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Article ; Online: Resuming elective surgical services in times of COVID-19 infection

Raul Coimbra / Sara Edwards / Bruno Cammarota Coimbra / Arnold Tabuenca

Trauma Surgery & Acute Care Open, Vol 5, Iss

2020 Volume 1

Abstract: The consequences of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus have been devastating to the healthcare system.As the positive effects of social distancing, mandatory masking, and societal lockdown on the spread of the disease ... ...

Abstract	The consequences of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus have been devastating to the healthcare system.As the positive effects of social distancing, mandatory masking, and societal lockdown on the spread of the disease and its incidence in the community were documented, societal and financial pressures mounted worldwide, prompting efforts to “re-open” countries, states, communities, businesses, and schools. The same happened with hospital, which had to start developing strategies to resume elective surgery activities. This manuscript describes the pre-requisites as well as the strategies for resuming surgical activity, be it in the outpatient or inpatient setting.
Keywords	Surgery ; RD1-811 ; Medical emergencies. Critical care. Intensive care. First aid ; RC86-88.9 ; covid19
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	BMJ Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Retrievable inferior vena cava filter use in trauma

Raul Coimbra / Todd Constantini

Jornal Vascular Brasileiro, Vol 8, Iss 3, Pp 204-

has the fever broken? Uso de filtro temporário em veia cava inferior em traumas: a febre passou?

2009 Volume 206

Keywords	Surgery ; RD1-811 ; Medicine ; R ; DOAJ:Surgery ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; DOAJ:Cardiovascular
Language	Portuguese
Publishing date	2009-09-01T00:00:00Z
Publisher	Sociedade Brasileira de Angiologia e de Cirurgia Vascular (SBACV)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Counter regulation of ECRG4 gene expression by hypermethylation-dependent inhibition and the Sp1 transcription factor-dependent stimulation of the c2orf40 promoter

Dang, Xitong / Andrew Baird / Brian P. Eliceiri / Raul Coimbra / Xiaorong Zeng

Gene. 2017 Dec. 15, v. 636

2017

Abstract: The human cytokine precursor ECRG4 has been associated with multiple physiological, developmental and pathophysiological processes involving cell proliferation, cell migration, innate immunity, inflammation, cancer progression and metastases. Although ... ...

Abstract	The human cytokine precursor ECRG4 has been associated with multiple physiological, developmental and pathophysiological processes involving cell proliferation, cell migration, innate immunity, inflammation, cancer progression and metastases. Although down-regulation of ECRG4 gene expression has been largely attributed to hypermethylation of CpG islands in the 5’untranslated region of the ECRG4 promoter, the mechanisms that underlie the dynamics of its regulation have never been systematically described. Here we show that the ECRG4 gene is widely expressed in human tissues and report that its core promoter lies between the −780 to +420 base pairs relative to the ATG start codon of the ECRG4 open reading frame. This sequence, which contains several CpG islands, also includes multiple overlapping Sp1 consensus binding sequences and a putative binding site for NF-kB activation. 5′RACE of mRNA derived from human leukocytes shows that ECRG4 transcription initiates from the guanidine at −11 from the initiation ATG of the ECRG4 open reading frame. While there is no canonical TATA- or CAAT-boxes proximal to this translational initiation site, there is a distal TATA-sequence in the 5′UTR. This region was identified as the sequence targeted by hypermethylation because in vitro methylation of plasmids encoding the ECRG4 promoter abolish promoter activity and the treatment of Jurkat cells (which naturally express ECRG4) with the methylation inhibitor 5-AzaC, increases endogenous ECRG4 expression. Because ChIP assays show that Sp1 binds the ECRG4 promoter, that forced Sp1 expression trans-activates the ECRG4 promoter and Sp1 inhibition with mithramycin inhibits ECRG4 expression, we conclude that the dynamic positive and negative regulatory elements controlling ECRG4 expression include a counter regulation between promoter methylation and Sp1 activation.
Keywords	5' untranslated regions ; binding sites ; cell movement ; cell proliferation ; cytokines ; gene expression ; genes ; genomic islands ; guanidines ; humans ; inflammation ; innate immunity ; leukocytes ; metastasis ; methylation ; neoplasms ; open reading frames ; plasmids ; start codon ; transcription factor NF-kappa B ; translation (genetics)
Language	English
Dates of publication	2017-1215
Size	p. 103-111.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	391792-7
ISSN	1879-0038 ; 0378-1119
ISSN (online)	1879-0038
ISSN	0378-1119
DOI	10.1016/j.gene.2017.08.041
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Modulating the Biologic Activity of Mesenteric Lymph after Traumatic Shock Decreases Systemic Inflammation and End Organ Injury.

Simone Langness / Todd W Costantini / Koji Morishita / Brian P Eliceiri / Raul Coimbra

PLoS ONE, Vol 11, Iss 12, p e

2016 Volume 0168322

Abstract: Trauma/hemorrhagic shock (T/HS) causes the release of pro-inflammatory mediators into the mesenteric lymph (ML), triggering a systemic inflammatory response and acute lung injury (ALI). Direct and pharmacologic vagal nerve stimulation prevents gut ... ...

Abstract	Trauma/hemorrhagic shock (T/HS) causes the release of pro-inflammatory mediators into the mesenteric lymph (ML), triggering a systemic inflammatory response and acute lung injury (ALI). Direct and pharmacologic vagal nerve stimulation prevents gut barrier failure and alters the biologic activity of ML after injury. We hypothesize that treatment with a pharmacologic vagal agonist after T/HS would attenuate the biologic activity of ML and prevent ALI.ML was collected from male Sprague-Dawley rats after T/HS, trauma-sham shock (T/SS) or T/HS with administration of the pharmacologic vagal agonist CPSI-121. ML samples from each experimental group were injected into naïve mice to assess biologic activity. Blood samples were analyzed for changes in STAT3 phosphorylation (pSTAT3). Lung injury was characterized by histology, permeability and immune cell recruitment.T/HS lymph injected in naïve mice caused a systemic inflammatory response characterized by hypotension and increased circulating monocyte pSTAT3 activity. Injection of T/HS lymph also resulted in ALI, confirmed by histology, lung permeability and increased recruitment of pulmonary macrophages and neutrophils to lung parenchyma. CPSI-121 attenuated T/HS lymph-induced systemic inflammatory response and ALI with stable hemodynamics and similar monocyte pSTAT3 levels, lung histology, lung permeability and lung immune cell recruitment compared to animals injected with lymph from T/SS.Treatment with CPSI-121 after T/HS attenuated the biologic activity of the ML and decreased ALI. Given the superior clinical feasibility of utilizing a pharmacologic approach to vagal nerve stimulation, CPSI-121 is a potential treatment strategy to limit end organ dysfunction after injury.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Filtro de veia cava

Luiz Guilherme Cintra Vidal Reys / Raul Coimbra / Dale Fortlage

Revista do Colégio Brasileiro de Cirurgiões, Vol 39, Iss 1, Pp 16-

uma década de experiência em um centro de trauma nível I

2012 Volume 21

Abstract: OBJETIVO: Avaliar os dados relativos à utilização de filtro de veia cava na Divisão de Trauma do Centro Médico da UCSD San Diego, CA/EUA. MÉTODOS: Estudo descritivo realizado na Divisão de Trauma visando avaliar a experiência acumulada e a conduta ... ...

Abstract	OBJETIVO: Avaliar os dados relativos à utilização de filtro de veia cava na Divisão de Trauma do Centro Médico da UCSD San Diego, CA/EUA. MÉTODOS: Estudo descritivo realizado na Divisão de Trauma visando avaliar a experiência acumulada e a conduta terapêutica nos doentes atendidos pela equipe da Divisão de Trauma e submetidos à colocação de filtro de veia cava como método de prevenção ou tratamento do TEP no período de janeiro de 1999 a dezembro de 2008. RESULTADOS: O estudo compreendeu 512 doentes, destacando-se o sexo masculino (73%). Quanto à causa do traumatismo predominou o acidente automobilístico, seguido por lesões provocadas por quedas. A relação homem/mulher foi 3:1. A faixa etária mais atingida foi 21 a 40 anos, representando 36% dos doentes. O percentual de filtros de cava profiláticos foi de 82% contra 18% de filtros terapêuticos. O traumatismo craniano foi a principal causa para indicação de filtros profiláticos seguido dos traumas raquimedulares. O índice de TVP pós-filtro foi 11%. CONCLUSÃO: Na presença de contraindicação ao uso de anticoagulantes em doentes vítimas de trauma grave, os filtros de veia cava inferior demonstraram ser uma opção efetiva e segura. Entretanto, deve-se aplicar rigor ao julgamento clínico para todas as indicações, mesmo após o advento de filtros "recuperáveis".
Keywords	Ferimentos e lesões ; Condutas terapêuticas ; Filtros de veia cava ; efeitos adversos ; utilização ; Surgery ; RD1-811 ; Medicine ; R
Language	Portuguese
Publishing date	2012-01-01T00:00:00Z
Publisher	Colégio Brasileiro de Cirurgiões
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Current diagnosis and management of blunt traumatic rupture of the thoracic aorta Estado atual do diagnóstico e tratamento das lesões traumáticas da aorta torácica

Vishal Bansal / Jeanne Lee / Raul Coimbra

Jornal Vascular Brasileiro, Vol 6, Iss 1, Pp 64-

2007 Volume 73

Abstract: The diagnosis and management of aortic lacerations has been gradually improving. Historically, aortic lacerations were a common cause of exsanguination with extremely high mortality rate. However, in modern trauma systems with advanced resuscitation and ... ...

Abstract	The diagnosis and management of aortic lacerations has been gradually improving. Historically, aortic lacerations were a common cause of exsanguination with extremely high mortality rate. However, in modern trauma systems with advanced resuscitation and rapid radiology imaging, the diagnosis of an aortic injury is improving with an emphasis on preventing the progression of intimal flaps and pseudoaneurysms to frank dissection or rupture. Both diagnostic modalities and the paradigm of immediate operative intervention have changed. The evolution of endovascular stenting may play a future role in definitive care. O diagnóstico e tratamento das lesões traumáticas da aorta torácica vêm gradualmente melhorando. Historicamente, as lesões traumáticas da aorta torácica eram causa freqüente de exanguinação, apresentando altas taxas de mortalidade. Por outro lado, após o desenvolvimento de sistemas modernos de atendimento às vítimas de traumatismos, com protocolos avançados de reanimação volêmica e rápida avaliação radiológica, o diagnóstico de lesões da aorta torácica tem melhorado significativamente. A ênfase atual está centrada na prevenção da progressão das lesões intimais menores e pseudo-aneurismas até a dissecção franca ou ruptura aórtica. As modalidades diagnósticas sofreram alterações, bem como o paradigma de intervenção cirúrgica imediata. A evolução de próteses endovasculares poderá desempenhar um importante papel no tratamento definitivo.
Keywords	Trauma torácico ; aorta torácica ; ruptura traumática da aorta torácica ; tratamento endovascular ; endoprótese ; paraplegia ; Thoracic trauma ; thoracic aorta ; thoracic aortic rupture ; endovascular repair ; endoprosthesis ; stent graft ; Surgery ; RD1-811 ; Medicine ; R ; DOAJ:Surgery ; DOAJ:Medicine (General) ; DOAJ:Health Sciences ; Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; DOAJ:Cardiovascular
Language	Portuguese
Publishing date	2007-03-01T00:00:00Z
Publisher	Sociedade Brasileira de Angiologia e de Cirurgia Vascular (SBACV)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Gastric Trichobezoar Causing Intermittent Small Bowel Obstruction

Nicole G. Coufal / Akash P. Kansagra / Jay Doucet / Jeanne Lee / Raul Coimbra / Vishal Bansal

Case Reports in Medicine, Vol

Report of a Case and Review of the Literature

2011 Volume 2011

Abstract: We report the unusual case of a 45-year-old woman who presented with multiple episodes of small bowel obstruction. Initial exploratory lap-roscopy did not reveal an etiology of the obstruction. Subsequent upper endoscopy identified a non-obstructing ... ...

Abstract	We report the unusual case of a 45-year-old woman who presented with multiple episodes of small bowel obstruction. Initial exploratory lap-roscopy did not reveal an etiology of the obstruction. Subsequent upper endoscopy identified a non-obstructing gastric trichobezoar which could not be removed endoscopically but was not thought to be responsible for the small bowel obstruction given its location. One week postoperatively, the patient experienced recurrence of small bowel obstruction. Repeat endoscopy disclosed that the trichobezoar was no longer located in the stomach and upon repeat laparotomy was extracted from the mid-jejunum. In the following 8 months, the patient had no further episodes of small bowel obstruction. Consequently, gastric bezoars should be included in the differential diagnosis of recurrent small bowel obstruction.
Keywords	Medicine ; R
Language	English
Publishing date	2011-01-01T00:00:00Z
Publisher	Hindawi Publishing Corporation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Ecrg4 attenuates the inflammatory proliferative response of mucosal epithelial cells to infection.

Arwa Kurabi / Kwang Pak / Xitong Dang / Raul Coimbra / Brian P Eliceiri / Allen F Ryan / Andrew Baird

PLoS ONE, Vol 8, Iss 4, p e

2013 Volume 61394

Abstract: We report an inverse relationship between expression of the orphan candidate tumor suppressor gene esophageal cancer related gene 4 (Ecrg4), and the mucosal epithelial cell response to infection in the middle ear (ME). First, we found constitutive Ecrg4 ... ...

Abstract	We report an inverse relationship between expression of the orphan candidate tumor suppressor gene esophageal cancer related gene 4 (Ecrg4), and the mucosal epithelial cell response to infection in the middle ear (ME). First, we found constitutive Ecrg4 mRNA expression in normal, quiescent ME mucosa that was confirmed by immunostainning of mucosal epithelial cells and immunoblotting of tissue lysates for the 14 kDa Ecrg4 protein. Upon experimental ME infection, Ecrg4 gene expression rapidly decreased by over 80%, between 3 to 48 hrs, post infection. When explants of this infected mucosa were placed in culture and transduced with an adenovirus (AD) encoding Ecrg4 gene (ADEcrg4), the proliferative and migratory responses of mucosal cells were significantly inhibited. ADEcrg4 transduction of control explants from uninfected MEs had no effect on basal growth and migration. Over-expression of Ecrg4 in vivo, by pre-injecting MEs with ADEcrg4 48 hrs prior to infection, prevented the natural down-regulation of Ecrg4, reduced mucosal proliferation and prevented inflammatory cell infiltration normally observed after infection. Taken together, these data support a hypothesis that Ecrg4 plays a role in coordinating the inflammatory and proliferative response to infection of mucosal epithelium suggesting a possible mechanism for its putative anti-tumor activity.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Enteric glia cells attenuate cytomix-induced intestinal epithelial barrier breakdown.

Gerald A Cheadle / Todd W Costantini / Nicole Lopez / Vishal Bansal / Brian P Eliceiri / Raul Coimbra

PLoS ONE, Vol 8, Iss 7, p e

2013 Volume 69042

Abstract: BACKGROUND: Intestinal barrier failure may lead to systemic inflammation and distant organ injury in patients following severe injury. Enteric glia cells (EGCs) have been shown to play an important role in maintaining gut barrier integrity through ... ...

Abstract	BACKGROUND: Intestinal barrier failure may lead to systemic inflammation and distant organ injury in patients following severe injury. Enteric glia cells (EGCs) have been shown to play an important role in maintaining gut barrier integrity through secretion of S-Nitrosoglutathione (GSNO). We have recently shown than Vagal Nerve Stimulation (VNS) increases EGC activation, which was associated with improved gut barrier integrity. Thus, we sought to further study the mechanism by which EGCs prevent intestinal barrier breakdown utilizing an in vitro model. We postulated that EGCs, through the secretion of GSNO, would improve intestinal barrier function through improved expression and localization of intestinal tight junction proteins. METHODS: Epithelial cells were co-cultured with EGCs or incubated with GSNO and exposed to Cytomix (TNF-α, INF-γ, IL-1β) for 24 hours. Barrier function was assessed by permeability to 4kDa FITC-Dextran. Changes in tight junction proteins ZO-1, occludin, and phospho-MLC (P-MLC) were assessed by immunohistochemistry and immunoblot. KEY RESULTS: Co-culture of Cytomix-stimulated epithelial monolayers with EGCs prevented increases in permeability and improved expression and localization of occludin, ZO-1, and P-MLC. Further, treatment of epithelial monolayers with GSNO also prevented Cytomix-induced increases in permeability and exhibited a similar improvement in expression and localization of occludin, ZO-1, and P-MLC. CONCLUSIONS & INFERENCES: The addition of EGCs, or their secreted mediator GSNO, prevents epithelial barrier failure after injury and improved expression of tight junction proteins. Thus, therapies that increase EGC activation, such as VNS, may be a novel strategy to limit barrier failure in patients following severe injury.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Insights into the regulation of TNF-a production in human mononuclear cells

Jessica Deree / Joilson O. Martins / Heidi Melbostad / William H. Loomis / Raul Coimbra

Clinics, Vol 63, Iss 3, Pp 321-

the effects of non-specific phosphodiesterase inhibition

2008 Volume 328

Abstract: OBJECTIVE: The objective of this study was to determine the effect of nonspecific phosphodiesterase inhibition on transcription factor activation and tumor necrosis factor-alpha (TNF-a) production in lipopolysaccharide (LPS)-stimulated human mononuclear ... ...

Abstract	OBJECTIVE: The objective of this study was to determine the effect of nonspecific phosphodiesterase inhibition on transcription factor activation and tumor necrosis factor-alpha (TNF-a) production in lipopolysaccharide (LPS)-stimulated human mononuclear cells. INTRODUCTION: The production of TNF-a following LPS stimulation is one of the key steps in bacterial sepsis and inflammation. The mechanism by which phosphodiesterase inhibition alters TNF-a production in the presence of LPS remains unclear. METHODS: Human mononuclear cells were stimulated with LPS (1 µg/mL), in the presence and absence of Pentoxifylline (PTX; 20 mM), a nonspecific phosphodiesterase inhibitor. Western blotting of phosphorylated cytoplasmic I-kBa, nuclear factor-kB p65 (NF-kB), and nuclear cAMP-response element binding protein (CREB) was performed. DNA binding of NF-kB and CREB was verified by electrophoretic mobility shift assay. TNF-a levels were determined in the supernatant of stimulated cells in the presence and absence Protein kinase A inhibition by an enzyme-linked immunosorbent assay (ELISA). RESULTS: PTX was demonstrated to significantly reduce cytoplasmic I-kBa phosphorylation, nuclear p65 phosphorylation, and the DNA binding activity of NF-kB. In contrast, PTX markedly enhanced the phosphorylation and DNA binding activity of CREB. Cells concomitantly treated with PTX and LPS secreted similar levels of TNF-a in the presence and absence Protein kinase A inhibition. DISCUSSION: The increased level of cAMP that results from phosphodiesterase inhibition affects cytoplasmic and nuclear events, resulting in the attenuation of NF-kB and the activation of CREB transcriptional DNA binding through pathways that are partially Protein kinase A-independent. CONCLUSION: PTX-mediated phosphodiesterase inhibition occurs partially through a Protein kinase A-independent pathway and may serve as a useful tool in the attenuation of LPS-induced inflammation.
Keywords	Sepsis ; Pentoxifylline ; Cyclic adenosine-3 ; 5-monophosphate (cAMP) ; cAMP-response element binding protein (CREB) ; Nuclear factor-kB (NF-kB) ; Medicine (General) ; R5-920
Subject code	571 ; 630
Language	English
Publishing date	2008-01-01T00:00:00Z
Publisher	Elsevier España
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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