Organizational Principles of Hyporheic Exchange Flow and Biogeochemical Cycling in River Networks Across Scales

Hyporheic zones increase freshwater ecosystem resilience to hydrological extremes and global environmental change. However, current conceptualizations of hyporheic exchange, residence time distributions, and the associated biogeochemical cycling in streambed sediments do not always accurately explain the hydrological and biogeochemical complexity observed in streams and rivers. Specifically, existing conceptual models insufficiently represent the coupled transport and reactivity along groundwater and surface water flow paths, the role of autochthonous organic matter in streambed biogeochemical functioning, and the feedbacks between surface-subsurface ecological processes, both within and across spatial and temporal scales. While simplified approaches to these issues are justifiable and necessary for transferability, the exclusion of important hyporheic processes from our conceptualizations can lead to erroneous conclusions and inadequate understanding and management of interconnected surface water and groundwater environments. This is particularly true at the landscape scale, where the organizational principles of spatio-temporal dynamics of hyporheic exchange flow (HEF) and biogeochemical processes remain largely uncharacterized. This article seeks to identify the most important drivers and controls of HEF and biogeochemical cycling based on a comprehensive synthesis of findings from a wide range of river systems. We use these observations to test current paradigms and conceptual models, discussing the interactions of local-to-regional hydrological, geomorphological, and ecological controls of hyporheic zone functioning. This improved conceptualization of the landscape organizational principles of drivers of HEF and biogeochemical processes from reach to catchment scales will inform future river research directions and watershed management strategies

Post-traumatic stress and future substance use outcomes: leveraging antecedent factors to stratify risk

Background: Post-traumatic stress disorder (PTSD) and substance use (tobacco, alcohol, and cannabis) are highly comorbid. Many factors affect this relationship, including sociodemographic and psychosocial characteristics, other prior traumas, and physical health. However, few prior studies have investigated this prospectively, examining new substance use and the extent to which a wide range of factors may modify the relationship to PTSD. Methods: The Advancing Understanding of RecOvery afteR traumA (AURORA) study is a prospective cohort of adults presenting at emergency departments (N = 2,943). Participants self-reported PTSD symptoms and the frequency and quantity of tobacco, alcohol, and cannabis use at six total timepoints. We assessed the associations of PTSD and future substance use, lagged by one timepoint, using the Poisson generalized estimating equations. We also stratified by incident and prevalent substance use and generated causal forests to identify the most important effect modifiers of this relationship out of 128 potential variables. Results: At baseline, 37.3% (N = 1,099) of participants reported likely PTSD. PTSD was associated with tobacco frequency (incidence rate ratio (IRR): 1.003, 95% CI: 1.00, 1.01, p = 0.02) and quantity (IRR: 1.01, 95% CI: 1.001, 1.01, p = 0.01), and alcohol frequency (IRR: 1.002, 95% CI: 1.00, 1.004, p = 0.03) and quantity (IRR: 1.003, 95% CI: 1.001, 1.01, p = 0.001), but not with cannabis use. There were slight differences in incident compared to prevalent tobacco frequency and quantity of use; prevalent tobacco frequency and quantity were associated with PTSD symptoms, while incident tobacco frequency and quantity were not. Using causal forests, lifetime worst use of cigarettes, overall self-rated physical health, and prior childhood trauma were major moderators of the relationship between PTSD symptoms and the three substances investigated. Conclusion: PTSD symptoms were highly associated with tobacco and alcohol use, while the association with prospective cannabis use is not clear. Findings suggest that understanding the different risk stratification that occurs can aid in tailoring interventions to populations at greatest risk to best mitigate the comorbidity between PTSD symptoms and future substance use outcomes. We demonstrate that this is particularly salient for tobacco use and, to some extent, alcohol use, while cannabis is less likely to be impacted by PTSD symptoms across the strata

Determination of the Form Factors for the Decay B0 --> D*-l+nu_l and of the CKM Matrix Element |Vcb|

We present a combined measurement of the Cabibbo-Kobayashi-Maskawa matrix element $|V_{cb}|$ and of the parameters $\rho^2$, $R_1$, and $R_2$, which fully characterize the form factors of the $B^0 \to D^{*-}\ell^{+}\nu_\ell$ decay in the framework of HQET, based on a sample of about 52,800 $B^0 \to D^{*-}\ell^{+}\nu_\ell$ decays recorded by the BABAR detector. The kinematical information of the fully reconstructed decay is used to extract the following values for the parameters (where the first errors are statistical and the second systematic): $\rho^2 = 1.156 \pm 0.094 \pm 0.028$, $R_1 = 1.329 \pm 0.131 \pm 0.044$, $R_2 = 0.859 \pm 0.077 \pm 0.022$, $\mathcal{F}(1)|V_{cb}| = (35.03 \pm 0.39 \pm 1.15) \times 10^{-3}$. By combining these measurements with the previous BABAR measurements of the form factors which employs a different technique on a partial sample of the data, we improve the statistical accuracy of the measurement, obtaining: $\rho^2 = 1.179 \pm 0.048 \pm 0.028, R_1 = 1.417 \pm 0.061 \pm 0.044, R_2 = 0.836 \pm 0.037 \pm 0.022,$ and $\mathcal{F}(1)|V_{cb}| = (34.68 \pm 0.32 \pm 1.15) \times 10^{-3}.$ Using the lattice calculations for the axial form factor $\mathcal{F}(1)$, we extract $|V_{cb}| =(37.74 \pm 0.35 \pm 1.25 \pm ^{1.23}_{1.44}) \times 10^{-3}$, where the third error is due to the uncertainty in $\mathcal{F}(1)$

Study of the Exclusive Initial-State Radiation Production of the DDˉD \bar D System

A study of exclusive production of the $D \bar D$ system through initial-state r adiation is performed in a search for charmonium states, where $D=D^0$ or $D^+$. The $D^0$ mesons are reconstructed in the $D^0 \to K^- \pi^+$, $D^0 \to K^- \pi^+ \pi^0$, and $D^0 \to K^- \pi^+ \pi^+ \pi^-$ decay modes. The $D^+$ is reconstructed through the $D^+ \to K^- \pi^+ \pi^+$ decay mode. The analysis makes use of an integrated luminosity of 288.5 fb$^{-1}$ collected by the BaBar experiment. The $D \bar D$ mass spectrum shows a clear $\psi(3770)$ signal. Further structures appear in the 3.9 and 4.1 GeV/$c^2$ regions. No evidence is found for Y(4260) decays to $D \bar D$, implying an up per limit \frac{\BR(Y(4260)\to D \bar D)}{\BR(Y(4260)\to J/\psi \pi^+ \pi^-)} < 7.6 (95 % confidence level)

Predicting at-risk opioid use three months after ed visit for trauma: Results from the AURORA study

OBJECTIVE: Whether short-term, low-potency opioid prescriptions for acute pain lead to future at-risk opioid use remains controversial and inadequately characterized. Our objective was to measure the association between emergency department (ED) opioid analgesic exposure after a physical, trauma-related event and subsequent opioid use. We hypothesized ED opioid analgesic exposure is associated with subsequent at-risk opioid use. METHODS: Participants were enrolled in AURORA, a prospective cohort study of adult patients in 29 U.S., urban EDs receiving care for a traumatic event. Exclusion criteria were hospital admission, persons reporting any non-medical opioid use (e.g., opioids without prescription or taking more than prescribed for euphoria) in the 30 days before enrollment, and missing or incomplete data regarding opioid exposure or pain. We used multivariable logistic regression to assess the relationship between ED opioid exposure and at-risk opioid use, defined as any self-reported non-medical opioid use after initial ED encounter or prescription opioid use at 3-months. RESULTS: Of 1441 subjects completing 3-month follow-up, 872 participants were included for analysis. At-risk opioid use occurred within 3 months in 33/620 (5.3%, CI: 3.7,7.4) participants without ED opioid analgesic exposure; 4/16 (25.0%, CI: 8.3, 52.6) with ED opioid prescription only; 17/146 (11.6%, CI: 7.1, 18.3) with ED opioid administration only; 12/90 (13.3%, CI: 7.4, 22.5) with both. Controlling for clinical factors, adjusted odds ratios (aORs) for at-risk opioid use after ED opioid exposure were: ED prescription only: 4.9 (95% CI 1.4, 17.4); ED administration for analgesia only: 2.0 (CI 1.0, 3.8); both: 2.8 (CI 1.2, 6.5). CONCLUSIONS: ED opioids were associated with subsequent at-risk opioid use within three months in a geographically diverse cohort of adult trauma patients. This supports need for prospective studies focused on the long-term consequences of ED opioid analgesic exposure to estimate individual risk and guide therapeutic decision-making

The AURORA Study: a longitudinal, multimodal library of brain biology and function after traumatic stress exposure

Adverse posttraumatic neuropsychiatric sequelae (APNS) are common among civilian trauma survivors and military veterans. These APNS, as traditionally classified, include posttraumatic stress, postconcussion syndrome, depression, and regional or widespread pain. Traditional classifications have come to hamper scientific progress because they artificially fragment APNS into siloed, syndromic diagnoses unmoored to discrete components of brain functioning and studied in isolation. These limitations in classification and ontology slow the discovery of pathophysiologic mechanisms, biobehavioral markers, risk prediction tools, and preventive/treatment interventions. Progress in overcoming these limitations has been challenging because such progress would require studies that both evaluate a broad spectrum of posttraumatic sequelae (to overcome fragmentation) and also perform in-depth biobehavioral evaluation (to index sequelae to domains of brain function). This article summarizes the methods of the Advancing Understanding of RecOvery afteR traumA (AURORA) Study. AURORA conducts a large-scale (n = 5000 target sample) in-depth assessment of APNS development using a state-of-the-art battery of self-report, neurocognitive, physiologic, digital phenotyping, psychophysical, neuroimaging, and genomic assessments, beginning in the early aftermath of trauma and continuing for 1 year. The goals of AURORA are to achieve improved phenotypes, prediction tools, and understanding of molecular mechanisms to inform the future development and testing of preventive and treatment interventions

Measurements of Branching Fractions, Polarizations, and Direct CP-Violation Asymmetries in B→ρK∗ and B→f0(980)K∗ Decays

We report searches for B -meson decays to the charmless final states ρ K ∗ and f 0 ( 980 ) K ∗ with a sample of 232 × 10 6 B ¯¯¯ B pairs collected with the BABAR detector at the PEP-II e + e − collider. We measure in units of 10 − 6 the following branching fractions, where the first error quoted is statistical and the second systematic, or upper limits are given at the 90% confidence level : B ( B + → ρ 0 K * + ) < 6.1 , B ( B + → ρ + K * 0 ) = 9.6 ± 1.7 ± 1.5 , B ( B 0 → ρ − K * + ) < 12.0 , B ( B 0 → ρ 0 K * 0 ) = 5.6 ± 0.9 ± 1.3 , B ( B + → f 0 ( 980 ) K * + ) = 5.2 ± 1.2 ± 0.5 , and B ( B 0 → f 0 ( 980 ) K * 0 ) < 4.3 . For the significant modes, we also measure the fraction of longitudinal polarization and the charge asymmetry: f L ( B + → ρ + K * 0 ) = 0.52 ± 0.10 ± 0.04 , f L ( B 0 → ρ 0 K * 0 ) = 0.57 ± 0.09 ± 0.08 , A C P ( B + → ρ + K * 0 ) = − 0.01 ± 0.16 ± 0.02 , A C P ( B 0 → ρ 0 K * 0 ) = 0.09 ± 0.19 ± 0.02 , and A C P ( B + → f 0 ( 980 ) K * + ) = − 0.34 ± 0.21 ± 0.03