Texas Water Development Board Report 108

Report on providing data collected on surface water quality in Texas to analyze oxygen, nutrients, and pesticides

Tailored voltage waveform capacitively coupled plasmas in electronegative gases : frequency dependence of asymmetry effects

Capacitively coupled radio frequency plasmas operated in an electronegative gas (CF4) and driven by voltage waveforms composed of four consecutive harmonics are investigated for different fundamental driving frequencies using PIC/MCC simulations and an analytical model. As has been observed previously for electropositive gases, the application of peak-shaped waveforms (that are characterized by a strong amplitude asymmetry) results in the development of a DC self-bias due to the electrical asymmetry effect (EAE), which increases the energy of ions arriving at the powered electrode. In contrast to the electropositive case (Korolov et al 2012 J. Phys. D: Appl. Phys. 45 465202) the absolute value of the DC self-bias is found to increase as the fundamental frequency is reduced in this electronegative discharge, providing an increased range over which the DC self-bias can be controlled. The analytical model reveals that this increased DC self-bias is caused by changes in the spatial profile and the mean value of the net charge density in the grounded electrode sheath. The spatio-temporally resolved simulation data show that as the frequency is reduced the grounded electrode sheath region becomes electronegative. The presence of negative ions in this sheath leads to very different dynamics of the power absorption of electrons, which in turn enhances the local electronegativity and plasma density via ionization and attachment processes. The ion flux to the grounded electrode (where the ion energy is lowest) can be up to twice that to the powered electrode. At the same time, while the mean ion energies at both electrodes are quite different, their ratio remains approximately constant for all base frequencies studied here

Dynamics of Glycoprotein Charge in the Evolutionary History of Human Influenza

Influenza viruses show a significant capacity to evade host immunity; this is manifest both as large occasional jumps in the antigenic phenotype of viral surface molecules and in gradual antigenic changes leading to annual influenza epidemics in humans. Recent mouse studies show that avidity for host cells can play an important role in polyclonal antibody escape, and further that electrostatic charge of the hemagglutinin glycoprotein can contribute to such avidity.We test the role of glycoprotein charge on sequence data from the three major subtypes of influenza A in humans, using a simple method of calculating net glycoprotein charge. Of all subtypes, H3N2 in humans shows a striking pattern of increasing positive charge since its introduction in 1968. Notably, this trend applies to both hemagglutinin and neuraminidase glycoproteins. In the late 1980s hemagglutinin charge reached a plateau, while neuraminidase charge started to decline. We identify key groups of amino acid sites involved in this charge trend.To our knowledge these are the first indications that, for human H3N2, net glycoprotein charge covaries strongly with antigenic drift on a global scale. Further work is needed to elucidate how such charge interacts with other immune escape mechanisms, such as glycosylation, and we discuss important questions arising for future study

Cardiovascular risk scoring and magnetic resonance imaging detected subclinical cerebrovascular disease

AIMS: Cardiovascular risk factors are used for risk stratification in primary prevention. We sought to determine if simple cardiac risk scores are associated with magnetic resonance imaging (MRI)-detected subclinical cerebrovascular disease including carotid wall volume (CWV), carotid intraplaque haemorrhage (IPH), and silent brain infarction (SBI). METHODS AND RESULTS: A total of 7594 adults with no history of cardiovascular disease (CVD) underwent risk factor assessment and a non-contrast enhanced MRI of the carotid arteries and brain using a standardized protocol in a population-based cohort recruited between 2014 and 2018. The non-lab-based INTERHEART risk score (IHRS) was calculated in all participants; the Framingham Risk Score was calculated in a subset who provided blood samples (n = 3889). The association between these risk scores and MRI measures of CWV, carotid IPH, and SBI was determined. The mean age of the cohort was 58 (8.9) years, 55% were women. Each 5-point increase (∼1 SD) in the IHRS was associated with a 9 mm3 increase in CWV, adjusted for sex (P \u3c 0.0001), a 23% increase in IPH [95% confidence interval (CI) 9-38%], and a 32% (95% CI 20-45%) increase in SBI. These associations were consistent for lacunar and non-lacunar brain infarction. The Framingham Risk Score was also significantly associated with CWV, IPH, and SBI. CWV was additive and independent to the risk scores in its association with IPH and SBI. CONCLUSION: Simple cardiovascular risk scores are significantly associated with the presence of MRI-detected subclinical cerebrovascular disease, including CWV, IPH, and SBI in an adult population without known clinical CVD

Tidal Disruption Event Demographics with the Zwicky Transient Facility: Volumetric Rates, Luminosity Function, and Implications for the Local Black Hole Mass Function

We conduct a systematic tidal disruption event (TDE) demographics analysis using the largest sample of optically selected TDEs. A flux-limited, spectroscopically complete sample of 33 TDEs is constructed using the Zwicky Transient Facility over three years (from October 2018 to September 2021). We infer the black hole (BH) mass ($M_{\rm BH}$) with host galaxy scaling relations, showing that the sample $M_{\rm BH}$ ranges from $10^{5.1}\,M_\odot$ to $10^{8.2}\,M_\odot$. We developed a survey efficiency corrected maximum volume method to infer the rates. The rest-frame $g$-band luminosity function (LF) can be well described by a broken power-law of $\phi (L_g)\propto [(L_g / L_{\rm bk})^{0.3} + (L_g / L_{\rm bk})^{2.6}]^{-1}$, with $L_{\rm bk}=10^{43.1}\,{\rm erg\,s^{-1}}$. In the BH mass regime of $10^{5.3}\lesssim (M_{\rm BH}/M_\odot) \lesssim 10^{7.3}$, the TDE mass function follows $\phi(M_{\rm BH})\propto M_{\rm BH}^{-0.25}$, which favors a flat local BH mass function ($dn_{\rm BH}/d{\rm log}M_{\rm BH}\approx{\rm constant}$). We confirm the significant rate suppression at the high-mass end ($M_{\rm BH}\gtrsim 10^{7.5}\,M_\odot$), which is consistent with theoretical predictions considering direct capture of hydrogen-burning stars by the event horizon. At a host galaxy mass of $M_{\rm gal}\sim 10^{10}\,M_\odot$, the average optical TDE rate is $\approx 3.2\times 10^{-5}\,{\rm galaxy^{-1}\,yr^{-1}}$. We constrain the optical TDE rate to be [3.7, 7.4, and 1.6$]\times 10^{-5}\,{\rm galaxy^{-1}\,yr^{-1}}$ in galaxies with red, green, and blue colors.Comment: Replaced following peer-review process. 38 pages, 23 figures. Accepted for publication in ApJ

Reduced Cognitive Assessment Scores Among Individuals With Magnetic Resonance Imaging-Detected Vascular Brain Injury

Background and Purpose- Little is known about the association between covert vascular brain injury and cognitive impairment in middle-aged populations. We investigated if scores on a cognitive screen were lower in individuals with higher cardiovascular risk, and those with covert vascular brain injury. Methods- Seven thousand five hundred forty-seven adults, aged 35 to 69 years, free of cardiovascular disease underwent a cognitive assessment using the Digital Symbol Substitution test and Montreal Cognitive Assessment, and magnetic resonance imaging (MRI) to detect covert vascular brain injury (high white matter hyperintensities, lacunar, and nonlacunar brain infarctions). Cardiovascular risk factors were quantified using the INTERHEART (A Global Study of Risk Factors for Acute Myocardial Infarction) risk score. Multivariable mixed models tested for independent determinants of reduced cognitive scores. The population attributable risk of risk factors and MRI vascular brain injury on low cognitive scores was calculated. Results- The mean age of participants was 58 (SD, 9) years; 55% were women. Montreal Cognitive Assessment and Digital Symbol Substitution test scores decreased significantly with increasing age

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Cadherin 2-Related Arrhythmogenic Cardiomyopathy Prevalence and Clinical Features

Background:Arrhythmogenic cardiomyopathy (ACM) is an inherited cardiac disease characterized by fibrofatty replacement of the right and left ventricle, often causing ventricular dysfunction and life-threatening arrhythmias. Variants in desmosomal genes account for up to 60% of cases. Our objective was to establish the prevalence and clinical features of ACM stemming from pathogenic variants in the nondesmosomal cadherin 2 (CDH2), a novel genetic substrate of ACM.Methods:A cohort of 500 unrelated patients with a definite diagnosis of ACM and no disease-causing variants in the main ACM genes was assembled. Genetic screening of CDH2 was performed through next-generation or Sanger sequencing. Whenever possible, cascade screening was initiated in the families of CDH2-positive probands, and clinical evaluation was performed.Results:Genetic screening of CDH2 led to the identification of 7 rare variants: 5, identified in 6 probands, were classified as pathogenic or likely pathogenic. The previously established p.D407N pathogenic variant was detected in 2 additional probands. Probands and family members with pathogenic/likely pathogenic variants in CDH2 were clinically evaluated, and along with previously published cases, altogether contributed to the identification of gene-specific features (13 cases from this cohort and 11 previously published, for a total of 9 probands and 15 family members). Ventricular arrhythmic events occurred in most CDH2-positive subjects (20/24, 83%), while the occurrence of heart failure was rare (2/24, 8.3%). Among probands, sustained ventricular tachycardia and sudden cardiac death occurred in 5/9 (56%).Conclusions:In this worldwide cohort of previously genotype-negative ACM patients, the prevalence of probands with CDH2 pathogenic/likely pathogenic variants was 1.2% (6/500). Our data show that this cohort of CDH2-ACM patients has a high incidence of ventricular arrhythmias, while evolution toward heart failure is rare.</p

Dramatic rebrightening of the type-changing stripped-envelope supernova SN 2023aew

Multi-peaked supernovae with precursors, dramatic light-curve rebrightenings, and spectral transformation are rare, but are being discovered in increasing numbers by modern night-sky transient surveys like the Zwicky Transient Facility (ZTF). Here, we present the observations and analysis of SN 2023aew, which showed a dramatic increase in brightness following an initial luminous (-17.4 mag) and long (~100 days) unusual first peak (possibly precursor). SN 2023aew was classified as a Type IIb supernova during the first peak but changed its type to resemble a stripped-envelope supernova (SESN) after the marked rebrightening. We present comparisons of SN 2023aew's spectral evolution with SESN subtypes and argue that it is similar to SNe Ibc during its main peak. P-Cygni Balmer lines are present during the first peak, but vanish during the second peak's photospheric phase, before H$\alpha$ resurfaces again during the nebular phase. The nebular lines ([O I], [Ca II], Mg I], H$\alpha$) exhibit a double-peaked structure which hints towards a clumpy or non-spherical ejecta. We analyze the second peak in the light curve of SN 2023aew and find it to be broader than normal SESNe as well as requiring a very high $^{56}$Ni mass to power the peak luminosity. We discuss the possible origins of SN 2023aew including an eruption scenario where a part of the envelope is ejected during the first peak which also powers the second peak of the light curve through SN-CSM interaction.Comment: 22 pages, 11 figures, 5 table

Prediction of Biological Functions on Glycosylation Site Migrations in Human Influenza H1N1 Viruses

Protein glycosylation alteration is typically employed by various viruses for escaping immune pressures from their hosts. Our previous work had shown that not only the increase of glycosylation sites (glycosites) numbers, but also glycosite migration might be involved in the evolution of human seasonal influenza H1N1 viruses. More importantly, glycosite migration was likely a more effectively alteration way for the host adaption of human influenza H1N1 viruses. In this study, we provided more bioinformatics and statistic evidences for further predicting the significant biological functions of glycosite migration in the host adaptation of human influenza H1N1 viruses, by employing homology modeling and in silico protein glycosylation of representative HA and NA proteins as well as amino acid variability analysis at antigenic sites of HA and NA. The results showed that glycosite migrations in human influenza viruses have at least five possible functions: to more effectively mask the antigenic sites, to more effectively protect the enzymatic cleavage sites of neuraminidase (NA), to stabilize the polymeric structures, to regulate the receptor binding and catalytic activities and to balance the binding activity of hemagglutinin (HA) with the release activity of NA. The information here can provide some constructive suggestions for the function research related to protein glycosylation of influenza viruses, although these predictions still need to be supported by experimental data