Density biases and temperature relations for DESIRED HII regions

We present a first study based on the analysis of the DEep Spectra of Ionized REgions Database (DESIRED). This is a compilation of 190 high signal-to-noise ratio optical spectra of HII regions and other photoionized nebulae, mostly observed with 8-10m telescopes and containing $\sim$29380 emission lines. We find that the electron density --$n_{\rm e}$-- of the objects is underestimated when [SII] $\lambda6731/\lambda6716$ and/or [OII] $\lambda3726/\lambda3729$ are the only density indicators available. This is produced by the non-linear density dependence of the indicators in the presence of density inhomogeneities. The average underestimate is $\sim 300$ cm$^{-3}$ in extragalactic HII regions, introducing systematic overestimates of $T_{\rm e}$([OII]) and $T_{\rm e}$([SII]) compared to $T_{\rm e}$([NII]). The high-sensitivity of [OII] $\lambda\lambda7319+20+30+31/\lambda\lambda3726+29$ and [SII] $\lambda\lambda4069+76/\lambda\lambda6716+31$ to density makes them more suitable for the diagnosis of the presence of high-density clumps. If $T_{\rm e}$([NII]) is adopted, the density underestimate has a small impact in the ionic abundances derived from optical spectra, being limited to up to $\sim$0.1 dex when auroral [SII] and/or [OII] lines are used. However, these density effects are critical for the analysis of infrared fine structure lines, such as those observed by the JWST in local star forming regions, implying strong underestimates of the ionic abundances. We present temperature relations between $T_{\rm e}$([OIII]), $T_{\rm e}$([ArIII]), $T_{\rm e}$([SIII]) and $T_{\rm e}$([NII]) for the extragalactic HII regions. We confirm a non-linear dependence between $T_{\rm e}$([OIII])-$T_{\rm e}$([NII]) due to a more rapid increase of $T_{\rm e}$([OIII]) at lower metallicities.Comment: Accepted for publication in MNRA

PDR-1/hParkin negatively regulates the phagocytosis of apoptotic cell corpses in Caenorhabditis elegans

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation

PDR-1/hParkin negatively regulates the phagocyosis of apoptotic cell corpses in Caenorhabditis elegans

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation

PDR-1/hParkin negatively regulates the phagocyosis of apoptotic cell corpses in Caenorhabditis elegans

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation

PDR-1/hParkin negatively regulates the phagocyosis of apoptotic cell corpses in Caenorhabditis elegans

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation

PDR-1/hParkin negatively regulates the phagocytosis of apoptotic cell corpses in Caenorhabditis elegans

Apoptotic cell death is an integral part of cell turnover in many tissues, and proper corpse clearance is vital to maintaining tissue homeostasis in all multicellular organisms. Even in tissues with high cellular turnover, apoptotic cells are rarely seen because of efficient clearance mechanisms in healthy individuals. In Caenorhabditis elegans, two parallel and partly redundant conserved pathways act in cell corpse engulfment. The pathway for cytoskeletal rearrangement requires the small GTPase CED-10 Rac1 acting for an efficient surround of the dead cell. The CED-10 Rac pathway is also required for the proper migration of the distal tip cells (DTCs) during the development of the C. elegans gonad. Parkin, the mammalian homolog of the C. elegans PDR-1, interacts with Rac1 in aged human brain and it is also implicated with actin dynamics and cytoskeletal rearrangements in Parkinsons's disease, suggesting that it might act on engulfment. Our genetic and biochemical studies indicate that PDR-1 inhibits apoptotic cell engulfment and DTC migration by ubiquitylating CED-10 for degradation

Clinicopathological features, MCPyV status and outcomes of Merkel cell carcinoma in solid-organ transplant recipients: a retrospective, multicentre cohort study

none25siBackground The proportion of Merkel cell carcinomas (MCCs) in solid-organ transplant recipients (SOTR) harbouring Merkel cell polyomavirus (MCPyV) is unknown, as are factors affecting their outcomes. Objective To describe clinicopathological features of MCC in SOTR, investigate the tumoral MCPyV-status and identify factors associated with tumour outcomes. Methods Retrospective, international, cohort-study. MCPyV-status was investigated by immunohistochemistry and polymerase chain reaction. Results A total of 30 SOTR and 44 consecutive immunocompetent patients with MCC were enrolled. SOTR were younger at diagnosis (69 vs. 78 years, P < 0.001). Thirty-three percent of SOTR MCCs were MCPyV-positive vs. 91% of immunocompetent MCCs (P = 0.001). Solid-organ transplantation was associated with an increased cumulative incidence of progression (SHR: 3.35 [1.57-7.14], P = 0.002), MCC-specific mortality (SHR: 2.55 [1.07-6.06], P = 0.034) and overall mortality (HR: 3.26 [1.54-6.9], P = 0.002). MCPyV-positivity and switching to an mTOR inhibitor (mTORi) after MCC diagnosis were associated with an increased incidence of progression (SHR: 4.3 [1.5-13], P = 0.008 and SHR: 3.6 [1.1-12], P = 0.032 respectively) in SOTR. Limitations Retrospective design and heterogeneity of SOTR cohort. Conclusions MCPyV appears to play a less prominent role in the aetiopathogenesis of MCC in SOTR. SOTR have a worse prognosis than their immunocompetent counterparts and switching to an mTORi after the diagnosis of MCC does not improve progression.Ferrándiz-Pulido, C; Gómez-Tomás, A; Llombart, B; Mendoza, D; Marcoval, J; Piaserico, S; Baykal, C; Bouwes-Bavinck, J N; Rácz, E; Kanitakis, J; Harwood, C A; Cetkovská, P; Geusau, A; Del Marmol, V; Masferrer, E; Orte Cano, C; Ricar, J; de Oliveira, W R; Salido-Vallejo, R; Ducroux, E; Gkini, M A; López-Guerrero, J A; Kutzner, H; Kempf, W; Seçkin, DFerrándiz-Pulido, C; Gómez-Tomás, A; Llombart, B; Mendoza, D; Marcoval, J; Piaserico, S; Baykal, C; Bouwes-Bavinck, J N; Rácz, E; Kanitakis, J; Harwood, C A; Cetkovská, P; Geusau, A; Del Marmol, V; Masferrer, E; Orte Cano, C; Ricar, J; de Oliveira, W R; Salido-Vallejo, R; Ducroux, E; Gkini, M A; López-Guerrero, J A; Kutzner, H; Kempf, W; Seçkin,