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The production of prompt Λ+c baryons at midrapidity (|y|<0.5) was measured in central (0-10%) and mid-central (30-50%) Pb-Pb collisions at the center-of-mass energy per nucleon-nucleon pair sNN−−−√=5.02 TeV with the ALICE detector. The Λ+c production yield, the Λ+c/D0 production ratio, and the Λ+c nuclear modification factor RAA are reported. The results are more precise and more differential in transverse momentum (pT) and centrality with respect to previous measurements. The Λ+c/D0 ratio, which is enhanced with respect to the pp measurement for 4<pT<8 GeV/c, is described by theoretical calculations that model the charm-quark transport in the quark-gluon plasma and include hadronization via both coalescence and fragmentation mechanisms.
A new, more precise measurement of the Λ hyperon lifetime is performed using a large data sample of Pb–Pb collisions at √sNN p ¼ 5.02 TeV with ALICE. The Λ and Λ¯ hyperons are reconstructed at midrapidity using their two-body weak decay channel Λ → p þ π− and Λ¯ → p¯ þ πþ. The measured value of the Λ lifetime is τΛ ¼ ½261.07 0.37ðstat:Þ 0.72ðsyst:Þ ps. The relative difference between the lifetime of Λ and Λ¯ , which represents an important test of CPT invariance in the strangeness sector, is also measured. The obtained value ðτΛ − τΛ¯Þ=τΛ ¼ 0.0013 0.0028ðstat:Þ 0.0021ðsyst:Þ is consistent with zero within the uncertainties. Both measurements of the Λ hyperon lifetime and of the relative difference between τΛ and τΛ¯ are in agreement with the corresponding world averages of the Particle Data Group and about a factor of three more precise.
First measurement of Λ+c production down to pT = 0 in pp and p-Pb collisions at √𝑠NN = 5.02 TeV
(2023)
The production of prompt +c baryons has been measured at midrapidity in the transverse momentum interval 0 < pT < 1 GeV/c for the first time, in pp and p–Pb collisions at a center-of-mass energy per nucleon-nucleon collision √sNN = 5.02 TeV. The measurement was performed in the decay channel +c → pK0S by applying new decay reconstruction techniques using a Kalman-Filter vertexing algorithm and adopting a machine-learning approach for the candidate selection. The pT -integrated +c production cross sections in both collision systems were determined and used along with the measured yields in Pb–Pb collisions to compute the pT -integrated nuclear modification factors RpPb and RAA of +c baryons, which are compared to model calculations that consider nuclear modification of the parton distribution functions. The +c /D0 baryon-to-meson yield ratio is reported for pp and p–Pb collisions. Comparisons with models that include modified hadronization processes are presented, and the implications of the results on the understanding of charm hadronization in hadronic collisions are discussed. A significant (3.7σ) modification of the mean transverse momentum of + c baryons is seen in p–Pb collisions with respect to pp collisions, while the pT -integrated +c /D0 yield ratio was found to be consistent between the two collision systems within the uncertainties.
The measurement of the production of deuterons, tritons and 3He and their antiparticles in Pb-Pb collisions at √sNN = 5.02 TeV is presented in this article. The measurements are carried out at midrapidity (y|< 0.5) as a function of collision centrality using the ALICE detector. The pT-integrated yields, the coalescence parameters and the ratios to protons and antiprotons are reported and compared with nucleosynthesis models. The comparison of these results in different collision systems at different center-of-mass collision energies reveals a suppression of nucleus production in small systems. In the Statistical Hadronisation Model framework, this can be explained by a small correlation volume where the baryon number is conserved, as already shown in previous fluctuation analyses. However, a different size of the correlation volume is required to describe the proton yields in the same data sets. The coalescence model can describe this suppression by the fact that the wave functions of the nuclei are large and the fireball size starts to become comparable and even much smaller than the actual nucleus at low multiplicities.
The ALICE experiment was proposed in 1993, to study strongly interacting matter at extreme energy densities via a comprehensive investigation of nuclear collisions at the LHC. Its physics programme initially focused on the determination of the properties of the Quark-Gluon Plasma (QGP), a deconfined state of quarks and gluons and was extended along the years, covering a diverse ensemble of observables related to Quantum Chromodynamics (QCD), the theory of strong interactions. The experiment has studied Pb-Pb, Xe-Xe, p-Pb and pp collisions in the multi-TeV energy range, during the Run 1 and Run 2 data taking periods at the LHC (2009-2018). The aim of this review article is to gather and summarise a selection of ALICE physics results and to discuss their implications on the current understanding of the macroscopic and microscopic properties of strongly interacting matter at the highest temperature reached in the laboratory. It will be shown that it is possible to have a quantitative description of the properties of the QGP produced in Pb--Pb collisions. We also show that various features, commonly ascribed to QGP formation, are detected for a wide range of interacting system sizes. Precision measurements of QCD-related observables not directly connected to the study of the QGP will also be discussed. Prospects for future measurements with the ALICE detector and its foreseen upgrades will also be briefly described.
Understanding the role of parton mass and Casimir colour factors in the quantum chromodynamics parton shower represents an important step in characterising the emission properties of heavy quarks. Recent experimental advances in jet substructure techniques have provided the opportunity to isolate and characterise gluon emissions from heavy quarks. In this work, the first direct experimental constraint on the charm-quark splitting function is presented, obtained via the measurement of the groomed shared momentum fraction of the first splitting in charm jets, tagged by a reconstructed D0 meson. The measurement is made in proton-proton collisions at s√ = 13 TeV, in the low jet transverse-momentum interval of 15≤pjet chT<30 GeV/c where the emission properties are sensitive to parton mass effects. In addition, the opening angle of the first perturbative emission of the charm quark, as well as the number of perturbative emissions it undergoes, is reported. Comparisons to measurements of an inclusive-jet sample show a steeper splitting function for charm quarks compared with gluons and light quarks. Charm quarks also undergo fewer perturbative emissions in the parton shower, with a reduced probability of large-angle emissions.
Understanding the role of parton mass and Casimir colour factors in the quantum chromodynamics parton shower represents an important step in characterising the emission properties of heavy quarks. Recent experimental advances in jet substructure techniques have provided the opportunity to isolate and characterise gluon emissions from heavy quarks. In this work, the first direct experimental constraint on the charm-quark splitting function is presented, obtained via the measurement of the groomed shared momentum fraction of the first splitting in charm jets, tagged by a reconstructed D0 meson. The measurement is made in proton-proton collisions at s√ = 13 TeV, in the low jet transverse-momentum interval of 15≤pjet chT<30 GeV/c where the emission properties are sensitive to parton mass effects. In addition, the opening angle of the first perturbative emission of the charm quark, as well as the number of perturbative emissions it undergoes, is reported. Comparisons to measurements of an inclusive-jet sample show a steeper splitting function for charm quarks compared with gluons and light quarks. Charm quarks also undergo fewer perturbative emissions in the parton shower, with a reduced probability of large-angle emissions.
Background: Obesity impairs a variety of cell types including adipose-derived mesenchymal stem cells (ASCs). ASCs are indispensable for tissue homeostasis/repair, immunomodulation, and cell renewal. It has been demonstrated that obese ASCs are defective in differentiation, motility, immunomodulation, and replication. We have recently reported that some of these defects are linked to impaired primary cilia, which are unable to properly convey and coordinate a variety of signaling pathways. We hypothesized that the rescue of the primary cilium in obese ASCs would restore their functional properties.
Methods: Obese ASCs derived from subcutaneous and visceral adipose tissues were treated with a specific inhibitor against Aurora A or with an inhibitor against extracellular signal-regulated kinase 1/2 (Erk1/2). Multiple molecular and cellular assays were performed to analyze the altered functionalities and their involved pathways.
Results: The treatment with low doses of these inhibitors extended the length of the primary cilium, restored the invasion and migration potential, and improved the differentiation capacity of obese ASCs. Associated with enhanced differentiation ability, the cells displayed an increased expression of self-renewal/stemness-related genes like SOX2, OCT4, and NANOG, mediated by reduced active glycogen synthase kinase 3 β (GSK3β).
Conclusion: This work describes a novel phenomenon whereby the primary cilium of obese ASCs is rescuable by the low-dose inhibition of Aurora A or Erk1/2, restoring functional ASCs with increased stemness. These cells might be able to improve tissue homeostasis in obese patients and thereby ameliorate obesity-associated diseases. Additionally, these functionally restored obese ASCs could be useful for novel autologous mesenchymal stem cell-based therapies.
The oncogene B-cell lymphoma 6 (BCL6) is associated with lymphomagenesis. Intriguingly, its expression is increased in preeclamptic placentas. Preeclampsia is one of the leading causes of maternal and perinatal mortality and morbidity. Preeclamptic placentas are characterized by various defects like deregulated differentiation and impaired fusion of trophoblasts. Its pathogenesis is however not totally understood. We show here that BCL6 is present throughout the cell fusion process in the fusogenic trophoblastic cell line BeWo. Suppression of BCL6 promotes trophoblast fusion, indicated by enhanced levels of fusion-related β-hCG, syncytin 1 and syncytin 2. Increased mRNA levels of these genes could also be observed in primary term cytotrophoblasts depleted of BCL6. Conversely, stable overexpression of BCL6 reduces the fusion capacity of BeWo cells. These data suggest that an accurately regulated expression of BCL6 is important for proper differentiation and successful syncytialization of trophoblasts. While deregulated BCL6 is linked to lymphomagenesis by blocking lymphocyte terminal differentiation, increased BCL6 in the placenta contributes to the development of preeclampsia by impairing trophoblast differentiation and fusion.
Preeclampsia (PE), a gestational hypertensive disease originating from the placenta, is characterized by an imbalance of various cellular processes. The cell cycle regulator p21Cip1/CDKN1A (p21) and its family members p27 and p57 regulate signaling pathways fundamental to placental development. The aim of the present study was to enlighten the individual roles of these cell cycle regulators in placental development and their molecular involvement in the pathogenesis of PE. The expression and localization of p21, phospho-p21 (Thr-145), p27, and p57 was immunohistochemically analyzed in placental tissues from patients with early-onset PE, early-onset PE complicated by the HELLP (hemolysis, elevated liver enzymes and low platelet count) syndrome as well as late-onset PE compared to their corresponding control tissues from well-matched women undergoing caesarean sections. The gene level was evaluated using real-time quantitative PCR. We demonstrate that the delivery mode strongly influenced placental gene expression, especially for CDKN1A (p21) and CDKN1B (p27), which were significantly upregulated in response to labor. Cell cycle regulators were highly expressed in first trimester placentas and impacted by hypoxic conditions. In support of these observations, p21 protein was abundant in trophoblast organoids and hypoxia reduced its gene expression. Microarray analysis of the trophoblastic BeWo cell line depleted of p21 revealed various interesting candidate genes and signaling pathways for the fusion process. The level of p21 was reduced in fusing cytotrophoblasts in early-onset PE placentas and depletion of p21 led to reduced expression of fusion-related genes such as syncytin-2 and human chorionic gonadotropin (β-hCG), which adversely affected the fusion capability of trophoblastic cells. These data highlight that cell cycle regulators are important for the development of the placenta. Interfering with p21 influences multiple pathways related to the pathogenesis of PE.
Preeclampsia (PE) remains a leading cause of maternal and perinatal mortality and morbidity worldwide. Its pathogenesis has not been fully elucidated and no causal therapy is currently available. It is of clinical relevance to decipher novel molecular biomarkers. RITA (RBP-J (recombination signal binding protein J)-interacting and tubulin-associated protein) has been identified as a negative modulator of the Notch pathway and as a microtubule-associated protein important for cell migration and invasion. In the present work, we have systematically studied RITA’s expression in primary placental tissues from patients with early- and late-onset PE as well as in various trophoblastic cell lines. RITA is expressed in primary placental tissues throughout gestation, especially in proliferative villous cytotrophoblasts, in the terminally differentiated syncytiotrophoblast, and in migrating extravillous trophoblasts. RITA’s messenger RNA (mRNA) level is decreased in primary tissue samples from early-onset PE patients. The deficiency of RITA impairs the motility and invasion capacity of trophoblastic cell lines, and compromises the fusion ability of trophoblast-derived choriocarcinoma cells. These data suggest that RITA may play important roles in the development of the placenta and possibly in the pathogenesis of PE.