Utilización de la cestilla de Moss en el tratamiento de fracturas patológicas vertebrales

Las fracturas patológicas vertebrales pueden inducir radículo o mielopatía compresiva, inestabilidad y deformidad, de tal forma que el objetivo del tratamiento consistiría en restablecer lo más rápidamente posible la anatomía y función. En este sentido la utilización de una malla cilindrica de titanio como la «cestilla de Moss» consigue una estabilidad inmediata y permite la carga precoz. Presentamos un estudio retrospectivo de 6 pacientes afectos de fractura patológica vertebral intervenidos mediante abordaje anterior y estabilización instrumentada combinada con la «cestilla de Moss» rellena de injerto óseo o cemento acrílico. La valoración clínica se realiza subjetivamente por la presencia de dolor y neurológicamente según los grados de Frankel pre y postoperatorios. Radiológicamente se valora la corrección de la cifosis/lordosis/acuñamiento según el método de Cobb. La utilización de la «cestilla de Moss» en fracturas patológicas vertebrales consigue una estabilidad completa sin dependencia de la fusión ósea.Pathological spinal fractures could induce neurological deficit, instability and deformity. Therefore, the objective of the treatment consists of re-establishing the most quickly possible the anatomy and normal function. In this sense, the utilization of a cylindrical mesh of titanium, like the Moss's mesh, provide an immediate stability permiting early loading. We report a retrospective study of 6 patients with pathological spinal fracture operated by anterior decompression and spine stabilization using the Moss's mesh padded of bone graft acrylic cement. Clinical assessment was made subjectively for the presence of pain and neurologic ally according to pre and postoperatively Frankel's grades. The correction of the kyphosis, lordosis and vertebral collapse was assessed according to the Cobb's method. The utilization of the Moss's mesh in pathological spinal fractures provides a complete stability without dependence of the status of bone fusion

Estudio clínico-radiológico de la osteosíntesis con clavo gamma en fracturas trocantéricas

Los autores realizan un estudio retrospectivo de 222 enfermos afectos de fractura del macizo trocantérico tratados con clavo gamma estándar. Se valoran los resultados desde el punto de vista clínico, teniendo en cuenta el resultado funcional y las complicaciones, y radioló- gico considerando el tipo de implante, la impresión de estabilidad, los defectos del montaje y el ángulo cervicodiafisario para estudiar sus repercusiones en la consolidación. Se realiza una comparación de esta serie con otras de la literatura con el mismo implante (clavo gamma) y con otras en las que se usaron otros sistemas de osteosíntesis como DHS y Ender. Concluimos que con una técnica depurada el clavo gamma estándar es un sistema de osteosíntesis ideal en las fracturas inestables del macizo trocantérico.Two hundred twenty two fractures of the trochanteric area treated with the gamma standard nail were evaluated retrospectively. The clinical outcome was assessed keeping in mind the functional result and complications. The type of implant, stability impression, anomalies of the assembly and valgus-varus angle were analyzed in order to study their repercussions in the consolidation. This series is compared with others in the literature with the same implant (gamma nail) and with others using other systems of osteosintesys, like DHS and Ender's nails. We conclued that with a purified technique the gamma standard nail is an ideal system for osteosinthesys of unstable fractures of the trochanteric area

Severe acute respiratory syndrome coronavirus E protein transports calcium ions and activates the NLRP3 inflammasome

Severe acute respiratory syndrome coronavirus (SARS-CoV) envelope (E) protein is a viroporin involved in virulence. E protein ion channel (IC) activity is specifically correlated with enhanced pulmonary damage, edema accumulation and death. IL-1β driven proinflammation is associated with those pathological signatures, however its link to IC activity remains unknown. In this report, we demonstrate that SARS-CoV E protein forms protein–lipid channels in ERGIC/Golgi membranes that are permeable to calcium ions, a highly relevant feature never reported before. Calcium ions together with pH modulated E protein pore charge and selectivity. Interestingly, E protein IC activity boosted the activation of the NLRP3 inflammasome, leading to IL-1β overproduction. Calcium transport through the E protein IC was the main trigger of this process. These findings strikingly link SARS-CoV E protein IC induced ionic disturbances at the cell level to immunopathological consequences and disease worsening in the infected organism

Severe Acute Respiratory Syndrome Coronavirus Envelope Protein Ion Channel Activity Promotes Virus Fitness and Pathogenesis

Deletion of Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) envelope (E) gene attenuates the virus. E gene encodes a small multifunctional protein that possesses ion channel (IC) activity, an important function in virus-host interaction. To test the contribution of E protein IC activity in virus pathogenesis, two recombinant mouse-adapted SARSCoVs, each containing one single amino acid mutation that suppressed ion conductivity, were engineered. After serial infections, mutant viruses, in general, incorporated compensatory mutations within E gene that rendered active ion channels. Furthermore, IC activity conferred better fitness in competition assays, suggesting that ion conductivity represents an advantage for the virus. Interestingly, mice infected with viruses displaying E protein IC activity, either with the wild-type E protein sequence or with the revertants that restored ion transport, rapidly lost weight and died. In contrast, mice infected with mutants lacking IC activity, which did not incorporate mutations within E gene during the experiment, recovered from disease and most survived. Knocking down E protein IC activity did not significantly affect virus growth in infected mice but decreased edema accumulation, the major determinant of acute respiratory distress syndrome (ARDS) leading to death. Reduced edema correlated with lung epithelia integrity and proper localization of Na+ /K+ ATPase, which participates in edema resolution. Levels of inflammasome-activated IL-1b were reduced in the lung airways of the animals infected with viruses lacking E protein IC activity, indicating that E protein IC function is required for inflammasome activation. Reduction of IL-1b was accompanied by diminished amounts of TNF and IL-6 in the absence of E protein ion conductivity. All these key cytokines promote the progression of lung damage and ARDS pathology. In conclusion, E protein IC activity represents a new determinant for SARS-CoV virulence

Challenge 8: Smart Cybersecurity

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Severe Acute Respiratory Syndrome Coronavirus Envelope Protein Regulates Cell Stress Response and Apoptosis

Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE

Severe acute respiratory syndrome coronavirus envelope protein regulates cell stress response and apoptosis

Severe acute respiratory syndrome virus (SARS-CoV) that lacks the envelope (E) gene (rSARS-CoV-ΔE) is attenuated in vivo. To identify factors that contribute to rSARS-CoV-ΔE attenuation, gene expression in cells infected by SARS-CoV with or without E gene was compared. Twenty-five stress response genes were preferentially upregulated during infection in the absence of the E gene. In addition, genes involved in signal transduction, transcription, cell metabolism, immunoregulation, inflammation, apoptosis and cell cycle and differentiation were differentially regulated in cells infected with rSARS-CoV with or without the E gene. Administration of E protein in trans reduced the stress response in cells infected with rSARS-CoV-ΔE or with respiratory syncytial virus, or treated with drugs, such as tunicamycin and thapsigargin that elicit cell stress by different mechanisms. In addition, SARS-CoV E protein down-regulated the signaling pathway inositol-requiring enzyme 1 (IRE-1) of the unfolded protein response, but not the PKR-like ER kinase (PERK) or activating transcription factor 6 (ATF-6) pathways, and reduced cell apoptosis. Overall, the activation of the IRE-1 pathway was not able to restore cell homeostasis, and apoptosis was induced probably as a measure to protect the host by limiting virus production and dissemination. The expression of proinflammatory cytokines was reduced in rSARS-CoV-ΔE-infected cells compared to rSARS-CoV-infected cells, suggesting that the increase in stress responses and the reduction of inflammation in the absence of the E gene contributed to the attenuation of rSARS-CoV-ΔE.Peer reviewe