Miracle-dz/UniFAR-FTUs huggingface dataset:
Phishing for Long Tails: Examining Organizational Repeat Clickers and Protective Stewards

Organizational cybersecurity efforts depend largely on the employees who reside within organizational walls. These individuals are central to the effectiveness of organizational actions to protect sensitive assets, and research has shown that they can be detrimental (e.g., sabotage and computer abuse) as well as beneficial (e.g., protective motivated behaviors) to their organizations. One major context where employees affect their organizations is phishing via email systems, which is a common attack vector used by external actors to penetrate organizational networks, steal employee credentials, and create other forms of harm. In analyzing the behavior of more than 6,000 employees at a large university in the Southeast United States during 20 mock phishing campaigns over a 19-month period, this research effort makes several contributions. First, employees’ negative behaviors like clicking links and then entering data are evaluated alongside the positive behaviors of reporting the suspected phishing attempts to the proper organizational representatives. The analysis displays evidence of both repeat clicker and repeat reporter phenomena and their frequency and Pareto distributions across the study time frame. Second, we find that employees can be categorized according to one of the four unique clusters with respect to their behavioral responses to phishing attacks—“Gaffes,” “Beacons,” “Spectators,” and “Gushers. ” While each of the clusters exhibits some level of phishing failures and reports, significant variation exists among the employee classifications. Our findings are helpful in driving a new and more holistic stream of research in the realm of all forms of employee responses to phishing attacks, and we provide avenues for such future research.
Uncertainty Avoidance as a Moderating Factor to the Self-Congruity Concept: The Development of a Conceptual Framework

The aim of this article was to propose a framework based on the theory of self-congruity and on Hofstede’s uncertainty avoidance. The framework was to combine destination personality, self-congruity, uncertainty avoidance, and tourists’ revisit intention. The present conceptual paper proposed an integrated model of self-congruity which incorporates the effect of uncertainty avoidance. More importantly, the uncertainty avoidance was introduced as a moderator between self-congruity and revisit intention. Based on the theoretical framework proposed in this article, the estimated results affirmed the applicability of the theory of self-congruity for tourism research. Moreover, by extending the theoretical model through the incorporation of a variable of uncertainty avoidance in the context of tourism, this article offers a significant contribution to the tourism literature. It is important to understand how the theory of self-congruity applies across a broad cultural spectrum. This article also offers several implications for destination marketing organizations from a practical perspective.
Epidermal Growth Factor Receptor Mutation Status and Response to Tyrosine Kinase Inhibitors in Advanced Chinese Female Lung Squamous Cell Carcinoma: A Retrospective Study

Background The frequency of epidermal growth factor receptor (EGFR) mutations and the efficacy of tyrosine kinase inhibitor (TKI) in Chinese female patients with lung squamous cell carcinoma (SCC) are unknown. This study was designed to investigate the incidence of EGFR mutations and the role of targeted therapy in advanced Chinese female lung SCC patients. Methods Advanced female patients diagnosed with lung SCC at the Shanghai Chest Hospital between January 2013 and December 2018 were retrospectively analyzed. Results A total of 4223 advanced lung SCC patients were screened, and there were 154 female lung SCC patients who had underwent EGFR mutation detection. Positive EGFR mutations were found in 29.9% (46/154) of female lung SCC patients, including twenty-three 19del mutation (14.9%), twenty-one 21L858R mutation (13.6%) and other mutations (1.4%, 21861Q and 20ins). For 45 EGFR positive mutation female SCC patients, the median progression-free survival (PFS) of patients who received EGFR-TKI therapy (n=38) was 8.0 months (95% CI, 5.4-10.7 months), which was significantly longer than patients who were treated with chemotherapy (8.0 vs. 3.2 months, p=0.024), and the median overall survival (OS) was also longer (24.9 months vs. 13.9 months, p=0.020). The objective response rate (ORR) was 44.7% (17/38), and the disease control rate (DCR) was 81.6% (31/38). For 105 female SCC patients with EGFR negative mutation, the median OS was 18.6 months (95% CI, 14.2-22.9 months) and it was no different from that of EGFR positive mutation patients (18.6 vs. 22.8 months, p=0.377). Conclusion For advanced Chinese female lung SCC patients with EGFR positive mutations, targeted therapy could confer longer PFS and OS than chemotherapy, but the survival was similar with patients who were negative EGFR mutations.
Testicular Growth and Pubertal Onset in GH-Deficient Children Treated With Growth Hormone: A Retrospective Study

The prevalence of idiopathic oligozoospermia has been esteemed as high as 75%. An Italian survey has reported bilateral testicular hypotrophy in 14% of final-year high school students. The search for determinants of testicular growth in childhood is important for the primary prevention of spermatogenic failure. Therefore, this retrospective study aimed to evaluate the testicular growth and pubertal onset in deficient children treated recombinant human growth hormone (rhGH). To accomplish this, the clinical charts of 93 patients with GH deficiency (GHD) were carefully reviewed. Their mean age at the time of diagnosis was 11.2 ± 2.4 years. rhGH was administered for 44.0 ± 22.4 months, and the onset of puberty was recorded after a mean of 25.8 ± 22.4 months from the first rhGH administration. As expected, serum insulin-like growth factor 1 (IGF1) levels increased significantly after treatment. Before rhGH therapy, the Tanner stage was I in 59 out of 70 boys (84.3%), II in 8/70 (11.4%), III in 3/70 (4.3%). No one was on stage IV or V. The mean Tanner stage was 1.19 ± 0.51. At the last visit, the Tanner stage was I in 8/72 boys (11.1%), II in 6/72 (8.3%), III in 6/72 (8.3%), IV in 16/72 (22.2%), and V in 36/72 (50.0%). After a mean of 44.0 ± 22.4 months of rhGH treatment, the mean Tanner stage was 4.05 ± 1.30. Patients treated with rhGH showed a significant testicular volume (TV) growth over time, whereas no growth was observed in age-matched but not yet treated patients, even when the age was compatible with a spontaneous start of puberty. The multivariate regression analysis showed that the duration of treatment and the mean rhGH dose significantly predicted the percentage of TV increase. In contrast, age, serum FSH, and IGF1 levels, and final rhGH dose did not impact TV growth over time. In conclusion, these findings suggest that GH may play a role in testicular growth and pubertal onset, despite the descriptive nature of this study. Further properly designed studies are needed to confirm these findings. This knowledge may be useful to implement the diagnostic-therapeutic algorithm in case of a lack of testicular growth in childhood.
Challenges in Clinicogenetic Correlations: One Gene – Many Phenotypes

Progress in genetics – particularly the advent of next‐generation sequencing (NGS) – has enabled an unparalleled gene discovery and revealed unmatched complexity of genotype–phenotype correlations in movement disorders. Among other things, it has emerged that mutations in one and the same gene can cause multiple, often markedly different phenotypes. Consequently, movement disorder specialists have increasingly experienced challenges in clinicogenetic correlations.
A Self‐Reported Clinical Tool Predicts Falls in People with Parkinson's Disease

A 3‐step clinical prediction tool including falling in the previous year, freezing of gait in the past month and self‐selected gait speed <1.1 m/s has shown high accuracy in predicting falls in people with Parkinson's disease (PD). The accuracy of this tool when including only self‐report measures is yet to be determined.
H2S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins

Endogenously produced hydrogen sulfide (H2S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H2S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present study was undertaken to investigate the effects of a novel H2S prodrug, SG-1002, on stress induced hypertrophic signaling in murine HL-1 cardiac muscle cells. Treatment of HL-1 cells with SG-1002 under serum starvation without or with H2O2 increased the levels of H2S, H2S producing enzyme, cystathionine β-synthase (CBS) as well as antioxidant protein levels, such as super oxide dismutase1 (SOD1) and catalase and decreased oxidative stress. SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in stressed HL-1 cells. Treatment with SG-1002 caused a significant induction of cell viability and a marked reduction of cellular cytotoxicity in HL-1 cells under serum starvation incubated or with H2O2. Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H2S levels or H2S producing enzyme, CBS and antioxidant proteins.
The strange role of brain lesion size in cognitive neuropsychology

The size of brain lesions is a variable that is frequently considered in cognitive neuropsychology. In particular, lesion-deficit inference studies often control for lesion size, and the association of lesion size with post-stroke cognitive deficits and its predictive value are studied. In the present article, the role of lesion size in cognitive deficits and its computational or design-wise consideration is discussed and questioned. First, I argue that the commonly discussed role or effect of lesion size in cognitive deficits eludes us. A generally valid understanding of the causal relation of lesion size, lesion location, and cognitive deficits is unachievable. Second, founded on the theory of covariate control, I argue that lesion size control is no valid covariate control. Instead, it is identified as a procedure with only situational benefits, which is supported by empirical data. This theoretical background is used to suggest possible research practices in lesion-deficit inference, post-stroke outcome prediction, and behavioural studies. Last, control for lesion size is put into a bigger methodological and also historical context – it is identified to relate to a long-known association problem in neuropsychology, which was previously discussed from the perspectives of a mislocalisation in lesion-deficit mapping and the symptom complex approach. Highlights - Lesion size is a factor that is often considered or controlled in neuropsychology - No general causal relation between lesion size, lesion location and deficit exists - Lesion size in brain mapping, outcome prediction and behavioural study is discussed - Lesion size control is no valid covariate control - Practical suggestions and guidelines how to consider lesion size are provided
Comparative Analysis of Public RNA-Sequencing Data from Human Intestinal Enteroid (HIEs) Infected with Enteric RNA Viruses Identifies Universal and Virus-Specific Epithelial Responses

Acute gastroenteritis (AGE) has a significant disease burden on society. Noroviruses, rotaviruses and astroviruses are important viral causes of AGE but are relatively understudied enteric pathogens. Recent developments in novel biomimetic human models of enteric disease are opening new possibilities for studying human-specific hostmicrobe interactions. Human intestinal enteroids (HIE), which are epithelium-only intestinal organoids derived from stem cells isolated from human intestinal biopsy tissues, have been successfully used to culture representative norovirus, rotavirus and astrovirus strains. Previous studies investigated host-virus interactions at the intestinal epithelial interface by individually profiling the epithelial transcriptional response to a member of each virus family by RNA sequencing (RNA-seq). We used these publicly available datasets to uniformly analyze these data and identify shared and unique transcriptional changes in the human intestinal epithelium upon human enteric virus infections.
Fast ontogenetic growth drives steep evolutionary scaling of metabolic rate

Metabolic rate (MR) changes with body mass (BM) as MR = aBMb, where a is a normalisation constant (log–log intercept) and b the scaling exponent (log–log slope). This scaling relationship is fundamental to biology and widely applied, yet a century of research has provided little consensus on why and how steeply metabolic rate scales with body mass. I here show that ontogenetic (within-individual) b can be strongly and positively related to growth rates of juvenile fish when food availability is naturally restricted, with fast growing individuals having steep and near-isometric metabolic scaling (b ≈ 1). I suggest that the steep evolutionary (among-species) scaling also found for fishes (b also approaching 1) is a by-product of natural selection for these fast growing individuals early in ontogeny, and that a weaker relationship between metabolic scaling and growth later in life causes variation in b at lower taxonomic levels (within orders or species). I support these ideas by showing that b within fish orders is linked to natural mortality rates of fish larvae.
Hybrid Histidine Kinase BinK Represses Vibrio fischeri Biofilm Signaling at Multiple Developmental Stages

Bacteria are often in a biofilm state, and transitions between planktonic and biofilm lifestyles are important for pathogenic, beneficial, and environmental microbes. The critical nature of biofilm formation during Vibrio fischeri colonization of the Hawaiian bobtail squid light organ provides an opportunity to study development of this process in vivo using a combination of genetic and imaging approaches. ABSTRACT The symbiosis between the Hawaiian bobtail squid, Euprymna scolopes, and its exclusive light organ symbiont, Vibrio fischeri, provides a natural system in which to study host-microbe specificity and gene regulation during the establishment of a mutually beneficial symbiosis. Colonization of the host relies on bacterial biofilm-like aggregation in the squid mucus field. Symbiotic biofilm formation is controlled by a two-component signaling (TCS) system consisting of regulators RscS-SypF-SypG, which together direct transcription of the symbiosis polysaccharide Syp. TCS systems are broadly important for bacteria to sense environmental cues and then direct changes in behavior. Previously, we identified the hybrid histidine kinase BinK as a strong negative regulator of V. fischeri biofilm regulation, and here we further explore the function of BinK. To inhibit biofilm formation, BinK requires the predicted phosphorylation sites in both the histidine kinase (H362) and receiver (D794) domains. Furthermore, we show that RscS is not essential for host colonization when binK is deleted from strain ES114, and imaging of aggregate size revealed no benefit to the presence of RscS in a background lacking BinK. Strains lacking RscS still suffered in competition. Finally, we show that BinK functions to inhibit biofilm gene expression in the light organ crypts, providing evidence for biofilm gene regulation at later stages of host colonization. Overall, this study provides direct evidence for opposing activities of RscS and BinK and yields novel insights into biofilm regulation during the maturation of a beneficial symbiosis. IMPORTANCE Bacteria are often in a biofilm state, and transitions between planktonic and biofilm lifestyles are important for pathogenic, beneficial, and environmental microbes. The critical nature of biofilm formation during Vibrio fischeri colonization of the Hawaiian bobtail squid light organ provides an opportunity to study development of this process in vivo using a combination of genetic and imaging approaches. The current work refines the signaling circuitry of the biofilm pathway in V. fischeri, provides evidence that biofilm regulatory changes occur in the host, and identifies BinK as one of the regulators of that process. This study provides information about how bacteria regulate biofilm gene expression in an intact animal host.
The CTEXT complex in Saccharomyces cerevisiae plays a crucial role in degrading distinct sets of aberrant mRNAs by the nuclear exosome

In Saccharomyces cerevisiae, DRN (Decay of RNA in the Nucleus) requiring Cbc1/2p, Tif4631p, and Upf3p promotes the exosomal degradation of aberrantly long 3′-extended-, export-defective transcripts and a small group of normal (special) mRNAs. In this study, using a systematic proteomic analysis we show that each of the known components interacts with one another and they exist as a separate complex, which was dubbed CTEXT (CBC-Tif4631p-dependent EXosome Targeting). We also identified a DEAD-box RNA helicase Dbp2p as an additional novel component of CTEXT during this analysis which was further bolstered by the finding that genomic deletions of Dbp2p led to the stabilization of all the signature nuclear messages. Interestingly, the RRM domain of Tif4631p located at the extreme N-termini of this polypeptide was found to play a vital role in in mediating the interaction of the CTEXT with the core exosome complex. These inferences were substantiated by the finding that deletion of this domain led to the functional impairment of the CTEXT complex. Thus, the CTEXT constitutes an independent complex that assists the nuclear exosome in degrading the select classes of nuclear transcripts in Saccharomyces cerevisiae.
Local density approximation and generalized gradient approximation calculations for oxygen and silicon vacancies in silica

Neutral oxygen and silicon vacancies’ energies in silica polytypes (α-quartz, β-cristobalite, and stishovite) have been studied using the local density approximation (LDA) and the generalized gradient approximation (GGA) for the exchange correlation. While the energies of formation of unrelaxed oxygen vacancies are remarkably constant (9.9 ±0.1 eV) in the three studied systems in GGA, the relaxation behavior is quite different: A strong Si–Si bond is formed in α-quartz, a weak one in β-cristobalite, while no bond at all is formed in stishovite. In α-quartz, peroxyl bridges are formed as the consequences of the relaxation of silicon vacancies. Their energy of formation from O2 (gas) is low (about 2 eV).
Subthalamic–Cortical Network Reorganization during Parkinson's Tremor

Tremor, a common and often primary symptom of Parkinson's disease, has been modeled with distinct onset and maintenance dynamics. To identify the neurophysiologic correlates of each state, we acquired intraoperative cortical and subthalamic nucleus recordings from 10 patients (9 male, 1 female) performing a naturalistic visual–motor task. From this task, we isolated short epochs of tremor onset and sustained tremor. Comparing these epochs, we found that the subthalamic nucleus was central to tremor onset, as it drove both motor cortical activity and tremor output. Once tremor became sustained, control of tremor shifted to cortex. At the same time, changes in directed functional connectivity across sensorimotor cortex further distinguished the sustained tremor state. SIGNIFICANCE STATEMENT Tremor is a common symptom of Parkinson's disease (PD). While tremor pathophysiology is thought to involve both basal ganglia and cerebello–thalamic–cortical circuits, it is unknown how these structures functionally interact to produce tremor. In this article, we analyzed intracranial recordings from the subthalamic nucleus and sensorimotor cortex in patients with PD undergoing deep brain stimulation surgery. Using an intraoperative task, we examined tremor in two separate dynamic contexts: when tremor first emerged, and when tremor was sustained. We believe that these findings reconcile several models of Parkinson's tremor, while describing the short-timescale dynamics of subcortical–cortical interactions during tremor for the first time. These findings may describe a framework for developing proactive and responsive neurostimulation models for specifically treating tremor.
SpeciesRax: A Tool for Maximum Likelihood Species Tree Inference from Gene Family Trees under Duplication, Transfer, and Loss

Species tree inference from gene family trees is becoming increasingly popular because it can account for discordance between the species tree and the corresponding gene family trees. In particular, methods that can account for multiple-copy gene families exhibit potential to leverage paralogy as informative signal. At present, there does not exist any widely adopted inference method for this purpose. Here, we present SpeciesRax, the first maximum likelihood method that can infer a rooted species tree from a set of gene family trees and can account for gene duplication, loss, and transfer events. By explicitly modelling events by which gene trees can depart from the species tree, SpeciesRax leverages the phylogenetic rooting signal in gene trees. SpeciesRax infers species tree branch lengths in units of expected substitutions per site and branch support values via paralogy-aware quartets extracted from the gene family trees. Using both empirical and simulated datasets we show that SpeciesRax is at least as accurate as the best competing methods while being one order of magnitude faster on large datasets at the same time. We used SpeciesRax to infer a biologically plausible rooted phylogeny of the vertebrates comprising 188 species from 31612 gene families in one hour using 40 cores. SpeciesRax is available under GNU GPL at https://github.com/BenoitMorel/GeneRax and on BioConda.
Revisiting the evolutionary history of pigs via de novo mutation rate estimation by deep genome sequencing on a three-generation pedigree

The mutation rate used in the previous analyses of pig evolution and demographics was cursory and brought potential bias in inferring its history. Herein, we estimated de novo mutation rate of pigs using high-quality whole-genome sequencing data from nine individuals in a three-generation pedigree through stringent filtering and validation. The estimated mutation rate was 3.6 × 10−9 per generation, corresponding to 1.2 × 10−9 per site per year. Using this mutation rate, we re-investigated the evolutionary history of pigs. Our estimates agreed to the divergence time of ~10 kiloyears ago (Kya) between European wild and domesticated pigs, consistent with the domestication time of European pigs based on archaeological evidence. However, other divergence events inferred here were not as ancient as previously described. Our estimates suggested that: Sus speciation occurred ~1.36 Million years ago (Mya); European pigs split up with Asian ones only ~219 Kya; South and North Chinese wild pig split ~25 Kya. Meanwhile, our results showed that the most recent divergence event between Chinese wild and domesticated pigs occurred in the Hetao plain, North China, approximately 20 Kya, supporting the possibly independent domestication in North China along the middle Yellow River. We also found the maximum effective population size of pigs was ~6 times larger than the previous estimate. Notably by simulation, we confirmed an archaic migration from other Sus species originating ~ 2 Mya to European pigs during pigs’ western colonization, which possibly interfered with the previous demographic inference. Our findings advance the understanding of pig evolutionary history.