{μ-N-[(Diphenyl­phosphino)meth­yl]pyridin-2-amine-κ2 N 1:P}bis­{[2-(2,2′-bipyridin-6-yl)phenyl-κ3 N,N′,C 1]platinum(II)} bis­(perchlorate)

The title compound, [Pt2(C16H11N2)2(C18H17N2P)](ClO4)2, contains two PtII atoms, bridged by an N-[(diphenyl­phosphino)meth­yl]pyridin-2-amine (dppmp) ligand. One Pt atom is coordinated by one P atom from the dppmp ligand, and one C atom and two N atoms from a 6-phenyl-2,2′-bipyridine (pbpy) ligand in a square-planar geometry. The other Pt atom is coordinated by one N atom from the dppmp ligand, and one C atom and two N atoms from another pbpy ligand in a square-planar geometry. There are intra­molecular π–π inter­actions between the pbpy ligands, with a centroid–centroid distance of 3.62 (1) Å between two pyridyl rings. The oxygen atoms of both perchlorate anions are disordered, each over two different positions [occupanicies 0.49 (3)/0.51 (3) and 0.48 (2)/0.52 (2)]

Reading Comprehension and Behavior in Children Using E-books vs. Printed Books

The purpose of this research is to investigate the influence that personalized, gamified, and PDF electronic reading practices have on the attitudes which fifth-grade students possess toward e-reading experiences, as well as how these stances affect the students' motivation and reading comprehension while they are learning English as a second/foreign language (EFL). For the purpose of the study, there were a total of 84 fifth-grade kids from public schools in Greece, who participated. These students were split up into three different experimental groups and a control one. Participants in the experimental groups read throughout the treatment period according to a preset schedule using one of three diverse electronic reading formats (PDF, gamified, or customized), whilst participants in the control group read utilizing a paper guided reading plan. The participants' experiences playing video games online were analyzed via a technique called the quasi-experimental approach. According to the findings of the research, the experimental group and the control group did not significantly vary from one another in terms of their levels of reading comprehension. On the other hand, in comparison to the participants in the control group, those who took part in the experiments reported having more favorable sentiments regarding their electronic reading experiences and were more inspired to read. As indicated from the research findings, kids may experience an increase in their desire to read when they use electronic gadgets. This study has implications for educators and policymakers as they consider incorporating digital reading practices into their teaching methods, particularly when it comes to improving students' motivation to read

Selective Oxidative Stress Induces Dual Damage to Telomeres and Mitochondria in Human T Cells

Oxidative stress caused by excess reactive oxygen species (ROS) accelerates telomere erosion and mitochondrial injury, leading to impaired cellular functions and cell death. Whether oxidative stress-mediated telomere erosion induces mitochondrial injury, or vice versa, in human T cells—the major effectors of host adaptive immunity against infection and malignancy—is poorly understood due to the pleiotropic effects of ROS. Here we employed a novel chemoptogenetic tool that selectively produces a single oxygen (1O2) only at telomeres or mitochondria in Jurkat T cells. We found that targeted 1O2 production at telomeres triggered not only telomeric DNA damage but also mitochondrial dysfunction, resulting in T cell apoptotic death. Conversely, targeted 1O2 formation at mitochondria induced not only mitochondrial injury but also telomeric DNA damage, leading to cellular crisis and apoptosis. Targeted oxidative stress at either telomeres or mitochondria increased ROS production, whereas blocking ROS formation during oxidative stress reversed the telomeric injury, mitochondrial dysfunction, and cellular apoptosis. Notably, the X-ray repair cross-complementing protein 1 (XRCC1) in the base excision repair (BER) pathway and multiple mitochondrial proteins in other cellular pathways were dysregulated by the targeted oxidative stress. By confining singlet 1O2 formation to a single organelle, this study suggests that oxidative stress induces dual injury in T cells via crosstalk between telomeres and mitochondria. Further identification of these oxidation pathways may offer a novel approach to preserve mitochondrial functions, protect telomere integrity, and maintain T cell survival, which can be exploited to combat various immune aging-associated diseases

Inhibition of TRF2 Accelerates Telomere Attrition and DNA Damage in Naïve CD4 T Cells During HCV Infection

T cells play a crucial role in viral clearance and vaccine responses; however, the mechanisms that regulate their homeostasis during viral infections remain unclear. In this study, we investigated the machineries of T-cell homeostasis and telomeric DNA damage using a human model of hepatitis C virus (HCV) infection. We found that naïve CD4 T cells in chronically HCV-infected patients (HCV T cells) were significantly reduced due to apoptosis compared with age-matched healthy subjects (HSs). These HCV T cells were not only senescent, as demonstrated by overexpression of aging markers and particularly shortened telomeres; but also DNA damaged, as evidenced by increased dysfunctional telomere-induced foci (TIF). Mechanistically, the telomere shelterin protein, in particular telomeric repeat binding factor 2 (TRF2) that functions to protect telomeres from DNA damage, was significantly inhibited posttranscriptionally via the p53-dependent Siah-1a ubiquitination. Importantly, knockdown of TRF2 in healthy T cells resulted in increases in telomeric DNA damage and T-cell apoptosis, whereas overexpression of TRF2 in HCV T cells alleviated telomeric DNA damage and T-cell apoptosis. To the best of our knowledge, this is the first report revealing that inhibition of TRF2 promotes T-cell telomere attrition and telomeric DNA damage that accelerates T-cell senescent and apoptotic programs, which contribute to naïve T-cell loss during viral infection. Thus, restoring the impaired T-cell telomeric shelterin machinery may offer a new strategy to improve immunotherapy and vaccine response against human viral diseases

Visible and Infrared Nanocrystal-Based Light Modulator with CMOS Compatible Bias Operation

Nanocrystals are now established light sources, and as synthesis and device integration have gained maturity, new functionalities can now be considered. So far, the emitted light from a nanocrystal population remains mostly driven by the structural properties (composition, size, and shape) of the particle, and only limited postsynthesis tunability has been demonstrated. Here, we explore the design of light amplitude modulators using a nanocrystal-based light-emitting diode operated under reverse bias. We demonstrate strong photoluminescence modulations for devices operating in the visible and near-telecom wavelengths using low bias operations (<3 V) compatible with conventional electronics. For a visible device based on 2D nanoplatelets, we demonstrate that the photoluminescence quenching is driven by the field-induced change of nonradiative decay rate and that the field is less involved than the particle charging. This work demonstrates that a simple diode stack can combine several functionalities (light-emitting diode, detector, and light modulator) simply by selecting the driving bias.The project is supported by ERC starting grant blackQD (Grant No. 756225) and Ne2Dem (Grant No. 853049). We acknowledge the use of clean-room facilities from the “Centrale de Proximité Paris-Centre”. This work has been supported by the Region Ile-de-France in the framework of DIM Nano-K (grant dopQD). This work is supported by French state funds managed by the ANR within the Investissements d’Avenir program under reference ANR-11-IDEX-0004-02, and more specifically within the framework of the Cluster of Excellence MATISSE and also by the grant IPER-Nano2 (ANR-18CE30-0023-01), Copin (ANR-19-CE24-0022), Frontal (ANR-19-CE09-0017), Graskop (ANR-19-CE09-0026), and NITQuantum (ANR-20-ASTR-0008–01), Bright (ANR-21-CE24–0012–02), MixDferro (ANR-21-CE09–0029) and QuickTera (ANR-22-CE09-0018). J.I.C. acknowledges support from UJI-B2021-06 and MICINN PID2021-128659NB-I00. H.Z. thanks China Scholarship Council for Ph.D. funding

Mitochondrial Functions Are Compromised in CD4 T Cells From ART-Controlled PLHIV

The hallmark of HIV/AIDS is a gradual depletion of CD4 T cells. Despite effective control by antiretroviral therapy (ART), a significant subgroup of people living with HIV (PLHIV) fails to achieve complete immune reconstitution, deemed as immune non-responders (INRs). The mechanisms underlying incomplete CD4 T cell recovery in PLHIV remain unclear. In this study, CD4 T cells from PLHIV were phenotyped and functionally characterized, focusing on their mitochondrial functions. The results show that while total CD4 T cells are diminished, cycling cells are expanded in PLHIV, especially in INRs. HIV-INR CD4 T cells are more activated, displaying exhausted and senescent phenotypes with compromised mitochondrial functions. Transcriptional profiling and flow cytometry analysis showed remarkable repression of mitochondrial transcription factor A (mtTFA) in CD4 T cells from PLHIV, leading to abnormal mitochondrial and T cell homeostasis. These results demonstrate a sequential cellular paradigm of T cell over-activation, proliferation, exhaustion, senescence, apoptosis, and depletion, which correlates with compromised mitochondrial functions. Therefore, reconstituting the mtTFA pathway may provide an adjunctive immunological approach to revitalizing CD4 T cells in ART-treated PLHIV, especially in INRs