The Measurement of Popularity and Prevalence of Software Vulnerability

Prioritizing bug fixes becomes a daunting task due to the increasing number of vulnerability disclosure programs. When making a decision, not only the Common Vulnerability Scoring System (CVSS) but also the probability of exploitation, the trend of particular security issues should be taken into account. This paper aims to discuss the sources and approaches for measuring degree of interest in a specific vulnerability at a particular point in real-time. This research presents а new metric and estimation model which is based on vulnerability assessment. We compared several techniques to determine the most suitable approach and relevant sources for improving vulnerability management and prioritization problems. We chose the Google Trend analytics tool to gather trend data, distinguish main features and build data set. The result of this study is the regression equation which helps efficiently prioritize vulnerabilities considering the public interest in the particular security issue. The proposed method provides the popularity estimation of Common Vulnerabilities and Exposures (CVE) using public resources.

The Challenge of Social Vulnerability Assessment in the Context of Land Use Changes for Sustainable Urban Planning—Case Studies: Developing Cities in Romania

Urban growth triggers massive changes in land use cover, exacerbating extreme natural and technological events. In order for land use planning to be efficient, it requires the integration of comprehensive risk and vulnerability assessment. This paper aims to create a bridge between the existing vulnerability theories and their implementation in land use planning policies and proposes an innovative approach to determine whether the changes in the territorial dynamics of cities draw considerable changes in communities’ social vulnerability. The methodology identifies and selects three case studies from the Urban Atlas inventory, representative of the dynamics of large Romanian cities, taking into consideration the following hazards: earthquakes, floods, and technological hazards. Vulnerability was then assessed by assigning each land use class a specific vulnerability level. The methodology involved assessing the level of vulnerability specific to the situation in 2018 compared to 2006. The results showed that major changes in land use are related to the transition of areas with a low level of vulnerability to areas with a higher level of vulnerability as a result of the urban areas expansion to the detriment of natural and agricultural areas. This is generally translated into a higher degree of vulnerability due to an increased density of artificial elements and of population in the residential areas. The findings of the study of territorial dynamics in the proximity of large industrial operators did not reveal a tendency that differed from the general trend. Although many territorial changes have been observed in the period 2006–2018, it is necessary to extend the analysis, with the issue of the new versions of the Urban Atlas, to confirm the identified trends and to express the up-to-date situation.

The NRF2-Dependent Transcriptional Regulation of Antioxidant Defense Pathways: Relevance for Cell Type-Specific Vulnerability to Neurodegeneration and Therapeutic Intervention

Oxidative stress has been implicated in the etiology and pathobiology of various neurodegenerative diseases. At baseline, the cells of the nervous system have the capability to regulate the genes for antioxidant defenses by engaging nuclear factor erythroid 2 (NFE2/NRF)-dependent transcriptional mechanisms, and a number of strategies have been proposed to activate these pathways to promote neuroprotection. Here, we briefly review the biology of the transcription factors of the NFE2/NRF family in the brain and provide evidence for the differential cellular localization of NFE2/NRF family members in the cells of the nervous system. We then discuss these findings in the context of the oxidative stress observed in two neurodegenerative diseases, Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), and present current strategies for activating NFE2/NRF-dependent transcription. Based on the expression of the NFE2/NRF family members in restricted populations of neurons and glia, we propose that, when designing strategies to engage these pathways for neuroprotection, the relative contributions of neuronal and non-neuronal cell types to the overall oxidative state of tissue should be considered, as well as the cell types which have the greatest intrinsic capacity for producing antioxidant enzymes.

Specific vulnerability of long telomeres to undergo end fusions revealed by mutational analysis of Rap1

The conserved Rap1 protein is part of the shelterin complex that plays critical roles in chromosome end protection and telomere length homeostasis. Previous studies addressed how fission yeast Rap1 contributes to telomere length maintenance, but the mechanism by which the protein inhibits end fusions has remained elusive. Here, we use a genetic screen in combination with high throughput sequencing to identify several amino acid positions in Rap1 that have a key role in end protection. Interestingly, mutations at these sites render cells susceptible to genome instability in a conditional manner with longer telomeres being prone to undergoing end fusions, while short telomeres are sufficiently protected. The protection of long telomeres requires their nuclear envelope attachment mediated by the Rap1-Bqt4 interaction. Our data demonstrates that longer telomeres pose an additional challenge for the maintenance of genome integrity and provides an explanation for a species-specific upper limit in telomere length.

The Gendered Nature of the Risk Factors of the COVID-19 Pandemic and Gender Equality: A Literature Review from a Vulnerability Perspective

The risk factors of COVID-19 are not gender-neutral but gendered. A vulnerability approach to pandemics suggests that females are more prone to risk exposure while there are inequalities in accessing resources and opportunities. These inequalities create a gendered pandemic vulnerability. The current article addresses the specific vulnerability on the gendered risk factors encountered by girls and women due to the gendered pandemic in a global context and their impacts on gender inequality. This study analyses the existing literature on the gendered pandemic and risk factors on females that lead to gender inequality during the COVID-19 pandemic. Thus, this study adopts a vulnerability approach to the pandemic as an analytical concept. Our findings from the systematic literature review suggest that women’s pre-existing vulnerabilities are exacerbated in the wake of the pandemic due to the gendered risk factors worsening the gender equality gap. We conclude by arguing that our study’s finding supports a vulnerability approach to disasters.

AR-negative prostate cancer is vulnerable to loss of JMJD1C demethylase

Prostate cancer is a leading cause of cancer-related mortality in men. The widespread use of androgen receptor (AR) inhibitors has generated an increased incidence of AR-negative prostate cancer, triggering the need for effective therapies for such patients. Here, analysis of public genome-wide CRISPR screens in human prostate cancer cell lines identified histone demethylase JMJD1C (KDM3C) as an AR-negative context-specific vulnerability. Secondary validation studies in multiple cell lines and organoids, including isogenic models, confirmed that small hairpin RNA (shRNA)–mediated depletion of JMJD1C potently inhibited growth specifically in AR-negative prostate cancer cells. To explore the cooperative interactions of AR and JMJD1C, we performed comparative transcriptomics of 1) isogenic AR-positive versus AR-negative prostate cancer cells, 2) AR-positive versus AR-negative prostate cancer tumors, and 3) isogenic JMJD1C-expressing versus JMJD1C-depleted AR-negative prostate cancer cells. Loss of AR or JMJD1C generates a modest tumor necrosis factor alpha (TNFα) signature, whereas combined loss of AR and JMJD1C strongly up-regulates the TNFα signature in human prostate cancer, suggesting TNFα signaling as a point of convergence for the combined actions of AR and JMJD1C. Correspondingly, AR-negative prostate cancer cells showed exquisite sensitivity to TNFα treatment and, conversely, TNFα pathway inhibition via inhibition of its downstream effector MAP4K4 partially reversed the growth defect of JMJD1C-depleted AR-negative prostate cancer cells. Given the deleterious systemic side effects of TNFα therapy in humans and the viability of JMJD1C-knockout mice, the identification of JMJD1C inhibition as a specific vulnerability in AR-negative prostate cancer may provide an alternative drug target for prostate cancer patients progressing on AR inhibitor therapy.

Mitigating the impact of SARS-CoV-2 on residential facilities for persons with intellectual disability and/or autism spectrum disorder: two experiences from the Italian red zone

Purpose Persons with intellectual disability and/or low-functioning autism spectrum didorder are with high support need (ID/ASD-HSN) are among the people who are most vulnerable to the COVID-19 pandemic. The specific vulnerability and the protective factors for persons with ID/LF-ASD attending residential and rehabilitative facilities have however received little attention. This paper aims to describe how two facilities located in the Italian COVID-19 red zone faced the risks associated with the spread of the pandemic and the results they have achieved so far. Design/methodology/approach Interventions to contrast the spread of the pandemic and preserve clients’ health conditions have been systematically monitored and recorded since the very beginning of the pandemic. Findings 26/138 clients had to undergo clinical screening and laboratory tests for COVID-like symptomatology, but only one resulted affected by COVID-19 and survived. Considering that Lombardy had 89,595 cases and 16,262 deaths (January–May 2020), one COVID-19 case/138 clients is a good result. Temporarily limiting physical contacts with friends/family in favor of reducing the burden of risk and adopting a system of prevention/safety strategies directed for persons with ID/LF-ASD attending and their caregivers have been useful measures. Research limitations/implications Structured or semi-structured interviews (using professional caregivers as informant) to confirm behavioral and emotional changes in the clients could not be carried out because of lack of time and resources (which were captured by the management of the pandemic) and could be the next goal for our residential facilities to implement the management of epidemic acute phases in a research-oriented view. Originality/value This study is a service evaluation report about facing COVID-19 pandemic. Only few such studies are present in medical literature about ID/ASD.

Integration of genome-level data to allow identification of subtype-specific vulnerability genes as novel therapeutic targets

The identification of cancer-specific vulnerability genes is one of the most promising approaches for developing more effective and less toxic cancer treatments. Cancer genomes exhibit thousands of changes in DNA methylation and gene expression, with the vast majority likely to be passenger changes. We hypothesised that, through integration of genome-wide DNA methylation/expression data, we could exploit this inherent variability to identify cancer subtype-specific vulnerability genes that would represent novel therapeutic targets that could allow cancer-specific cell killing. We developed a bioinformatics pipeline integrating genome-wide DNA methylation/gene expression data to identify candidate subtype-specific vulnerability partner genes for the genetic drivers of individual genetic/molecular subtypes. Using acute lymphoblastic leukaemia as an initial model, 21 candidate subtype-specific vulnerability genes were identified across the five common genetic subtypes, with at least one per subtype. To confirm the approach was applicable across cancer types, we also assessed medulloblastoma, identifying 15 candidate subtype-specific vulnerability genes across three of four established subtypes. Almost all identified genes had not previously been implicated in these diseases. Functional analysis of seven candidate subtype-specific vulnerability genes across the two tumour types confirmed that siRNA-mediated knockdown induced significant inhibition of proliferation/induction of apoptosis, which was specific to the cancer subtype in which the gene was predicted to be specifically lethal. Thus, we present a novel approach that integrates genome-wide DNA methylation/expression data to identify cancer subtype-specific vulnerability genes as novel therapeutic targets. We demonstrate this approach is applicable to multiple cancer types and identifies true functional subtype-specific vulnerability genes with high efficiency.