Multiple stellar populations at less evolved stages: detection of chemical variations among main-sequence dwarfs in NGC 1978

Multiple stellar populations (MPs) with different chemical compositions are not exclusive features of old GCs (older than 10 Gyr). Indeed, recent studies reveal that younger clusters ($\sim$2--6 Gyr-old) in the Magellanic Clouds also exhibit star-to-star chemical variations among evolved stars. However, whether MPs are present among less evolved dwarfs of these intermediate-age clusters is still unclear. In this work, we search for chemical variations among GK-type dwarfs in the $\sim$2 Gyr-old cluster NGC 1978, which is the youngest cluster with MPs. We exploit deep ultraviolet and visual observations from the Hubble Space Telescope to constrain the nitrogen (N) and oxygen (O) variations among MS stars. To do this, we compare appropriate photometric diagrams that are sensitive to N and O with synthetic diagrams of simple stellar populations and MPs. We conclude that the G- and K-type MS stars in NGC\,1978 host MPs. Our statistical analysis shows that the fraction of N-rich stars ranges from $\sim$40\% to $\sim$80\%, depending on the detailed distributions of nitrogen and oxygen.Comment: 16 pages, 10 figures, ApJ accepte

On the identification of N-rich metal-poor field stars with future China space station telescope

During the long term evolution of globular clusters (GCs), a part of member stars are lost to the field. The recently found nitrogen-rich (N-rich) metal-poor field stars are promising candidates of these GC escapees, since N enhancement is the fingerprint of chemically enhanced populations in GCs. In this work, we discuss the possibility of identifying N-rich metal-poor field stars with the upcoming China space station telescope (CSST). We focus on the main survey camera with NUV, u, g, r, i, z, y filters and slitless spectrograph with a resolution about 200. The combination of UV sensitive equipment and prominent N-related molecular lines in the UV band bodes well for the identification: the color-color diagram of (u-g) versus (g-r) is capable of separating N-rich field stars and normal halo stars, if metallicity can be estimated without using the information of u-band photometry. Besides, the synthetic spectra show that a signal-to-noise ratio of 10 is sufficient to identify N-rich field stars. In the near future, a large sample of N-rich field stars found by CSST, combined with state-of-the-art N-body simulations will be crucial to decipher the GC-Galaxy co-evolution.Comment: 13+2 pages, 11+2 figures, 4 tables, accepted by RA

Activation of BNIP3-mediated mitophagy protects against renal ischemia-reperfusion injury

Acute kidney injury (AKI) is a syndrome of abrupt loss of renal functions. The underlying pathological mechanisms of AKI remain largely unknown. BCL2-interacting protein 3 (BNIP3) has dual functions of regulating cell death and mitophagy, but its pathophysiological role in AKI remains unclear. Here, we demonstrated an increase of BNIP3 expression in cultured renal proximal tubular epithelial cells following oxygen-glucose deprivation-reperfusion (OGD-R) and in renal tubules after renal ischemia-reperfusion (IR)-induced injury in mice. Functionally, silencing Bnip3 by specific short hairpin RNAs in cultured renal tubular cells reduced OGD-R-induced mitophagy, and potentiated OGD-R-induced cell death. In vivo, Bnip3 knockout worsened renal IR injury, as manifested by more severe renal dysfunction and tissue injury. We further showed that Bnip3 knockout reduced mitophagy, which resulted in the accumulation of damaged mitochondria, increased production of reactive oxygen species, and enhanced cell death and inflammatory response in kidneys following renal IR. Taken together, these findings suggest that BNIP3-mediated mitophagy has a critical role in mitochondrial quality control and tubular cell survival during AKI

Binary Star Evolution in Different Environments: Filamentary, Fractal, Halo and Tidal-tail Clusters

Using membership of 85 open clusters from previous studies (Pang et al. 2021a,b, 2022b; Li et al. 2021) based on Gaia DR3 data, we identify binary candidates in the color-magnitude diagram, for systems with mass ratio q > 0.4. The binary fraction is corrected for incompleteness at different distances due to the Gaia angular resolution limit. We find a decreasing binary fraction with increasing cluster age, with substantial scatter. For clusters with a total mass > 200$M_\odot$, the binary fraction is independent of cluster mass. The binary fraction depends strongly on stellar density. Among four types of cluster environments, the lowest-density filamentary and fractal stellar groups have the highest mean binary fraction: 23.6% and 23.2%, respectively. The mean binary fraction in tidal-tail clusters is 20.8%, and is lowest in the densest halo-type clusters: 14.8%. We find clear evidence of early disruptions of binary stars in the cluster sample. The radial binary fraction depends strongly on the cluster-centric distance across all four types of environments, with the smallest binary fraction within the half-mass radius $r_h$, and increasing towards a few $r_h$. Only hints of mass segregation is found in the target clusters. The observed amount of mass segregation is not significant to generate a global effect inside the target clusters. We evaluate the bias of unresolved binary systems (assuming a primary mass of 1$M_\odot$) in 1D tangential velocity, which is 0.1-1$\,\rm km\,s^{-1}$. Further studies are required to characterize the internal star cluster kinematics using Gaia proper motions

The role of tidal interactions in the formation of slowly rotating early-type stars in young star clusters

The split main sequences found in the colour-magnitude diagrams of star clusters younger than ~600 Myr are suggested to be caused by the dichotomy of stellar rotation rates of upper main-sequence stars. Tidal interactions have been suggested as a possible explanation of the dichotomy of the stellar rotation rates. This hypothesis proposes that the slow rotation rates of stars along the split main sequences are caused by tidal interactions in binaries. To test this scenario, we measured the variations in the radial velocities of slowly rotating stars along the split main sequence of the young Galactic cluster NGC 2422 (~90 Myr) using spectra obtained at multiple epochs with the Canada-France-Hawai'i Telescope. Our results show that most slowly rotating stars are not radial-velocity variables. Using the theory of dynamical tides, we find that the binary separations necessary to fully or partially synchronise our spectroscopic targets, on time-scales shorter than the cluster age, predict much larger radial velocity variations across multiple-epoch observations, or a much larger radial velocity dispersion at a single epoch, than the observed values. This indicates that tidal interactions are not the dominant mechanism to form slowly rotating stars along the split main sequences. As the observations of the rotation velocity distribution among B- and A-type stars in binaries of larger separations hint at a much stronger effect of braking with age, we discuss the consequences of relaxing the constraints of the dynamical tides theory.Comment: 14 pages, 10 figures, 2 tables, accepted for publication in MNRA

Mitochondrial quality control in kidney injury and repair

Mitochondria are essential for the activity, function and viability of eukaryotic cells and mitochondrial dysfunction is involved in the pathogenesis of acute kidney injury (AKI) and chronic kidney disease, as well as in abnormal kidney repair after AKI. Multiple quality control mechanisms, including antioxidant defence, protein quality control, mitochondrial DNA repair, mitochondrial dynamics, mitophagy and mitochondrial biogenesis, have evolved to preserve mitochondrial homeostasis under physiological and pathological conditions. Loss of these mechanisms may induce mitochondrial damage and dysfunction, leading to cell death, tissue injury and, potentially, organ failure. Accumulating evidence suggests a role of disturbances in mitochondrial quality control in the pathogenesis of AKI, incomplete or maladaptive kidney repair and chronic kidney disease. Moreover, specific interventions that target mitochondrial quality control mechanisms to preserve and restore mitochondrial function have emerged as promising therapeutic strategies to prevent and treat kidney injury and accelerate kidney repair. However, clinical translation of these findings is challenging owing to potential adverse effects, unclear mechanisms of action and a lack of knowledge of the specific roles and regulation of mitochondrial quality control mechanisms in kidney resident and circulating cell types during injury and repair of the kidney

The influence of the China GLIM standards on the diagnosis of malnutrition in patients with hematopoietic stem cell transplant

BackgroundThe muscle-related indicator is removed from Global Leadership Initiative on Malnutrition (GLIM) criteria implemented in China for many reasons. Patients with hematopoietic stem cell transplants are at nutrition risk and can enter into the second step of GLIM; thus, they are suitable for learning the diagnosing malnutrition significance between primary GLIM and GLIM-China criteria. This article aims to explore the role of muscle mass in the diagnostic criteria of malnutrition and the effects of GLIM-China for diagnosing malnutrition.MethodsA total of 98 inpatients with hematopoietic stem cell transplants (HSCT) were recruited. Nutrition risk was assessed by using the Nutritional Risk Screening 2002 (NRS-2002). Appendicular skeletal muscle mass (ASMI) and fat-free mass index (FFMI) were determined using the bioelectrical impedance analysis (BIA) method. Malnutrition is defined by GLIM-China, GLIM, and PG-SGA. We use erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) to assess inflammation in GLIM and GLIM-China. The correlation or consistency among ASMI, FFMI, ESR, CRP, GLIM-China, GLIM, and PG-SGA was evaluated, respectively.ResultsOne hundred percent instead of the patients had nutritional risk. The magnitude of malnutrition using PG-SGA, GLIM, and GLIM-China was 75.5, 80.6, and 64.3%, respectively. GLIM-China and PG-SGA showed the same performance (p = 0.052 vs. 1.00) and agreement (kappa = 0.404 vs. 0.433, p < 0.0001) with the FFMI. Consistency was noted between ASMI and PG-SGA in the assessment of malnutrition (p = 0.664) with a good agreement (kappa = 0.562, p = 0.084). ASMI and FFMI could determine muscle mass reduction, which could not be determined by BMI, albumin (ALB), and pre-albumin (pre-ALB); 34% of GLIM-China (–) patients were with low ASMI, and 40% with low FFMI; 30.0% of patients with PG-SGA (<4) still have low ASMI, and 38.2% have low FFMI.ConclusionIf only the PG-SGA scale is used as a diagnostic criterion for evaluating malnutrition, a large proportion of patients with reduced muscle mass will be missed, but more patients with muscle loss will be missed via GLIM-China. Muscle-related indicators will help diagnose malnutrition

Pathogenic Connexin-31 Forms Constitutively Active Hemichannels to Promote Necrotic Cell Death

Mutations in Connexin-31 (Cx31) are associated with multiple human diseases including erythrokeratodermia variabilis (EKV). The molecular action of Cx31 pathogenic mutants remains largely elusive. We report here that expression of EKV pathogenic mutant Cx31R42P induces cell death with necrotic characteristics. Inhibition of hemichannel activity by a connexin hemichannel inhibitor or high extracellular calcium suppresses Cx31R42P-induced cell death. Expression of Cx31R42P induces ER stress resulting in reactive oxygen species (ROS) production, in turn, to regulate gating of Cx31R42P hemichannels and Cx31R42P induced cell death. Moreover, Cx31R42P hemichannels play an important role in mediating ATP release from the cell. In contrast, no hemichannel activity was detected with cells expressing wildtype Cx31. Together, the results suggest that Cx31R42P forms constitutively active hemichannels to promote necrotic cell death. The Cx31R42P active hemichannels are likely resulted by an ER stress mediated ROS overproduction. The study identifies a mechanism of EKV pathogenesis induced by a Cx31 mutant and provides a new avenue for potential treatment strategy of the disease