Abstract The production of $$\Sigma ^{0}$$ Σ 0 hyperons in proton proton collisions at a beam kinetic energy of 3.5 GeV impinging on a liquid hydrogen target was investigated using data collected ...with the HADES setup. The total production cross section is found to be $${\sigma (pK^{+}\Sigma ^{0}) = 17.7 \pm 1.7 (stat) \pm 1.6 (syst)}$$ σ ( p K + Σ 0 ) = 17.7 ± 1.7 ( s t a t ) ± 1.6 ( s y s t ) µb. Differential cross section distributions of the exclusive channel $${pp \rightarrow pK^{+}\Sigma ^{0}}$$ p p → p K + Σ 0 were analyzed in the center-of-mass, Gottfried–Jackson and helicity reference frames for the first time at the excess energy of 556 MeV. The data support the interplay between pion and kaon exchange mechanisms and clearly demonstrate the contribution of interfering nucleon resonances decaying to $$\textrm{K}^{+}\Sigma ^{0}$$ K + Σ 0 . The Bonn–Gatchina partial wave analysis was employed to analyse the data. Due to the limited statistics, it was not possible to obtain an unambiguous determination of the relative contribution of intermediate nucleon resonances to the final state. However nucleon resonances with masses around 1.710 $${\textrm{GeV}/\textrm{c}^{2}}$$ GeV / c 2 ( $${\textrm{N}^{*}(1710)}$$ N ∗ ( 1710 ) ) and 1.900 $${\textrm{GeV}/\textrm{c}^{2}}$$ GeV / c 2 ( $${\textrm{N}^{*}(1900)}$$ N ∗ ( 1900 ) or $${\Delta ^{*}(1900)}$$ Δ ∗ ( 1900 ) ) are preferred by the fit.
The production of
Σ
0
hyperons in proton proton collisions at a beam kinetic energy of 3.5 GeV impinging on a liquid hydrogen target was investigated using data collected with the HADES setup. The ...total production cross section is found to be
σ
(
p
K
+
Σ
0
)
=
17.7
±
1.7
(
s
t
a
t
)
±
1.6
(
s
y
s
t
)
µb. Differential cross section distributions of the exclusive channel
p
p
→
p
K
+
Σ
0
were analyzed in the center-of-mass, Gottfried–Jackson and helicity reference frames for the first time at the excess energy of 556 MeV. The data support the interplay between pion and kaon exchange mechanisms and clearly demonstrate the contribution of interfering nucleon resonances decaying to
K
+
Σ
0
. The Bonn–Gatchina partial wave analysis was employed to analyse the data. Due to the limited statistics, it was not possible to obtain an unambiguous determination of the relative contribution of intermediate nucleon resonances to the final state. However nucleon resonances with masses around 1.710
GeV
/
c
2
(
N
∗
(
1710
)
) and 1.900
GeV
/
c
2
(
N
∗
(
1900
)
or
Δ
∗
(
1900
)
) are preferred by the fit.
The global polarization of {\Lambda} hyperons along the total orbital angular momentum of a relativistic heavy-ion collision is presented based on the high statistics data samples collected in Au+Au ...collisions at \sqrt{s_{NN}} = 2.4 GeV and Ag+Ag at 2.55 GeV with the High-Acceptance Di-Electron Spectrometer (HADES) at GSI, Darmstadt. This is the first measurement below the strangeness production threshold in nucleon-nucleon collisions. Results are reported as a function of the collision centrality as well as a function of the hyperon transverse momentum (p_T) and rapidity (y_{CM}) for the range of centrality 0--40%. We observe a strong centrality dependence of the polarization with an increasing signal towards peripheral collisions. For mid-central (20--40%) collisions the polarization magnitudes are <P_{\Lambda}>(%) = 6.8 \pm 1.3 (stat.) \pm 2.1 (syst.) for Au+Au and <P_{\Lambda}>(%) = 6.2 \pm 0.4 (stat.) \pm 0.6 (syst.) for Ag+Ag, which are the largest values observed so far. This observation thus provides a continuation of the increasing trend previously observed by STAR and contrasts expectations from recent theoretical calculations predicting a maximum in the region of collision energies about 3 GeV. The observed polarization is of a similar magnitude as predicted by 3D fluid dynamics and the UrQMD plus thermal vorticity model and significantly above results from the AMPT model.
Hadron production (\(\pi^\pm\), proton, \(\Lambda\), \(K_S^0\), \(K^\pm\)) in \(\pi^- + \mathrm{C}\) and \(\pi^- + \mathrm{W}\) collisions is investigated at an incident pion beam momentum of ...\(1.7~\mathrm{GeV}/c\). This comprehensive set of data measured with HADES at SIS18/GSI significantly extends the existing world data on hadron production in pion induced reactions and provides a new reference for models that are commonly used for the interpretation of heavy-ion collisions. The measured inclusive differential production cross-sections are compared with state-of-the-art transport model (GiBUU, SMASH) calculations. The (semi-) exclusive channel \(\pi^- + A \rightarrow \Lambda + K_S^0 +X\), in which the kinematics of the strange hadrons are correlated, is also investigated and compared to a model calculation. Agreement and remaining tensions between data and the current version of the considered transport models are discussed.
The production of $\Sigma^0$ hyperons in proton proton collisions at a beam
kinetic energy of 3.5 GeV impinging on a liquid hydrogen target was
investigated using data collected with the HADES setup. ...The total production
cross section is found to be $\mathrm{\sigma (pK^{+}\Sigma^{0}) \mu b = 17.7
\pm 1.7 (stat) \pm 1.6 (syst)}$. Differential cross section distributions of
the exclusive channel $\mathrm{pp \rightarrow pK^{+}\Sigma^{0}}$ were analyzed
in the center-of-mass, Gottfried-Jackson and helicity reference frames for the
first time at the excess energy of 556 MeV. The data support the interplay
between pion and kaon exchange mechanisms and clearly demonstrate the
contribution of interfering nucleon resonances decaying to
$\mathrm{K^{+}\Sigma^{0}}$. The Bonn-Gatchina partial wave analysis was
employed to analyse the data. Due to the limited statistics, it was not
possible to obtain an unambiguous determination of the relative contribution of
intermediate nucleon resonances to the final state. However nucleon resonances
with masses around 1.710 $\mathrm{GeV/c^{2}}$ ($\mathrm{N^{*}(1710)}$) and
1.900 $\mathrm{GeV/c^{2}}$ ($\mathrm{N^{*}(1900)}$ or
$\mathrm{\Delta^{*}(1900)}$) are preferred by the fit.
Experiences over the last three decades of war have demonstrated a high incidence of traumatic brain injury (TBI) resulting in a persistent need for a neurosurgical capability within the deployed ...theater of operations. Despite this, no doctrinal requirement for a deployed neurosurgical capability exists. Through an iterative process, the Joint Trauma System Committee on Surgical Combat Casualty Care (CoSCCC) developed a position statement to inform medical and nonmedical military leaders about the risks of the lack of a specialized neurosurgical capability.
The need for deployed neurosurgical capability position statement was identified during the spring 2021 CoSCCC meeting. A triservice working group of experienced forward-deployed caregivers developed a preliminary statement. An extensive iterative review process was then conducted to ensure that the intended messaging was clear to senior medical leaders and operational commanders. To provide additional context and a civilian perspective, statement commentaries were solicited from civilian clinical experts including a recently retired military trauma surgeon boarded in neurocritical care, a trauma surgeon instrumental in developing the Brain Injury Guidelines, a practicing neurosurgeon with world-renowned expertise in TBI, and the chair of the Committee on Trauma.
After multiple revisions, the position statement was finalized, and approved by the CoSCCC membership in February 2023. Challenges identified include (1) military neurosurgeon attrition, (2) the lack of a doctrinal neurosurgical capabilities requirement during deployed combat operations, and (3) the need for neurosurgical telemedicine capability and in-theater computed tomography scans to triage TBI casualties requiring neurosurgical care.
Challenges identified regarding neurosurgical capabilities within the deployed trauma system include military neurosurgeon attrition and the lack of a doctrinal requirement for neurosurgical capability during deployed combat operations. To mitigate risk to the force in a future peer-peer conflict, several evidence-based recommendations are made. The solicited civilian commentaries strengthen these recommendations by putting them into the context of civilian TBI management. This neurosurgical capabilities position statement is intended to be a forcing function and a communication tool to inform operational commanders and military medical leaders on the use of these teams on current and future battlefields.
Prognostic and Epidemiological; Level V.
The production of \(\Sigma^0\) hyperons in proton proton collisions at a beam kinetic energy of 3.5 GeV impinging on a liquid hydrogen target was investigated using data collected with the HADES ...setup. The total production cross section is found to be \(\mathrm{\sigma (pK^{+}\Sigma^{0}) \mu b = 17.7 \pm 1.7 (stat) \pm 1.6 (syst)}\). Differential cross section distributions of the exclusive channel \(\mathrm{pp \rightarrow pK^{+}\Sigma^{0}}\) were analyzed in the center-of-mass, Gottfried-Jackson and helicity reference frames for the first time at the excess energy of 556 MeV. The data support the interplay between pion and kaon exchange mechanisms and clearly demonstrate the contribution of interfering nucleon resonances decaying to \(\mathrm{K^{+}\Sigma^{0}}\). The Bonn-Gatchina partial wave analysis was employed to analyse the data. Due to the limited statistics, it was not possible to obtain an unambiguous determination of the relative contribution of intermediate nucleon resonances to the final state. However nucleon resonances with masses around 1.710 \(\mathrm{GeV/c^{2}}\) (\(\mathrm{N^{*}(1710)}\)) and 1.900 \(\mathrm{GeV/c^{2}}\) (\(\mathrm{N^{*}(1900)}\) or \(\mathrm{\Delta^{*}(1900)}\)) are preferred by the fit.
The biological response to DNA double-strand breaks acts to preserve genome integrity. Individuals bearing inactivating mutations in components of this response exhibit clinical symptoms that include ...cellular radiosensitivity, immunodeficiency, and cancer predisposition. The archetype for such disorders is Ataxia-Telangiectasia caused by biallelic mutation in ATM, a central component of the DNA damage response. Here, we report that the ubiquitin ligase RNF168 is mutated in the RIDDLE syndrome, a recently discovered immunodeficiency and radiosensitivity disorder. We show that RNF168 is recruited to sites of DNA damage by binding to ubiquitylated histone H2A. RNF168 acts with UBC13 to amplify the RNF8-dependent histone ubiquitylation by targeting H2A-type histones and by promoting the formation of lysine 63-linked ubiquitin conjugates. These RNF168-dependent chromatin modifications orchestrate the accumulation of 53BP1 and BRCA1 to DNA lesions, and their loss is the likely cause of the cellular and developmental phenotypes associated with RIDDLE syndrome.
Cells respond to DNA double-strand breaks by recruiting factors such as the DNA-damage mediator protein MDC1, the p53-binding protein 1 (53BP1), and the breast cancer susceptibility protein BRCA1 to ...sites of damaged DNA. Here, we reveal that the ubiquitin ligase RNF8 mediates ubiquitin conjugation and 53BP1 and BRCA1 focal accumulation at sites of DNA lesions. Moreover, we establish that MDC1 recruits RNF8 through phosphodependent interactions between the RNF8 forkhead-associated domain and motifs in MDC1 that are phosphorylated by the DNA-damage activated protein kinase ataxia telangiectasia mutated (ATM). We also show that depletion of the E2 enzyme UBC13 impairs 53BP1 recruitment to sites of damage, which suggests that it cooperates with RNF8. Finally, we reveal that RNF8 promotes the G₂/M DNA damage checkpoint and resistance to ionizing radiation. These results demonstrate how the DNA-damage response is orchestrated by ATM-dependent phosphorylation of MDC1 and RNF8-mediated ubiquitination.
Exonuclease 1 (Exo1) is a 5'-3' exonuclease that interacts with MutS and MutL homologs and has been implicated in the excision step of DNA mismatch repair. To investigate the role of Exo1 in ...mammalian mismatch repair and assess its importance for tumorigenesis and meiosis, we generated an Exo1 mutant mouse line. Analysis of Exo1(-/-) cells for mismatch repair activity in vitro showed that Exo1 is required for the repair of base:base and single-base insertion/deletion mismatches in both 5' and 3' nick-directed repair. The repair defect in Exo1(-/-) cells also caused elevated microsatellite instability at a mononucleotide repeat marker and a significant increase in mutation rate at the Hprt locus. Exo1(-/-) animals displayed reduced survival and increased susceptibility to the development of lymphomas. In addition, Exo1(-/-) male and female mice were sterile because of a meiotic defect. Meiosis in Exo1(-/-) animals proceeded through prophase I; however, the chromosomes exhibited dynamic loss of chiasmata during metaphase I, resulting in meiotic failure and apoptosis. Our results show that mammalian Exo1 functions in mutation avoidance and is essential for male and female meiosis.
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