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  1. Article ; Online: FATAL INTRACEREBRAL HEMORRHAGE IN A PATIENT WITH SEVERE COVID-19 INFECTION

    Sanchez Fernandez, Lady / Anis, Karim / Maltseva, Anastasia

    Chest

    2020  Volume 158, Issue 4, Page(s) A835

    Keywords Critical Care and Intensive Care Medicine ; Pulmonary and Respiratory Medicine ; Cardiology and Cardiovascular Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1016/j.chest.2020.08.777
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: REPEATED PRONATION IN A MORBIDLY OBESE PATIENT OVERCOME BY A SEVERE COVID-19 INFECTION

    Fernandez, Lady Sanchez / Anis, Karim / Maltseva, Anastasia

    Chest

    2020  Volume 158, Issue 4, Page(s) A2575

    Keywords Critical Care and Intensive Care Medicine ; Pulmonary and Respiratory Medicine ; Cardiology and Cardiovascular Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 1032552-9
    ISSN 1931-3543 ; 0012-3692
    ISSN (online) 1931-3543
    ISSN 0012-3692
    DOI 10.1016/j.chest.2020.09.171
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Long-term outcomes after liver transplantation in the Hispanic population.

    Ochoa-Allemant, Pedro / Ezaz, Ghideon / Trivedi, Hirsh D / Sanchez-Fernandez, Lady / Bonder, Alan

    Liver international : official journal of the International Association for the Study of the Liver

    2019  Volume 40, Issue 2, Page(s) 437–446

    Abstract: Background & aims: Racial/ethnic disparities in liver transplantation (LT) are well-recognized. Although Hispanics represent the largest and youngest minority group in the United States, limited data exist on long-term outcomes. We aimed to investigate ... ...

    Abstract Background & aims: Racial/ethnic disparities in liver transplantation (LT) are well-recognized. Although Hispanics represent the largest and youngest minority group in the United States, limited data exist on long-term outcomes. We aimed to investigate long-term post-liver transplant outcomes in Hispanic patients and identify potential disparities compared to a baseline demographic of non-Hispanic white patients.
    Methods: We performed a retrospective cohort study of first-time liver transplant recipients using the United Network for Organ Sharing database from 2002 to 2013, with follow-up through 2018. The primary outcomes of interest were overall patient and graft survival after LT.
    Results: 45 767 patients underwent LT (85.0% non-Hispanic white, 15.0% Hispanic). Hispanics had lower socioeconomic status, higher prevalence of pretransplant comorbidities and more severe liver disease compared to non-Hispanic whites. Hispanics had similar patient (76.6% vs 75.6%; P = .12) and graft (71.7% vs 70.8%; P = .28) survival at 5 years and significantly better patient (62.9% vs 59.7%; P < .001) and graft (58.6% vs 55.6%; P = .002) survival at 10 years. In multivariable analysis, Hispanics had lower associated all-cause mortality (HR 0.86, 95% CI, 0.82-0.91; P < .001) and graft failure (HR 0.89, 95% CI, 0.85-0.93; P < .001) compared to non-Hispanic whites. In etiology-specific subanalysis, Hispanics transplanted for ALD, NASH and HCV had lower all-cause mortality compared to non-Hispanic whites.
    Conclusions: Hispanics have similar or better long-term post-LT outcomes compared to non-Hispanic whites despite a worse pretransplant risk factor profile. Further research is needed to clarify if this survival advantage reflects uncaptured protective factors or more stringent transplant selection in the Hispanic population.
    MeSH term(s) Ethnicity ; Hispanic or Latino ; Humans ; Liver Transplantation ; Racial Groups ; Retrospective Studies ; Risk Factors ; United States/epidemiology
    Language English
    Publishing date 2019-09-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2102783-3
    ISSN 1478-3231 ; 1478-3223
    ISSN (online) 1478-3231
    ISSN 1478-3223
    DOI 10.1111/liv.14248
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  4. Article ; Online: Maltodextrin-induced intestinal injury in a neonatal mouse model.

    Singh, Pratibha / Sanchez-Fernandez, Lady Leidy / Ramiro-Cortijo, David / Ochoa-Allemant, Pedro / Perides, George / Liu, Yan / Medina-Morales, Esli / Yakah, William / Freedman, Steven D / Martin, Camilia R

    Disease models & mechanisms

    2020  Volume 13, Issue 8

    Abstract: Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of ...

    Abstract Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of this study was to test in neonatal mice the effect of maltodextrin, a complex carbohydrate, on the risk of intestinal injury. The goal was to develop a robust and highly reproducible murine model of intestinal injury that allows insight into the pathogenesis and therapeutic interventions of nutrient-driven intestinal injury. Five- to 6-day-old C57BL/6 mice were assigned to the following groups: dam fed (D); D+hypoxia+
    MeSH term(s) Animals ; Animals, Newborn ; Cytokines/metabolism ; Disease Models, Animal ; Enterocolitis, Necrotizing/chemically induced ; Enterocolitis, Necrotizing/metabolism ; Enterocolitis, Necrotizing/microbiology ; Enterocolitis, Necrotizing/pathology ; Goblet Cells/metabolism ; Goblet Cells/microbiology ; Goblet Cells/pathology ; Hypoxia/complications ; Inflammation Mediators/metabolism ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/microbiology ; Intestinal Mucosa/pathology ; Intestine, Small/metabolism ; Intestine, Small/microbiology ; Intestine, Small/pathology ; Klebsiella pneumoniae/pathogenicity ; Mice, Inbred C57BL ; Microvilli/pathology ; Mucin-2/metabolism ; Permeability ; Polysaccharides ; Tight Junction Proteins/metabolism
    Chemical Substances Cytokines ; Inflammation Mediators ; Muc2 protein, mouse ; Mucin-2 ; Polysaccharides ; Tight Junction Proteins ; maltodextrin (7CVR7L4A2D)
    Language English
    Publishing date 2020-08-27
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.044776
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  5. Article ; Online: Maltodextrin-induced intestinal injury in a neonatal mouse model

    Pratibha Singh / Lady Leidy Sanchez-Fernandez / David Ramiro-Cortijo / Pedro Ochoa-Allemant / George Perides / Yan Liu / Esli Medina-Morales / William Yakah / Steven D. Freedman / Camilia R. Martin

    Disease Models & Mechanisms, Vol 13, Iss

    2020  Volume 8

    Abstract: Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of ...

    Abstract Prematurity and enteral feedings are major risk factors for intestinal injury leading to necrotizing enterocolitis (NEC). An immature digestive system can lead to maldigestion of macronutrients and increased vulnerability to intestinal injury. The aim of this study was to test in neonatal mice the effect of maltodextrin, a complex carbohydrate, on the risk of intestinal injury. The goal was to develop a robust and highly reproducible murine model of intestinal injury that allows insight into the pathogenesis and therapeutic interventions of nutrient-driven intestinal injury. Five- to 6-day-old C57BL/6 mice were assigned to the following groups: dam fed (D); D+hypoxia+Klebsiella pneumoniae; maltodextrin-dominant human infant formula (M) only; M+hypoxia; and M+hypoxia+K. pneumoniae. The mice in all M groups were gavage fed five times a day for 4 days. Mice were exposed to hypoxia twice a day for 10 min prior to the first and last feedings, and K. pneumoniae was added to feedings as per group assignment. Mice in all M groups demonstrated reduced body weight, increased small intestinal dilatation and increased intestinal injury scores. Maltodextrin-dominant infant formula with hypoxia led to intestinal injury in neonatal mice accompanied by loss of villi, increased MUC2 production, altered expression of tight junction proteins, enhanced intestinal permeability, increased cell death and higher levels of intestinal inflammatory mediators. This robust and highly reproducible model allows for further interrogation of the effects of nutrients on pathogenic factors leading to intestinal injury and NEC in preterm infants. This article has an associated First Person interview with the first author of the paper.
    Keywords intestinal injury ; maltodextrin ; necrotizing enterocolitis ; neonatal mouse model ; Medicine ; R ; Pathology ; RB1-214
    Subject code 610
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher The Company of Biologists
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Generation of one iPSC line (IMEDEAi006-A) from an early-onset familial Alzheimer's Disease (fAD) patient carrying the E280A mutation in the PSEN1 gene.

    Vallejo-Diez, Sara / Fleischer, Aarne / Martín-Fernández, Jose María / Sánchez-Gilabert, Almudena / Castresana, Mónica / Aguillón, David / Villegas, Andrés / Mastronardi, Claudio A / Espinosa, Lady G / Arcos-Burgos, Mauricio / Del Pozo, Ángel / Herrán, Enara / Gainza, Eusebio / Isaza-Ruget, Mario / Lopera, Francisco / Bachiller, Daniel

    Stem cell research

    2019  Volume 37, Page(s) 101440

    Abstract: The mutation E280A in PSEN1 (presenilin-1) is the most common cause of early-onset familial Alzheimer's Disease (fAD). It presents autosomal dominant inheritance and frequently leads to the manifestation of the disease in relatively young individuals. ... ...

    Abstract The mutation E280A in PSEN1 (presenilin-1) is the most common cause of early-onset familial Alzheimer's Disease (fAD). It presents autosomal dominant inheritance and frequently leads to the manifestation of the disease in relatively young individuals. Here we report the generation of one PSEN1 E280A iPSC line derived from an early-onset patient. OriP/EBNA1-based episomal plasmids containing OCT3/4, SOX2, KLF4, L-MYC, LIN28, BCL-xL and shp53 were used to reprogram oral mucosa fibroblasts. The iPSC line generated has normal karyotype, carry the E280A mutation, is free of plasmid integration, express high levels of pluripotency markers and can differentiate into all three germ layers.
    MeSH term(s) Age of Onset ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Cell Differentiation ; Cells, Cultured ; Cellular Reprogramming ; Female ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Heterozygote ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/pathology ; Middle Aged ; Mutation ; Phenotype ; Presenilin-1/genetics
    Chemical Substances PSEN1 protein, human ; Presenilin-1
    Language English
    Publishing date 2019-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1876-7753
    ISSN (online) 1876-7753
    DOI 10.1016/j.scr.2019.101440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Generation of one iPSC line (IMEDEAi006-A) from an early-onset familial Alzheimer's Disease (fAD) patient carrying the E280A mutation in the PSEN1 gene

    Sara Vallejo-Diez / Aarne Fleischer / Jose María Martín-Fernández / Almudena Sánchez-Gilabert / Mónica Castresana / David Aguillón / Andrés Villegas / Claudio A. Mastronardi / Lady G. Espinosa / Mauricio Arcos-Burgos / Ángel del Pozo / Enara Herrán / Eusebio Gainza / Mario Isaza-Ruget / Francisco Lopera / Daniel Bachiller

    Stem Cell Research, Vol 37, Iss , Pp - (2019)

    2019  

    Abstract: The mutation E280A in PSEN1 (presenilin-1) is the most common cause of early-onset familial Alzheimer's Disease (fAD). It presents autosomal dominant inheritance and frequently leads to the manifestation of the disease in relatively young individuals. ... ...

    Abstract The mutation E280A in PSEN1 (presenilin-1) is the most common cause of early-onset familial Alzheimer's Disease (fAD). It presents autosomal dominant inheritance and frequently leads to the manifestation of the disease in relatively young individuals. Here we report the generation of one PSEN1 E280A iPSC line derived from an early-onset patient. OriP/EBNA1-based episomal plasmids containing OCT3/4, SOX2, KLF4, L-MYC, LIN28, BCL-xL and shp53 were used to reprogram oral mucosa fibroblasts. The iPSC line generated has normal karyotype, carry the E280A mutation, is free of plasmid integration, express high levels of pluripotency markers and can differentiate into all three germ layers.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2019-05-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Early Enteral Administration of a Complex Lipid Emulsion Supplement Prevents Postnatal Deficits in Docosahexaenoic and Arachidonic Acids and Increases Tissue Accretion of Lipophilic Nutrients in Preterm Piglets.

    Akinsulire, Olajumoke / Perides, George / Anez-Bustillos, Lorenzo / Cluette-Brown, Joanne / Nedder, Arthur / Pollack, Elizabeth / Singh, Pratibha / Liu, Yan / Sanchez-Fernandez, Lady Leidy / Obregon, Evelyn / Bicak, Ece / Kiefer, Savanna / Yakah, William / Gutierrez, Hilda V / Dao, Duy T / Vurma, Mustafa / Ehling, Stefan / Gordon, Douglas / DeMichele, Stephen /
    Freedman, Steven D / Martin, Camilia R

    JPEN. Journal of parenteral and enteral nutrition

    2019  Volume 44, Issue 1, Page(s) 69–79

    Abstract: Background: Preterm delivery and current nutrition strategies result in deficiencies of critical long-chain fatty acids (FAs) and lipophilic nutrients, increasing the risk of preterm morbidities. We sought to determine the efficacy of preventing ... ...

    Abstract Background: Preterm delivery and current nutrition strategies result in deficiencies of critical long-chain fatty acids (FAs) and lipophilic nutrients, increasing the risk of preterm morbidities. We sought to determine the efficacy of preventing postnatal deficits in FAs and lipophilic nutrients using an enteral concentrated lipid supplement in preterm piglets.
    Methods: Preterm piglets were fed a baseline diet devoid of arachidonic acid (AA) and docosahexaenoic acid (DHA) and randomized to enteral supplementation as follows: (1) Intralipid (IL), (2) complex lipid supplement 1 (CLS1) with an AA:DHA ratio of 0.25, or (3) CLS2 with an AA:DHA ratio of 1.2. On day 8, plasma and tissue levels of FAs and lipophilic nutrients were measured and ileum histology performed.
    Results: Plasma DHA levels decreased in the IL group by day 2. In contrast, DHA increased by day 2 compared with birth levels in both CLS1 and CLS2 groups. The IL and CLS1 groups demonstrated a continued decline in AA levels during the 8-day protocol, whereas AA levels in the CLS2 group on day 8 were comparable to birth levels. Preserving AA levels in the CLS2 group was associated with greater ileal villus height and muscular layer thickness. Lipophilic nutrients were effectively absorbed in plasma and tissues.
    Conclusions: Enteral administration of CLS1 and CLS2 demonstrated similar increases in DHA levels compared with birth levels. Only CLS2 maintained AA birth levels. Providing a concentrated complex lipid emulsion with an AA:DHA ratio > 1 is important in preventing postnatal AA deficits.
    MeSH term(s) Animal Feed ; Animal Nutritional Physiological Phenomena ; Animals ; Animals, Newborn ; Arachidonic Acids/deficiency ; Arachidonic Acids/metabolism ; Dietary Supplements ; Docosahexaenoic Acids/deficiency ; Docosahexaenoic Acids/metabolism ; Emulsions/administration & dosage ; Enteral Nutrition/veterinary ; Nutrients ; Random Allocation ; Swine
    Chemical Substances Arachidonic Acids ; Emulsions ; Docosahexaenoic Acids (25167-62-8)
    Language English
    Publishing date 2019-08-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 800861-9
    ISSN 1941-2444 ; 0148-6071
    ISSN (online) 1941-2444
    ISSN 0148-6071
    DOI 10.1002/jpen.1697
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  9. Article: Fatal Intracerebral Hemorrhage in a Patient with Severe Covid-19 Infection

    Sanchez Fernandez, L. / Anis, K. / Maltseva, A.

    Chest

    Abstract: ... source=Web Response No relevant relationships by Lady Sanchez Fernandez, source=Web Response ...

    Abstract SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Stroke like lesions has been documented in COVID-19 patients Although the exact stroke-incidence is unknown, it was reported to be around 5 % in a hospitalized cohort in Wuhan and 1 1 % in a study in New York City CASE PRESENTATION: A 73-year-old male with a past medical history of hypertension and hyperlipidemia presents to ER with fever, cough, myalgia, increasing shortness of breath, and confusion for one day His daughter is known COVID-19 positive The patient was noted to be febrile, tachypneic, and hypoxic to 90% at room air Chest X-ray showed bilateral infiltrates and the COVID-19 test was positive The patient was immediately intubated due to his significant acute respiratory distress Inflammatory markers were significantly elevated: Troponin T: 5 86, Lactate dehydrogenase: 542, CRP: 350 mg/l, Ferritin: 1878, D-dimer: >20, fibrinogen: 1094, Total Creatinine kinase: 2260 and creatinine: 5 7 His course was complicated by septic shock requiring three vasopressors;acute kidney injury requiring hemodialysis;Enterococcus Faecalis bacteremia treated with Ampicillin, and Klebsiella pneumonia sensitive to ceftriaxone EKGs showed new onset of atrial fibrillation without ST changes Echocardiogram showed normal ejection fraction without wall motion abnormalities His significant troponin elevation was likely due to myonecrosis related to COVID-19 infection and he was started on heparin drip The patient respiratory status continued to improve however he remained obtunded Head CT showed acute right frontal hemorrhage and focal hyperdense foci in the left frontal lobe and basal ganglia Brain MRI showed a 2 8 x 2 4 cm lesion situated in the right sub-frontal region with appearances of abscess versus necrotic tissue and extensive bilateral scattered deep white matter infarcts Neurosurgery didn’t recommend any intervention due to poor prognosis After 27 days of intubation, the family requested comfort measures, and the patient was terminally extubated DISCUSSION: ‘Sepsis-induced coagulopathy’ is one of the hallmarks of severe COVID-19, usually manifests as a high D-dimer and elevated fibrinogen It induces a systemic inflammatory response with endothelial dysfunction and microthrombosis predisposing to acute strokes The risk of developing a cerebrovascular disease is multifactorial and includes cardiovascular risk factors, old age, and severe COVID-19 disease manifestations with sings of hypercoagulability In this case, the stroke like-lesions could be related to septic emboli with the conversation to hemorrhage due to heparin use in the setting of severe COVID-19 infection CONCLUSIONS: Ischemic and hemorrhagic stroke has been reported as a complication of severe COVID-19 infection The definite mechanism is unknown, but these findings can indicate poor prognosis with potential neurological sequelae and increased mortality Reference #1: https://www ncbi nlm nih gov/pmc/articles/PMC7202903/ Reference #2: https://www ncbi nlm nih gov/pmc/articles/PMC7236667/ Reference #3: https://jamanetwork com/journals/jamaneurology/fullarticle/2766766 DISCLOSURES: No relevant relationships by Karim Anis, source=Web Response No relevant relationships by Anastasia Maltseva, source=Web Response No relevant relationships by Lady Sanchez Fernandez, source=Web Response
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #866564
    Database COVID19

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