Multidifferential study of identified charged hadron distributions in ZZ-tagged jets in proton-proton collisions at s=\sqrt{s}=13 TeV

Jet fragmentation functions are measured for the first time in proton-proton collisions for charged pions, kaons, and protons within jets recoiling against a $Z$ boson. The charged-hadron distributions are studied longitudinally and transversely to the jet direction for jets with transverse momentum 20 $< p_{\textrm{T}} < 100$ GeV and in the pseudorapidity range $2.5 < \eta < 4$. The data sample was collected with the LHCb experiment at a center-of-mass energy of 13 TeV, corresponding to an integrated luminosity of 1.64 fb$^{-1}$. Triple differential distributions as a function of the hadron longitudinal momentum fraction, hadron transverse momentum, and jet transverse momentum are also measured for the first time. This helps constrain transverse-momentum-dependent fragmentation functions. Differences in the shapes and magnitudes of the measured distributions for the different hadron species provide insights into the hadronization process for jets predominantly initiated by light quarks.Comment: All figures and tables, along with machine-readable versions and any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-013.html (LHCb public pages

Study of the B−→Λc+Λˉc−K−B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-} decay

The decay $B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-}$ is studied in proton-proton collisions at a center-of-mass energy of $\sqrt{s}=13$ TeV using data corresponding to an integrated luminosity of 5 $\mathrm{fb}^{-1}$ collected by the LHCb experiment. In the $\Lambda_{c}^+ K^{-}$ system, the $\Xi_{c}(2930)^{0}$ state observed at the BaBar and Belle experiments is resolved into two narrower states, $\Xi_{c}(2923)^{0}$ and $\Xi_{c}(2939)^{0}$, whose masses and widths are measured to be $$m(\Xi_{c}(2923)^{0}) = 2924.5 \pm 0.4 \pm 1.1 \,\mathrm{MeV}, \\ m(\Xi_{c}(2939)^{0}) = 2938.5 \pm 0.9 \pm 2.3 \,\mathrm{MeV}, \\ \Gamma(\Xi_{c}(2923)^{0}) = \phantom{000}4.8 \pm 0.9 \pm 1.5 \,\mathrm{MeV},\\ \Gamma(\Xi_{c}(2939)^{0}) = \phantom{00}11.0 \pm 1.9 \pm 7.5 \,\mathrm{MeV},$$ where the first uncertainties are statistical and the second systematic. The results are consistent with a previous LHCb measurement using a prompt $\Lambda_{c}^{+} K^{-}$ sample. Evidence of a new $\Xi_{c}(2880)^{0}$ state is found with a local significance of $3.8\,\sigma$, whose mass and width are measured to be $2881.8 \pm 3.1 \pm 8.5\,\mathrm{MeV}$ and $12.4 \pm 5.3 \pm 5.8 \,\mathrm{MeV}$, respectively. In addition, evidence of a new decay mode $\Xi_{c}(2790)^{0} \to \Lambda_{c}^{+} K^{-}$ is found with a significance of $3.7\,\sigma$. The relative branching fraction of $B^{-} \to \Lambda_{c}^{+} \bar{\Lambda}_{c}^{-} K^{-}$ with respect to the $B^{-} \to D^{+} D^{-} K^{-}$ decay is measured to be $2.36 \pm 0.11 \pm 0.22 \pm 0.25$, where the first uncertainty is statistical, the second systematic and the third originates from the branching fractions of charm hadron decays.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-028.html (LHCb public pages

Measurement of the ratios of branching fractions R(D∗)\mathcal{R}(D^{*}) and R(D0)\mathcal{R}(D^{0})

The ratios of branching fractions $\mathcal{R}(D^{*})\equiv\mathcal{B}(\bar{B}\to D^{*}\tau^{-}\bar{\nu}_{\tau})/\mathcal{B}(\bar{B}\to D^{*}\mu^{-}\bar{\nu}_{\mu})$ and $\mathcal{R}(D^{0})\equiv\mathcal{B}(B^{-}\to D^{0}\tau^{-}\bar{\nu}_{\tau})/\mathcal{B}(B^{-}\to D^{0}\mu^{-}\bar{\nu}_{\mu})$ are measured, assuming isospin symmetry, using a sample of proton-proton collision data corresponding to 3.0 fb${ }^{-1}$ of integrated luminosity recorded by the LHCb experiment during 2011 and 2012. The tau lepton is identified in the decay mode $\tau^{-}\to\mu^{-}\nu_{\tau}\bar{\nu}_{\mu}$. The measured values are $\mathcal{R}(D^{*})=0.281\pm0.018\pm0.024$ and $\mathcal{R}(D^{0})=0.441\pm0.060\pm0.066$, where the first uncertainty is statistical and the second is systematic. The correlation between these measurements is $\rho=-0.43$. Results are consistent with the current average of these quantities and are at a combined 1.9 standard deviations from the predictions based on lepton flavor universality in the Standard Model.Comment: All figures and tables, along with any supplementary material and additional information, are available at https://cern.ch/lhcbproject/Publications/p/LHCb-PAPER-2022-039.html (LHCb public pages

"X" Marks the Spot

This 24 year-old man presented with several months of progressive visual loss in both eyes. His past medical, surgical and ocular history was unremarkable. There was no family history of phacomatosis. He complained of occasional binocular diplopia, but denied headaches or any other neurological symptoms. He denied galactorrhea, fatigue, and abdominal pain. On exam, his visual acuity was 20/125 OD and 20/50 OS. He had incomplete atypical bitemporal defects that respected the vertical meridian and pallor of both optic nerves, right more than left. Magnetic resonance imaging (MRI) of the brain showed an enlarged optic chiasm and a hyperintense left frontal periventricular lesion that was abutting the genu of the corpus callosum. Both lesions showed mild contrast enhancement. The differential diagnosis included a primary intrinsic chiasmal glioma versus an inflammatory etiology. An extensive infectious, inflammatory, and rheumatologic work-up was unrevealing. Cerebrospinal fluid (CSF) evaluation showed a mild lymphocytic pleocytosis (11/mL) and mildly increased protein concentration (54 mg/dL). The CSF showed 3 oligoclonal bands. CSF cytology and cultures were negative. Based on these findings, he received a 1-month course of high dose steroid treatment without clinical improvement and further visual loss in both eyes. Repeat MRI brain showed no radiological improvement. At this point, the patient started complaining of increased thirst. A diagnostic procedure was performed

'X' Marks the Spot

This 24 year-old man presented with several months of progressive visual loss in both eyes. His past medical, surgical and ocular history was unremarkable. There was no family history of phacomatosis. He complained of occasional binocular diplopia, but denied headaches or any other neurological symptoms. He denied galactorrhea, fatigue, and abdominal pain. On exam, his visual acuity was 20/125 OD and 20/50 OS. He had incomplete atypical bitemporal defects that respected the vertical meridian and pallor of both optic nerves, right more than left. Magnetic resonance imaging (MRI) of the brain showed an enlarged optic chiasm and a hyperintense left frontal periventricular lesion that was abutting the genu of the corpus callosum. Both lesions showed mild contrast enhancement. The differential diagnosis included a primary intrinsic chiasmal glioma versus an inflammatory etiology. An extensive infectious, inflammatory, and rheumatologic work-up was unrevealing. Cerebrospinal fluid (CSF) evaluation showed a mild lymphocytic pleocytosis (11/mL) and mildly increased protein concentration (54 mg/dL). The CSF showed 3 oligoclonal bands. CSF cytology and cultures were negative. Based on these findings, he received a 1-month course of high dose steroid treatment without clinical improvement and further visual loss in both eyes. Repeat MRI brain showed no radiological improvement. At this point, the patient started complaining of increased thirst. A diagnostic procedure was performed

'X' Marks the Spot

This 24 year-old man presented with several months of progressive visual loss in both eyes. His past medical, surgical and ocular history was unremarkable. There was no family history of phacomatosis. He complained of occasional binocular diplopia, but denied headaches or any other neurological symptoms. He denied galactorrhea, fatigue, and abdominal pain. On exam, his visual acuity was 20/125 OD and 20/50 OS. He had incomplete atypical bitemporal defects that respected the vertical meridian and pallor of both optic nerves, right more than left. Magnetic resonance imaging (MRI) of the brain showed an enlarged optic chiasm and a hyperintense left frontal periventricular lesion that was abutting the genu of the corpus callosum. Both lesions showed mild contrast enhancement. The differential diagnosis included a primary intrinsic chiasmal glioma versus an inflammatory etiology. An extensive infectious, inflammatory, and rheumatologic work-up was unrevealing. Cerebrospinal fluid (CSF) evaluation showed a mild lymphocytic pleocytosis (11/mL) and mildly increased protein concentration (54 mg/dL). The CSF showed 3 oligoclonal bands. CSF cytology and cultures were negative. Based on these findings, he received a 1-month course of high dose steroid treatment without clinical improvement and further visual loss in both eyes. Repeat MRI brain showed no radiological improvement. At this point, the patient started complaining of increased thirst. A diagnostic procedure was performed

Intracranial glioblastoma with drop metastases to the spine after stereotactic biopsy.

BACKGROUND: Glioblastoma (GBM) is the most common primary intracranial tumor, but metastases are rarely reported. Previous reports have documented the occurrence of drop metastases to the spine. However, few of these reports have demonstrated the occurrence of spinal metastases after biopsy with stable intracranial disease. Here we present such a case. CASE DESCRIPTION: We present a case of GBM metastatic to the spinal cord after a stereotactic biopsy with stable intracranial disease. To our knowledge, this occurrence has only been reported in one previous case. CONCLUSION: We propose that traversing the lateral ventricle at the time of biopsy contributed to cerebrospinal fluid seeding with tumor cells and subsequent development of spinal disease