ribosome complex, with modest affinity (Kd ∼ 4 muM), in an eEF-1alpha dependent manner. In the presence of didemnin B, eEF-2 is blocked from binding to the ribosome complex and therefore translocation is inhibited. We propose that the interaction between didemnin B and eEF-1alpha on the ribosome locks the ribosome complex in a conformation unfavorable for eEF-2 binding; alternatively, on associating with ribosome-bound eEF-1alpha, didemnin B occupies eEF-2's binding site, thus physically occluding eEF-2 from accessing the ribosome. Currently, there is no way to distinguish between these modes of inhibition. We have shown that inhibition of cellular protein biosynthesis by didemnin B is sufficient to inhibit cell proliferation, but not sufficient to trigger apoptosis. Thus, at low concentrations, didemnin B is a cytostatic agent, but not cytotoxic.Ph.D.BiochemistryPure SciencesUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/131837/2/9938389.pd

A Secure Image Encryption Algorithm Based on Hill Cipher System

We present a technique of image encryption based on Hill cipher system that provides better security than existing approach of Bibhudendra Acharya et al. by rendering the image content completely scrambled using multiple self-invertible keys, block shuffling and a new developed pel transformation. The Hill cipher algorithm is one of the symmetric key algorithms having several advantages in encryption. However, the inverse of the matrix used for encrypting the plain text in this algorithm may not always exist. Moreover this algorithm is susceptible to known plain text attack. Our proposed algorithm is aimed at better encryption of all types of images even ones with uniform background and makes the image encryption scheme more secure

p53 and HuR combinatorially control the biphasic dynamics of microRNA-125b in response to genotoxic stress

Post-transcriptional regulation of p53, by the microRNA miR-125b and the RNA-binding protein HuR, controls p53 expression under genotoxic stress. p53 mRNA translation is repressed by miR-125b, tightly regulating its basal level of expression. The repression is relieved upon DNA damage by a decrease in miR-125b level, contributing to pulsatile expression of p53. The pulse of p53, as also of HuR, in response to UV irradiation coincides with a time-dependent biphasic change in miR-125b level. We show that the cause for the decrease in miR-125b level immediately post DNA-damage is enhanced exosomal export mediated by HuR. The subsequent increase in miR-125b level is due to p53-mediated transcriptional upregulation and enhanced processing, demonstrating miR-125b as a transcriptional and processing target of p53. p53 activates the transcription of primary miR-125b RNA from a cryptic promoter in response to UV irradiation. Together, these regulatory processes constitute reciprocal feedback loops that determine the biphasic change in miR-125b level, ultimately contributing to the fine-tuned temporal regulation of p53 expression in response to genotoxic stress

A TORC2–Akt Feed-Forward Topology Underlies HER3 Resiliency in HER2-Amplified Cancers

The requisite role of HER3 in HER2-amplified cancers is beyond what would be expected as a dimerization partner or effector substrate and it exhibits a substantial degree of resiliency that mitigates the effects of HER2-inhibitor therapies. To better understand the roots of this resiliency, we conducted an in-depth chemical-genetic interrogation of the signaling network downstream of HER3. A unique attribute of these tumors is the deregulation of TORC2. The upstream signals that ordinarily maintain TORC2 signaling are lost in these tumors, and instead TORC2 is driven by Akt. We find that in these cancers HER3 functions as a buffering arm of an Akt-TORC2 feed-forward loop that functions as a self-perpetuating module. This network topology alters the role of HER3 from a conditionally engaged ligand-driven upstream physiologic signaling input to an essential component of a concentric signaling throughput highly competent at preservation of homeostasis. The competence of this signaling topology is evident in its response to perturbation at any of its nodes. Thus, a critical pathophysiologic event in the evolution of HER2-amplified cancers is the loss of the input signals that normally drive TORC2 signaling, repositioning it under Akt dependency, and fundamentally altering the role of HER3. This reprogramming of the downstream network topology is a key aspect in the pathogenesis of HER2-amplified cancers and constitutes a formidable barrier in the targeted therapy of these cancers

A TORC2–Akt Feed-Forward Topology Underlies HER3 Resiliency in HER2-Amplified Cancers

The requisite role of HER3 in HER2-amplified cancers is beyond what would be expected as a dimerization partner or effector substrate and it exhibits a substantial degree of resiliency that mitigates the effects of HER2-inhibitor therapies. To better understand the roots of this resiliency, we conducted an in-depth chemical-genetic interrogation of the signaling network downstream of HER3. A unique attribute of these tumors is the deregulation of TORC2. The upstream signals that ordinarily maintain TORC2 signaling are lost in these tumors, and instead TORC2 is driven by Akt. We find that in these cancers HER3 functions as a buffering arm of an Akt-TORC2 feed-forward loop that functions as a self-perpetuating module. This network topology alters the role of HER3 from a conditionally engaged ligand-driven upstream physiologic signaling input to an essential component of a concentric signaling throughput highly competent at preservation of homeostasis. The competence of this signaling topology is evident in its response to perturbation at any of its nodes. Thus a critical pathophysiological event in the evolution of HER2-amplified cancers is the loss of the input signals that normally drive TORC2 signaling, repositioning it under Akt dependency and fundamentally altering the role of HER3. This reprogramming of the downstream network topology is a key aspect in the pathogenesis of HER2-amplified cancers and constitutes a formidable barrier in the targeted therapy of these cancers