Ambulatory models for autologous stem-cell transplantation: a systematic review of the health impact.

Autologous stem-cell transplantation (ASCT) is the standard of care for the management of multiple myeloma and has a well-established role in the treatment of some types of lymphoma. Over the last decades, the number of ASCT performed has increased significantly, leading to elevated pressure and cost for healthcare services. Conventional model of ASCT includes the admission of patients to a specialized Transplant Unit at any stage of the procedure. To optimize healthcare provision, ambulatory (outpatient/at-home) setting should be the focus moving forward. Thus, ambulatory ASCT model permits reducing average hospital stays and pressures on healthcare services, with significant cost-saving benefits and high degree of patient and caregiver satisfaction. In addition, it facilitates the bed resource for other complex procedures such as allografts or CAR-T cell therapy. The aim of this systematic review is to document the health impact, feasibility and safety of the outpatient/at-home ASCT models, which are increasingly being applied around the world.

Human tNeurons reveal aging-linked proteostasis deficits driving Alzheimer's phenotypes.

Aging is a prominent risk factor for Alzheimer's disease (AD), but the cellular mechanisms underlying neuronal phenotypes remain elusive. Both accumulation of amyloid plaques and neurofibrillary tangles in the brain1 and age-linked organelle deficits2-7 are proposed as causes of AD phenotypes but the relationship between these events is unclear. Here, we address this question using a transdifferentiated neuron (tNeuron) model directly from human dermal fibroblasts. Patient-derived tNeurons retain aging hallmarks and exhibit AD-linked deficits. Quantitative tNeuron proteomic analyses identify aging and AD-linked deficits in proteostasis and organelle homeostasis, particularly affecting endosome-lysosomal components. The proteostasis and lysosomal homeostasis deficits in aged tNeurons are exacerbated in sporadic and familial AD tNeurons, promoting constitutive lysosomal damage and defects in ESCRT-mediated repair. We find deficits in neuronal lysosomal homeostasis lead to inflammatory cytokine secretion, cell death and spontaneous development of Aß and phospho-Tau deposits. These proteotoxic inclusions co-localize with lysosomes and damage markers and resemble inclusions in brain tissue from AD patients and APP-transgenic mice. Supporting the centrality of lysosomal deficits driving AD phenotypes, lysosome-function enhancing compounds reduce AD-associated cytokine secretion and Aß deposits. We conclude that proteostasis and organelle deficits are upstream initiating factors leading to neuronal aging and AD phenotypes.

Targetable leukaemia dependency on noncanonical PI3Kγ signalling.

Phosphoinositide-3-kinase-γ (PI3Kγ) is implicated as a target to repolarize tumour-associated macrophages and promote antitumour immune responses in solid cancers1-4. However, cancer cell-intrinsic roles of PI3Kγ are unclear. Here, by integrating unbiased genome-wide CRISPR interference screening with functional analyses across acute leukaemias, we define a selective dependency on the PI3Kγ complex in a high-risk subset that includes myeloid, lymphoid and dendritic lineages. This dependency is characterized by innate inflammatory signalling and activation of phosphoinositide 3-kinase regulatory subunit 5 (PIK3R5), which encodes a regulatory subunit of PI3Kγ5 and stabilizes the active enzymatic complex. We identify p21 (RAC1)-activated kinase 1 (PAK1) as a noncanonical substrate of PI3Kγ that mediates this cell-intrinsic dependency and find that dephosphorylation of PAK1 by PI3Kγ inhibition impairs mitochondrial oxidative phosphorylation. Treatment with the selective PI3Kγ inhibitor eganelisib is effective in leukaemias with activated PIK3R5. In addition, the combination of eganelisib and cytarabine prolongs survival over either agent alone, even in patient-derived leukaemia xenografts with low baseline PIK3R5 expression, as residual leukaemia cells after cytarabine treatment have elevated G protein-coupled purinergic receptor activity and PAK1 phosphorylation. Together, our study reveals a targetable dependency on PI3Kγ-PAK1 signalling that is amenable to near-term evaluation in patients with acute leukaemia.

Biallelic USP14 variants cause a syndromic neurodevelopmental disorder.

PURPOSE: Imbalances in protein homeostasis affect human brain development, with the ubiquitin-proteasome system (UPS) and autophagy playing crucial roles in neurodevelopmental disorders (NDD). This study explores the impact of biallelic USP14 variants on neurodevelopment, focusing on its role as a key hub connecting UPS and autophagy. METHODS: Here, we identified biallelic USP14 variants in 4 individuals from 3 unrelated families: 1 fetus, a newborn with a syndromic NDD and 2 siblings affected by a progressive neurological disease. Specifically, the 2 siblings from the latter family carried 2 compound heterozygous variants c.8T>C p.(Leu3Pro) and c.988C>T p.(Arg330∗), whereas the fetus had a homozygous frameshift c.899_902del p.(Lys300Serfs∗24) variant, and the newborn patient harbored a homozygous frameshift c.233_236del p.(Leu78Glnfs∗11) variant. Functional studies were conducted using sodium dodecyl-sulfate polyacrylamide gel electrophoresis, western blotting, and mass spectrometry analyses in both patient-derived and CRISPR-Cas9-generated cells. RESULTS: Our investigations indicated that the USP14 variants correlated with reduced N-terminal methionine excision, along with profound alterations in proteasome, autophagy, and mitophagy activities. CONCLUSION: Biallelic USP14 variants in NDD patients perturbed protein degradation pathways, potentially contributing to disorder etiology. Altered UPS, autophagy, and mitophagy activities underscore the intricate interplay, elucidating their significance in maintaining proper protein homeostasis during brain development.

Mapping Malaria Vector Habitats in West Africa: Drone Imagery and Deep Learning Analysis for Targeted Vector Surveillance.

Disease control programs are needed to identify the breeding sites of mosquitoes, which transmit malaria and other diseases, in order to target interventions and identify environmental risk factors. The increasing availability of very-high-resolution drone data provides new opportunities to find and characterize these vector breeding sites. Within this study, drone images from two malaria-endemic regions in Burkina Faso and Côte d'Ivoire were assembled and labeled using open-source tools. We developed and applied a workflow using region-of-interest-based and deep learning methods to identify land cover types associated with vector breeding sites from very-high-resolution natural color imagery. Analysis methods were assessed using cross-validation and achieved maximum Dice coefficients of 0.68 and 0.75 for vegetated and non-vegetated water bodies, respectively. This classifier consistently identified the presence of other land cover types associated with the breeding sites, obtaining Dice coefficients of 0.88 for tillage and crops, 0.87 for buildings and 0.71 for roads. This study establishes a framework for developing deep learning approaches to identify vector breeding sites and highlights the need to evaluate how results will be used by control programs.

Proteostasis and lysosomal quality control deficits in Alzheimer's disease neurons.

The role of proteostasis and organelle homeostasis dysfunction in human aging and Alzheimer's disease (AD) remains unclear. Analyzing proteome-wide changes in human donor fibroblasts and their corresponding transdifferentiated neurons (tNeurons), we find aging and AD synergistically impair multiple proteostasis pathways, most notably lysosomal quality control (LQC). In particular, we show that ESCRT-mediated lysosomal repair defects are associated with both sporadic and PSEN1 familial AD. Aging- and AD-linked defects are detected in fibroblasts but highly exacerbated in tNeurons, leading to enhanced neuronal vulnerability, unrepaired lysosomal damage, inflammatory factor secretion and cytotoxicity. Surprisingly, tNeurons from aged and AD donors spontaneously develop amyloid-ß inclusions co-localizing with LQC markers, LAMP1/2-positive lysosomes and proteostasis factors; we observe similar inclusions in brain tissue from AD patients and APP-transgenic mice. Importantly, compounds enhancing lysosomal function broadly ameliorate these AD-associated pathologies. Our findings establish cell-autonomous LQC dysfunction in neurons as a central vulnerability in aging and AD pathogenesis.

Assigning Viscosity Values in the Glass Softening Temperature Range.

A new optical method for assigning glass viscosity values in the softening temperature range is presented. In this method, an irregular particle, a few millimeters in size, laying on an alumina plate, is heated up to temperature T, and then remains at this temperature. T should be within the softening temperature range of the glass. There are no external applied shear stresses, the only acting shear forces are those coming from the particle's own surface energy. At the fixed temperature T, the surface free energy of the sample decreases by viscous flow while its shape evolves from a polyhedron or irregular shape towards a spherical or rounded shape. This shape evolution is recorded using a photographic camera. From each image, the sample's roundness is determined, obtaining a characteristic time τ from the roundness against time. Simultaneously, using the available software, a value for the viscosity η was calculated, at temperature T, allowing for building sets of T, τ, η, namely three data values. Accordingly, if T, τ are considered as independent variables, a master function η = η (T, τ) can be built. Now, if we measure T, τ data on a glass of an unknown viscosity, the master function makes it possible to assign a η value. When incipient crystallization or liquid-liquid phase separations are present, effective viscosity values are obtained. This method requires a high temperature microscope, as well as tridimmensional samples with a few cubic millimeters of volume. Each isothermal τ determination can take from minutes to several hours. We tested the method with two glasses of known viscosity values: borosilicate glass (VG98) and alumimoborosilicate glass (SG7), both of which are used for radioactive waste immobilization and have assigned log(η) values between 6 and 7.3 with η in Pa s. The discrepancy between the log(η) values assigned here and those values fitted with a VFT function on the values measured for the SG7 and VG98 glasses were within ±14%.

Targeting pleckstrin-2/Akt signaling reduces proliferation in myeloproliferative neoplasm models.

Myeloproliferative neoplasms (MPNs) are characterized by the activated JAK2/STAT pathway. Pleckstrin-2 (Plek2) is a downstream target of the JAK2/STAT5 pathway and is overexpressed in patients with MPNs. We previously revealed that Plek2 plays critical roles in the pathogenesis of JAK2-mutated MPNs. The nonessential roles of Plek2 under physiologic conditions make it an ideal target for MPN therapy. Here, we identified first-in-class Plek2 inhibitors through an in silico high-throughput screening approach and cell-based assays, followed by the synthesis of analogs. Plek2-specific small-molecule inhibitors showed potent inhibitory effects on cell proliferation. Mechanistically, Plek2 interacts with and enhances the activity of Akt through the recruitment of downstream effector proteins. The Plek2-signaling complex also includes Hsp72, which protects Akt from degradation. These functions were blocked by Plek2 inhibitors via their direct binding to the Plek2 dishevelled, Egl-10 and pleckstrin (DEP) domain. The role of Plek2 in activating Akt signaling was further confirmed in vivo using a hematopoietic-specific Pten-knockout mouse model. We next tested Plek2 inhibitors alone or in combination with an Akt inhibitor in various MPN mouse models, which showed significant therapeutic efficacies similar to that seen with the genetic depletion of Plek2. The Plek2 inhibitor was also effective in reducing proliferation of CD34-positive cells from MPN patients. Our studies reveal a Plek2/Akt complex that drives cell proliferation and can be targeted by a class of antiproliferative compounds for MPN therapy.

Measuring accessibility to public services and infrastructure criticality for disasters risk management.

Component criticality analysis of infrastructure systems has traditionally focused on physical networks rather than infrastructure services. As an example, a key objective of transport infrastructure is to ensure mobility and resilient access to public services, including for the population, service providers, and associated supply chains. We introduce a new user-centric measure for estimating infrastructure criticality and urban accessibility to critical public services - particularly healthcare facilities without loss of generality - and the effects of disaster-induced infrastructure disruptions. Accessibility measures include individuals' choices of all services in each sector. The approach is scalable and modular while preserving detailed features necessary for local planning decisions. It relies on open data to simulate various disaster scenarios, including floods, seismic, and compound shocks. We present results for Lima, Peru, and Manila, Philippines, to illustrate how the approach identifies the most affected areas by shocks, underserved populations, and changes in accessibility and critical infrastructure components. We capture the changes in people's choices of health service providers under each scenario. For Lima, we show that the floods of 2020 caused an increase in average access times to all health services from 33 minutes to 48 minutes. We identify specific critical road segments for ensuring access under each scenario. For Manila, we locate the 22% of the population who lost complete access to all higher health services due to flooding of over 15 cm. The approach is used to identify and prioritize targeted measures to strengthen the resilience of critical public services and their supporting infrastructure systems, while putting the population at the center of decision-making.

Frontotemporal Dementia Patient Neurons With Progranulin Deficiency Display Protein Dyshomeostasis.

Haploinsufficiency of progranulin (PGRN) causes frontotemporal dementia (FTD), a devastating neurodegenerative disease with no effective treatment. PGRN is required for efficient proteostasis, as loss of neuronal PGRN results in dysfunctional lysosomes and impaired clearance and cytoplasmic aggregation of TDP-43, a protein involved in neurodegeneration in FTD. These and other events lead to neurodegeneration and neuroinflammation. However, the detailed mechanisms leading to protein dyshomeostasis in PGRN-deficient cells remain unclear. We report here the development of human cell models of FTD with PGRN-deficiency to explore the molecular mechanisms underlying proteostasis breakdown and TDP-43 aggregation in FTD. Neurons differentiated from FTD patient induced pluripotent stem cells (iPSCs) have reduced PGRN levels, and the neurons recapitulate key disease features, including impaired lysosomal function, defective TDP-43 turnover and accumulation, neurodegeneration, and death. Proteomic analysis revealed altered levels of proteins linked to the autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS) in FTD patient neurons, providing new mechanistic insights into the link between PGRN-deficiency and disease pathobiology.

Targetable leukemia dependency on noncanonical PI3Kγ signaling.

Phosphoinositide 3-kinase gamma (PI3Kγ) is implicated as a target to repolarize tumor-associated macrophages and promote anti-tumor immune responses in solid cancers. However, cancer cell-intrinsic roles of PI3Kγ are unclear. Here, by integrating unbiased genome-wide CRISPR interference screening with functional analyses across acute leukemias, we define a selective dependency on the PI3Kγ complex in a high-risk subset that includes myeloid, lymphoid, and dendritic lineages. This dependency is characterized by innate inflammatory signaling and activation of phosphoinositide 3-kinase regulatory subunit 5 ( PIK3R5 ), which encodes a regulatory subunit of PI3Kγ and stabilizes the active enzymatic complex. Mechanistically, we identify p21 (RAC1) activated kinase 1 (PAK1) as a noncanonical substrate of PI3Kγ that mediates this cell-intrinsic dependency independently of Akt kinase. PI3Kγ inhibition dephosphorylates PAK1, activates a transcriptional network of NFκB-related tumor suppressor genes, and impairs mitochondrial oxidative phosphorylation. We find that treatment with the selective PI3Kγ inhibitor eganelisib is effective in leukemias with activated PIK3R5 , either at baseline or by exogenous inflammatory stimulation. Notably, the combination of eganelisib and cytarabine prolongs survival over either agent alone, even in patient-derived leukemia xenografts with low baseline PIK3R5 expression, as residual leukemia cells after cytarabine treatment have elevated G protein-coupled purinergic receptor activity and PAK1 phosphorylation. Taken together, our study reveals a targetable dependency on PI3Kγ/PAK1 signaling that is amenable to near-term evaluation in patients with acute leukemia.

Liver RBFOX2 regulates cholesterol homeostasis via Scarb1 alternative splicing in mice.

RNA alternative splicing (AS) expands the regulatory potential of eukaryotic genomes. The mechanisms regulating liver-specific AS profiles and their contribution to liver function are poorly understood. Here, we identify a key role for the splicing factor RNA-binding Fox protein 2 (RBFOX2) in maintaining cholesterol homeostasis in a lipogenic environment in the liver. Using enhanced individual-nucleotide-resolution ultra-violet cross-linking and immunoprecipitation, we identify physiologically relevant targets of RBFOX2 in mouse liver, including the scavenger receptor class B type I (Scarb1). RBFOX2 function is decreased in the liver in diet-induced obesity, causing a Scarb1 isoform switch and alteration of hepatocyte lipid homeostasis. Our findings demonstrate that specific AS programmes actively maintain liver physiology, and underlie the lipotoxic effects of obesogenic diets when dysregulated. Splice-switching oligonucleotides targeting this network alleviate obesity-induced inflammation in the liver and promote an anti-atherogenic lipoprotein profile in the blood, underscoring the potential of isoform-specific RNA therapeutics for treating metabolism-associated diseases.

From a Lose-Lose to a Win-Win Situation: User-Friendly Biomass Models for Acacia longifolia to Aid Research, Management and Valorisation.

Woody invasive species pose a big threat to ecosystems worldwide. Among them, Acacia longifolia is especially aggressive, fundamentally changing ecosystem structure through massive biomass input. This biomass is rarely harvested for usage; thus, these plants constitute a nuisance for stakeholders who invest time and money for control without monetary return. Simultaneously, there is an increased effort to valorise its biomass, e.g., for compost, growth substrate or as biofuel. However, to incentivise A. longifolia harvest and usage, stakeholders need to be able to estimate what can be obtained from management actions. Thus, the total biomass and its quality (C/N ratio) need to be predicted to perform cost-benefit analyses for usage and determine the level of invasion that has already occurred. Here, we report allometric biomass models for major biomass pools, as well as give an overview of biomass quality. Subsequently, we derive a simplified volume-based model (BM ~ 6.297 + 0.982 × Vol; BM = total dry biomass and Vol = plant volume), which can be applied to remote sensing data or with in situ manual measurements. This toolkit will help local stakeholders, forest managers or municipalities to predict the impact and valorisation potential of this invasive species and could ultimately encourage its management.

Prevalence of individual brain and eye defects potentially related to Zika virus in pregnancy in 22 U.S. states and territories, January 2016 to June 2017.

During the Centers for Disease Control and Prevention's Zika Virus Response, birth defects surveillance programs adapted to monitor birth defects potentially related to Zika virus (ZIKV) infection during pregnancy. Pregnancy outcomes occurring during January 2016 to June 2017 in 22 U.S. states and territories were used to estimate the prevalence of those brain and eye defects potentially related to ZIKV. Jurisdictions were divided into three groups: areas with widespread ZIKV transmission, areas with limited local ZIKV transmission, and areas without local ZIKV transmission. Prevalence estimates for selected brain and eye defects and microcephaly per 10,000 live births were estimated. Prevalence ratios (PRs) and 95% confidence intervals (CIs) were estimated using Poisson regression for areas with widespread and limited ZIKV transmission compared with areas without local ZIKV transmission. Defects with significantly higher prevalence in areas of widespread transmission were pooled, and PRs were calculated by quarter, comparing subsequent quarters to the first quarter (January-March 2016). Nine defects had significantly higher prevalence in areas of widespread transmission. The highest PRs were seen in intracranial calcifications (PR = 12.6, 95% CI [7.4, 21.3]), chorioretinal abnormalities (12.5 [7.1, 22.3]), brainstem abnormalities (9.3 [4.7, 18.4]), and cerebral/cortical atrophy (6.7 [4.2, 10.8]). The PR of the nine pooled defects was significantly higher in three quarters in areas with widespread transmission. The largest difference in prevalence was observed for defects consistently reported in infants with congenital ZIKV infection. Birth defects surveillance programs could consider monitoring a subset of birth defects potentially related to ZIKV in pregnancy.

Proof of concept for the use of trained sniffer dogs to detect osteosarcoma.

Sarcomas are mesenchymal cancers which often show an aggressive behavior and patient survival largely depends on an early detection. In last years, much attention has been given to the fact that cancer patients release specific odorous volatile organic compounds (VOCs) that can be efficiently detected by properly trained sniffer dogs. Here, we have evaluated for the first time the ability of sniffer dogs (n = 2) to detect osteosarcoma cell cultures and patient samples. One of the two dogs was successfully trained to discriminate osteosarcoma patient-derived primary cells from mesenchymal stem/stromal cells (MSCs) obtained from healthy individuals. After the training phase, the dog was able to detect osteosarcoma specific odor cues in a different panel of 6 osteosarcoma cell lines with sensitivity and specificity rates between 95 and 100%. Moreover, the same VOCs were also detected by the sniffer dog in saliva samples from osteosarcoma patients (n = 2) and discriminated from samples from healthy individuals with a similar efficacy. Altogether, these results indicate that there are common odor profiles shared by cultures of osteosarcoma cells and body fluid samples from patients and provide a first proof of concept about the potential of canine odor detection as a non-invasive screening method to detect osteosarcomas.

Identifying possible inaccuracy in reported birth head circumference measurements among infants in the US Zika Pregnancy and Infant Registry.

BACKGROUND: The US Zika Pregnancy and Infant Registry (USZPIR) monitors infants born to mothers with confirmed or possible Zika virus infection during pregnancy. The surveillance case definition for Zika-associated birth defects includes microcephaly based on head circumference (HC). METHODS: We assessed birth and follow-up data from infants with birth HC measurements <3rd percentile and birthweight ≥10th percentile to determine possible misclassification of microcephaly. We developed a schema informed by literature review and expert opinion to identify possible HC measurement inaccuracy using HC growth velocity and longitudinal HC measurements between 2 and 12 months of age. Two or more HC measurements were required for assessment. Inaccuracy in birth HC measurement was suspected if growth velocity was >3 cm/month in the first 3 months or HC was consistently >25th percentile during follow-up. RESULTS: Of 6,799 liveborn infants in USZPIR, 351 (5.2%) had Zika-associated birth defects, of which 111 had birth HC measurements <3rd percentile and birthweight ≥10th percentile. Of 84/111 infants with sufficient follow-up, 38/84 (45%) were classified as having possible inaccuracy of birth HC measurement, 19/84 (23%) had HC ≥3rd percentile on follow-up without meeting criteria for possible inaccuracy, and 27/84 (32%) had continued HC <3rd percentile. After excluding possible inaccuracies, the proportion of infants with Zika-associated birth defects including microcephaly decreased from 5.2% to 4.6%. CONCLUSIONS: About one-third of infants in USZPIR with Zika-associated birth defects had only microcephaly, but indications of possible measurement inaccuracy were common. Implementation of this schema in longitudinal studies can reduce misclassification of microcephaly.

Recurrent SARS-CoV-2 RNA Detection after COVID-19 Illness Onset during Pregnancy.

The Surveillance for Emerging Threats to Mothers and Babies Network conducts longitudinal surveillance of pregnant persons in the United States with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 infection during pregnancy. Of 6,551 infected pregnant persons in this analysis, 142 (2.2%) had positive RNA tests >90 days and up to 416 days after infection.

Zika-Associated Birth Defects Reported in Pregnancies with Laboratory Evidence of Confirmed or Possible Zika Virus Infection - U.S. Zika Pregnancy and Infant Registry, December 1, 2015-March 31, 2018.

Zika virus infection during pregnancy can cause serious birth defects of the brain and eyes, including intracranial calcifications, cerebral or cortical atrophy, chorioretinal abnormalities, and optic nerve abnormalities (1,2). The frequency of these Zika-associated brain and eye defects, based on data from the U.S. Zika Pregnancy and Infant Registry (USZPIR), has been previously reported in aggregate (3,4). This report describes the frequency of individual Zika-associated brain and eye defects among infants from pregnancies with laboratory evidence of confirmed or possible Zika virus infection. Among 6,799 live-born infants in USZPIR born during December 1, 2015-March 31, 2018, 4.6% had any Zika-associated birth defect; in a subgroup of pregnancies with a positive nucleic acid amplification test (NAAT) for Zika virus infection, the percentage was 6.1% of live-born infants. The brain and eye defects most frequently reported included microcephaly, corpus callosum abnormalities, intracranial calcification, abnormal cortical gyral patterns, ventriculomegaly, cerebral or cortical atrophy, chorioretinal abnormalities, and optic nerve abnormalities. Among infants with any Zika-associated birth defect, one third had more than one defect reported. Certain brain and eye defects in an infant might prompt suspicion of prenatal Zika virus infection. These findings can help target surveillance efforts to the most common brain and eye defects associated with Zika virus infection during pregnancy should a Zika virus outbreak reemerge, and might provide a signal to the reemergence of Zika virus, particularly in geographic regions without ongoing comprehensive Zika virus surveillance.

Impacto en el patrón de atención en cirugía de cabeza y cuello y las medidas sanitarias adoptadas durante los primeros 150 días de la era COVID-19 / Impact on the pattern of care in Head and Neck Surgery and the regional and institutional policy changes adopted during the first 150 days of the COVID-19 era

Resumen Introducción: La pandemia COVID-19 generó una reestructuración en la atención quirúrgica mundialmente debido a su alta transmisibilidad y la inherente limitación de los recursos humanos y materiales disponibles. Objetivo: Describir el impacto de la pandemia COVID-19 en el Equipo de Cirugía Cabeza y Cuello del Complejo Asistencial Barros Luco Trudeau (CABL) en su ejecución clínico-quirúrgica y la secuenciación organizada de las medidas sanitarias aplicadas a lo largo del tiempo durante los primeros 150 días de iniciada la pandemia en Chile. Materiales y Método: Realizamos una revisión retrospectiva de los pacientes sometidos a cirugía y/o evaluados ambulatoriamente durante el período COVID-19 comprendido entre el 3 de marzo y el 31 de julio de 2020, comparado con el mismo intervalo de tiempo de 2019. Características clínicas y medidas sanitarias empleadas durante este período fueron sintetizadas. Resultados: Detectamos un descenso del 64% en atención ambulatoria y un descenso del 58% en la carga quirúrgica, comparado con el año 2019. Durante el período COVID-19 de 2020, un total de 61 pacientes fueron sometidos a intervención quirúrgica. La principal indicación de cirugía fue cáncer en un 75,4% (46). No se reportaron pacientes contagiados por COVID-19 en los 14 días siguientes a la hospitalización. Se discuten las consideraciones perioperatorias empleadas y restricciones nacionales/institucionales sanitarias. Conclusión: La crisis sanitaria mundial secundaria al COVID-19 generó una reducción en las atenciones ambulatorias y cirugías realizadas por Equipo de Cabeza y Cuello CABL. A pesar de las restricciones sanitarias, organizamos estratificadamente la atención para preservar la resolución de casos críticos no diferibles en cabeza y cuello.

Introduction: The COVID-19 pandemic generated a restructuring of surgical care worldwide due to the disease's high transmissibility and the inherent limitation of available human and material resources. Aim: The study's aim was to describe the impact of the COVID-19 pandemic on the head and neck surgery team at Complejo Asistencial Barros Luco Trudeau (CABL) in clinical-surgical execution and organization of sanitary sequencing measures implemented over time during the first 150 days after the pandemic started in Chile. Materials and Method: We performed a retrospective review of patients undergoing surgery or outpatient evaluation during the COVID-19 period from 03-03-2020 to 07-31-2020, compared to the same time interval in 2019. Clinical characteristics and sanitary measures used during this period were synthesized. Results: We detected a 64% decrease in outpatient care and a 58% decrease in surgical load from 2019. During the COVID-19 period of 2020, a total of 61 patients underwent surgical intervention. The main indication for surgery was cancer, in 75.4% of patients (46). COVID-19 was not reported in any patients in the 14 days following hospitalization. We discussed the perioperative considerations used and the national/institutional sanitary restrictions. Conclusions: The global health crisis to COVID-19 generated a reduction in outpatient care and surgeries performed by the CABL head and neck team. Despite health restrictions, we organized care stratified to preserve critical head and neck non-deferrable cases.