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\"Battling both inner and external demons, Stephanie must learn to balance school and crime-fighting or face the wrath of Barbara Gordon! With guest appearences from Batman and Robin and villains like Man-Bat and Clayface, Batgirl must step up to the mantle! Batgirl must battle the Calculator and stop his plan to unleash a nanovirus upon the citizens of Gotham City that will turn them into mindless techno-zombies, enter the FLOOD!\"-- Provided by publisher.

Plasmas in various astrophysical systems are in nonequilibrium states, as evidenced by direct in situ measurements in the solar wind, solar corona, and planetary environments, as well as by indirect observations of nonthermal sources of waves and emissions. Specific to observed nonequilibrium plasmas are non-Maxwellian velocity distributions with suprathermal tails, most often described by kappa (power-law) distributions. In this paper, we introduce an alternative modeling for linear waves in plasmas described by the generalized Druyvesteyn distribution model. This model can reproduce not only high-energy tails, but also low-energy flat tops in velocity distributions, like those of electrons in interplanetary shocks and the solar transition region. The wave dispersion relation of longitudinal waves is derived in terms of the newly introduced Druyvesteyn dispersion function. The dispersion curves as well as damping rates of high-frequency Langmuir waves are numerically computed for the isotropic case, and their analytical approximations are provided in the limit of weak damping. We thus offer a new tool for modeling longitudinal waves, and in particular Langmuir waves under the specific conditions of Druyvesteyn distributions.

\"With the aid of Kelvin, a dinosaur from the past, Amber must save her father--and the rest of us--from the very same danger that caused the dinosaurs to flee--and from the dinosaurs themselves as they return to Earth\"-- Back cover.

Background Type 2 diabetes (T2D) is associated with generalized vascular dysfunction characterized by increases in large artery stiffness, endothelial dysfunction, and vascular smooth muscle dysfunction. Sodium glucose cotransporter 2 inhibitors (SGLT2i) represent the most recently approved class of oral medications for the treatment of T2D, and have been shown to reduce cardiovascular and overall mortality. Although it is currently unclear how SGLT2i decrease cardiovascular risk, an improvement in vascular function is one potential mechanism. The aim of the current study was to examine if dapagliflozin, a widely prescribed STLT2i, improves generalized vascular dysfunction in type 2 diabetic mice. In light of several studies demonstrating a bi-directional relation between orally ingested medications and the gut microbiota, a secondary aim was to determine the effects of dapagliflozin on the gut microbiota. Methods Male diabetic mice (Db, n = 24) and control littermates (Con; n = 23) were randomized to receive either a standard diet or a standard diet containing dapagliflozin (60 mg dapagliflozin/kg diet; 0.006%) for 8 weeks. Arterial stiffness was assessed by aortic pulse wave velocity; endothelial function and vascular smooth muscle dysfunction were assessed by dilatory responses to acetylcholine and sodium nitroprusside, respectively. Results Compared to untreated diabetic mice, diabetic mice treated with dapagliflozin displayed significantly lower arterial stiffness (Db = 469 cm/s vs. Db + dapa = 435 cm/s, p < 0.05), and improvements in endothelial dysfunction (area under the curve [AUC] Db = 57.2 vs. Db + dapa = 117.0, p < 0.05) and vascular smooth muscle dysfunction (AUC, Db = 201.7 vs. Db + dapa = 285.5, p < 0.05). These vascular improvements were accompanied by reductions in hyperglycemia and circulating markers of inflammation. The microbiota of Db and Con mice were distinctly different, and dapagliflozin treatment was associated with minor alterations in gut microbiota composition, particularly in Db mice, although these effects did not conclusively mediate the improvements in vascular function. Conclusions Dapagliflozin treatment improves arterial stiffness, endothelial dysfunction and vascular smooth muscle dysfunction, and subtly alters microbiota composition in type 2 diabetic mice. Collectively, the improvements in generalized vascular function may represent an important mechanism underlying the cardiovascular benefits of SGLT2i treatment.

Diets high in saturated fatty acids are linked to increased cardiovascular disease risk, whereas monounsaturated fatty acids have been associated with improved cardiovascular outcomes. Accordingly, cell culture studies have demonstrated that saturated fatty acids, particularly long chain saturated fatty acids such as palmitate, induce dysfunction and cell death in a variety of cell types, and monounsaturated fatty acids may confer protection against palmitate-mediated damage. The aim of the present study was to examine whether monounsaturated fatty acids could protect against palmitate-mediated cell death in endothelial cells, to determine if AMPK inactivation and activation (via compound C and AICAR, respectively) underlies both palmitate-induced damage and monounsaturated fatty acid-mediated protection, and to explore the role of ER stress in this context. Human umbilical vein endothelial cells were examined for cell viability and apoptosis following treatment for 24 hours with palmitate (0.25 and 0.5mM) alone or in combination with the monounsaturated fatty acids oleate or palmitoleate (0.25 and 0.5mM), AICAR, compound C, 4μ8C, or TUDCA. Compared to control cells, palmitate significantly decreased cell viability and increased apoptosis in a dose-dependent manner. The monounsaturated fatty acids oleate and palmitoleate completely prevented the cytotoxic effects of palmitate. Although palmitate induced markers of ER stress, chemical inhibition of ER stress did not prevent palmitate-induced lipoapoptosis. Conversely, the AMPK activator AICAR (0.1 and 0.5mM) conferred protection from palmitate mediated-alterations in viability, apoptosis and ER stress, whereas the AMPK inhibitor compound C (20 and 40μM) significantly exacerbated palmitate-mediated damage. Lastly, co-incubation with palmitate, monounsaturated fatty acids, and compound C significantly mitigated the protective effects of both oleate and palmitoleate. In conclusion, monounsaturated fatty acids confer protection against the cytotoxic effects of palmitate in vascular endothelial cells; and palmitate-mediated damage, as well as monounsaturated-mediated protection, are due in part to inactivation and activation, respectively, of the metabolic regulator AMPK. These results may have implications for understanding the deleterious effects of high saturated fat diets on cardiovascular dysfunction and disease risk.

Individuals with anterior cruciate ligament reconstruction (ACLR) have quadriceps dysfunction that contributes to physical disability and posttraumatic knee osteoarthritis. Quadriceps function in the ACLR limb is commonly evaluated relative to the contralateral uninjured limb. Bilateral quadriceps dysfunction is common in individuals with ACLR, potentially biasing these evaluations.   To compare quadriceps function between individuals with ACLR and uninjured control participants.   Cross-sectional study.   Research laboratory.   Twenty individuals with unilateral ACLR (age = 21.1 ± 1.7 years, mass = 68.3 ± 14.9 kg, time since ACLR = 50.7 ± 21.3 months; females = 14; Tegner Score = 7.1 ± 0.3; 16 patellar tendon autografts, 3 hamstrings autografts, 1 allograft) matched to 20 control participants (age = 21.2 ± 1.2 years, mass = 67.9 ± 11.3 kg; females = 14; Tegner Score = 7.1 ± 0.4) on age, sex, body mass index, and Tegner Activity Scale.   Maximal voluntary isometric knee extension was performed on an isokinetic dynamometer. Peak torque (PT), rate of torque development (RTD), electromyographic (EMG) amplitude, central activation ratio (CAR), and hamstrings EMG amplitude were assessed during maximal voluntary isometric knee extension and compared between groups using independent-samples t tests. Relationships between hamstrings co-activation and quadriceps function were assessed using Pearson correlations.   Participants with anterior cruciate ligament reconstruction displayed lesser quadriceps PT (1.86 ± 0.74 versus 2.56 ± 0.37 Nm/kg, P = .001), RTD (39.4 ± 18.7 versus 52.9 ± 16.4 Nm/s/kg, P = .03), EMG amplitude (0.25 ± 0.12 versus 0.37 ± 0.26 mV, P = .04), and CAR (83.3% ± 11.1% versus 93.7% ± 3.2%, P = .002) and greater hamstrings co-activation (27.2% ± 12.8% versus 14.3% ± 3.7%, P < .001) compared with control participants. Correlations were found between hamstrings co-activation and PT (r = -0.39, P = .007), RTD (r = -0.30, P = .03), and EMG amplitude (r = -0.30, P = .03).   Individuals with ACLR possessed deficits in PT, RTD, and CAR compared with control participants. Peak torque is the net result of all agonist and antagonist activity, and lesser PT in individuals with ACLR is partially attributable to greater hamstrings co-activation.

Purpose of Review The goal of this article is to summarize the treatment-focused literature on cannabis and tobacco co-use and the treatment implications of co-use. This review will focus on the following: (1) the impact of co-use on cessation outcomes, (2) compensatory use/substitution of the non-treated substance among co-users, and (3) treatment interventions to address co-use. This article will highlight the limitations to co-use captured in the literature and offer considerations and directives for co-use research and treatment moving forward. Recent Findings The degree to which co-use affects cessation for a single, targeted substance remains in question, as the literature is largely mixed. Cannabis treatment trials are better equipped to answer these questions given that they do not typically exclude tobacco users. While the relationship between tobacco use and poorer cannabis outcomes appears to have some evidence, the reverse relationship (cannabis use affecting tobacco outcomes) is not consistently supported. Summary The co-use of cannabis and tobacco and its impact on single substance cessation and/or compensatory substance use during cessation is generally overlooked in treatment trials, while interventions to address both substances are rare. Capturing co-use adds burden for researchers, clinicians, and participants, but is warranted given the prevalence of co-use and a rapidly changing cannabis and tobacco regulatory environment, which may further complicate co-occurring substance use. Co-users are a heterogeneous population; trials focused on co-users, in addition to better data capture and consistent terminology, will aid in an understanding of nuanced patterns of co-use critical to inform treatment interventions.

Investigating the ramifications of site-specific protein redox modification in cells is challenging. This protocol uses HaloTagged proteins and a HaloTag-targetable photocaged 4-hydroxynonenal to elicit target-specific modifications and to trace their effects. This protocol describes targetable reactive electrophiles and oxidants (T-REX)—a live-cell-based tool designed to (i) interrogate the consequences of specific and time-resolved redox events, and (ii) screen for bona fide redox-sensor targets. A small-molecule toolset comprising photocaged precursors to specific reactive redox signals is constructed such that these inert precursors specifically and irreversibly tag any HaloTag-fused protein of interest (POI) in mammalian and Escherichia coli cells. Syntheses of the alkyne-functionalized endogenous reactive signal 4-hydroxynonenal (HNE(alkyne)) and the HaloTag-targetable photocaged precursor to HNE(alkyne) (also known as Ht-PreHNE or HtPHA) are described. Low-energy light prompts photo-uncaging ( t 1/2 <1–2 min) and target-specific modification. The targeted modification of the POI enables precisely timed and spatially controlled redox events with no off-target modification. Two independent pathways are described, along with a simple setup to functionally validate known targets or discover novel sensors. T-REX sidesteps mixed responses caused by uncontrolled whole-cell swamping with reactive signals. Modification and downstream response can be analyzed by in-gel fluorescence, proteomics, qRT-PCR, immunofluorescence, fluorescence resonance energy transfer (FRET)-based and dual-luciferase reporters, or flow cytometry assays. T-REX targeting takes 4 h from initial probe treatment. Analysis of targeted redox responses takes an additional 4–24 h, depending on the nature of the pathway and the type of readouts used.

Purpose of Review This report provides an updated overview of pre-clinical and clinical research on the etiology and biological substrates of the cannabis withdrawal syndrome. Recent Findings Long-term cannabis use is associated with downregulation of type-1 cannabinoid receptors (CB 1 ). Reduced CB 1 receptor density is related to increased withdrawal during early abstinence, and the reduction in CB 1 receptor density reverses with extended abstinence. Females have been shown to have increased rate and severity of a subset of cannabis withdrawal symptoms compared with men. Summary Recent studies have extended knowledge of the biological processes and individual difference variables that influence cannabis withdrawal. However, caveats include small sample sizes in clinical studies, participant samples that are predominantly male, and limited examinations of endocannabinoids, enzymes that degrade endocannabinoids, negative allosteric modulators, and other neurobiological systems that may directly impact cannabis withdrawal symptom expression.

Background: Chronic hamstring tears can result in challenging surgical repairs. Allografts may be used to augment the repair; however, there is limited clinical evidence supporting their use. Purposes: To (1) evaluate clinical outcomes of patients who underwent proximal hamstring repair with allograft augmentation or interposition and (2) compare them to matched controls who underwent primary hamstring repair. Study Design: Cohort study; Level of evidence, 3. Methods: A total of 117 patients who underwent proximal hamstring repair were included, consisting of 19 allograft augmentations, 20 allograft interpositions, and 78 primary repairs. Allograft cohorts were propensity-matched with those who underwent primary repair in a 1 to 2 ratio. Clinical outcomes were obtained at the final follow-up. Data were extracted using continuous variables, with normality reported as mean values ± standard deviation, and non-normality reported as median values with interquartile ranges (IQR). Results: The median follow-up of the augmentation cohort was 1.9 [IQR, 0.8-3.9] years, while it was 3.2 [IQR, 1.6-5.1] years (P = .182) for the primary repair cohort. The mean follow-up for the interposition cohort was 3.5 ± 2.4 years, while it was 4.2 ± 2.5 years for the primary repair cohort (P = .227). Forty-two percent of the augmentation cohort had undergone previous surgery, compared with 5% of the interposition cohort. The time from injury to surgery for the augmentation and primary repair cohorts was 6.4 and 1.3 months, respectively (P < .001). For the interposition and primary repair cohorts, the durations were 17.8 and 1 months, respectively (P < .001). Clinical outcomes, including the Tegner Activity Scale (3 vs 3), pain with activity (47.4% vs 23.7%), and muscle spasms (36.8% vs 26.3%), did not show significant differences between the augmentation and primary repair cohorts. The augmentation cohort had a significantly worse Lower Extremity Functional Scale (LEFS) score (64 vs 75; P < .001) and were more likely to experience pain with sitting (52.6% vs 21.1%; P = .034) than the primary repair cohort. There was no significant difference in clinical outcomes between the interposition and primary repair cohorts (LEFS: 69 vs 75.5, Tegner Activity Scale: 4 vs 4; pain with sitting: 26.3% vs 27.5%; pain with activity: 42.1% vs 30%; muscle spasms: 26.3% vs 30%). Revision rates were similar between cohorts (P≥ .255). Conclusion: Proximal hamstring repair for chronic tears with allograft augmentation or interposition is a reproducible procedure that results in satisfactory, yet poorer clinical outcomes compared with patients who underwent primary hamstring repair. These procedures should be considered in symptomatic patients with chronic tears that are not amenable to primary repair.