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1.
Int J Surg Pathol ; : 10668969241260207, 2024 Jul 21.
Artigo em Inglês | MEDLINE | ID: mdl-39034536

RESUMO

Introduction. Sarcina organisms are rare, gram-positive, sugar-fermenting cocci, identifiable in tissues only by histologic examination or molecular testing. Since its discovery, the pathogenicity and relevance of Sarcina in the human gastrointestinal tract has remained ill-defined. A recent literature review of 66 reported examples demonstrated the potential for severe complications such as emphysematous gastritis and gastric perforation. In pediatrics, colonization is associated with mucosal alterations and/or gastrointestinal dysmotility/obstruction with variable outcomes, including death secondary to gastric perforation. Yet, the features of Sarcina colonization within the gastrointestinal tract of adolescents are poorly understood and rarely reported. Methods. We present the gastrointestinal histopathological findings and the complete history of 4 pediatric patients with Sarcina colonization at our institution. Additionally a literature review with focus in the keywords "Sarcina" and "gastrointestinal' was performed, and the clinical and histopathological features of all previously reported examples of Sarcina in the gastrointestinal tract of pediatric patients were summarized. Results. All 4 patients had delayed gastric emptying, 3 of them due to neurologic disease, and one with pyloric obstruction due to duodenal ulceration with Helicobacter gastritis. In the 3 patients with available esophageal biopsies, it was associated to esophagitis with increased intraepithelial eosinophils. Conclusion. The potential pathogenicity of Sarcina colonization in the gastrointestinal tract of pediatric patients needs to be reevaluated. Due to potential serious complications, the identification of these organisms in the gastrointestinal tract sample should be reported and warrants further evaluation for possible gastrointestinal dysmotility or other mucosal alterations.

2.
Urology ; 187: 82-85, 2024 May.
Artigo em Inglês | MEDLINE | ID: mdl-38401809

RESUMO

Neuroblastoma accounts for a significant portion of childhood tumors and can present in a variety of ways. Pelvic neuroblastoma has been reported but few cases exist of neuroblastoma invading or originating from the bladder or prostate. We present a 4-year-old patient with pelvic neuroblastoma arising from the prostate and describe the medical and surgical management of this challenging case. While pelvic neuroblastoma may have an improved prognosis, this case demonstrates the challenging surgical decisions that accompany these patients to maintain quality of life while balancing oncologic efficacy of treatment.


Assuntos
Neuroblastoma , Neoplasias da Próstata , Humanos , Neuroblastoma/cirurgia , Neuroblastoma/diagnóstico , Neuroblastoma/patologia , Masculino , Neoplasias da Próstata/patologia , Neoplasias da Próstata/cirurgia , Pré-Escolar , Neoplasias Pélvicas/cirurgia , Neoplasias Pélvicas/patologia , Neoplasias Pélvicas/diagnóstico
3.
J Pediatr Surg ; 59(3): 451-458, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-37865575

RESUMO

BACKGROUND: Infants with congenital diaphragmatic hernia (CDH) experience high morbidity and mortality due to pulmonary arterial hypertension and hypoplasia. Mechanical ventilation is a central component of CDH management. Our objective was to evaluate the impact of a standardized clinical practice guideline (implemented in January 2012) on ventilator management for infants with CDH, and associate management changes with short-term outcomes, specifically extracorporeal membrane oxygenation (ECMO) utilization and survival to discharge. METHODS: We conducted a retrospective pre-post study of 103 CDH infants admitted from January 2007-July 2021, divided pre- (n = 40) and post-guideline (n = 63). Clinical outcomes, ventilator settings, and blood gas values in the first 7 days of mechanical ventilation were compared between the pre- and post-guideline cohorts. RESULTS: Post-guideline, ECMO utilization decreased (11% vs 38%, p = 0.001) and survival to discharge improved (92% vs 68%, p = 0.001). More post-guideline patients remained on conventional mechanical ventilation without need for escalation to high-frequency ventilation or ECMO, and had higher pressures and PaCO2 with lower FiO2 and PaO2 (p < 0.05). CONCLUSIONS: Standardized ventilator management optimizing pressures for adequate lung expansion and minimizing oxygen toxicity improves outcomes for infants with CDH. LEVEL OF EVIDENCE: III.


Assuntos
Hérnias Diafragmáticas Congênitas , Humanos , Hérnias Diafragmáticas Congênitas/terapia , Estudos Retrospectivos , Pulmão/anormalidades , Respiração Artificial , Ventiladores Mecânicos
4.
J Pediatr Surg ; 58(3): 389-396, 2023 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-35965150

RESUMO

BACKGROUND: Infants with congenital diaphragmatic hernia (CDH) are at high risk of death, even despite extracorporeal membrane oxygenation (ECMO) support. In January 2012 we implemented a standardized clinical practice guideline (CPG) to manage infants with CDH. We hypothesized that infants with CDH managed with CPG had better clinical outcomes, less ECMO utilization, and increased survival to discharge. METHODS: We conducted a retrospective pre-post study of infants with CDH admitted between January 2007 and July 2021 (n = 133). Patients were divided into Cohort 1, pre-CPG (January 2007 to December 2011, n = 54), and Cohort 2, post-CPG (January 2012 to July 2021, n = 79). RESULTS: More patients in Cohort 1 were small for gestational age than in Cohort 2. No other patient demographics were different between cohorts. Cohort 2 had significantly lower ECMO utilization as compared to Cohort 1 (18% vs 50%, p<0.001). Cohort 2 had significantly higher survival to discharge compared to Cohort 1 (85% vs 57%, p<0.001). Survival for ECMO-treated patients in Cohort 2 was significantly higher than in Cohort 1 (71% vs 26%, p = 0.005). In Cohort 1, 70% of the non-survivors were repaired, of which 81% were repaired on ECMO. In Cohort 2, 8% of the non-survivors were repaired, none on ECMO. Only 3% in Cohort 2 were discharged with pulmonary hypertension medication. CONCLUSIONS: A standardized CPG to manage patients with CDH decreased ECMO utilization and improved clinical outcomes including survival to discharge. Refinement of management strategies, implementation of new interventions, and meticulous care can improve outcomes in patients with CDH.


Assuntos
Hérnias Diafragmáticas Congênitas , Hipertensão Pulmonar , Doenças do Recém-Nascido , Recém-Nascido , Humanos , Lactente , Hérnias Diafragmáticas Congênitas/cirurgia , Estudos Retrospectivos , Taxa de Sobrevida
5.
Oxid Med Cell Longev ; 2019: 4745067, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31772705

RESUMO

BACKGROUND: Organ injury and dysfunction in sepsis accounts for significant morbidity and mortality. Adaptive cellular responses in the setting of sepsis prevent injury and allow for organ recovery. We and others have shown that part of the adaptive response includes regulation of cellular respiration and maintenance of a healthy mitochondrial population. Herein, we hypothesized that endotoxin-induced changes in hepatocyte mitochondrial respiration and homeostasis are regulated by an inducible nitric oxide synthase/nitric oxide (iNOS/NO)-mitochondrial reactive oxygen species (mtROS) signaling axis, involving activation of the NRF2 signaling pathway. METHODS: Wild-type (C57Bl/6) or iNos-/- male mice were subjected to intraperitoneal lipopolysaccharide (LPS) injections to simulate endotoxemia. Individual mice were randomized to treatment with NO-releasing agent DPTA-NONOate, mtROS scavenger MitoTEMPO, or vehicle controls. Other mice were treated with scramble or Nrf2-specific siRNA via tail vein injection. Primary murine hepatocytes were utilized for in vitro studies with or without LPS stimulation. Oxygen consumption rates were measured to establish mitochondrial respiratory parameters. Western blotting, confocal microscopy with immunocytochemistry, and rtPCR were performed for analysis of iNOS as well as markers of both autophagy and mitochondrial biogenesis. RESULTS: LPS treatment inhibited aerobic respiration in vitro in wild-type but not iNos -/- cells. Experimental endotoxemia in vivo or in vitro induced iNOS protein and mtROS production. However, induction of mtROS was dependent on iNOS expression. Furthermore, LPS-induced hepatic autophagy/mitophagy and mitochondrial biogenesis were significantly attenuated in iNos -/- mice or cells with NO or mtROS scavenging. These responses were rescued in iNos -/- mice via delivery of NO both in vivo and in vitro. Conclusions. These data suggest that regulation of mitochondrial quality control following hepatocyte LPS exposure is dependent at least in part on a NO-mtROS signaling network. Further investigation to identify specific agents that modulate this process may facilitate the prevention of organ injury in sepsis.


Assuntos
Endotoxinas/metabolismo , Hepatócitos/metabolismo , Mitocôndrias/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Animais , Humanos , Masculino , Camundongos , Controle de Qualidade , Espécies Reativas de Oxigênio , Transdução de Sinais
6.
Oxid Med Cell Longev ; 2018: 2021645, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29849867

RESUMO

Hypoxia occurs as a part of multiple disease states, including hemorrhagic shock. Adaptive responses occur within the cell to limit the consequences of hypoxia. This includes changes in mitochondrial respiration, stress-induced cell signaling, and gene expression that is regulated by hypoxia inducible factor-1α (HIF-1α). Heme oxygenase-2 (HO-2) has been shown to be involved in oxygen sensing in several cell types. The purpose of these experiments was to test the hypothesis that HO-2 is a critical regulator of mitochondrial oxygen consumption and reactive oxygen species (ROS) production to influence hypoxia-adaptive responses such as HIF-1α protein levels and JNK signaling. Methods and Results. In vitro studies were performed in primary mouse hepatocytes. HO-2, but not HO-1, was expressed in mitochondria at baseline. Decreased oxygen consumption and increased mitochondrial ROS production in response to hypoxia were dependent upon HO-2 expression. HO-2 expression regulated HIF-1α and JNK signaling in a mitochondrial ROS-dependent manner. Furthermore, knockdown of HO-2 led to increased organ damage, systemic inflammation, tissue hypoxia, and shock in a murine model of hemorrhage and resuscitation. Conclusion. HO-2 signaling plays a role in hypoxic signaling and hemorrhagic shock. This pathway may be able to be harnessed for therapeutic effects.


Assuntos
Hipóxia Celular/fisiologia , Heme Oxigenase (Desciclizante)/metabolismo , Hepatócitos/metabolismo , Mitocôndrias Hepáticas/metabolismo , Animais , Técnicas de Silenciamento de Genes , Heme Oxigenase (Desciclizante)/antagonistas & inibidores , Hepatócitos/enzimologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Sistema de Sinalização das MAP Quinases , Camundongos , Camundongos Endogâmicos C57BL , Oxigênio/metabolismo , Consumo de Oxigênio , Choque Hemorrágico/enzimologia , Choque Hemorrágico/metabolismo
7.
Crit Care Med ; 46(8): e779-e787, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29727369

RESUMO

OBJECTIVES: The physiology of nearly all mammalian organisms are entrained by light and exhibit circadian rhythm. The data derived from animal studies show that light influences immunity, and these neurophysiologic pathways are maximally entrained by the blue spectrum. Here, we hypothesize that bright blue light reduces acute kidney injury by comparison with either bright red or standard, white fluorescent light in mice subjected to sepsis. To further translational relevance, we performed a pilot clinical trial of blue light therapy in human subjects with appendicitis. DESIGN: Laboratory animal research, pilot human feasibility trial. SETTING: University basic science laboratory and tertiary care hospital. SUBJECTS: Male C57BL/6J mice, adult (> 17 yr) patients with acute appendicitis. INTERVENTIONS: Mice underwent cecal ligation and puncture and were randomly assigned to a 24-hour photoperiod of bright blue, bright red, or ambient white fluorescent light. Subjects with appendicitis were randomized to receive postoperatively standard care or standard care plus high-illuminance blue light. MEASUREMENTS AND MAIN RESULTS: Exposure to bright blue light enhanced bacterial clearance from the peritoneum, reduced bacteremia and systemic inflammation, and attenuated the degree of acute kidney injury. The mechanism involved an elevation in cholinergic tone that augmented tissue expression of the nuclear orphan receptor REV-ERBα and occurred independent of alterations in melatonin or corticosterone concentrations. Clinically, exposure to blue light after appendectomy was feasible and reduced serum interleukin-6 and interleukin-10 concentrations. CONCLUSIONS: Modifying the spectrum of light may offer therapeutic utility in sepsis.


Assuntos
Injúria Renal Aguda/etiologia , Injúria Renal Aguda/terapia , Apendicite/terapia , Fototerapia/métodos , Sepse/complicações , Adulto , Animais , Citocinas/biossíntese , Feminino , Humanos , Hidrocortisona/sangue , Mediadores da Inflamação/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Técnicas Microbiológicas , Pessoa de Meia-Idade , Escores de Disfunção Orgânica , Distribuição Aleatória
8.
Surg Infect (Larchmt) ; 18(4): 447-450, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28448197

RESUMO

Surgical site infection (SSI) contributes significantly to surgical morbidity. Patient factors and operative factors contribute to the risk of development of SSI. This review focuses on understanding operative characteristics that are associated with an increased risk of SSI. Much attention has been given to protocol care to reduce SSI, such as hair removal, skin preparation, and pre-operative antibiotic agents. Even with this, the appropriate antibiotic and re-dosing regimens often remain a challenge. Other operative factors such as blood loss/transfusion, emergency/urgent cases, duration of the operation, type of anesthesia, and resident involvement are also potentially modifiable to reduce the risk of SSI. Data are reviewed to highlight the increased risk associated with such factors. Strategies to reduce risk, such as operative care bundles, have significant promise to reduce the incidence of SSI for any given procedure.


Assuntos
Infecção da Ferida Cirúrgica , Humanos , Infecção da Ferida Cirúrgica/classificação , Infecção da Ferida Cirúrgica/epidemiologia , Infecção da Ferida Cirúrgica/prevenção & controle , Infecção da Ferida Cirúrgica/terapia
10.
J Steroid Biochem Mol Biol ; 104(1-2): 11-21, 2007 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-17197171

RESUMO

The role of estrogen in the motility and invasion of breast cancer cells is controversial. Although estrogen receptor (ER)-positive breast tumors are considered less aggressive and more differentiated they still undergo metastasis. In many types of epithelial cancers, the ability to undergo metastasis has been associated with a loss of epithelial features and acquisition of mesenchymal properties leading to migration of individual cells, a process known as epithelial-to-mesenchymal transition (EMT). In this report, we show that a subset of ER-positive breast cancer cells can acquire mesenchymal-like features and motility in a reversible manner. In MCF-7 breast cancer cells estrogen-promoted acquisition of mesenchymal-like features while antiestrogens, such as tamoxifen, prevented this transition. Moreover, pharmacological inhibition of Src family kinases decreased the ability of estrogen to promote epithelial-to-mesenchymal-like transition. In addition to mesenchymal-like motility, a subset of estrogen-treated cells also moved as cell clusters (collective motility). While membrane localization of E-cadherin/beta-catenin was decreased in fibroblast-like cells, enhanced levels of E-cadherin/beta-catenin were detected in motile cell clusters. Thus, during tumor progression, estrogen may foster motility and invasion of ER-positive breast cancer by promoting simultaneously reversible EMT-like changes and collective motility. These studies suggest that antiestrogen therapy and Src family kinase inhibitors may decrease development of metastases in ER-positive breast cancer by blocking estrogen-dependent migration of human breast cancer cells.


Assuntos
Neoplasias da Mama/patologia , Movimento Celular/efeitos dos fármacos , Epitélio/efeitos dos fármacos , Estrogênios/farmacologia , Mesoderma/efeitos dos fármacos , Antineoplásicos Hormonais/farmacologia , Western Blotting , Caderinas/metabolismo , Adesão Celular , Epitélio/metabolismo , Imunofluorescência , Humanos , Mesoderma/metabolismo , Fenótipo , Receptores de Estrogênio/metabolismo , Tamoxifeno/farmacologia , Células Tumorais Cultivadas/efeitos dos fármacos , beta Catenina/metabolismo
11.
J Steroid Biochem Mol Biol ; 98(4-5): 193-8, 2006 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-16464573

RESUMO

A common problem in breast cancer therapy is resistance to the antiestrogen tamoxifen. However, tamoxifen-resistant breast tumors can still respond to other hormonal therapies. In animal models of tamoxifen-resistant breast cancer cells, physiological levels of estrogen can induce tumor regression. Recently, the estrogen receptor downregulator fulvestrant was shown to promote tumor growth of tamoxifen-resistant cells when added in combination with physiological levels of estrogen. Here, we show, using a cell culture model, that continuous exposure of tamoxifen-resistant cells to physiological levels of estrogen leads to cell death. Addition of the estrogen receptor downregulator fulvestrant prevents estrogen-induced death in a dose-dependent manner. Our data indicate that endogenous levels of estrogen affect the response of tamoxifen-resistant cells to fulvestrant. These results suggest that failure of fulvestrant to inhibit tumor growth in some tamoxifen-resistant patients may be due to endogenous estrogen levels. Moreover, these studies support short-term treatment with estrogen as a second-line hormonal therapy for tamoxifen-resistant breast cancer.


Assuntos
Apoptose/efeitos dos fármacos , Neoplasias da Mama/tratamento farmacológico , Resistencia a Medicamentos Antineoplásicos , Estradiol/análogos & derivados , Estrogênios/farmacologia , Receptores de Estrogênio/antagonistas & inibidores , Tamoxifeno/farmacologia , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Proliferação de Células/efeitos dos fármacos , Regulação para Baixo , Estradiol/farmacologia , Antagonistas de Estrogênios/farmacologia , Moduladores de Receptor Estrogênico/farmacologia , Feminino , Fulvestranto , Humanos , Neoplasias Hormônio-Dependentes/tratamento farmacológico , Neoplasias Hormônio-Dependentes/metabolismo , Neoplasias Hormônio-Dependentes/patologia , Receptores de Estrogênio/metabolismo , Células Tumorais Cultivadas
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