Turbulent cold flows gave birth to the first quasars.

How quasars powered by supermassive black holes formed less than a billion years after the Big Bang is still one of the outstanding problems in astrophysics, 20 years after their discovery1-4. Cosmological simulations suggest that rare cold flows converging on primordial haloes in low-shear environments could have created these quasars if they were 104-105 solar masses at birth, but could not resolve their formation5-8. Semi-analytical studies of the progenitor halo of a primordial quasar found that it favours the formation of such seeds, but could not verify if one actually appeared9. Here we show that a halo at the rare convergence of strong, cold accretion flows creates massive black holes seeds without the need for ultraviolet backgrounds, supersonic streaming motions or even atomic cooling. Cold flows drive violent, supersonic turbulence in the halo, which prevents star formation until it reaches a mass that triggers sudden, catastrophic baryon collapse that forms 31,000 and 40,000 solar-mass stars. This simple, robust process ensures that haloes capable of forming quasars by a redshift of z > 6 produce massive seeds. The first quasars were thus a natural consequence of structure formation in cold dark matter cosmologies, and not exotic, finely tuned environments as previously thought10-14.

Hohlraum Reheating from Burning NIF Implosions.

As fusion experiments at the National Ignition Facility (NIF) approach and exceed breakeven, energy from the burning capsule is predicted to couple to the gold walls and reheat the hohlraum. On December 5, 2022, experiment N221204 exceeded target breakeven, historically achieving 3.15 MJ of fusion energy from 2.05 MJ of laser drive; for the first time, energy from the igniting capsule reheated the hohlraum beyond the peak laser-driven radiation temperature of 313 eV to a peak of 350 eV, in less than half a nanosecond. This reheating effect has now been unambiguously observed by the two independent Dante calorimeter systems across multiple experiments, and is shown to result from reheating of the remnant tungsten-doped ablator by the exploding core, which is heated by alpha deposition.

Diabetes is accompanied by secretion of pro-atherosclerotic exosomes from vascular smooth muscle cells.

BACKGROUND: Atherosclerosis is a common co-morbidity of type 2 diabetes mellitus. Monocyte recruitment by an activated endothelium and the pro-inflammatory activity of the resulting macrophages are critical components of atherosclerosis. Exosomal transfer of microRNAs has emerged as a paracrine signaling mechanism regulating atherosclerotic plaque development. MicroRNAs-221 and -222 (miR-221/222) are elevated in vascular smooth muscle cells (VSMCs) of diabetic patients. We hypothesized that the transfer of miR-221/222 via VSMC-derived exosomes from diabetic sources (DVEs) promotes increased vascular inflammation and atherosclerotic plaque development. METHODS: Exosomes were obtained from VSMCs, following exposure to non-targeting or miR-221/-222 siRNA (-KD), isolated from diabetic (DVEs) and non-diabetic (NVEs) sources and their miR-221/-222 content was measured using droplet digital PCR (ddPCR). Expression of adhesion molecules and the adhesion of monocytes was measured following exposure to DVEs and NVEs. Macrophage phenotype following exposure to DVEs was determined by measuring mRNA markers and secreted cytokines. Age-matched apolipoprotein-E-deficient mice null (ApoE-/-) mice were maintained on Western diet for 6 weeks and received injections of saline, NVEs, NVE-KDs, DVEs or DVE-KDs every other day. Atherosclerotic plaque formation was measured using Oil Red Oil staining. RESULTS: Exposure of human umbilical vein and coronary artery endothelial cells to DVEs, but not NVEs, NVE-KDs, or DVE-KDs promoted increased intercellular adhesion molecule-1 expression and monocyte adhesion. DVEs but not NVEs, NVE-KDs, or DVE-KDs also promoted pro-inflammatory polarization of human monocytes in a miR-221/222 dependent manner. Finally, intravenous administration of DVEs, but not NVEs, resulted in a significant increase in atherosclerotic plaque development. CONCLUSION: These data identify a novel paracrine signaling pathway that promotes the cardiovascular complications of diabetes mellitus.

Incubation with porcine urinary bladder matrix yields a late-stage wound transcriptome in endothelial cells and keratinocytes isolated from both diabetic and non-diabetic subjects.

Proper wound closure requires the functional coordination of endothelial cells (ECs) and keratinocytes. In the late stages of wound healing, keratinocytes become activated and ECs promote the maturation of nascent blood vessels. In diabetes mellitus, decreased keratinocyte activation and impaired angiogenic action of ECs delay wound healing. Porcine urinary bladder matrix (UBM) improves the rate of wound healing, but the effect of exposure to UBM under diabetic conditions remains unclear. We hypothesized that keratinocytes and ECs isolated from both diabetic and non-diabetic donors would exhibit a similar transcriptome representative of the later stages of wound healing following incubation with UBM. Human keratinocytes and dermal ECs isolated from non-diabetic and diabetic donors were incubated with and without UBM particulate. RNA-Seq analysis was performed to identify changes in the transcriptome of these cells associated with exposure to UBM. While diabetic and non-diabetic cells exhibited different transcriptomes, these differences were minimized following incubation with UBM. ECs exposed to UBM exhibited changes in the expression of transcripts suggesting an increase in the endothelial-mesenchymal transition (EndoMT) associated with vessel maturation. Keratinocytes incubated with UBM demonstrated an increase in markers of activation. Comparison of the whole transcriptomes with public datasets suggested increased EndoMT and keratinocyte activation following UBM exposure. Both cell types exhibited loss of pro-inflammatory cytokines and adhesion molecules. These data suggest that application of UBM may accelerate healing by promoting a transition to the later stages of wound healing. This healing phenotype is achieved in cells isolated from both diabetic and non-diabetic donors.

HIV Care Engagement Among Trans Women of Color in San Francisco Bay Area Demonstration Projects: Findings from the Brandy Martell Project and TransAccess.

In the San Francisco Bay Area (SFBA), trans women of color are disproportionately affected by HIV and have poor HIV care outcomes. The Brandy Martell Project and TransAccess were two demonstration projects aimed at increasing HIV care engagement and retention among trans women of color in the SFBA. Both projects took place in clinics with a long history of providing trans health care and social services. Both also relied on peer navigation to address systems barriers and promote HIV care linkage and engagement. Our analysis was to identify associations between intervention exposure and primary HIV care visits, ART prescription, and retention in HIV care. Using GEE, we estimated the association between intervention exposure measures (receipt of intervention, intervention dose, intervention provider, and peer dose) and any primary HIV care visit or ART prescription over the 12-month period. Overall, the Brandy Martell Project and TransAccess interventions had significantly positive associations with HIV care outcomes measured. Peer navigation also had a significantly positive association with HIV care outcomes. These interventions demonstrate promise for engaging and retaining trans women of color in HIV care, and call for future investment in this highly underserved community.

The TSIS-1 Hybrid Solar Reference Spectrum.

We present a new solar irradiance reference spectrum representative of solar minimum conditions between solar cycles 24 and 25. The Total and Spectral Solar Irradiance Sensor-1 (TSIS-1) Hybrid Solar Reference Spectrum (HSRS) is developed by applying a modified spectral ratio method to normalize very high spectral resolution solar line data to the absolute irradiance scale of the TSIS-1 Spectral Irradiance Monitor (SIM) and the CubeSat Compact SIM (CSIM). The high spectral resolution solar line data are the Air Force Geophysical Laboratory ultraviolet solar irradiance balloon observations, the ground-based Quality Assurance of Spectral Ultraviolet Measurements In Europe Fourier transform spectrometer solar irradiance observations, the Kitt Peak National Observatory solar transmittance atlas, and the semi-empirical Solar Pseudo-Transmittance Spectrum atlas. The TSIS-1 HSRS spans 202-2730 nm at 0.01 to ∼0.001 nm spectral resolution with uncertainties of 0.3% between 460 and 2365 nm and 1.3% at wavelengths outside that range.

Blockade of sodium-glucose cotransporter 2 suppresses high glucose-induced angiotensinogen augmentation in renal proximal tubular cells.

Renal proximal tubular angiotensinogen (AGT) is increased by hyperglycemia (HG) in diabetes mellitus, which augments intrarenal angiotensin II formation, contributing to the development of hypertension and kidney injury. Sodium-glucose cotransporter 2 (SGLT2) is abundantly expressed in proximal tubular cells (PTCs). The present study investigated the effects of canagliflozin (CANA), a SGLT2 inhibitor, on HG-induced AGT elevation in cultured PTCs. Mouse PTCs were treated with 5-25 mM glucose. CANA (0-10 µM) was applied 1 h before glucose treatment. Glucose (10 mM) increased AGT mRNA and protein levels at 12 h (3.06 ± 0.48-fold in protein), and 1 and 10 µM CANA as well as SGLT2 shRNA attenuated the AGT augmentation. CANA did not suppress the elevated AGT levels induced by 25 mM glucose. Increased AGT expression induced by treatment with pyruvate, a glucose metabolite that does not require SGLT2 for uptake, was not attenuated by CANA. In HG-treated PTCs, intracellular reactive oxygen species levels were elevated compared with baseline (4.24 ± 0.23-fold), and these were also inhibited by CANA. Furthermore, tempol, an antioxidant, attenuated AGT upregulation in HG-treated PTCs. HG-induced AGT upregulation was not inhibited by an angiotensin II receptor antagonist, indicating that HG stimulates AGT expression in an angiotensin II-independent manner. These results indicate that enhanced glucose entry via SGLT2 into PTCs elevates intracellular reactive oxygen species generation by stimulation of glycolysis and consequent AGT augmentation. SGLT2 blockade limits HG-induced AGT stimulation, thus reducing the development of kidney injury in diabetes mellitus.

Endothelial deficiency of insulin-like growth factor-1 receptor reduces endothelial barrier function and promotes atherosclerosis in Apoe-deficient mice.

Insulin-like growth factor-1 (IGF-1) decreases atherosclerosis in apolipoprotein E (Apoe)-deficient mice when administered systemically. However, mechanisms for its atheroprotective effect are not fully understood. We generated endothelium-specific IGF-1 receptor (IGF1R)-deficient mice on an Apoe-deficient background to assess effects of IGF-1 on the endothelium in the context of hyperlipidemia-induced atherosclerosis. Endothelial deficiency of IGF1R promoted atherosclerotic burden, when animals were fed on a high-fat diet for 12 wk or normal chow for 12 mo. Under the normal chow feeding condition, the vascular relaxation response to acetylcholine was increased in the endothelial IGF1R-deficient aorta; however, feeding of a high-fat diet substantially attenuated the relaxation response, and there was no difference between endothelial IGF1R-deficient and control mice. The endothelium and its intercellular junctions provide a barrier function to the vasculature. In human aortic endothelial cells, IGF-1 upregulated occludin, claudin 5, VE-cadherin, JAM-A, and CD31 expression levels, and vice versa, specific IGF1R inhibitor, picropodophyllin, an IGF1R-neutralizing antibody (αIR3), or siRNA to IGF1R abolished the IGF-1 effects on junction and adherens proteins, suggesting that IGF-1 promoted endothelial barrier function. Moreover, endothelial transwell permeability assays indicated that inhibition of IGF-1 signaling elevated solute permeability through the monolayer of human aortic endothelial cells. In summary, endothelial IGF1R deficiency increases atherosclerosis, and IGF-1 positively regulates tight junction protein and adherens junction protein levels and endothelial barrier function. Our findings suggest that the elevation of the endothelial junction protein level is, at least in part, the mechanism for antiatherogenic effects of IGF-1.NEW & NOTEWORTHY Endothelial insulin-like growth factor-1 (IGF-1) receptor deficiency significantly elevated atherosclerotic burden in apolipoprotein E-deficient mice, mediated at least in part by downregulation of intercellular junction proteins and, thus, elevated endothelial permeability. This study revealed a novel role for IGF-1 in supporting endothelial barrier function. These findings suggest that IGF-1's ability to promote endothelial barrier function may offer a novel therapeutic strategy for vascular diseases such as atherosclerosis.

Canagliflozin Prevents Intrarenal Angiotensinogen Augmentation and Mitigates Kidney Injury and Hypertension in Mouse Model of Type 2 Diabetes Mellitus.

BACKGROUND: Hypertension and renal injury are common complications of type 2 diabetes mellitus (T2DM). Hyperglycemia stimulates renal proximal tubular angiotensinogen (AGT) expression via elevated oxidative stress contributing to the development of high blood pressure and diabetic nephropathy. The sodium glucose cotransporter 2 (SGLT2) in proximal tubules is responsible for the majority of glucose reabsorption by renal tubules. We tested the hypothesis that SGLT2 inhibition with canagliflozin (CANA) prevents intrarenal AGT augmentation and ameliorates kidney injury and hypertension in T2DM. METHODS: We induced T2DM in New Zealand obese mice with a high fat diet (DM, 30% fat) with control mice receiving regular fat diet (ND, 4% fat). When DM mice exhibited > 350 mg/dL blood glucose levels, both DM- and ND-fed mice were treated with 10 mg/kg/day CANA or vehicle by oral gavage for 6 weeks. We evaluated intrarenal AGT, blood pressure, and the development of kidney injury. RESULTS: Systolic blood pressure in DM mice (133.9 ± 2.0 mm Hg) was normalized by CANA (113.9 ± 4.0 mm Hg). CANA treatment ameliorated hyperglycemia-associated augmentation of renal AGT mRNA (148 ± 21 copies/ng RNA in DM, and 90 ± 16 copies/ng RNA in DM + CANA) and protein levels as well as elevation of urinary 8-isoprostane levels. Tubular fibrosis in DM mice (3.4 ± 0.9-fold, fibrotic score, ratio to ND) was suppressed by CANA (0.9 ± 0.3-fold). Furthermore, CANA attenuated DM associated increased macrophage infiltration and cell proliferation in kidneys of DM mice. CONCLUSIONS: CANA prevents intrarenal AGT upregulation and oxidative stress and which may mitigate high blood pressure, renal tubular fibrosis, and renal inflammation in T2DM.

SM22α (Smooth Muscle Protein 22-α) Promoter-Driven IGF1R (Insulin-Like Growth Factor 1 Receptor) Deficiency Promotes Atherosclerosis.

Objective- IGF-1 (insulin-like growth factor 1) is a major autocrine/paracrine growth factor, which promotes cell proliferation, migration, and survival. We have shown previously that IGF-1 reduced atherosclerosis and promoted features of stable atherosclerotic plaque in Apoe-/- mice-an animal model of atherosclerosis. The aim of this study was to assess effects of smooth muscle cell (SMC) IGF-1 signaling on the atherosclerotic plaque. Approach and Results- We generated Apoe-/- mice with IGF1R (IGF-1 receptor) deficiency in SMC and fibroblasts (SM22α [smooth muscle protein 22 α]-CreKI/IGF1R-flox mice). IGF1R was decreased in the aorta and adventitia of SM22α-CreKI/IGF1R-flox mice and also in aortic SMC, embryonic, skin, and lung fibroblasts isolated from SM22α-CreKI/IGF1R-flox mice. IGF1R deficiency downregulated collagen mRNA-binding protein LARP6 (La ribonucleoprotein domain family, member 6) and vascular collagen, and mice exhibited growth retardation. The high-fat diet-fed SM22α-CreKI/IGF1R-flox mice had increased atherosclerotic burden and inflammatory responses. α-SMA (α-smooth muscle actin)-positive plaque cells had reduced proliferation and elevated apoptosis. SMC/fibroblast-targeted decline in IGF-1 signaling decreased atherosclerotic plaque SMC, markedly depleted collagen, reduced plaque fibrous cap, and increased plaque necrotic cores. Aortic SMC isolated from SM22α-CreKI/IGF1R-flox mice had decreased cell proliferation, migration, increased sensitivity to apoptosis, and these effects were associated with disruption of IGF-1-induced Akt signaling. Conclusions- IGF-1 signaling in SMC and in fibroblast is a critical determinant of normal vascular wall development and atheroprotection.

High-Performance Indirect-Drive Cryogenic Implosions at High Adiabat on the National Ignition Facility.

To reach the pressures and densities required for ignition, it may be necessary to develop an approach to design that makes it easier for simulations to guide experiments. Here, we report on a new short-pulse inertial confinement fusion platform that is specifically designed to be more predictable. The platform has demonstrated 99%+0.5% laser coupling into the hohlraum, high implosion velocity (411 km/s), high hotspot pressure (220+60 Gbar), and high cold fuel areal density compression ratio (>400), while maintaining controlled implosion symmetry, providing a promising new physics platform to study ignition physics.

Housing and income effects on HIV-related health outcomes in the San Francisco Bay Area - findings from the SPNS transwomen of color initiative.

Transwomen of color are disproportionately impacted by HIV and may have worse health outcomes than other populations. This analysis was conducted to examine structural factors associated with poor health outcomes among transwomen of color living with HIV in the San Francisco Bay Area (N = 159). Univariate and multivariable analyses were conducted to determine if structural factors were associated with poor HIV-related health outcomes. A majority of participants were Black or African American (110/159, 69.2%), 32 (20.1%) identified their primary race/ethnicity as Hispanic or Latino/a or Spanish, and 17 (10.7%) identified as another race/ethnicity. Transwomen of color in our sample faced extreme structural barriers, including residential transience, extreme low income, high prevalence of running out of money in the last six months, high rates of food insecurity, high prevalence of income via entitlement programs, engagement in sex work and other illicit activities for income. Unstable housing was the structural factor most consistently associated with poor health outcomes along the HIV care continuum and may explain engagement in other sources of income generation. Interventions are needed that go beyond the individual and health care-level to address needs for housing and economic opportunities to improve HIV care outcomes among transwomen of color living with HIV in the San Francisco Bay Area.

Clear cell changes in salivary gland neoplasms: A 20-year retrospective study.

BACKGROUND: Clear cells are observed histopathologically in both benign and malignant neoplasms but their presence in salivary gland tumors has not been extensively documented. MATERIAL AND METHODS: With IRB approval, the archive of the University of Florida College of Dentistry oral pathology biopsy service was retrospectively searched from 1994-2014 for all benign and malignant salivary tumors. Epidemiological data, tumor location and duration, and type of tumor were recorded. A four reviewer panel examined the original slides. Reviewers scaled each case as 0 (no clear cells present), 1 (few to focal clear cells), 2 (less than 50% clear cells), and 3 (greater than 50% clear cells). RESULTS: A total of 535 cases were included of which 48% of tumors displayed 0 clear cells (257/535), 31.4% (168/535) scored 1, 13.6% (73/535) scored 2, and 7% (37/535) scored 3. Of the 251 (47%) malignant neoplasms, 64% (160/251) demonstrated 0-1 clear cell change, while 36% (91/251) showed a score of 2-3. For the total 284 (53%) benign tumors, 93% (265/535) scored 0-1 and 7% (19/535) scored a 2-3 range. No statistical difference was noted for gender, age, or duration of time present in regards to presence or absence of clear cells. Statistically significant differences in clear cell presence were found between location groups, between benign and malignant diagnosis, and between specific diagnostic groups. CONCLUSIONS: This study demonstrates the frequent presence of increased numbers of clear cells in oral salivary malignancies and highlights salivary gland differential diagnoses when presented with clear cell changes.

Factor VIII assay variability in postinfusion samples containing full length and B-domain deleted FVIII.

INTRODUCTION: Although the variability in factor VIII (FVIII):C measurement is well recognized, this has not been widely reported for post-FVIII infusion samples. AIM/METHODS: Three samples from haemophilia A patients were distributed in a UK National External Quality Assessment Scheme survey, each after treatment with either ReFacto AF, Kogenate FS or Advate. Fifty-two UK haemophilia centres performed FVIII assays using one-stage (n = 46) and chromogenic (n = 10) assays. Centres calibrated assays with the local plasma standard and with ReFacto AF laboratory standard for the ReFacto AF sample. RESULTS/CONCLUSIONS: Chromogenic assays gave significantly higher results than one-stage assays (P < 0.0001, 32% difference) in the post-Kogenate sample but not in the post-ReFacto AF (11% higher by chromogenic assay, ns) or post-Advate samples (3% lower by chromogenic, ns) when assays were calibrated with plasma standards. Twenty centres used all Instrumentation Laboratory (IL)-activated partial thromboplastin time reagents (Synthasil)/IL deficient plasma/reference plasma) in the one-stage assay and 15 used all Siemens reagents (Actin FS/Siemens deficient plasma/reference plasma); this made a significant difference to results post-ReFacto AF (41% higher by IL reagents, P < 0.0001) and Advate (39% higher by IL reagents, P < 0.0001), but not Kogenate (7% higher by IL, ns) when calibrated with plasma standards. Differences between results obtained with different one-stage assay reagents for monitoring Advate have implications for dosing patients. Furthermore, there was considerable inter-laboratory variation as indicated by CVs in the range 15-26% for chromogenic assay and 12-19% for one-stage assay results. This study suggests that external quality assessment schemes should offer participation in post-FVIII infusion schemes where haemophilic patients are monitored.

Application of a Sub-set of Skinfold Sites for Ultrasound Measurement of Subcutaneous Adiposity and Percentage Body Fat Estimation in Athletes.

Body composition assessment is an integral feature of elite sport as optimization facilitates successful performance. This study aims to refine the use of B-mode ultrasound in the assessment of athlete body composition by determining suitable sites for measurement. 67 elite athletes recruited from the Human Performance Laboratory, University College Cork, Ireland, underwent dual measurement of body composition. Subcutaneous adipose tissue thickness at 7 anatomical sites were measured using ultrasound and compared to percentage body fat values determined using Dual-Energy X-ray Absorptiometry. Multiple linear regressions were performed and an equation to predict percentage body fat was derived. The present study found subcutaneous adipose tissue depths at the triceps, biceps, anterior thigh and supraspinale sites correlated significantly with percentage body fat by X-ray absorptiometry (all p<0.05). Summation of the depths at these locations correlated strongly with percentage body fat by Dual-Energy X-ray Absorptiometry (R²=0.879). The triceps, biceps, anterior thigh and supraspinale sites are suitable anatomical landmarks for the estimation of %BF using B-mode ultrasound. Use of B-mode ultrasound in the assessment of athlete body composition confers many benefits including lack of ionising radiation and its potential to be used as a portable field tool.

Acute Loss of miR-221 and miR-222 in the Atherosclerotic Plaque Shoulder Accompanies Plaque Rupture.

BACKGROUND AND PURPOSE: Atherosclerotic plaque vulnerability is accompanied by changes in the molecular and cellular function in the plaque shoulder, including a decrease in vascular smooth muscle cell proliferation. We aimed to determine whether the expression of 3 miRNAs that regulate vascular smooth muscle cell proliferation (miR-145, miR-221, and miR-222) is altered with plaque rupture, suggesting a role in regulating plaque stability. METHODS: miRNAs were measured in the plaque shoulder of carotid plaques obtained from patients undergoing carotid endarterectomy (CEA) for 3 distinct clinical scenarios: (1) patients without previous neurological events but high-grade carotid stenosis (asymptomatic), (2) patients with an acute neurological event within 5 days of the CEA (urgent), and (3) patients undergoing CEA>5 days after a neurological event (symptomatic). RESULTS: Mean time from plaque rupture event to CEA was 2.4 days in the urgent group. The urgent group exhibited a significant decrease in miR-221 and miR-222 expression in the plaque shoulder, whereas no significant differences were seen in miR-145 across the 3 groups. Regression analysis demonstrated a significant correlation between time from the neurological event to CEA and increasing miR-221 and miR-222, but not miR-145. mRNA encoding p27Kip1, a target of miR-221 and miR-222 that inhibits vascular smooth muscle cell proliferation, was increased in the urgent group. CONCLUSIONS: Atherosclerotic plaque rupture is accompanied by a loss of miR-221 and miR-222 and an increase in p27Kip1 mRNA expression in the plaque shoulder, suggesting an association between these miRNAs and atherosclerotic plaque stability.

Renal Autotransplantation in Lynch Syndrome: A Viable Option in a Patient With Contralateral Metachronous Ureteral Cancer.

The success of human kidney allotransplantation was realized over six decades ago. First described 50 years ago, renal autotransplantation has been utilized sparingly as a salvage procedure for patients at risk of losing renal function, either from a benign or malignant condition. While classically associated with colorectal malignancies, Lynch syndrome also carries a small yet significant risk for the development of ureteral carcinoma. For these patients who develop chronic kidney disease, allotransplantation may not be an option due to the lifelong risk of several malignancies. We report the first known case of renal autotransplantation in a patient with metachronous ureteral cancer due to Lynch syndrome.

The use of skill tests to predict status in junior Australian football.

This study examined whether skill tests were predictive of status in junior Australian football. Players were recruited from the 2013 under 18 (U18) West Australian Football League competition and classified into two groups: elite (state U18 squad representative; n = 25; 17.9 ± 0.5 years) and subelite (nonstate U18 squad representative; n = 25; 17.3 ± 0.6 years). Both groups completed the Australian football kicking (AFK) and Australian football handballing (AFHB) tests, assessing kicking accuracy/ball speed and handballing accuracy on dominant and nondominant sides. A multivariate analysis of variance (MANOVA) modelled the main effect of "status", whilst logistic regression models were built for the predictive analysis using the same test parameters. Between-group differences were noted across all parameters, with the combination of kicking accuracy and ball speed on the dominant and nondominant sides being the best predictor of status for the AFK test (wi = 0.25, AUC = 89.4%) and the combination of accuracy on the dominant and nondominant sides being the best predictor of status for the AFHB test (wi = 0.80, AUC = 88.4%). The AFK and AFHB tests are predictive of status, suggesting that their use is warranted as a means of talent identification in junior Australian football.

Vitamin D2 from light-exposed edible mushrooms is safe, bioavailable and effectively supports bone growth in rats.

UNLABELLED: Widespread poor vitamin D status, a health risk for bone disease, increases the need for new food sources of vitamin D. Light-exposed edible mushrooms synthesize vitamin D(2). Bioavailability, safety, and efficacy of high levels of vitamin D(2) from mushrooms to support bone health was established in chronically fed growing rats. INTRODUCTION: Poor vitamin D status from reduced sun exposure is made worse by limited access to vitamin D-containing foods. Exposing white button mushrooms to ultraviolet B (UVB) light markedly increases their vitamin D(2) content, creating a new food source of vitamin D. We used a growing rat model to determine safety, bioavailability, and efficacy in support of bone growth by vitamin D(2) from UVB-exposed mushrooms. METHODS: We fed 150 weanling female rats one of five diets for 10 weeks, all formulated on AIN-93 G. Control diets contained no mushrooms either with or without vitamin D(3). Other diets contained 2.5% and 5.0% of UVB-exposed or -unexposed mushrooms. Safety of the high levels of vitamin D(2) from mushrooms was assessed by animal growth and by Von Kossa staining for soft tissue calcification. Bioavailability was determined from changes in circulating levels of 25-hydroxyvitamin D [25(OH)D] and parathyroid hormone (PTH). Efficacy in support of bone growth was determined from measures of femur bending properties, size, mineralization, and microarchitecture. RESULTS: Diets containing 2.5% and 5.0% light-exposed mushrooms significantly raised 25(OH)D and suppressed PTH levels compared to control-fed rats or rats fed 5.0% mushroom unexposed to light. Microarchitecture and trabecular mineralization were only modestly higher in the light-treated mushroom-fed rats compared to the controls. Von Kossa staining revealed no soft tissue calcification despite very high plasma 25(OH)D. CONCLUSIONS: Vitamin D(2) from UVB-exposed mushrooms is bioavailable, safe, and functional in supporting bone growth and mineralization in a growing rat model without evidence of toxicity.

Alpha heating of indirect-drive layered implosions on the National Ignition Facility.

In order to understand how close current layered implosions in indirect-drive inertial confinement fusion are to ignition, it is necessary to measure the level of alpha heating present. To this end, pairs of experiments were performed that consisted of a low-yield tritium-hydrogen-deuterium (THD) layered implosion and a high-yield deuterium-tritium (DT) layered implosion to validate experimentally current simulation-based methods of determining yield amplification. The THD capsules were designed to reduce simultaneously DT neutron yield (alpha heating) and maintain hydrodynamic similarity with the higher yield DT capsules. The ratio of the yields measured in these experiments then allowed the alpha heating level of the DT layered implosions to be determined. The level of alpha heating inferred is consistent with fits to simulations expressed in terms of experimentally measurable quantities and enables us to infer the level of alpha heating in recent high-performing implosions.