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ABSTRACT: Laparoscopic liver resections are being performed with increasing frequency, with several groups having reported minimally invasive approaches for major anatomic hepatic resections. Some surgeons favor a pure laparoscopic approach, while others prefer a hand-assisted approach for major laparoscopic liver resections. There are clear advantages and disadvantages to a hand-assisted technique. The purpose of this study is to summarize the literature comparing pure laparoscopic and hand-assisted approaches for minimally invasive hepatic resection, and to describe our approach in 432 laparoscopic liver resections.
Journal of hepato-biliary-pancreatic sciences. 10/2012;
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ABSTRACT: Laparoscopic liver surgery has evolved significantly over the past decade. Increasing understanding of hepatic anatomy and advancements in technology have extended the scope of the minimally invasive approach. Robotic-assisted technology offers solutions to the fundamental limitations of conventional laparoscopic liver resection. Several centers have begun to utilize robotic technology to perform complex liver surgeries. The purpose of this review is to provide a comprehensive analysis of published literature about the role of robotic-assisted laparoscopic technology in liver surgery. A literature search of Pubmed was used to identify all English publications about robotic liver surgery. Publications were selected to examine all unique patient series. Outcomes analyzed included operative time, estimated blood loss, length of stay, complication rate, conversion rate to open, cost, and oncologic outcomes. A total of eight series containing 134 unique patients were selected for review. Sixty-nine percent of patients had malignant lesions resected, while 31% had benign lesions. Segmentectomy/wedge (36%) was the most common resection performed, followed by left lateral sectionectomy (28%) right hepatectomy (16%) and left hepatectomy (9%). A meta-analysis of the remaining data was not possible due to heterogeneity in methods for reporting. Outcomes varied widely between studies. Based on analysis of early published series, robotic liver surgery is a feasible and safe tool for the minimally invasive resection of hepatic lesions. Further evaluation is required to assess for improvement in outcomes, and long-term oncologic outcomes are still pending.
Minerva chirurgica 08/2011; 66(4):281-93. · 0.77 Impact Factor
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ABSTRACT: With the aging population, more elderly patients are being considered for hepatic resection. We investigated whether advanced age was associated with higher rate and severity of postoperative complications.
A total of 75 patients aged ≥70 years (group E) were matched with 75 patients aged <70 years (group Y) by the extent of liver resection and by operative indications. Primary outcome measures were rates and severity of complications. Secondary outcome measures were length of hospital stay and discharge destination. Univariate analysis was also performed to identify variables associated with higher surgical risk.
Male-to-female ratio was 43:32 in both groups. Overall complication rates were 44 and 33.3% in group E and Y, respectively (P = 0.241; odds ratio = 1.57; 95% confidence interval [95% CI], 0.81-3.05). There was no mortality in both groups. The only postoperative age-related morbidity was confusion in the elderly. There was no difference in the rates of severe complications (grade ≥3) between group E and group Y (16 vs. 14.7%; P = 0.744; odds ratio = 1.11; 95% CI, 0.46-2.70). Median length of hospital stay were 7 and 6 days, respectively (P = 0.01). Nineteen percent and 1% of patients in group E and group Y were discharge to rehabilitation facilities, respectively (P = 0.001). Univariate analysis showed that preoperative systemic chemotherapy and longer operative time were associated with higher morbidity in the elderly.
Liver resection can be performed in patients aged ≥70 years as safely as in younger patients. Duration and timing of systemic chemotherapy before liver resection should be optimized to minimize postoperative morbidity.
Annals of Surgical Oncology 11/2010; 18(4):1088-95. · 4.17 Impact Factor
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Journal of Surgical Research 02/2010; 158(2):350. · 2.25 Impact Factor
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Journal of Surgical Research 02/2010; 158(2):347-8. · 2.25 Impact Factor
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ABSTRACT: High mobility group box 1 (HMGB1) is a nuclear factor released extracellularly as a late mediator of lethality in sepsis and as an early mediator of inflammation following injury. In contrast to the proinflammatory role of HMGB1, recent evidence suggests beneficial applications of HMGB1 in injury states. One such application is the use of HMGB1 as a preconditioning stimulus. Preconditioning is a phenomenon whereby a low level of stressful stimuli confers protection against subsequent injury. Preconditioning has been demonstrated in multiple species, can be induced by various stimuli, and is applicable in different organ systems. Only with the recent introduction of the concept of endogenous molecules, such as HMGB1, as signals and mediators for inflammation during injury states has the use of endogenous molecules been investigated for this use. This review will focus on the use of endogenous molecules, specifically HMGB1, as a preconditioning stimulus and its mechanism of protection, as well as other protective applications for HMGB1.
Journal of Leukocyte Biology 04/2008; 83(3):558-63. · 4.99 Impact Factor
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J Kohmoto,
A Nakao,
D B Stolz,
T Kaizu, A Tsung,
A Ikeda,
H Shimizu,
T Takahashi,
K Tomiyama,
R Sugimoto,
A M K Choi,
T R Billiar,
N Murase,
K R McCurry
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ABSTRACT: Carbon monoxide (CO) provides protection against oxidative stress via anti-inflammatory and cytoprotective actions. In this study, we tested the hypothesis that a low concentration of exogenous (inhaled) CO would protect transplanted lung grafts from cold ischemia-reperfusion injury via a mechanism involving the mitogen-activated protein kinase (MAPK) signaling pathway. Lewis rats underwent orthotopic syngeneic or allogeneic left lung transplantation with 6 h of cold static preservation. Exposure of donors and recipients (1 h before and then continuously post-transplant) to 250 ppm CO resulted in significant improvement in gas exchange, reduced leukocyte sequestration, preservation of parenchymal and endothelial cell ultrastructure and reduced inflammation compared to animals exposed to air. The beneficial effects of CO were associated with p38 MAPK phosphorylation and were significantly prevented by treatment with a p38 MAPK inhibitor, suggesting that CO's efficacy is at least partially mediated by activation of p38 MAPK. Furthermore, CO markedly suppressed inflammatory events in the contralateral naïve lung. This study demonstrates that perioperative exposure of donors and recipients to CO at a low concentration can impart potent anti-inflammatory and cytoprotective effects in a clinically relevant model of lung transplantation and support further evaluation for potential clinical use.
American Journal of Transplantation 11/2007; 7(10):2279-90. · 6.39 Impact Factor
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12/2006: pages 383-391;
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ABSTRACT: Hepatic I/R (ischaemia/reperfusion) injury occurs in a variety of clinical settings including transplantation, elective liver resections and trauma. One of the challenges in studying the pathophysiology of I/R injury is the fact that the liver plays a central role in a variety of metabolic pathways in addition to governing aspects of immune surveillance and tolerance. The pathways activated in response to insults as varied as toxins, microbial and endogenous ligands and I/R may share common elements. The multiple intracellular signalling cascades involved in this process and the initiating events are still under investigation. Recent work on the role of TLRs (Toll-like receptors) in I/R injury has elucidated some of the more proximal signalling events in the pathway. In addition to the well-established role of signalling molecules such as NO (nitric oxide) in mediating damage or protection following hepatic I/R, more recent studies have focused on the participation of endogenous danger signals or DAMPs (damage-associated molecular patterns) such as HMGB1 (high-mobility group box 1). The complex interplay between HMGB1, TLRs and the many intracellular signalling molecules and pathways is illustrative of how our understanding of hepatic I/R injury is continually evolving.
Biochemical Society Transactions 12/2006; 34(Pt 5):957-9. · 3.71 Impact Factor
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A Nakao,
H Toyokawa, A Tsung,
M A Nalesnik,
D B Stolz,
J Kohmoto,
A Ikeda,
K Tomiyama,
T Harada,
T Takahashi,
R Yang,
M P Fink,
K Morita,
A M K Choi,
N Murase
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ABSTRACT: Carbon monoxide (CO), a byproduct of heme catalysis, was shown to have potent cytoprotective and anti-inflammatory effects. In vivo recipient CO inhalation at low concentrations prevented ischemia/reperfusion (I/R) injury associated with small intestinal transplantation (SITx). This study examined whether ex vivo delivery of CO in University of Wisconsin (UW) solution could ameliorate intestinal I/R injury. Orthotopic syngenic SITx was performed in Lewis rats after 6 h cold preservation in control UW or UW that was bubbled with CO gas (0.1-5%) (CO-UW). Recipient survival with intestinal grafts preserved in 5%, but not 0.1%, CO-UW improved to 86.7% (13/15) from 53% (9/17) with control UW. At 3 h after SITx, grafts stored in 5% CO-UW showed improved intestinal barrier function, less mucosal denudation and reduced inflammatory mediator upregulation compared to those in control UW. Preservation in CO-UW associated with reduced vascular resistance (end preservation), increased graft cyclic guanosine monophosphate levels (1 h), and improved graft blood flow (1 h). Protective effects of CO-UW were reversed by ODQ, an inhibitor of soluble guanylyl cyclase. In vitro culture experiment also showed better preservation of vascular endothelial cells with CO-UW. The study suggests that ex vivo CO delivery into UW solution would be a simple and innovative therapeutic strategy to prevent transplant-induced I/R injury.
American Journal of Transplantation 11/2006; 6(10):2243-55. · 6.39 Impact Factor
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M.R. Metukuri,
D. Beer-Stolz,
R.A. Namas,
R. Dhupar,
A. Torres,
P.A. Loughran,
B.S. Jefferson, A. Tsung,
T.R. Billiar,
Y. Vodovotz,
R. Zamora
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ABSTRACT: We have previously demonstrated that the Bcl-2/adenovirus EIB 19-kDa interacting protein 3 (BNIP3), a cell death-related member of the Bcl-2 family, is upregulated in vitro and in vivo in both experimental and clinical settings of redox stress and that nitric oxide (NO) downregulates its expression. In this study we sought to examine the expression and localization of BNIP3 in murine hepatocytes and in a murine model of hemorrhagic shock (HS) and ischemia-reperfusion (I/R). Freshly isolated mouse hepatocytes were exposed to 1% hypoxia for 6 h followed by reoxygenation for 18 h, and protein was isolated for Western blot analysis. Hepatocytes grown on coverslips were fixed for localization studies. Similarly, livers from surgically cannulated C57Bl/6 mice and from mice cannulated and subjected to 1-4 h of HS were processed for protein isolation and Western blot analysis. In hepatocytes, BNIP3 was expressed constitutively but was upregulated under hypoxic conditions, and this upregulation was countered by treatment with a NO donor. Surprisingly, BNIP3 was localized in the nucleus of normoxic hepatocytes, in the cytoplasm following hypoxia, and again in the nucleus following reoxygenation. Upregulation of BNIP3 partially required p38 MAPK activation. BNIP3 contributed to hypoxic injury in hepatocytes, since this injury was diminished by knockdown of BNIP3 mRNA. Hepatic BNIP3 was also upregulated in two different models of liver stress in vivo, suggesting that a multitude of inflammatory stresses can lead to the modulation of BNIP3. In turn, the upregulation of BNIP3 appears to be one mechanism of hepatocyte cell death and liver damage in these settings
Am.J.Physiol Gastrointest.Liver Physiol. 01/2003; 296(3):G499-G509.
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ABSTRACT: Dendritic cells (DCs) are potent antigen-presenting cells critical in regulating the adaptive immune response. The role of DCs is dichotomous; they may both present antigens and the appropriate stimulatory molecules to initiate an adaptive immune response, or they may induce tolerance and release anti-inflammatory signals. The activation of immature DCs, required for the expression of the necessary costimulatory T cell molecules, is dependent on pattern recognition receptors. In addition to the pathogen-derived ligands of pattern recognition receptors, several damage-associated molecular patterns (DAMPs) have recently been shown to interact with DCs and dramatically affect their ultimate function. The complex interplay of DAMPs on DCs is clinically important, with implications for transplantation, tumor immunity, autoimmunity, chronic inflammation and other conditions of sterile inflammation such as ischemia reperfusion injury. In this review, we will focus on the role of DAMPs in DC function.
Journal of Innate Immunity 08/1970; 4(1):6-15. · 4.21 Impact Factor
