| 1. |
- Feng, Shaohong, et al.
(author)
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Dense sampling of bird diversity increases power of comparative genomics
- 2020
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In: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 587:7833
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Journal article (peer-reviewed)abstract
- Whole-genome sequencing projects are increasingly populating the tree of life and characterizing biodiversity(1-4). Sparse taxon sampling has previously been proposed to confound phylogenetic inference(5), and captures only a fraction of the genomic diversity. Here we report a substantial step towards the dense representation of avian phylogenetic and molecular diversity, by analysing 363 genomes from 92.4% of bird families-including 267 newly sequenced genomes produced for phase II of the Bird 10,000 Genomes (B10K) Project. We use this comparative genome dataset in combination with a pipeline that leverages a reference-free whole-genome alignment to identify orthologous regions in greater numbers than has previously been possible and to recognize genomic novelties in particular bird lineages. The densely sampled alignment provides a single-base-pair map of selection, has more than doubled the fraction of bases that are confidently predicted to be under conservation and reveals extensive patterns of weak selection in predominantly non-coding DNA. Our results demonstrate that increasing the diversity of genomes used in comparative studies can reveal more shared and lineage-specific variation, and improve the investigation of genomic characteristics. We anticipate that this genomic resource will offer new perspectives on evolutionary processes in cross-species comparative analyses and assist in efforts to conserve species. A dataset of the genomes of 363 species from the Bird 10,000 Genomes Project shows increased power to detect shared and lineage-specific variation, demonstrating the importance of phylogenetically diverse taxon sampling in whole-genome sequencing.
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| 2. |
- Razavi-Shearer, Devin M., et al.
(author)
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Adjusted estimate of the prevalence of hepatitis delta virus in 25 countries and territories
- 2024
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In: JOURNAL OF HEPATOLOGY. - 0168-8278 .- 1600-0641. ; 80:2, s. 232-242
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Journal article (peer-reviewed)abstract
- Background & Aims: Hepatitis delta virus (HDV) is a satellite RNA virus that requires the hepatitis B virus (HBV) for assembly and propagation. Individuals infected with HDV progress to advanced liver disease faster than HBV-monoinfected individuals. Recent studies have estimated the global prevalence of anti-HDV antibodies among the HBV-infected population to be 5-15%. This study aimed to better understand HDV prevalence at the population level in 25 countries/territories. Methods: We conducted a literature review to determine the prevalence of anti-HDV and HDV RNA in hepatitis B surface antigen (HBsAg)-positive individuals in 25 countries/territories. Virtual meetings were held with experts from each setting to discuss the findings and collect unpublished data. Data were weighted for patient segments and regional heterogeneity to estimate the prevalence in the HBV-infected population. The findings were then combined with The Polaris Observatory HBV data to estimate the anti-HDV and HDV RNA prevalence in each country/territory at the population level. Results: After adjusting for geographical distribution, disease stage and special populations, the anti-HDV prevalence among the HBsAg+ population changed from the literature estimate in 19 countries. The highest anti-HDV prevalence was 60.1% in Mongolia. Once adjusted for the size of the HBsAg+ population and HDV RNA positivity rate, China had the highest absolute number of HDV RNA+ cases. Conclusions: We found substantially lower HDV prevalence than previously reported, as prior meta-analyses primarily focused on studies conducted in groups/regions that have a higher probability of HBV infection: tertiary care centers, specific risk groups or geographical regions. There is large uncertainty in HDV prevalence estimates. The implementation of reflex testing would improve estimates, while also allowing earlier linkage to care for HDV RNA+ individuals. The logistical and economic burden of reflex testing on the health system would be limited, as only HBsAg+ cases would be screened.
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| 3. |
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| 4. |
- Ni, Yuan Qi, et al.
(author)
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Infant-phase reddening by surface Fe-peak elements in a normal type Ia supernova
- 2022
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In: Nature Astronomy. - : Springer Science and Business Media LLC. - 2397-3366. ; 6:5, s. 568-576
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Journal article (peer-reviewed)abstract
- Type Ia supernovae are thermonuclear explosions of white dwarf stars. They play a central role in the chemical evolution of the Universe and are an important measure of cosmological distances. However, outstanding questions remain about their origins. Despite extensive efforts to obtain natal information from their earliest signals, observations have thus far failed to identify how the majority of them explode. Here, we present infant-phase detections of SN 2018aoz from a very low brightness of −10.5 AB absolute magnitude, revealing a hitherto unseen plateau in the B band that results in a rapid redward colour evolution between 1.0 and 12.4 hours after the estimated epoch of first light. The missing B-band flux is best explained by line-blanket absorption from Fe-peak elements in the outer 1% of the ejected mass. The observed B − V colour evolution of the supernova also matches the prediction from an over-density of Fe-peak elements in the same outer 1% of the ejected mass, whereas bluer colours are expected from a purely monotonic distribution of Fe-peak elements. The presence of excess nucleosynthetic material in the extreme outer layers of the ejecta points to enhanced surface nuclear burning or extended subsonic mixing processes in some normal type Ia SN explosions.
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| 5. |
- Ni, Yuan Qi, et al.
(author)
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The Origin and Evolution of the Normal Type Ia SN 2018aoz with Infant-phase Reddening and Excess Emission
- 2023
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In: Astrophysical Journal. - : American Astronomical Society. - 0004-637X .- 1538-4357. ; 946:1
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Journal article (peer-reviewed)abstract
- SN 2018aoz is a Type Ia SN with a B-band plateau and excess emission in infant-phase light curves ≲1 day after the first light, evidencing an over-density of surface iron-peak elements as shown in our previous study. Here, we advance the constraints on the nature and origin of SN 2018aoz based on its evolution until the nebular phase. Near-peak spectroscopic features show that the SN is intermediate between two subtypes of normal Type Ia: core normal and broad line. The excess emission may be attributable to the radioactive decay of surface iron-peak elements as well as the interaction of ejecta with either the binary companion or a small torus of circumstellar material. Nebular-phase limits on Hα and He i favor a white dwarf companion, consistent with the small companion size constrained by the low early SN luminosity, while the absence of [O I] and He i disfavors a violent merger of the progenitor. Of the two main explosion mechanisms proposed to explain the distribution of surface iron-peak elements in SN 2018aoz, the asymmetric Chandrasekhar-mass explosion is less consistent with the progenitor constraints and the observed blueshifts of nebular-phase [Fe II] and [Ni II]. The helium-shell double-detonation explosion is compatible with the observed lack of C spectral features, but current 1D models are incompatible with the infant-phase excess emission, Bmax–Vmax color, and weak strength of nebular-phase [Ca II]. Although the explosion processes of SN 2018aoz still need to be more precisely understood, the same processes could produce a significant fraction of Type Ia SNe that appear to be normal after ∼1 day.
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| 6. |
- Ryder, Jeffrey W
(author)
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Mechanisms regulating metabolic and mitogenic events in skeletal muscle : implications for insulin resistance and exercise
- 2000
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Doctoral thesis (other academic/artistic)abstract
- Reduced glucose transport in skeletal muscle is a hallmark feature of Type II diabetes. Numerous mechanisms acutely or chronically regulate skeletal muscle glucose transport. The role of GLUT4, mitogen-activated protein kinases (MAPK), and peroxisome proliferator-activated receptor [gamma] (PPAR[gamma]) were examined in skeletal muscle. The role of GLUT4 was first considered. Insulin increased 2-deoxyglucose uptake 2.8-and 2.1-fold in Wild-type versus GLUT4-deficient (GLUT4-null) soleus muscle. GLUT4 ablation did not increase GLUT3 or GLUT5 protein in soleus muscle. Insulin-stimulated cell surface GLUT1 content was similar in Wild-type and GLUT4-null soleus muscle. Hypoxia stimulated glucose uptake 2- to 2.5- fold in Wild-type EDL or soleus muscle, but was without effect in GLUT4-null muscle. Introduction of the MLC-GLUT4 transgene into GLUT4-null mice restored hypoxia-stimulated glucose uptake in EDL muscle. Exercise, but not insulin, significantly increased glucose uptake in EDL muscle from fed GLUT4-null mice. However, the exercise effect was reduced compared to Wild-type mice. Exercise led to a similar degree of muscle glycogen depletion in Wild-type and GLUT-null mice. Glycogen was restored in Wild-type mice by 5 h after exercise, whereas restoration of glycogen in GLUT4-null mice was observed 24 h post-exercise. In muscle from healthy human subjects, insulin and hypoxia similarly stimulated glucose transport and GLUT4 translocation. Glucose transport and GLUT4 translocation were markedly reduced in diabetic skeletal muscle in response to either insulin or hypoxia. A greater defect was observed in GLUT4 translocation. Mitogenic events are under control of the MAPK-signaling pathways. In vitro muscle contraction increased ERK1/2 and p38 MAPK phosphorylation and p90Rsk, MAPKAP-K2, and MSK1 activity in rat epitrochlearis muscle. The MEK1 inhibitor, PD98059, completely abolished contraction-mediated ERK1/2, p90Rsk, and MSK1 activity. The p38 MAPK inhibitor, SB203580, prevented p38 MAPK, MAPKAP-K2, and MSK1 activation. Thiazolidinediones (TZD: PPAR[gamma] agonists) are a new class of anti-diabetic drugs. Oral TZD-treatment partially restored in vivo glucose uptake and normalized in vitro glucose uptake in ZDF rat and ob/ob mouse skeletal muscle, respectively. However, in vitro TZD-exposure (5-9h) did not improve insulin-stimulated glucose uptake in soleus muscle from ob/ob mice. In conclusion, GLUT4 is a major regulatory factory for both insulin- and exercise stimulated glucose transport. However, GLUT4-independent mechanisms exist in skeletal muscle. Furthermore, defects in GLUT4 translocation may contribute to Type II diabetes. Exercise-induced improvements in skeletal muscle insulin action likely involve direct activation of MAPK-signaling pathways in response to muscle contraction, whereas improved insulin action in muscle following TZD treatment is secondary to PPAR[gamma] activation in other tissues.
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