Global collaborative healthcare: assessing the resource requirements at a leading Academic Medical Center.

Introduction: Academic Medical Centers ("AMCs") have served as a hub of the United States ("US") health system and represented the state-of-the art in American health care for well over a century. Currently, the global healthcare market is both massive and expanding and is being altered by the unprecedented impact of technological advances and globalization. This provides AMCs a platform to enter into trans-national collaborative partnerships with healthcare organizations around the world, thus providing a means to deliver on its promise globally while also expanding and diversifying its resources.

Acute kidney injury is surprisingly common and a powerful predictor of mortality in surgical sepsis.

Background: Acute kidney injury (AKI) is a common and often catastrophic complication in hospitalized patients; however, the impact of AKI in surgical sepsis remains unknown. We used Risk, Injury, Failure, Loss, End stage (RIFLE) consensus criteria to define the incidence of AKI in surgical sepsis and characterize the impact of AKI on patient morbidity and mortality.

Methods: Our prospective, institutional review board-approved sepsis research database was retrospectively queried for the incidence of AKI by RIFLE criteria, excluding those with chronic kidney disease.

Single-stage repair of a complex type B aortic dissection associated with a pressurized infrarenal abdominal aortic aneurysm.

The decision-making involved in managing type 2 aortic dissections remains challenging despite the advances in endovascular technology. We report a challenging case of a patient presenting with a type 2 aortic dissection and false lumen extension into an infrarenal abdominal aortic aneurysm (AAA). Severe back pain and hypertension were the patient's initial complaints, and dynamic magnetic resonance angiography revealed 1-way pulsatile flow into the AAA sac from the false lumen.

Lung T lymphocyte trafficking and activation during ischemic acute kidney injury.

Despite advances in renal replacement therapy, the mortality rate for acute kidney injury (AKI) remains unacceptably high, likely owing to extrarenal organ dysfunction. Kidney ischemia-reperfusion injury (IRI) activates cellular and soluble mediators that facilitate organ crosstalk and induce caspase-dependent lung apoptosis and injury through a TNFR1-dependent pathway. Given that T lymphocytes mediate local IRI in the kidney and are known to drive TNFR1-mediated apoptosis, we hypothesized that T lymphocytes activated during kidney IRI would traffic to the lung and mediate pulmonary apoptosis during AKI.

Lung endothelial cell apoptosis during ischemic acute kidney injury.

Kidney ischemia-reperfusion injury (IRI) activates cellular and soluble mediators that drive lung inflammatory cascades, tumor necrosis factor receptor 1 (TNFR1)-mediated programmed cell death, and microvascular barrier dysfunction, leading to acute lung injury. We hypothesized that lung microvascular endothelial cells (ECs), with their integral role in maintaining the lung-semipermeable barrier, were key cellular targets of TNFR1-mediated apoptosis during ischemic AKI. Male C57/BL6 mice and Sprague-Dawley rats underwent 60 min of bilateral renal pedicle occlusion (IRI) or sham laparotomy (sham) and were killed at 4 or 24 h.

TNFR1-dependent pulmonary apoptosis during ischemic acute kidney injury.

Despite advancements in renal replacement therapy, the mortality rate for acute kidney injury (AKI) remains unacceptably high, likely due to remote organ injury. Kidney ischemia-reperfusion injury (IRI) activates cellular and soluble mediators that incite a distinct pulmonary proinflammatory and proapoptotic response. Tumor necrosis factor receptor 1 (TNFR1) has been identified as a prominent death receptor activated in the lungs during ischemic AKI.

Endovascular management of carotid artery stenosis secondary to sclerosing mediastinitis.

Sclerosing mediastinitis is a rare, progressive condition characterized by extensive fibrotic reaction. We report the first known case of symptomatic, extrinsic compression of the carotid artery by fibrotic extension of sclerosing mediastinitis. A 54-year-old woman began experiencing neurologic symptoms from extension of a known mediastinal mass resulting in 70% to 79% stenosis of the right internal carotid artery.

Endovascular repair of ruptured abdominal and thoracic aortic aneurysms.

Management of acute pathology remains one of the most challenging clinical entities, with a persistently high mortality rate both prior to and upon arrival to a hospital. Responding to the distinct advantages of endovascular approaches to aortic disease, many high-volume cardiovascular centers have focused on endovascular therapies for managing patients with ruptured or leaking aortic aneurysms and other acute aortic syndromes. Nonetheless, similar to outcomes for other surgical emergencies, time and efficiency are critical in managing these conditions.

Inflammatory Mechanisms of Organ Crosstalk during Ischemic Acute Kidney Injury.

Acute kidney injury (AKI) is a common complication during inpatient hospitalization, and clinical outcomes remain poor despite advancements in renal replacement therapy. AKI in the setting of multiple organ failure (MOF) remains a formidable challenge to clinicians and incurs an unacceptably high mortality rate. Kidney ischemia-reperfusion injury (IRI) incites a proinflammatory cascade and releases cellular and soluble mediators with systemic implications for remote organ injury.

Pulmonary endothelial cell activation during experimental acute kidney injury.

Acute kidney injury (AKI) leads to increased lung microvascular permeability, leukocyte infiltration, and upregulation of soluble inflammatory proteins in rodents. Most work investigating connections between AKI and pulmonary dysfunction, however, has focused on characterizing whole lung tissue changes associated with AKI. Studies at the cellular level are essential to understanding the molecular basis of lung changes during AKI.

Surgical sepsis and organ crosstalk: the role of the kidney.

Acute kidney injury (AKI) is a common complication of hospitalized patients, and clinical outcomes remain poor despite advances in renal replacement therapy. The accepted pathophysiology of AKI in the setting of sepsis has evolved from one of simple decreased renal blood flow to one that involves a more complex interaction of intra-glomerular microcirculatory vasodilation combined with the local release of inflammatory mediators and apoptosis. Evidence from preclinical AKI models suggests that crosstalk occurs between kidneys and other organ systems via soluble and cellular inflammatory mediators and that this involves both the innate and adaptive immune systems.

Secondary stroke prevention in the era of carotid stenting: update on recent trials.

Stroke is a leading cause of morbidity and mortality worldwide. Traditional therapy for extracranial carotid artery occlusive disease, a significant risk factor for stroke, consists of optimal medical management and selective surgical treatment with carotid endarterectomy (CEA) for stroke risk reduction. Buoyed by the widespread application of percutaneous interventions for the treatment of coronary artery disease, carotid artery stenting (CAS) has steadily developed during the past decade as an alternative to CEA for patients who might benefit from surgical treatment.

Therapeutic distant organ effects of regional hypothermia during mesenteric ischemia-reperfusion injury.

Introduction: Mesenteric ischemia-reperfusion injury (IRI) leads to systemic inflammation and multiple organ failure in clinical and laboratory settings. We investigated the lung structural, functional, and genomic response to mesenteric IRI with and without regional intraischemic hypothermia (RIH) in rodents and hypothesized that RIH would protect the lung and preferentially modulate the distant organ transcriptome under these conditions.

Methods: Sprague-Dawley rats underwent sham laparotomy or superior mesenteric artery occlusion (SMAO) for 60 minutes with or without RIH.

Organ crosstalk: the role of the kidney.

Purpose Of Review: Acute kidney injury (AKI) continues to contribute significantly to morbidity and mortality in the ICU setting, especially when associated with distant organ dysfunction. There is increasing evidence that AKI directly contributes to organ dysfunction in lung, brain, liver, heart and other organs. This review will examine our current understanding of the deleterious organ crosstalk in the critically ill, which can provide a framework for developing novel therapeutics.

Academic needs in developing countries: a survey of the West African College of Surgeons.

Background: The inaugural Fundamentals of Surgical Research Course was held in Sierra Leone in conjunction with the West African College of Surgeons (WACS). We subsequently performed a formal assessment of the academic needs of West African surgeons to plan for future courses, and hypothesized that they would differ from the goals of the U.S.

Kidney-lung crosstalk in the critically ill patient.

Despite advances in renal replacement therapy, the mortality of acute kidney injury (AKI) has remained high, especially when associated with distant organ dysfunction such as acute lung injury (ALI). Mortality rates for combined AKI/ALI reach 80% in critically ill patients. While the clinical presentation of AKI-associated ALI is characterized by increased pulmonary edema, a defining feature of the syndrome, the AKI-induced lung effects extend beyond simple volume overload.

Kidney ischemia-reperfusion injury induces caspase-dependent pulmonary apoptosis.

Distant organ effects of acute kidney injury (AKI) are a leading cause of morbidity and mortality. While little is known about the underlying mechanisms, limited data suggest a role for inflammation and apoptosis. Utilizing a lung candidate gene discovery approach in a mouse model of ischemic AKI-induced lung dysfunction, we identified prominent lung activation of 66 apoptosis-related genes at 6 and/or 36 h following ischemia, of which 6 genes represent the tumor necrosis factor receptor (TNFR) superfamily, and another 23 genes are associated with the TNFR pathway.

Multiple treatment algorithms for successful outcomes in venous thoracic outlet syndrome.

Background: We sought to determine the outcomes in patients presenting with venous thoracic outlet syndrome.

Methods: Prospectively collected data from 67 patients between October 2003 and December 2007. The average age was 31 years (range, 16-54); the 37 males and 30 females presented on average 9.

Renal ischemia-reperfusion leads to long term infiltration of activated and effector-memory T lymphocytes.

It is well-established that significant ischemia-reperfusion injury during kidney transplantation results in increased incidence of long-term fibrosis and rejection. To test for a role of T cell infiltration and activation following ischemic injury, we induced both bilateral and unilateral renal ischemia in mice, followed by reperfusion, and then isolated mononuclear cells. Analysis of these cells by flow cytometry showed that 2 weeks after bilateral ischemia there was a significant increase of CD8(+) T cells.

Interactive effects of mechanical ventilation and kidney health on lung function in an in vivo mouse model.

We hypothesized that the influence of acute kidney injury (AKI) on the sensitivity of the lung to an injurious process varies with the severity of the injurious process. Thus, we thought that AKI would exacerbate lung injury from low degrees of lung trauma but attenuate lung injury from higher degrees of lung trauma. C57BL/6 mice underwent AKI (30-min kidney ischemia) or sham surgery, followed at 24 h by 4 h of spontaneous breathing (SB), mechanical ventilation with low tidal volume (7 ml/kg, LTV), or mechanical ventilation with high tidal volume (30 ml/kg, HTV).

The local and systemic inflammatory transcriptome after acute kidney injury.

Studies in humans and animal models have demonstrated that acute kidney injury (AKI) has a significant effect on the function of extrarenal organs. The combination of AKI and lung dysfunction is associated with 80% mortality; the lung, because of its extensive capillary network, is a prime target for AKI-induced effects. The study presented here tested the hypothesis that AKI leads to a vigorous inflammatory response and produces distinct genomic signatures in the kidney and lung.