Miracle-dz/UniFAR-FTUs huggingface dataset:
Seismic constraints on caldera dynamics from the 2015 Axial Seamount eruption

Volcano monitoring goes into the deep Axial Seamount is a large and active submarine volcano along the Juan de Fuca midocean ridge off the coast of the western United States. Eruptions in 1998 and 2011 were followed by periods of magma recharge, making it an ideal location to include in the Ocean Observatories Initiative Cabled Array. Wilcock et al. present real-time seismic data from the most recent eruption in April 2015 that allow the tracking of magma before and during eruption. Nooner and Chadwick show that eruptions are predictable on the basis of deformation data. As magma pools underneath it, Axial Seamount inflates and erupts when the inflation hits a threshold. Both studies elucidate the dynamics of submarine volcanoes, which vastly outnumber their aboveground counterparts. Science, this issue p. 1395, p. 1399 Seismic data track the movement of magma during the April 2015 Axial Seamount eruption. Seismic observations in volcanically active calderas are challenging. A new cabled observatory atop Axial Seamount on the Juan de Fuca ridge allows unprecedented real-time monitoring of a submarine caldera. Beginning on 24 April 2015, the seismic network captured an eruption that culminated in explosive acoustic signals where lava erupted on the seafloor. Extensive seismic activity preceding the eruption shows that inflation is accommodated by the reactivation of an outward-dipping caldera ring fault, with strong tidal triggering indicating a critically stressed system. The ring fault accommodated deflation during the eruption and provided a pathway for a dike that propagated south and north beneath the caldera’s east wall. Once north of the caldera, the eruption stepped westward, and a dike propagated along the extensional north rift.
Frankixalus, a New Rhacophorid Genus of Tree Hole Breeding Frogs with Oophagous Tadpoles

Despite renewed interest in the biogeography and evolutionary history of Old World tree frogs (Rhacophoridae), this family still includes enigmatic frogs with ambiguous phylogenetic placement. During fieldwork in four northeastern states of India, we discovered several populations of tree hole breeding frogs with oophagous tadpoles. We used molecular data, consisting of two nuclear and three mitochondrial gene fragments for all known rhacophorid genera, to investigate the phylogenetic position of these new frogs. Our analyses identify a previously overlooked, yet distinct evolutionary lineage of frogs that warrants recognition as a new genus and is here described as Frankixalus gen. nov. This genus, which contains the enigmatic ‘Polypedates’ jerdonii described by Günther in 1876, forms the sister group of a clade containing Kurixalus, Pseudophilautus, Raorchestes, Mercurana and Beddomixalus. The distinctiveness of this evolutionary lineage is also corroborated by the external morphology of adults and tadpoles, adult osteology, breeding ecology, and life history features.
SPECT in patients with cortical visual loss.

Single-photon emission computed tomography (SPECT) with 99mTc-hexamethylpropyleneamine oxime (HMPAO) was used to investigate changes in cerebral blood flow in seven patients with cortical visual impairment. Traumatic brain injury (TBI) was the cause of cortical damage in two patients, cerebral ischemia in two patients and carbon monoxide (CO) poisoning, status epilepticus and Alzheimer's Disease (AD) each in three separate patients. The SPECT scans of the seven patients were compared to T2-weighted magnetic resonance image (MRI) scans of the brain to determine the correlation between functional and anatomical findings. In six of the seven patients, the qualitative interpretation of the SPECT studies supported the clinical findings (i.e., the visual field defect) by revealing altered regional cerebral blood flow (rCBF) in the appropriate regions of the visual pathway. MR scans in all of the patients, on the other hand, were either normal or disclosed smaller lesions than those detected by SPECT. We conclude that SPECT may reveal altered rCBF in patients with cortical visual impairment of various etiologies, even when MRI studies are normal or nondiagnostic.
Segmental enhancement inversion of small renal oncocytoma: differences in prevalence according to tumor size.

OBJECTIVE The purpose of this study was to retrospectively assess the prevalence of segmental enhancement inversion of small renal oncocytomas according to tumor size. MATERIALS AND METHODS Thirty-three patients (19 men, 14 women; mean age, 61 years; range, 40-74 years) with 33 oncocytomas diagnosed at surgical resection who had undergone contrast-enhanced biphasic CT between January 2000 and December 2011 were included. CT scans were analyzed by two radiologists blinded to the specifics of the pathology report for size, presence of segmental enhancement inversion, enhancement pattern, and homogeneity. Segmental enhancement inversion was present when a renal mass was divided into two differently enhanced segments in the corticomedullary phase (30-40 seconds after contrast injection) with the degree of enhancement reversed in the nephrographic phase (120-180 seconds after contrast injection). The masses were further assessed for fibrous septa, cystic change, hemorrhage, and necrosis. For statistical analysis, the Pearson chi-square test and linear regression were used to evaluate the relation between the prevalence of segmental enhancement inversion and tumor size or pathologic changes. RESULTS The mean diameter of 33 renal oncocytomas was 2.65 cm (range, 0.8-4.8 cm). There was no significant linear trend according to size (p = 0.762), although segmental enhancement inversion was significantly (p = 0.006) more common (10/12) in tumors measuring 1.5-2.9 cm. Pathologic change was present in 14 oncocytomas. There was no significant linear trend according to size (p = 0.068), but 2.5-cm and larger tumors had a significantly higher prevalence (57.9%) (p = 0.036). Segmental enhancement inversion was more common (13/19) in tumors without pathologic change (p = 0.024). CONCLUSION Segmental enhancement inversion was a characteristic finding in our series of small renal oncocytomas and was more common in tumors measuring 1.5-2.9 cm. Pathologic changes such as central scar were more common in oncocytomas larger than 2.5 cm and may be related to the low occurrence of segmental enhancement inversion.
Interactions between perception and action programming: Evidence from visual extinction and optic ataxia

We report a series of 7 experiments examining the interaction between visual perception and action programming, contrasting 2 neuropsychological cases: a case of visual extinction and a case with extinction and optic ataxia. The patients had to make pointing responses to left and right locations, whilst identifying briefly presented shapes. Different patterns of performance emerged with the two cases. The patient with “pure” extinction (i.e., extinction without optic ataxia) showed dramatic effects of action programming on perceptual report. Programming an action to the ipsilesional side increased extinction (on 2-item trials) and tended to induce neglect (on 1-item trials); this was ameliorated when the action was programmed to the contralesional side. Separable effects of using the contralesional hand and pointing to the contralesional side were apparent. In contrast, the optic ataxic patient showed few effects of congruency between the visual stimulus and the action, but extinction when an action was programmed. This effect was particularly marked when actions had to be made to peripheral locations, suggesting that it reflected reduced resources to stimuli. These effects all occurred using stimulus exposures that were completed well before actions were effected. The data demonstrate interactions between action programming and visual perception. Programming an action to the affected side with the contralesional limb reduces “pure” extinction because attention is coupled to the end point of the action. However, in a patient with deficient visuo-motor coupling (optic ataxia), programming an action can increase a spatial deficit by recruiting resources away from perceptual processing. The implications for models of perception and action are discussed.
Nucleotide Oligomerization and Binding Domain 2-Dependent Dendritic Cell Activation Is Necessary for Innate Immunity and Optimal CD8+ T Cell Responses to Influenza A Virus Infection

ABSTRACT Nucleotide oligomerization and binding domain (NOD)-like receptors (NLRs) are important in the innate immune response to viral infection. Recent findings have implicated NLRP3, NOD2, and NLRX1 as important players in the innate antiviral response, but their roles in the generation of adaptive immunity to viruses are less clear. We demonstrate here that NOD2 is critical for both innate and adaptive immune responses necessary for controlling viral replication and survival during influenza A virus (IAV) infection. Nod2 −/− mice have reduced beta interferon (IFN-β) levels and fewer activated dendritic cells (DCs), and the DCs are more prone to cell death in the lungs of Nod2 −/− mice during IAV infection. In agreement with the role for DCs in priming adaptive immunity, the generation of virus-specific CD8+ T cells and their activation and production of IFN-γ were lower in Nod2 −/− mice. Furthermore, Nod2 −/− DCs, when cocultured with T cells in vitro, have a lower costimulatory capacity. Thus, Nod2 −/− DCs are unable to efficiently prime CD8+ T cells. These findings demonstrate that Nod2 is critical for the generation of both innate and adaptive immune responses necessary for controlling IAV infection. IMPORTANCE The innate immune system is the host's first line of defense against invading pathogens and is also necessary for alerting and activating T and B cells to initiate the adaptive immune response. We demonstrate here that the innate immune receptor NOD2 is required for the production of antiviral type I interferons and the activation and survival of dendritic cells that, in turn, alert T cells to the presence of influenza A virus infection. In mice that are missing NOD2, interferon levels are lower, and the CD8+ T cell response is impaired. As a result, the animals cannot control virus replication in their lungs as efficiently. This discovery helps us understand how the body naturally responds to virus infection and may help in the development of vaccines that use NOD2 to stimulate the CD8+ T cell response, thus providing better protection against influenza A virus infection.
Antenatal differential diagnosis of congenital chloride diarrhea: A case report

Congenital chloride diarrhea (CCD) is a rare disease characterized by profound, watery diarrhea. It is inherited as an autosomal recessive trait and is caused by a dysfunction of electrolyte transport in the brush border of the ileum. CCD is a medically treatable condition but is frequently misdiagnosed as a surgically treatable condition, such as bowel obstruction, because of similar antenatal ultrasonographic findings. Therefore, a correct diagnosis is of upmost importance before treatment initiation. Although some methods for antenatal differential diagnosis were reported, antenatal diagnosis of CCD remains difficult. Here, we report the case of a patient with CCD, which was presumed antenatally and confirmed postnatally. We also discuss the results of antenatal ultrasonography and amniocentesis and provide some tips regarding ultrasonographic findings for the antenatal differential diagnosis of CCD. Further, we present a brief literature review.
The Notch pathway in colorectal cancer

Colorectal cancer (CRC) is the third leading cause of cancer death worldwide. It is also the third most common cancer diagnosis among men, and the second most common cancer diagnosis among women. Globally, CRC can account for nearly 694,000 annual deaths. It is widely appreciated that CRC is the result of dysregulated cellular pathways that promote an inappropriate stem‐cell‐like phenotype, apoptotic resistance, unchecked proliferation and metastatic spread. While no single pathway is responsible for all of these attributes, an array of recent studies suggests a pivotal role for abnormal Notch‐1 signaling in CRC, in part due to interconnectivity of Notch with other pathways. This review will summarize recent evidence for a role of Notch signaling in CRC, will consider interconnectivity between Notch and other pathways involved in CRC and will discuss the possible utility of targeting Notch as a CRC therapeutic.
In‐vitro evaluation of bioadhesion in particulate systems and possible improvement using interactive mixtures

The bioadhesion of tablet components was tested using the fracture method (maximum tensile stress in detaching the sample from mucus membrane) and comparing traditional tablet specimens with powder monolayers. Both nonadhesive excipients and established mucoadhesive materials were investigated. Some nonadhesive materials showed unexpectedly good adhesive properties when tested as tablets but not as powders. Conversely, some bioadhesive materials had unexpectedly low adhesive properties when tested as tablets. Thus, powder specimens of some materials appear to give more realistic results than tablet specimens in this respect. The use of powder specimens seems particularly applicable for testing dispersible tablets intended fortransmucosal absorption. Potential for increasing the bioadhesive properties of coarse, nonadhesive carrier particles by coating them with fine particles of bioadhesive materials during dry mixing (forming interactive mixtures) was also studied. The tensile strength of the adhesive bond between the mucosa and the nonadhesive excipients was improved when fine cross‐linked carboxymethyl cellulose sodium (Ac‐Di‐Sol) particles were added. The addition of increased proportions of Ac‐Di‐Sol initially improved the bioadhesive properties until a plateau was reached. A standardised test of bioadhesive capacity could therefore involve the addition of fine bioadhesive powders to coarse carriers in proportions close to those providing monoparticulate surface coverage. Interactive mixtures such as these may also offer potential as a tool for use in the development of bioadhesive drug formulations.
Factors associated with coronary artery calcification in young female patients with SLE

Background: With improved survival rates of patients with systemic lupus erythematosus (SLE), damage such as accelerated atherosclerosis gains increasing importance. Objective: To identify the prevalence of coronary artery calcifications (CAC) in asymptomatic patients. Methods: Electron beam tomography (EBT) was performed in 75 female patients with SLE aged <50. The results were correlated with traditional and SLE related factors associated with CAC. 49 women with symptomatic coronary heart disease (CHD) and 279 women without CHD were also analysed. Results: Overall, 21/75 (28%) patients had CAC. Low HDL cholesterol levels <1.40 mmol/l (p=0.03, OR=1.8, 67% v 39%) and cigarette smoking (p=0.01, OR=5.7, 76% v 44%) were identified as factors associated with CAC. Hypertension and high cholesterol were more common in women with CHD (p<0.01) than in those without CHD. SLE related factors were proteinuria (1331 v 465 mg/day, p=0.02), impaired renal function (p=0.02, OR=2.6, 26% v 6%), and high C3 levels (p=0.04, OR=1.8, 65% v 38%). High C3 levels were also more common in symptomatic CHD (p=0.02). The prevalence of Sm antibodies was lower in patients with CAC (15% v 42%, p=0.03). In a multivariate analysis, cigarette smoking, reduced renal function, high C3, and a cumulative steroid dose above 30 g were the most important CAC associated factors in the lupus cohort. Conclusion: A subgroup of patients with SLE with CAC without any clinical symptoms of CHD was identified by EBT. Therefore, EBT is useful for assessing asymptomatic atherosclerosis in this group.
Characterizing on-road driving performance in individuals with traumatic brain injury who pass or fail an on-road driving assessment

Abstract Objective: To characterise on-road driving performance in individuals with traumatic brain injury who fail on-road driving assessment, compared with both those who pass assessment and healthy controls, and the injury and cognitive factors associated with driving performance. Study design: Cross-sectional. Methods: Forty eight participants with traumatic brain injury (Age M = 40.50 SD = 14.62, 77% male, post-traumatic amnesia days M = 28.74 SD =27.68) and 48 healthy matched controls completed a standardised on-road driving assessment in addition to cognitive measures. Results: Individuals with traumatic brain injury who passed on-road driving assessment performed no differently from controls while individuals with traumatic brain injury who failed the assessment demonstrated significantly worse driving performance relative to controls across a range of driving manoeuvres and error types including observation of on-road environment, speed control, gap selection, lane position, following distance and basic car control. Longer time post-injury and reduced visual perception were both significantly correlated with reduced driving skills. Conclusions: This exploratory study indicated that drivers with traumatic brain injury who failed on-road assessment demonstrated a heterogeneous pattern of impaired driving manoeuvres, characterised by skill deficits across both operational (e.g., basic car control and lane position) and tactical domains (e.g., following distance, gap selection, and observation) of driving. These preliminary findings can be used for implementation of future driving assessments and rehabilitation programs. Implications for rehabilitation Clinicians should be aware that the majority of individuals with traumatic brain injury were deemed fit to resume driving following formal on-road assessment, despite having moderate to very severe traumatic brain injuries. Drivers with traumatic brain injury who failed an on-road assessment demonstrated a heterogeneous pattern of impaired skills including errors with observation, speed regulation, gap selection, and vehicle control and accordingly had difficulty executing a diverse range of common driving manoeuvres. Comprehensive, formal on-road assessments, incorporating a range of skills, and manoeuvres, are needed to evaluate readiness to return to driving following traumatic brain injury. Individually tailored driver rehabilitation programs need to address these heterogeneous skill deficits to best support individuals to make a successful return to driving post-traumatic brain injury.
The effects of childlessness on the care and psychological well-being of older adults with disabilities

Objectives: Adult children are a primary focus of family and caregiver research. In contrast, relatively little is known about childless elders with a disability, including their care needs and the state of their overall well-being compared to elderly parents. We addressed this gap by examining the relationship between childlessness and the care and well-being of adults aged 75 and older with a disability. Methods: Parents and childless persons aged 75 and older were compared using data from the 1998 to 2004 waves of the Health and Retirement Study (HRS). We used logistic regression to examine the relationship between childlessness and care provision (personal care and assistive devise use) and ordinal regression to examine the relationships of parental status, personal care, and use of assistive devices with well-being. The analysis was based on 2048 observations from 1456 community-dwelling respondents who had difficulty walking across a room or getting into or out of bed. Results: Compared to parents, childless elders with a disability generally do not receive less care or have worse psychological well-being. However, being unmarried reduces the likelihood of having personal care and is associated with depressive affect. Use of assistive devices is associated with less depressive affect. Conclusion: Childless older adults are similar to parents on measures of psychological well-being and care provision. This finding has important implications, as it is projected that 30% of baby boomers who will need assistance will lack care from spouses or adult children. Further exploration of compensatory resources is suggested.
Opposing effects of histidine phosphorylation regulate the AtxA virulence transcription factor in Bacillus anthracis

Expression of genes for Bacillus anthracis toxin and capsule virulence factors are dependent upon the AtxA transcription factor. The mechanism by which AtxA regulates the transcription of its target genes is unknown. Here we report that bioinformatic analyses suggested the presence in AtxA of two PTS (phosphenolpyruvate : sugar phosphotransferase system) regulation domains (PRD) generally regulated by phosphorylation/dephosphorylation at conserved histidine residues. By means of amino acid substitutions that mimic the phosphorylated (H to D) or the unphosphorylated (H to A) state of the protein, we showed that phosphorylation of H199 of PRD1 is likely to be necessary for AtxA activation while phosphorylation of H379 in PRD2 is inhibitory to toxin gene transcription. In vivo labelling experiments with radioactive phosphate allowed us to propose that H199 and H379 are AtxA residues subject to regulated phosphorylation. In support to these notions, we also show that deletion of ptsHI, encoding the HPr intermediate and the EI enzymes of PTS, or growth in the presence of glucose affect positively and negatively, respectively, the activity of AtxA. Our results link virulence factor production in B. anthracis to carbohydrate metabolism and, for the first time, provide a mechanistic explanation for AtxA transcriptional activity.
Application of AgaR repressor and dominant repressor variants for verification of a gene cluster involved in N‐acetylgalactosamine metabolism in Escherichia coli K‐12

The agaZVWEFASYBCDI gene cluster encodes the phosphotransferase systems and enzymes responsible for the uptake and metabolism of N‐acetylgalactosamine and galactosamine in Escherichia coli. In some strains of E. coli, particularly the common K‐12 strain, a portion of this cluster is missing because of a site‐specific recombination event that occurred between sites in agaW and agaA. Strains that have undergone this recombination event have lost the ability to utilize either N‐acetylgalactosamine or galactosamine as sole sources of carbon. Divergently transcribed from this gene cluster is the gene agaR encoding a transcriptional repressor belonging to the DeoR/GlpR family of transcriptional regulators. Promoters upstream of agaR, agaZ and agaS were characterized. All three promoters had elevated activity in the presence of N‐acetylgalactosamine or galactosamine, were regulated in vivo by AgaR and possessed specific DNA‐binding sites for AgaR upstream from the start sites of transcription as determined by DNase I footprinting. In vivo analysis and DNase I footprinting indicated that the promoter specific for agaZ also requires activation by cAMP‐CRP. Previous work with GlpR and other members of the DeoR/GlpR family have identified highly conserved amino acid residues that function in DNA‐binding or response to inducer. These residues of AgaR were targeted for site‐directed mutagenesis and yielded variants of AgaR that were either negatively dominant or non‐inducible. The apparent ability to produce negatively dominant and non‐inducible variants of proteins of the DeoR/GlpR family of currently unknown function will likely facilitate screening for function.