Occurrence of the Asiatic Weatherfish, Misgurnus Anguillicaudatus (Cantor, 1842), in Alabama, USA

The Asiatic weatherfish, Misgurnus anguillicaudatus, is a generalist species that has invaded numerous physiographic niches worldwide. Asiatic weatherfish populations have been observed to compete with native fish populations in Hawaii and are of major concern in Australia due to the concomitant introduction of an exotic parasite. Asiatic weatherfish populations have been observed in 16 of the contiguous United States (US) since the 1940s. Alabama is the most recent US state to report sustaining Asiatic weatherfish populations. Asiatic weatherfish were first observed by local fishermen in 2000, but reported established in Alabama in 2009 and, more recently, in 2012. From 2013 to 2014, surveys were conducted in NE Alabama on the Coosa River near Logan Martin Reservoir, as well as the surrounding watershed on the eastern side of the reservoir, specifically investigating for Asiatic weatherfish. Sites were surveyed using standard protocols for the surveying of wadeable streams using a backpack electrofisher and seine nets. Weatherfish were collected at 5 of 15 sites surveyed between 2013 and 2014. A total of 112 fish were collected, comprising 15% (112/738) of total catch. At 2 of the 5 sites, weatherfish occurrence was \u3e50% of the total species observed. Weatherfish were collected in numerous habitats including lentic pools, lotic riffles, as well as in dense vegetation. Numerous size class individuals were collected (27–114mm SL) indicating populations are reproducing. Based on its occurrence in Logan Martin Reservoir and surrounding tributaries, the species appears to be expanding its range utilizing Logan Martin Reservoir as a “stepping stone” for migration. Little is known about competition between Asiatic weatherfish and native US fishes although many conservationists suggest competition is inevitable. Currently, Asiatic weatherfish co-occur in Alabama springs alongside a rare endemic fish species (coldwater dater, Etheostoma ditrema) and it is likely to encounter other sensitive species as it expands its range

Physiological Ecology of Four Endemic Alabama Species and the Exotic Asiatic Weatherfish, \u3ci\u3eMisgurnus anguillicaudatus\u3c/i\u3e (Cantor, 1842)

The occurrence of Asiatic Weatherfish, Misgurnus anguillicaudatus, in Alabama, a state known for its rich biodiversity, has generated concern among conservation managers. The current study used respirometry techniques to investigate the effects of increasing temperature on four native southeastern fishes (one cyprinid, two percids, and one elassomid) and the non-native M. anguillicaudatus. A minimum of five individuals of each species were used, and three experimental temperatures were chosen to represent spring and summer averages of northeast Alabama streams (15, 20, and 25°C). Overall, mean standard metabolic rates (SMRs) for M. anguillicaudatus were low (97.01, 127.75, and 158.50 mg O2 kg-1h-1 at 15, 20, and 25°C, respectively); M. anguillicaudatus was the only species for which SMR did not significantly increase with temperature (p = 0.467). In contrast, mean SMRs for all native species examined were higher than M. anguillicaudatus rates at a given temperature, and mean SMRs for Cyprinella caerulea, Etheostoma brevirostrum, and Etheostoma ditrema exhibited significant increases in SMR when temperatures were increased (e.g. 403.46, 704.42, and 1150.03 mg O2 kg-1h-1 at 25°C, respectively) (p \u3c 0.01). Elassoma zonatum displayed highly significant increases in SMR when temperature increased from 15-20°C (p \u3c 0.001). Overall, the abiotic tolerances of M. anguillicaudatus may facilitate further establishment that could lead to negative impacts on native species

Analyses of ionizing radiation effects in – vitro in peripheral blood 1 lymphocytes with Raman spectroscopy

The use of Raman spectroscopy to measure the biochemical profile of healthy and diseased cells and tissues may be a potential solution to many diagnostic problems in the clinic. Although extensively used to identify changes in the biochemical profiles of cancerous cells and tissue, Raman spectroscopy has been used less often for analyzing changes to the cellular environment by external factors such as ionizing radiation. In tandem with this, the biological impact of low doses of ionizing radiation remains poorly understood. Extensive studies have been performed on the radiobiological effects associated with radiation doses above 0.1 Gy, and are well characterized, but recent studies on low-dose radiation exposure have revealed complex and highly variable responses. We report here the novel finding that demonstrate the capability of Raman spectroscopy to detect radiation-induced damage responses in isolated lymphocytes irradiated with doses of 0.05 and 0.5 Gy. Lymphocytes were isolated from peripheral blood in a cohort of volunteers, cultured ex vivo and then irradiated. Within 1 h after irradiation spectral effects were observed with Raman microspectroscopy and principal component analysis and linear discriminant analysis at both doses relative to the sham-irradiated control (0 Gy). Cellular DNA damage was confirmed using parallel γ-H2AX fluorescence measurements on the extracted lymphocytes per donor and per dose. DNA damage measurements exhibited interindividual variability among both donors and dose, which matched that seen in the spectral variability in the lymphocyte cohort. Further evidence of links between spectral features and DNA damage was also observed, which may potentially allow noninvasive insight into the DNA remodeling that occurs after exposure to ionizing radiation

Embedded Star Formation in the Eagle Nebula with Spitzer/GLIMPSE

We present new Spitzer photometry of the Eagle Nebula (M16, containing the optical cluster NGC 6611) combined with near-infrared photometry from 2MASS. We use dust radiative transfer models, mid-infrared and near-infrared color-color analysis, and mid-infrared spectral indices to analyze point source spectral energy distributions, select candidate young stellar objects (YSOs), and constrain their mass and evolutionary state. Comparison of the different protostellar selection methods shows that mid-infrared methods are consistent, but as has been known for some time, near-infrared-only analysis misses some young objects. We reveal more than 400 protostellar candidates, including one massive young stellar object (YSO) that has not been previously highlighted. The YSO distribution supports a picture of distributed low-level star formation, with no strong evidence of triggered star formation in the ``pillars''. We confirm the youth of NGC 6611 by a large fraction of infrared-excess sources, and reveal a younger cluster of YSOs in the nearby molecular cloud. Analysis of the YSO clustering properties shows a possible imprint of the molecular cloud's Jeans length. Multiwavelength mid-IR imaging thus allows us to analyze the protostellar population, to measure the dust temperature and column density, and to relate these in a consistent picture of star formation in M16.Comment: 16p preprint - ApJ accepte

MicroRNA Analysis of ATM-Deficient Cells Indicate PTEN and CCDN1 as Potential Biomarkers of Radiation Response

Genetic and epigenetic profile changes associated with individual radiation sensitivity are well documented and have led to enhanced understanding of the mechanisms of the radiation-induced DNA damage response. However, the search continues to identify reliable biomarkers of individual radiation sensitivity. Herein, we report on a multi-biomarker approach using traditional cytogenetic biomarkers, DNA damage biomarkers and transcriptional microRNA (miR) biomarkers coupled with their potential gene targets to identify radiosensitivity in ataxia-telangiectasia mutated (ATM)-deficient lymphoblastoid cell lines (LCL); ATM-proficient cell lines were used as controls. Cells were 0.05 and 0.5 Gy irradiated, using a linear accelerator, with sham-irradiated cells as controls. At 1 h postirradiation, cells were fixed for γ-H2AX analysis as a measurement of DNA damage, and cytogenetic analysis using the G2 chromosomal sensitivity assay, G-banding and FISH techniques. RNA was also isolated for genetic profiling by microRNA (miR) and RT-PCR analysis. A panel of 752 miR were analyzed, and potential target genes, phosphatase and tensin homolog (PTEN) and cyclin D1 (CCND1), were measured. The cytogenetic assays revealed that although the control cell line had functional cell cycle checkpoints, the radiosensitivity of the control and AT cell lines were similar. Analysis of DNA damage in all cell lines, including an additional control cell line, showed elevated γ-H2AX levels for only one AT cell line. Of the 752 miR analyzed, eight miR were upregulated, and six miR were downregulated in the AT cells compared to the control. Upregulated miR-152-3p, miR-24-5p and miR-92-15p and all downregulated miR were indicated as modulators of PTEN and CCDN1. Further measurement of both genes validated their potential role as radiation-response biomarkers. The multi-biomarker approach not only revealed potential candidates for radiation response, but provided additional mechanistic insights into the response in AT-deficient cells

Peak flow rate and death due to coronary heart disease: 30-year results from the Northwick Park Heart cohort study.

OBJECTIVE: Numerous studies have reported that chronic obstructive pulmonary disease or impaired lung function are associated with later coronary heart disease (CHD). However, it is unclear if lung function is an independent risk factor, as many of these studies have included only limited measures of other factors associated with CHD. METHODS: In total 2167 men of all ages in the first Northwick Park Heart Study were followed for a median of 30 years. Cox regression models were used to assess the relationship between peak flow rate (PFR) and CHD mortality adjusted for potential confounders measured at baseline. Analyses allowed for missing data, and secondary analyses for repeat measures on some men and competing risks of CHD death. RESULTS: There were 254 CHD deaths with some evidence of an association between PFR and CHD mortality. The adjusted HRs (95% CIs) from the lowest to the highest of four PFR quartiles were 1.53 (1.04 to 2.25), <430 L/min; 1.43 (0.99 to 2.08), 430 - <490 L/min; and 1.31 (0.93 to 1.86), 490 - <550 L/min; compared with the reference group of ≥550 L/min (trend test p=0.025). Other associations with CHD mortality were observed for systolic blood pressure (p<0.0001), body mass index (p=0.0002), smoking status (p=0.015), blood cholesterol (p=0.005), plasma fibrinogen (p=0.001) and high-risk ECG (p=0.021). There were no strong associations for factors V and VIII or platelet count. CONCLUSIONS: After allowing for a range of other risk factors associated with CHD, there was only limited evidence of a relation between PFR and CHD mortality

Quality of Life Associated with Physical Activity but not Sedentary Time in Youth

Purpose: It has been reported that youth who engaged in more screen time had lower quality of life scores compared to those that were more physically active. Furthermore, increased sedentary behavior increases health risks particularly the risk for obesity. A cross-sectional analysis was completed to examine the relationship between healthrelated quality-of-life (HRQOL) and accelerometer-measured sedentary time (ST) and physical activity (PA) in 9-10-yearold youth who were recruited for the family-based, childhood obesity intervention, iCook 4-H. It was hypothesized that objectively measured ST would be negatively correlated and PA would be positively correlated with HRQOL.Methods: A subset of participants (n=118) wore Actigraph GT3X+ accelerometers for 7 days and completed the Pediatric Quality of Life survey (PedsQLTM, version 4.0) to assess HRQOL. Mean daily minutes of accelerometermeasured ST (547 ± 60) and PA including light-intensity (LPA=240 ± 49), moderate-intensity (MPA=35 ± 11), vigorous-intensity (VPA=17 ± 9), and moderate-to vigorousintensity (MVPA=52 ± 19) were evaluated during waking hours. Multiple linear regressions were used to assess relationship between ST and PA intensities with HRQOL. Statistical significance was set at p ≤ 0.05.Results: There were no significant associations between ST or LPA with HRQOL. MPA, VPA and MVPA were positively associated with multiple HRQOL domains.Conclusion: The lack of relationship between objectively measured ST and LPA with the total HRQOL score and subscales merits further investigation. The findings of the current study support the need for lifestyle interventions that engage families in behavior that increases MVPA

Molnupiravir inhibits SARS-CoV-2 variants including Omicron in the hamster model.

The recent emergence of the SARS-CoV-2 Omicron variant of concern (VOC) containing a heavily mutated spike protein capable of escaping preexisting immunity identifies a continued need for interventional measures. Molnupiravir (MK-4482), an orally administered nucleoside analog, has demonstrated efficacy against earlier SARS-CoV-2 lineages and was recently approved for SARS-CoV-2 infections in high-risk adults. Here we assessed the efficacy of MK-4482 against the earlier Alpha, Beta and Delta VOCs and Omicron in the hamster COVID-19 model. Omicron replication and associated lung disease in vehicle treated hamsters was reduced compared to the earlier VOCs. MK-4482 treatment inhibited virus replication in the lungs of Alpha, Beta and Delta VOC infected hamsters. Importantly, MK-4482 profoundly inhibited virus replication in the upper and lower respiratory tract of hamsters infected with the Omicron VOC. Consistent with its mutagenic mechanism, MK-4482 treatment had a more pronounced inhibitory effect on infectious titers compared to viral RNA genome load. Histopathologic analysis showed that MK-4482 treatment caused a concomitant reduction in the level of lung disease and viral antigen load in infected hamsters across all VOCs examined. Together, our data indicate the potential of MK-4482 as an effective antiviral against known SARS-CoV-2 VOCs, especially Omicron, and likely future SARS-CoV-2 variants

Lymphoid Enhancer Factor-1 Links Two Hereditary Leukemia Syndromes through Core-binding Factor α Regulation of ELA2

Two hereditary human leukemia syndromes are severe congenital neutropenia (SCN), caused by mutations in the gene ELA2, encoding the protease neutrophil elastase, and familial platelet disorder with acute myelogenous leukemia (AML), caused by mutations in the gene AML1, encoding the transcription factor core-binding factor α (CBFα). In mice, CBFα regulates the expression of ELA2, suggesting a common link for both diseases. However, gene-targeted mouse models have failed to reproduce either human disease, thus prohibiting further in vivo studies in mice. Here we investigate CBFα regulation of the human ELA2 promoter, taking advantage of bone marrow obtained from patients with either illness. In particular, we have identified novel ELA2 promoter substitutions (-199 C to A) within a potential motif for lymphoid enhancer factor-1 (LEF-1), a transcriptional mediator of Wnt/β-catenin signaling, in SCN patients. The LEF-1 motif lies adjacent to a potential CBFα binding site that is in a different position in human compared with mouse ELA2. We find that LEF-1 and CBFα co-activate ELA2 expression. In vitro, the high mobility group domain of LEF-1 interacts with the runt DNA binding and proline-, serine-, threonine-rich activation domains of CBFα. ELA2 transcript levels are up-regulated in bone marrow of an SCN patient with the -199 C to A substitution. Conversely, a mutation of the CBFα activation domain, found in a patient with familial platelet disorder with AML, fails to stimulate the ELA2 promoter in vitro, and bone marrow correspondingly demonstrates reduced ELA2 transcript. Observations in these complementary patients indicate that LEF-1 cooperates with CBFα to activate ELA2 in vivo and also suggest the possibility that up-regulating promoter mutations can contribute to SCN. Two hereditary AML predisposition syndromes may therefore intersect via LEF-1, potentially linking them to more generalized cancer mechanisms