The Start Matters: A Comparative Analysis of Climate Equity Among UNFCCC Country Parties and Country Groups

Incorrect indicators and starting years for emission cumulation can lead to confusion regarding the concepts of climate equity and climate responsibility. This article examines the variations in the results obtained by using different indicators and starting years to calculate climate equity and climate responsibilities among country parties and country groups of the UNFCCC. The article utilizes historical greenhouse gas (GHG) emissions data from 193 countries spanning the period 1850 to 2021. The data is aggregated from various sources including EDGAR, Climate Watch, and Global Carbon Budget (GCB). The article calculates cumulative GHG emissions and cumulative GHG emissions per capita, with starting years 1850, 1970, and 1990. By highlighting differences in various indicators, the article aims to provide a better understanding of climate responsibilities, climate beneficiaries, and climate equity. The results demonstrate that cumulative emissions and cumulative emissions per capita are scientific indicators that reveal a country’s level of climate responsibility and climate equity. Negotiators can achieve consensus more easily in the complex system if they have a comprehensive and scientific understanding of climate equity. It is suggested that country groups under the UNFCCC use scientific indicators and methodologies to reveal climate responsibilities and climate equity

Traumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders.

The complexity of the traumatic brain injury (TBI) pathology, particularly concussive injury, is a serious obstacle for diagnosis, treatment, and long-term prognosis. Here we utilize modern systems biology in a rodent model of concussive injury to gain a thorough view of the impact of TBI on fundamental aspects of gene regulation, which have the potential to drive or alter the course of the TBI pathology. TBI perturbed epigenomic programming, transcriptional activities (expression level and alternative splicing), and the organization of genes in networks centered around genes such as Anax2, Ogn, and Fmod. Transcriptomic signatures in the hippocampus are involved in neuronal signaling, metabolism, inflammation, and blood function, and they overlap with those in leukocytes from peripheral blood. The homology between genomic signatures from blood and brain elicited by TBI provides proof of concept information for development of biomarkers of TBI based on composite genomic patterns. By intersecting with human genome-wide association studies, many TBI signature genes and network regulators identified in our rodent model were causally associated with brain disorders with relevant link to TBI. The overall results show that concussive brain injury reprograms genes which could lead to predisposition to neurological and psychiatric disorders, and that genomic information from peripheral leukocytes has the potential to predict TBI pathogenesis in the brain

Astrocyte elevated gene 1: biological functions and molecular mechanism in cancer and beyond

Since its discovery, nearly one decade of research on astrocyte elevated gene 1 (AEG-1) has witnessed expanding knowledge of this molecule, ranging from its role in cancer biology to molecular mechanisms underlying the biological functions. As a multifunctional oncoprotein, AEG-1 has been shown to overexpress in multiple types of human cancer, and the elevation of AEG-1 in tumor cells leads to enhanced phenotypes characteristic of malignant aggressiveness, including increased abilities to proliferate robustly, to invade surrounding tissues, to migrate, to induce neovascularization, and to enhance chemoresistance. The multifunctional role of AEG-1 in tumor development and progression has been found to be associated with several signaling cascades, namely, 1) activation of NF-kappa B, partially through direct interaction with p65; 2) PI3K/AKT signaling triggered by AEG-1 indirectly; 3) enhancement of the transcriptional activity of beta-catenin by indirect activation of MAPK and induction of LEF1; 4) regulation of mi/siRNA-mediated gene silencing by interacting with SND1; and 5) promotion of protective autophagy; in addition to possibly unknown mechanisms. Elevated AEG-1 expression is seen in nearly all tumor types, and in most cases AEG-1 positively correlates with tumor progression and poorer patient survival. Taken together, AEG-1 might represent a potential prognostic biomarker and therapeutic target

BadSQA: Stealthy Backdoor Attacks Using Presence Events as Triggers in Non-Intrusive Speech Quality Assessment

Non-Intrusive speech quality assessment (NISQA) has gained significant attention for predicting the mean opinion score (MOS) of speech without requiring the reference speech. In practical NISQA scenarios, untrusted third-party resources are often employed during deep neural network training to reduce costs. However, it would introduce a potential security vulnerability as specially designed untrusted resources can launch backdoor attacks against NISQA systems. Existing backdoor attacks primarily focus on classification tasks and are not directly applicable to NISQA which is a regression task. In this paper, we propose a novel backdoor attack on NISQA tasks, leveraging presence events as triggers to achieving highly stealthy attacks. To evaluate the effectiveness of our proposed approach, we conducted experiments on four benchmark datasets and employed two state-of-the-art NISQA models. The results demonstrate that the proposed backdoor attack achieved an average attack success rate of up to 99% with a poisoning rate of only 3%.Comment: 5 pages, 6 figures,conferenc