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1.
Ann Plast Surg ; 82(1): 85-88, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30516557

RESUMO

Open abdominal surgery continues to be most commonly complicated by postoperative herniation at the incision line. In 2012, Novitsky et al described a novel hernia repair technique that utilized a transversus abdominis release coupled with a posterior (retrorectus) component separation (TAR-PCS) of the ventral abdominal wall. Early reports attest to the versatility and low recurrence rate of this technique, particularly when repairing large and complex defects. We present a rare case of herniation below the linea arcuate (LAH) following repair via TAR-PCS. Given its novelty compared with more widely utilized techniques, literature review revealed less discussion regarding potential pitfalls associated with this type of reconstruction, in particular the potential for LAH. To date, only 9 cases of symptomatic LAH have been described, although 2 previously described "suprapubic" herniations following TAR-PCS may represent previously mischaracterized cases of this type of complication. Nonetheless, none of these reports were in the setting of ventral hernia repair.


Assuntos
Músculos Abdominais/cirurgia , Hérnia Ventral/cirurgia , Herniorrafia/efeitos adversos , Hérnia Incisional/cirurgia , Complicações Pós-Operatórias/cirurgia , Reoperação/métodos , Doença Aguda , Idoso , Feminino , Seguimentos , Herniorrafia/métodos , Humanos , Laparotomia/efeitos adversos , Laparotomia/métodos , Complicações Pós-Operatórias/diagnóstico por imagem , Medição de Risco , Telas Cirúrgicas , Fatores de Tempo , Tomografia Computadorizada por Raios X/métodos , Resultado do Tratamento , Cicatrização/fisiologia
4.
Radiat Oncol J ; 34(2): 156-9, 2016 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-27306770

RESUMO

Although carbohydrate antigen (CA) 19-9 is a useful tumor marker for pancreatic cancer, it can also become elevated from a variety of benign and malignant conditions. Herein we describe an unusual presentation of elevated CA 19-9 in an asymptomatic patient who had previously undergone adjuvant chemotherapy and radiation therapy for resected early stage pancreatic cancer. The rise in CA 19-9 might be due to delayed radiation-induced inflammation related to previous intra-abdominal radiation therapy with or without radiation recall induced by gemcitabine. After treatment with corticosteroids the CA 19-9 level decreased to normal, and the patient has not developed any evidence of recurrent cancer to date.

5.
HPB (Oxford) ; 15(3): 210-7, 2013 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-23374361

RESUMO

OBJECTIVES: This study aimed to compare survival outcomes after hepatic resection (HR) and radiofrequency ablation (RFA) in early-stage hepatocellular carcinoma (HCC) at a Western hepatobiliary centre. METHODS: Demographic details, clinicopathologic tumour characteristics and survival outcomes were compared among non-transplant candidate patients undergoing HR (n= 50) and RFA (n= 60) for early-stage HCC during 2001-2011. RESULTS: Patients who underwent HR had larger tumours, a longer length of stay and a higher rate of postoperative complications. After a median follow-up of 29 months, there were no significant differences between the treatment groups in 1-, 3- and 5-year overall survival (OS) [RFA group: 86%, 50%, 35%, respectively; HR group: 88%, 68%, 47%, respectively (P= 0.222)] or disease-free survival (DFS) [RFA group: 68%, 42%, 28%, respectively; HR group: 66%, 42%, 34%, respectively (P= 0.823)]. The 58 patients who underwent RFA demonstrated ablation success on follow-up computed tomography at 3 months. Of these, 96.5% of patients showed sustained ablation success over the entire follow-up period. In a subgroup analysis of patients with tumours measuring 2-5 cm, no differences in OS or DFS emerged between the HR and RFA groups. Similarly, no significant differences in outcomes in patients with Child-Pugh class A cirrhosis were seen between the RFA and HR groups. CONCLUSIONS: Radiofrequency ablation is comparable with HR in terms of OS and DFS. It is a reasonable alternative as a first-line treatment for HCC in well-selected patients who are not candidates for transplant.


Assuntos
Carcinoma Hepatocelular/cirurgia , Ablação por Cateter , Hepatectomia , Neoplasias Hepáticas/cirurgia , Idoso , Carcinoma Hepatocelular/diagnóstico por imagem , Carcinoma Hepatocelular/mortalidade , Carcinoma Hepatocelular/secundário , Ablação por Cateter/efeitos adversos , Ablação por Cateter/mortalidade , Distribuição de Qui-Quadrado , Intervalo Livre de Doença , Feminino , Hepatectomia/efeitos adversos , Hepatectomia/mortalidade , Humanos , Estimativa de Kaplan-Meier , Tempo de Internação , Neoplasias Hepáticas/diagnóstico por imagem , Neoplasias Hepáticas/mortalidade , Neoplasias Hepáticas/patologia , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Estadiamento de Neoplasias , Pennsylvania , Complicações Pós-Operatórias/etiologia , Estudos Retrospectivos , Fatores de Tempo , Tomografia Computadorizada por Raios X , Resultado do Tratamento , Carga Tumoral
6.
J Gastrointest Surg ; 16(12): 2256-9, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23086449

RESUMO

INTRODUCTION: Despite detection on imaging before resection of hepatic malignancies, the natural history of indeterminate pulmonary nodules (IPN) is unknown. The objective of this study is to determine how often IPN detected on imaging before surgery for hepatic malignancies represent lung metastases. METHODS: Demographics, comorbidities, tumor characteristics, and surgical treatments of patients with pre-operative IPN who underwent liver resection and/or radiofrequency ablation for malignant diagnoses were reviewed. RESULTS: From 2000 to 2010, 90 patients with at least one IPN underwent liver resection or radiofrequency ablation for malignancy. Of these, 44 (48.9 %), 32 (35.6 %), and 14 (15.6 %) patients had colorectal cancer liver metastases (CRCLM), primary hepatobiliary malignancies (HB), and other cancers, respectively. The median number of IPN was 1. The median size was 4 mm. Twenty (22 %) patients had isolated lung recurrence after hepatic surgical therapy. Eighty percent occurred in the exact location of the pre-operative IPN. Isolated lung recurrence was more common among patients with CRCLM compared to those with HB and other cancers (42.9 vs. 9.4 vs. 14.3 %, p = 0.004). CONCLUSION: Pre-operatively detected IPN represent lung metastases in a substantial portion of patients undergoing surgery for hepatic malignancy. IPN are more likely to represent lung metastases in patients with CRCLM compared to those with primary HB and other cancers.


Assuntos
Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/cirurgia , Neoplasias Pulmonares/secundário , Idoso , Feminino , Hepatectomia , Humanos , Neoplasias Pulmonares/epidemiologia , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
7.
Am J Physiol Gastrointest Liver Physiol ; 303(2): G189-98, 2012 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-22575222

RESUMO

Sterile inflammatory insults, such as ischemia-reperfusion (I/R) injury, result from pathogenic factors, including damage-associated molecular pattern signaling, activation of innate immunity, and upregulation of proinflammatory cytokines. At the same time, a number of protective, or prosurvival, pathways are also activated, and the extent of end-organ damage is ultimately determined by the balance between these two systems. In liver I/R, members of the calcium/calmodulin-dependent protein kinase (CaMK) family are known to be activated, but their individual roles are largely unknown. In this study, we show that one CaMK member, CaMKIV, is protective in hepatic I/R by activating the prosurvival pathway of autophagy in hepatocytes. CaMKIV knockout mice experience significantly worse organ damage after I/R and are deficient in hepatocyte autophagic signaling. Restoration of autophagic signaling with rapamycin reduces organ damage in CaMKIV knockout mice to wild-type levels. In vitro, we show that CaMKIV activation induces autophagy in mouse hepatocytes, and that CaMKIV activation protects hepatocytes from oxidative stress-induced cell death. In conclusion, the protective autophagic signaling pathway serves to reduce organ damage following I/R and is regulated by activation of CaMKIV signaling in hepatocytes.


Assuntos
Autofagia/fisiologia , Proteína Quinase Tipo 4 Dependente de Cálcio-Calmodulina/fisiologia , Hepatócitos/enzimologia , Fígado/irrigação sanguínea , Fígado/enzimologia , Traumatismo por Reperfusão/enzimologia , Animais , Autofagia/efeitos dos fármacos , Autofagia/genética , Proteína Quinase Tipo 4 Dependente de Cálcio-Calmodulina/genética , Células Cultivadas , Hepatócitos/efeitos dos fármacos , Hepatócitos/fisiologia , Fígado/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Estresse Oxidativo/fisiologia , Traumatismo por Reperfusão/tratamento farmacológico , Transdução de Sinais/genética , Sirolimo/farmacologia
8.
Shock ; 37(5): 511-7, 2012 May.
Artigo em Inglês | MEDLINE | ID: mdl-22266972

RESUMO

Sepsis-induced lymphocyte and dendritic cell apoptosis contributes to immunosuppression, which results in an inability to eradicate the primary infection as well as a propensity to acquire new, secondary infections. Another cellular process, autophagy, is also activated in immune cells and plays a protective role. In the present study, we demonstrate that interferon regulatory factor 1 (IRF-1) regulates both immune cell apoptosis and autophagy in a murine endotoxemia model. Interferon regulatory factor 1 is activated at an early phase through a Toll-like receptor 4-dependent, myeloid differentiation primary response gene 88-independent manner in splenocytes. Furthermore, IRF-1 knockout (KO) mice are protected from a lethal endotoxemia model. This protection is associated with decreased apoptosis and increased autophagy in splenocytes. Interferon regulatory factor 1 KO mice experience decreased apoptotic cell loss, especially in CD4⁺ T lymphocytes and myeloid antigen-presenting cells. Meanwhile, IRF-1 KO mice demonstrate increased autophagy and improved mitochondrial integrity. This increased autophagy in KO mice is attributable, at least in part, to deactivation of mammalian target of rapamycin/P70S6 signaling--a main negative regulator of autophagy. Therefore, we propose a novel role for IRF-1 in regulating both apoptosis and autophagy in splenocytes in the setting of endotoxemia with IRF-1 promoting apoptosis and inhibiting autophagy.


Assuntos
Apoptose , Autofagia , Endotoxemia/metabolismo , Fator Regulador 1 de Interferon/metabolismo , Baço/metabolismo , Animais , Linfócitos T CD4-Positivos/metabolismo , Linfócitos T CD4-Positivos/patologia , Modelos Animais de Doenças , Endotoxemia/genética , Endotoxemia/patologia , Fator Regulador 1 de Interferon/genética , Lipopolissacarídeos/toxicidade , Masculino , Camundongos , Camundongos Knockout , Fator 88 de Diferenciação Mieloide/genética , Fator 88 de Diferenciação Mieloide/metabolismo , Proteínas Quinases S6 Ribossômicas 70-kDa/genética , Proteínas Quinases S6 Ribossômicas 70-kDa/metabolismo , Baço/patologia , Serina-Treonina Quinases TOR/genética , Serina-Treonina Quinases TOR/metabolismo , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/metabolismo
9.
Hepatology ; 55(6): 1863-75, 2012 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-22234969

RESUMO

UNLABELLED: Hypoxia is often found in solid tumors and is associated with tumor progression and poor clinical outcomes. The exact mechanisms related to hypoxia-induced invasion and metastasis remain unclear. We elucidated the mechanism by which the nuclear-damage-associated molecular pattern molecule, high-mobility group box 1 (HMGB1), released under hypoxic stress, can induce an inflammatory response to promote invasion and metastasis in hepatocellular carcinoma (HCC) cells. Caspase-1 activation was found to occur in hypoxic HCC cells in a process that was dependent on the extracellular release of HMGB1 and subsequent activation of both Toll-like receptor 4 (TLR4)- and receptor for advanced glycation endproducts (RAGE)-signaling pathways. Downstream from hypoxia-induced caspase-1 activation, cleavage and release of proinflammatory cytokines interleukin (IL)-1ß and -18 occurred. We further demonstrate that overexpression of HMGB1 or treatment with recombinant HMGB1 enhanced the invasiveness of HCC cells, whereas stable knockdown of HMGB1 remarkably reduced HCC invasion. Moreover, in a murine model of HCC pulmonary metastasis, stable knockdown of HMGB1 suppressed HCC invasion and metastasis. CONCLUSION: These results suggest that in hypoxic HCC cells, HMGB1 activates TLR4- and RAGE-signaling pathways to induce caspase-1 activation with the subsequent production of multiple inflammatory mediators, which, in turn, promote cancer invasion and metastasis.


Assuntos
Carcinoma Hepatocelular/patologia , Caspase 1/metabolismo , Proteína HMGB1/fisiologia , Neoplasias Hepáticas/patologia , Animais , Hipóxia Celular , Linhagem Celular Tumoral , Ativação Enzimática , Humanos , Interleucina-1beta/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Invasividade Neoplásica , Receptor para Produtos Finais de Glicação Avançada , Receptores Imunológicos/fisiologia , Transdução de Sinais , Receptor 4 Toll-Like/fisiologia
10.
Mol Med ; 18: 201-8, 2012 Mar 27.
Artigo em Inglês | MEDLINE | ID: mdl-22105605

RESUMO

The pathogenesis of sepsis is complex and, unfortunately, poorly understood. The cellular process of autophagy is believed to play a protective role in sepsis; however, the mechanisms responsible for its regulation in this setting are ill defined. In the present study, interferon regulatory factor 1 (IRF-1) was found to regulate the autophagic response in lipopolysaccharide (LPS)-stimulated macrophages. In vivo, tissue macrophages obtained from LPS-stimulated IRF-1 knockout (KO) mice demonstrated increased autophagy and decreased apoptosis compared to those isolated from IRF-1 wild-type (WT) mice. In vitro, LPS-stimulated peritoneal macrophages obtained from IRF-1 KO mice experienced increased autophagy and decreased apoptosis. IRF-1 mediates the inhibition of autophagy by modulating the activation of the mammalian target of rapamycin (mTOR). LPS induced the activation of mTOR in WT peritoneal macrophages, but not in IRF-1 KO macrophages. In contrast, overexpression of IRF-1 alone increased the activation of mTOR and consequently decreased autophagic flux. Furthermore, the inhibitory effects of IRF-1 mTOR activity were mediated by nitric oxide (NO). Therefore, we propose a novel role for IRF-1 and NO in the regulation of macrophage autophagy during LPS stimulation in which IRF-1/NO inhibits autophagy through mTOR activation.


Assuntos
Autofagia/efeitos dos fármacos , Fator Regulador 1 de Interferon/metabolismo , Lipopolissacarídeos/toxicidade , Macrófagos/citologia , Macrófagos/metabolismo , Óxido Nítrico/metabolismo , Animais , Apoptose/efeitos dos fármacos , Proteínas Reguladoras de Apoptose/metabolismo , Autofagia/genética , Proteína Beclina-1 , Western Blotting , Linhagem Celular , Sobrevivência Celular , Células Cultivadas , Eletroforese em Gel de Poliacrilamida , Endotoxemia/metabolismo , Marcação In Situ das Extremidades Cortadas , Fator Regulador 1 de Interferon/genética , Macrófagos/efeitos dos fármacos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Microscopia Eletrônica de Transmissão
11.
Kidney Int ; 77(2): 101-9, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-19907413

RESUMO

Reactive oxygen species (ROS) contribute to the development of interstitial fibrosis and tubular atrophy seen in chronic allograft nephropathy (CAN). As molecular hydrogen gas can act as a scavenger of ROS, we tested the effect of treatment with hydrogen water (HW) in a model of kidney transplantation, in which allografts from Lewis rats were orthotopically transplanted into Brown Norway recipients that had undergone bilateral nephrectomy. Molecular hydrogen was dissolved in water and recipients were given HW from day 0 until day 150. Rats that were treated with regular water (RW) gradually developed proteinuria and their creatinine clearance declined, ultimately leading to graft failure secondary to CAN. In contrast, treatment with HW improved allograft function, slowed the progression of CAN, reduced oxidant injury and inflammatory mediator production, and improved overall survival. Inflammatory signaling pathways, such as mitogen-activated protein kinases, were less activated in renal allografts from HW-treated rats as compared with RW-treated rats. Hence, oral HW is an effective antioxidant and antiinflammatory agent that prevented CAN, improved survival of rat renal allografts, and may be of therapeutic value in the setting of transplantation.


Assuntos
Antioxidantes/uso terapêutico , Hidrogênio/uso terapêutico , Transplante de Rim/efeitos adversos , Insuficiência Renal Crônica/prevenção & controle , Administração Oral , Animais , Antioxidantes/administração & dosagem , Biomarcadores/metabolismo , Sobrevivência de Enxerto/efeitos dos fármacos , Hidrogênio/administração & dosagem , Inflamação/metabolismo , Testes de Função Renal , Masculino , Ratos , Ratos Endogâmicos Lew , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/metabolismo , Transdução de Sinais/efeitos dos fármacos , Transplante Homólogo , Aumento de Peso/efeitos dos fármacos
12.
J Heart Lung Transplant ; 29(5): 544-53, 2010 May.
Artigo em Inglês | MEDLINE | ID: mdl-20036162

RESUMO

BACKGROUND: Recent advances in novel medical gases, including hydrogen and carbon monoxide (CO), have demonstrated significant opportunities for therapeutic use. This study was designed to evaluate the effects of inhaled hydrogen or CO, or both, on cold ischemia/reperfusion (I/R) injury of the myocardium. METHODS: Syngeneic heterotopic heart transplantation was performed in rats after 6 or 18 hours of cold ischemia in Celsior solution. Survival, morphology, apoptosis and marker gene expression were assessed in the grafts after in vivo inhalation of hydrogen (1% to 3%), CO (50 to 250 ppm), both or neither. Both donors and recipients were treated for 1 hour before and 1 hour after reperfusion. RESULTS: After 6-hour cold ischemia, inhalation of hydrogen (>2%) or CO (250 ppm) alone attenuated myocardial injury. Prolonged cold ischemia for 18 hours resulted in severe myocardial injury, and treatment with hydrogen or CO alone failed to demonstrate significant protection. Dual treatment with hydrogen and CO significantly attenuated I/R graft injury, reducing the infarcted area and decreasing in serum troponin I and creatine phosphokinase (CPK). Hydrogen treatment alone significantly reduced malondialdehyde levels and serum high-mobility group box 1 protein levels as compared with air-treated controls. In contrast, CO only marginally prevented lipid peroxidation, but it suppressed I/R-induced mRNA upregulation for several pro-inflammatory mediators and reduced graft apoptosis. CONCLUSIONS: Combined therapy with hydrogen and CO demonstrated enhanced therapeutic efficacy via both anti-oxidant and anti-inflammatory mechanisms, and may be a clinically feasible approach for preventing cold I/R injury of the myocardium.


Assuntos
Monóxido de Carbono/farmacologia , Isquemia Fria , Transplante de Coração/patologia , Hidrogênio/farmacologia , Transplante Heterotópico , Administração por Inalação , Animais , Apoptose/efeitos dos fármacos , Western Blotting , Quimioterapia Combinada , Marcação In Situ das Extremidades Cortadas , Mediadores da Inflamação/análise , Macrófagos/patologia , Masculino , Malondialdeído/análise , Traumatismo por Reperfusão Miocárdica , Miocárdio/patologia , Ratos , Ratos Endogâmicos Lew , Síndrome de Resposta Inflamatória Sistêmica/patologia
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