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Altered translation elongation contributes to key hallmarks of aging in the killifish brain
No full textAging is a major risk factor for neurodegeneration and is characterized by diverse cellular and molecular hallmarks. To understand the origin of these hallmarks, we studied the effects of aging on the transcriptome, translatome, and proteome in the brain of short-lived killifish. We identified a cascade of events in which aberrant translation pausing led to altered abundance of proteins independently of transcriptional regulation. In particular, aging caused increased ribosome stalling and widespread depletion of proteins enriched in basic amino acids. These findings uncover a potential vulnerable point in the aging brain’s biology—the biogenesis of basic DNA and RNA binding proteins. This vulnerability may represent a unifying principle that connects various aging hallmarks, encompassing genome integrity, proteostasis, and the biosynthesis of macromolecules.Editor’s summary To get a handle on what falls apart during aging in the brain, Di Fraia et al . turned to the short-lived killifish (see the Perspective by Dionne and Laurent). The authors monitored changes in protein and RNA abundance, protein solubility, post-translational modification, and organelle composition as the fish aged. As organisms age, protein abundance is less closely coupled to transcript abundance. In the fish, this appeared to have less to do with protein stability and was more likely influenced by altered translation. Proteins rich in basic amino acids, a characteristic of RNA and DNA binding proteins, had delays in translation and decreased in abundance. Changes in mitochondrial composition were also noted as likely contributors to loss of function in aging. —L. Bryan RayINTRODUCTION Aging brains are characterized by a series of molecular and cellular changes known as aging hallmarks. Among these, a decline in protein homeostasis (proteostasis) marked by reduced clearance and increased protein damage and aggregation has received particular attention as a plausible link between brain aging and those neurodegenerative diseases also characterized by protein aggregation. A notable phenomenon in brain aging is a loss of concordance between mRNA and protein levels, whereby age-linked changes in mRNA do not necessarily lead to proportional changes in protein levels. In this study, we set out to investigate the causes of this “protein-transcript decoupling” and how impaired protein synthesis might contribute to other hallmarks of brain aging. RATIONALE We used the short-lived African turquoise killifish, which exhibits a naturally compressed life span and accelerated brain aging, to undertake a comprehensive investigation of age-related decline in brain proteostasis. We compared young, adult, and old killifish brains at the levels of amino acid concentrations, tRNAs, mRNAs (transcriptome), actively translated mRNAs (translatome), proteins (proteome), protein modifications [phosphorylation (Ph), ubiquitylation (Ub), and acetylation (Ac)], and protein solubility and subcellular localization. We also tested whether reduced protein degradation caused by proteasome impairment contributes to protein-transcript decoupling and other aging hallmarks in the killifish brain. Our comprehensive design allowed us to pinpoint aging-vulnerable steps in protein biogenesis and reveal mechanisms connecting proteostasis decline to other aging hallmarks. RESULTS We observed alterations in all molecular signatures investigated, ranging from amino acid concentrations to protein solubility and localization. A clear pattern of proteostasis dysfunction emerged: Although the synthesis of some proteins was enhanced, there was a widespread reduction of proteins enriched in positively charged (basic) amino acids. Notably, many DNA and RNA binding proteins exhibited reduced abundance in old brains, decreasing at the protein but not the transcript levels. Ribosome profiling (Ribo-seq) revealed that brain aging increased ribosome stalling. Accordingly, ribosome collisions were more frequent in old brains. Crucially, stalling events occurred disproportionately on stretches enriched in lysine and arginine codons, thus affecting translation of mRNAs encoding proteins enriched in these basic amino acids, leading to a decline in their protein levels in old brains. Aging-affected proteins included ribosomal subunits and proteins involved in DNA repair, transcription, chromatin maintenance, and RNA splicing and export, which all mediate processes influenced by aging. Ribosome stalling was also associated with increased protein insolubility, likely owing to nascent polypeptide misfolding. Partial proteasome inhibition affected aging hallmarks distinct from those linked to translation dysfunction and primarily influenced lysosomes and mitochondria. CONCLUSION This work identifies altered translation elongation and impaired protein biogenesis as hallmarks of brain aging in a short-lived vertebrate. Increased ribosome pausing is proposed as a key mechanism contributing to the mismatch between mRNA and protein changes observed in aged brains, leading to proteome aging by altering the production of proteins essential for genome integrity, mRNA transcription, splicing, protein synthesis, and mitochondrial function. This mechanism thereby links translation and proteostasis decline to other hallmarks of aging and may also be implicated in neurodegenerative diseases where similar ribosome dysfunction and protein misfolding occur. Altered protein synthesis remodels the aging brain proteome. Age-related mRNA and protein changes are decoupled. Ribosome profiling reveals increased translation elongation pausing, occurring preferentially at codons encoding for basic residues. Ribosome pausing contributes to protein-transcript decoupling and is associated with a depletion in RNA and DNA binding proteins. These changes also contribute to protein misfolding and insolubility, linking protein synthesis defects to other aging hallmarks. PTMs, posttranslational modifications.Aging is a major risk factor for neurodegeneration and is characterized by diverse cellular and molecular hallmarks. To understand the origin of these hallmarks, we studied the effects of aging on the transcriptome, translatome, and proteome in the brain of short-lived killifish. We identified a cascade of events in which aberrant translation pausing led to altered abundance of proteins independently of transcriptional regulation. In particular, aging caused increased ribosome stalling and widespread depletion of proteins enriched in basic amino acids. These findings uncover a potential vulnerable point in the aging brain’s biology—the biogenesis of basic DNA and RNA binding proteins. This vulnerability may represent a unifying principle that connects various aging hallmarks, encompassing genome integrity, proteostasis, and the biosynthesis of macromolecules.Editor’s summary To get a handle on what falls apart during aging in the brain, Di Fraia et al . turned to the short-lived killifish (see the Perspective by Dionne and Laurent). The authors monitored changes in protein and RNA abundance, protein solubility, post-translational modification, and organelle composition as the fish aged. As organisms age, protein abundance is less closely coupled to transcript abundance. In the fish, this appeared to have less to do with protein stability and was more likely influenced by altered translation. Proteins rich in basic amino acids, a characteristic of RNA and DNA binding proteins, had delays in translation and decreased in abundance. Changes in mitochondrial composition were also noted as likely contributors to loss of function in aging. —L. Bryan RayINTRODUCTION Aging brains are characterized by a series of molecular and cellular changes known as aging hallmarks. Among these, a decline in protein homeostasis (proteostasis) marked by reduced clearance and increased protein damage and aggregation has received particular attention as a plausible link between brain aging and those neurodegenerative diseases also characterized by protein aggregation. A notable phenomenon in brain aging is a loss of concordance between mRNA and protein levels, whereby age-linked changes in mRNA do not necessarily lead to proportional changes in protein levels. In this study, we set out to investigate the causes of this “protein-transcript decoupling” and how impaired protein synthesis might contribute to other hallmarks of brain aging. RATIONALE We used the short-lived African turquoise killifish, which exhibits a naturally compressed life span and accelerated brain aging, to undertake a comprehensive investigation of age-related decline in brain proteostasis. We compared young, adult, and old killifish brains at the levels of amino acid concentrations, tRNAs, mRNAs (transcriptome), actively translated mRNAs (translatome), proteins (proteome), protein modifications [phosphorylation (Ph), ubiquitylation (Ub), and acetylation (Ac)], and protein solubility and subcellular localization. We also tested whether reduced protein degradation caused by proteasome impairment contributes to protein-transcript decoupling and other aging hallmarks in the killifish brain. Our comprehensive design allowed us to pinpoint aging-vulnerable steps in protein biogenesis and reveal mechanisms connecting proteostasis decline to other aging hallmarks. RESULTS We observed alterations in all molecular signatures investigated, ranging from amino acid concentrations to protein solubility and localization. A clear pattern of proteostasis dysfunction emerged: Although the synthesis of some proteins was enhanced, there was a widespread reduction of proteins enriched in positively charged (basic) amino acids. Notably, many DNA and RNA binding proteins exhibited reduced abundance in old brains, decreasing at the protein but not the transcript levels. Ribosome profiling (Ribo-seq) revealed that brain aging increased ribosome stalling. Accordingly, ribosome collisions were more frequent in old brains. Crucially, stalling events occurred disproportionately on stretches enriched in lysine and arginine codons, thus affecting translation of mRNAs encoding proteins enriched in these basic amino acids, leading to a decline in their protein levels in old brains. Aging-affected proteins included ribosomal subunits and proteins involved in DNA repair, transcription, chromatin maintenance, and RNA splicing and export, which all mediate processes influenced by aging. Ribosome stalling was also associated with increased protein insolubility, likely owing to nascent polypeptide misfolding. Partial proteasome inhibition affected aging hallmarks distinct from those linked to translation dysfunction and primarily influenced lysosomes and mitochondria. CONCLUSION This work identifies altered translation elongation and impaired protein biogenesis as hallmarks of brain aging in a short-lived vertebrate. Increased ribosome pausing is proposed as a key mechanism contributing to the mismatch between mRNA and protein changes observed in aged brains, leading to proteome aging by altering the production of proteins essential for genome integrity, mRNA transcription, splicing, protein synthesis, and mitochondrial function. This mechanism thereby links translation and proteostasis decline to other hallmarks of aging and may also be implicated in neurodegenerative diseases where similar ribosome dysfunction and protein misfolding occur. Altered protein synthesis remodels the aging brain proteome. Age-related mRNA and protein changes are decoupled. Ribosome profiling reveals increased translation elongation pausing, occurring preferentially at codons encoding for basic residues. Ribosome pausing contributes to protein-transcript decoupling and is associated with a depletion in RNA and DNA binding proteins. These changes also contribute to protein misfolding and insolubility, linking protein synthesis defects to other aging hallmarks. PTMs, posttranslational modifications.Aging is a major risk factor for neurodegeneration and is characterized by diverse cellular and molecular hallmarks. To understand the origin of these hallmarks, we studied the effects of aging on the transcriptome, translatome, and proteome in the brain of short-lived killifish. We identified a cascade of events in which aberrant translation pausing led to altered abundance of proteins independently of transcriptional regulation. In particular, aging caused increased ribosome stalling and widespread depletion of proteins enriched in basic amino acids. These findings uncover a potential vulnerable point in the aging brain’s biology—the biogenesis of basic DNA and RNA binding proteins. This vulnerability may represent a unifying principle that connects various aging hallmarks, encompassing genome integrity, proteostasis, and the biosynthesis of macromolecules.Editor’s summary To get a handle on what falls apart during aging in the brain, Di Fraia et al . turned to the short-lived killifish (see the Perspective by Dionne and Laurent). The authors monitored changes in protein and RNA abundance, protein solubility, post-translational modification, and organelle composition as the fish aged. As organisms age, protein abundance is less closely coupled to transcript abundance. In the fish, this appeared to have less to do with protein stability and was more likely influenced by altered translation. Proteins rich in basic amino acids, a characteristic of RNA and DNA binding proteins, had delays in translation and decreased in abundance. Changes in mitochondrial composition were also noted as likely contributors to loss of function in aging. —L. Bryan RayINTRODUCTION Aging brains are characterized by a series of molecular and cellular changes known as aging hallmarks. Among these, a decline in protein homeostasis (proteostasis) marked by reduced clearance and increased protein damage and aggregation has received particular attention as a plausible link between brain aging and those neurodegenerative diseases also characterized by protein aggregation. A notable phenomenon in brain aging is a loss of concordance between mRNA and protein levels, whereby age-linked changes in mRNA do not necessarily lead to proportional changes in protein levels. In this study, we set out to investigate the causes of this “protein-transcript decoupling” and how impaired protein synthesis might contribute to other hallmarks of brain aging. RATIONALE We used the short-lived African turquoise killifish, which exhibits a naturally compressed life span and accelerated brain aging, to undertake a comprehensive investigation of age-related decline in brain proteostasis. We compared young, adult, and old killifish brains at the levels of amino acid concentrations, tRNAs, mRNAs (transcriptome), actively translated mRNAs (translatome), proteins (proteome), protein modifications [phosphorylation (Ph), ubiquitylation (Ub), and acetylation (Ac)], and protein solubility and subcellular localization. We also tested whether reduced protein degradation caused by proteasome impairment contributes to protein-transcript decoupling and other aging hallmarks in the killifish brain. Our comprehensive design allowed us to pinpoint aging-vulnerable steps in protein biogenesis and reveal mechanisms connecting proteostasis decline to other aging hallmarks. RESULTS We observed alterations in all molecular signatures investigated, ranging from amino acid concentrations to protein solubility and localization. A clear pattern of proteostasis dysfunction emerged: Although the synthesis of some proteins was enhanced, there was a widespread reduction of proteins enriched in positively charged (basic) amino acids. Notably, many DNA and RNA binding proteins exhibited reduced abundance in old brains, decreasing at the protein but not the transcript levels. Ribosome profiling (Ribo-seq) revealed that brain aging increased ribosome stalling. Accordingly, ribosome collisions were more frequent in old brains. Crucially, stalling events occurred disproportionately on stretches enriched in lysine and arginine codons, thus affecting translation of mRNAs encoding proteins enriched in these basic amino acids, leading to a decline in their protein levels in old brains. Aging-affected proteins included ribosomal subunits and proteins involved in DNA repair, transcription, chromatin maintenance, and RNA splicing and export, which all mediate processes influenced by aging. Ribosome stalling was also associated with increased protein insolubility, likely owing to nascent polypeptide misfolding. Partial proteasome inhibition affected aging hallmarks distinct from those linked to translation dysfunction and primarily influenced lysosomes and mitochondria. CONCLUSION This work identifies altered translation elongation and impaired protein biogenesis as hallmarks of brain aging in a short-lived vertebrate. Increased ribosome pausing is proposed as a key mechanism contributing to the mismatch between mRNA and protein changes observed in aged brains, leading to proteome aging by altering the production of proteins essential for genome integrity, mRNA transcription, splicing, protein synthesis, and mitochondrial function. This mechanism thereby links translation and proteostasis decline to other hallmarks of aging and may also be implicated in neurodegenerative diseases where similar ribosome dysfunction and protein misfolding occur. Altered protein synthesis remodels the aging brain proteome. Age-related mRNA and protein changes are decoupled. Ribosome profiling reveals increased translation elongation pausing, occurring preferentially at codons encoding for basic residues. Ribosome pausing contributes to protein-transcript decoupling and is associated with a depletion in RNA and DNA binding proteins. These changes also contribute to protein misfolding and insolubility, linking protein synthesis defects to other aging hallmarks. PTMs, posttranslational modifications
The intracellular Ca 2+ sensitivity of transmitter release in glutamatergic neocortical boutons
No full textSynaptotagmin-1 (Syt1) and Syt2 are the main calcium (Ca 2+ ) sensors triggering synchronous release in the brain. In this work, we studied the mechanisms mediating Syt1-triggered release from neocortical synapses. We measured the Ca 2+ dependency of release in layer 5 pyramidal neuron synapses by laser photolysis of caged Ca 2+ . Release had high Ca 2+ affinity and positive cooperativity. Measurements at cerebellar Purkinje cell synapses and kinetic models indicate substantial differences compared with Syt2-triggered release. Our results suggest that Syt1-controlled release machineries are optimized for high reliability at moderate Ca 2+ elevations and high plastic controllability.Editor’s summary Calcium-dependent neurotransmitter release from presynaptic terminals is one of the main mechanisms mediating neuronal communication. Synaptotagmin 1 (Syt1) is the main calcium sensor in the neocortex. Bornschein et al . examined the calcium sensitivity of neurotransmitter release at small neocortical synapses in rodent brain slices using electrophysiology, quantitative analysis, and modeling. Syt1-mediated release has high affinity for calcium and a steep dose-response curve in the range of action potential–evoked calcium concentrations, suggesting substantial differences to the published work on Syt2-triggered neurotransmitter release in the hindbrain. These results pave the way for a better understanding of neocortical synaptic transmission. —Mattia MarosoSynaptotagmin-1 (Syt1) and Syt2 are the main calcium (Ca 2+ ) sensors triggering synchronous release in the brain. In this work, we studied the mechanisms mediating Syt1-triggered release from neocortical synapses. We measured the Ca 2+ dependency of release in layer 5 pyramidal neuron synapses by laser photolysis of caged Ca 2+ . Release had high Ca 2+ affinity and positive cooperativity. Measurements at cerebellar Purkinje cell synapses and kinetic models indicate substantial differences compared with Syt2-triggered release. Our results suggest that Syt1-controlled release machineries are optimized for high reliability at moderate Ca 2+ elevations and high plastic controllability.Editor’s summary Calcium-dependent neurotransmitter release from presynaptic terminals is one of the main mechanisms mediating neuronal communication. Synaptotagmin 1 (Syt1) is the main calcium sensor in the neocortex. Bornschein et al . examined the calcium sensitivity of neurotransmitter release at small neocortical synapses in rodent brain slices using electrophysiology, quantitative analysis, and modeling. Syt1-mediated release has high affinity for calcium and a steep dose-response curve in the range of action potential–evoked calcium concentrations, suggesting substantial differences to the published work on Syt2-triggered neurotransmitter release in the hindbrain. These results pave the way for a better understanding of neocortical synaptic transmission. —Mattia Maros
Efficacy of team‑based collaborative care for distressed patients in secondary prevention of chronic coronary heart disease: Results from the multicenter, randomized controlled TEACH trial
No full textIntroduction: Coronary heart disease (CHD) has serious implications for patients´ quality of life (QoL). Psychological distress affects 15 to 40% of patients with CHD and is robustly associated with poorer prognosis. Blended collaborative care (BCC), a telephone-delivered intervention involving non-physician care managers that address both psychological and medical factors can be applied for secondary prevention of CHD. Methods: We conducted the multicenter, randomized controlled TEACH trial that investigated the efficacy of a BCC intervention (TeamCare) in distressed CHD patients. The primary aim was to examine the treatment response rate of TeamCare defined as ≥ 50% improvements in health-related QoL (HRQoL, assessed by HeartQoL) after 12 months compared to usual care (UC). Secondary endpoints were changes in HRQoL, psychological and medical factors, and satisfaction with care. Results: In total, 457 patients (mean age 62.9 ± 9.5 years, 23% females) were randomized to TeamCare (n=230) or UC (n=227). At 12 months, TeamCare patients showed a significantly higher proportion of treatment response on HeartQoL compared to UC (19% vs. 10%, respectively). TeamCare yielded significantly greater improvements in HeartQoL scores: global (d=0.338), physical (d=0.270), and emotional (d=0.382). Further, TeamCare led to a significantly greater decrease in depression (d=-0.329), anxiety (d=-0.300), perceived stress (d=-0.233), and medical risk score (d=-0.235). Finally, BCC patients showed a higher satisfaction with overall treatment and psychosocial care. Conclusion: The TEACH study is the first ever performed BCC trial in distressed CHD patients in Europe. The BCC intervention has the potential to significantly improve secondary prevention in distressed CHD patients
Behavioral phenotyping identifies autism-like repetitive stereotypies in a Tsc2 haploinsufficient rat model
No full textAbstract Besides deficits in social communication and interaction, repetitive behavior patterns are core manifestations of autism spectrum disorder (ASD). Phenotypes are heterogeneous and can range from simple lower-order motor stereotypies to more complex higher-order cognitive inflexibility and fixated interests. Due to ASD’s multifaceted etiology, animal models are often generated from monogenic diseases associated with ASD, such as Tuberous Sclerosis Complex (TSC), and are expected to copy behavioral core deficits to increase the model´s translational value for ASD disease research and novel treatment development. The global haploinsufficient Tsc2 +/− Eker rat model has been shown to display ASD core symptoms in the social domain. However, the presence and extent of aberrant repetitive behavior patterns in the Eker rat remain to be investigated. Thus, the present study applied a set of behavioral tests to determine the repetitive behavioral profile in Tsc2 +/− Eker rats and used brain-region-specific neurotransmitter analysis to support findings on a molecular level. Tsc2 +/− animals demonstrated lower-order repetitive behavior in the form of excessive self-grooming and nestlet shredding under non-stressful conditions that co-occurred alongside social interaction deficits. However, no higher-order repetitive behavior was detected in Tsc2 +/− rats. Interestingly, Tsc2 +/− rats exhibited increased levels of homeostatic dopamine in the prefrontal cortex, supporting the link between aberrant cortical dopaminergic transmission and the appearance of lower-order repetitive phenotypes. Together, our results support the Tsc2 +/− Eker rat as a model of ASD-like behavior for further investigation of ASD-related development and neurobiology
Attribute non-attendance in the choice experiment with machine Learning: WTP for organic apples in Germany
No full textAbstract Choice experiments (CE) have been widely applied as an important method for estimating consumer preferences and predicting consumer behaviors. However, it is well known that the non-attended attributes in CE could lead to some bias and estimation inefficiency. Therefore, it is crucial to accurately filter out the attribute non-attendance (ANA) and to ensure that there is no effect from the change in correlation structure while increasing the fitting degree of the estimation model. In addition to the general approaches for identifying ANA, we applied a machine learning algorithm, namely, the Least Absolute Shrinkage and Selection Operator (LASSO), to tackle this problem. The approach is empirically applied to analyze consumers’ willingness to pay (WTP) for organic apples in Germany where promoting organic agriculture is an important policy. The results show that when the penalty factor ( λ ) takes different values, the attribute of Organic can been screened out when countries of origin and size are considered. It implies that ANA might be linked to niche market or hypothetical market. Furthermore, German consumers prefer apples produced in France and Italy over those produced in China, paying a premium of €1.53 and €1.40, respectively. Meanwhile, apple size is negatively correlated with consumers’ purchase preferences. Lasso performs efficiently and conveniently in identifying ANA in CE
Immunopathogenic and clinical implications of advanced tissue analysis in non-tuberculous mycobacterial infections in children
No full textObjectives Infections with non-tuberculous mycobacteria (NTM) in children usually affect the lymph nodes and surrounding tissue. Although the infection is typically self-limiting, it carries a substantial risk of complications due to persistent inflammation and invasive therapeutic interventions. Yet, the immunopathogenesis of the disease is obscure, as are biomarkers guiding treatment decisions. Methods In this observational study, we analyzed histological samples collected in the NTMkids study to identify parameters associated with impaired wound healing and complicated disease progression. Samples from 33 patients (median age at first presentation 33 months) were investigated, with two consecutive biopsies in 9 patients. Results Germinal centers, a scattered distribution of granuloma associated CD4+ T-cells, higher CD8+ T-cell density inside the necrosis and foamy epitheloid cells were associated with a favorable outcome. Tissue damage presenting clinically as liquefaction was associated with an adverse outcome. Conclusions The identified tissue reaction patterns in NTM infections provide insights into the biology of NTM lymphadenitis in children and may aid in more precise treatment decisions
Clinical Predictors and Recurrence Characteristics Following Radiotherapy for Primary Central Nervous System Lymphoma: A Retrospective Cohort Study
No full textBackground/Objectives: Primary central nervous system lymphoma (PCNSL) is a rare but aggressive tumor, primarily affecting elderly patients. Radiotherapy (RT) remains an important treatment option, particularly for patients who are ineligible for systemic chemotherapy. This study aims to identify prognostic factors and evaluate recurrence patterns in a real-world cohort of PCNSL patients treated with RT. Methods: We retrospectively analyzed 64 PCNSL patients treated with radiotherapy at our institution between 2000 and 2022. Clinical characteristics, treatment details, and outcomes were collected by chart review. Overall survival (OS) was analyzed using Kaplan–Meier and Cox regression methods. Recurrence patterns were assessed based on available post-treatment imaging. Results: Median patient age was 71 years (range: 31–83); 53.1% had an Eastern Cooperative Oncology Group (ECOG) performance status ≥2. Radiotherapy was used as first-line treatment in 62.5% of cases, primarily due to contraindications to chemotherapy. Median OS was 10 months from diagnosis. Age, poor performance status, seizures at presentation, absence of systemic therapy, incomplete radiotherapy, and <80% applied dose of planned radiotherapy were associated with inferior OS in our univariable analysis. Multivariable analysis confirmed age, systemic therapy, seizures, and radiotherapy dose <80% as independent predictors. Among twenty-nine patients with imaging follow-up, eight recurrences after RT were documented: six of those within, and two outside of the initially affected areas. All recurrences occurred within previously irradiated areas. Conclusions: This study confirms known negative prognostic factors in PCNSL and underscores the importance of systemic chemotherapy for curatively intended treatments aiming for prolonged survival. The recurrence patterns observed question the added benefit of whole-brain irradiation in preventing distant relapses. These findings support the need for prospective trials to optimize radiotherapy strategies while balancing efficacy and neurotoxicity
Observational Parameters of Blue Large-amplitude Pulsators *
No full textAbstract Blue large-amplitude pulsators (BLAPs) are a recently discovered class of short-period pulsating variable stars. In this work, we present new information on these stars based on photometric and spectroscopic data obtained for known and new objects detected by the Optical Gravitational Lensing Experiment (OGLE) survey. BLAPs are evolved objects with pulsation periods in the range of 3–75 minutes, stretching between subdwarf B-type stars and upper main-sequence stars in the Hertzsprung–Russell diagram. In general, BLAPs are single-mode stars pulsating in the fundamental radial mode. Their phase-folded light curves are typically sawtooth-shaped, but many longer-period objects exhibit an additional bump. The long-term OGLE observations show that the period change rates of BLAPs are usually of the order of 10 −7 yr −1 and in a quarter of the sample are negative. The spectroscopic data indicate that BLAPs form a homogeneous group in the period, surface gravity, and effective temperature spaces. However, we observe a split into two groups in terms of helium-to-hydrogen content. The atmospheres of He-enriched BLAPs are more abundant in metals (about 5 times) than the atmosphere of the Sun. We discover that BLAPs obey a period–gravity relationship and we use the distance to OGLE-BLAP-009 to derive a period–luminosity relation. Most of the stars observed in the OGLE Galactic bulge fields seem to reside in the bulge, while the remaining objects likely are in the foreground Galactic disk
Changes in grazing patterns explain post-Soviet fire trends on the Eurasian steppe better than climate
No full textAbstract In grassland ecosystems, fire plays an important role in maintaining biodiversity and ecological functioning but also causes substantial greenhouse gas emissions. Both climate and herbivory are key determinants of fire regimes, yet the relative importance of these factors remains debated. We focused on the steppes of Kazakhstan—one of the world’s largest grasslands and a global fire hotspot—to assess the relative importance of climate and grazing patterns on fire regimes. Specifically, we made use of the natural experiment that the post-Soviet collapse of the Kazakh livestock sector provided. We used the MODIS Burned Area Product and calculated annual livestock grazing demand (required forage intake) from 2001 to 2019. We estimated a binomial mixed-effects model to extricate the impact of grazing demand and climate factors on fire occurrence. Our results show that fire regimes changed markedly on the Kazakh steppes, with exceptionally high fire frequencies and extent in the 2000s. We found a clearly negative association between grazing demand and burned area; in other words, more heavily grazed areas burned less frequently. Moreover, annual grazing demand appeared in more of the best-performing models than precipitation, temperature, relative humidity, or growing degree days. Given that livestock herding is declining in many grassland regions, and native grazers have been lost or greatly reduced in the past, our study highlights the increasing risk of fire with less grazing, but also the potential for grazing restoration to mitigate such risks in the world’s grassland regions.Volkswagen Foundation http://dx.doi.org/10.13039/501100001663Leibniz-Institut für Agrarentwicklung in Transformationsökonomien (IAMO