Feasibility of diagnosis of postcardiotomy tamponade by miniaturized transesophageal echocardiography.

BACKGROUND: Pericardial tamponade after cardiac surgery is a critical diagnosis that can be difficult to diagnose using conventional cardiac monitoring. Transesophageal echocardiography can provide comprehensive information to make the diagnosis but is not always available, whereas transthoracic echocardiography has its utility limited because of the body habitus or other surgical effects. New monitoring devices, miniaturized hemodynamic transesophageal echocardiography (hTEE), which allows point of care assessment of cardiac filling and functions, may aid in diagnosis of postcardiotomy tamponade. METHODS: From May 2011 to July 2013, 21 patients underwent hTEE to rule out pericardial tamponade for clinical suspicion of tamponade after open heart surgery. The hTEE images were reviewed, and the patient outcomes were analyzed. RESULTS: Nine patients showed no evidence of pericardial collection and did not require reexploration. Two patients showed a presence of small hematoma without ventricular compression and also did not undergo exploration. Ten patients were positive for pericardial tamponade (effusion or hematoma with ventricular compression); eight of these cases underwent emergent surgical exploration. Of the two patients who did not undergo immediate reoperation, one was managed by chest tube manipulation and the other patient underwent subsequent surgical exploration after his extensive coagulopathy was corrected by medical treatment. CONCLUSIONS: The diagnosis of pericardial tamponade postcardiotomy is feasible using a disposable hTEE based on our limited experience. We avoided unnecessary explorations while concomitantly made prompt diagnosis in emergent situations. The hTEE device was a valuable tool in hemodynamic management in the intensive care unit, allowing rapid evaluations

Case Series on Veno - venous extracorporeal membrane oxygenation (VV-ECMO) as a bridge to complete recovery in influenza type A related refractory ARDS

Introduction: Influenza A sequelae range from mild symptoms to acute respiratory distress syndrome (ARDS), which can be refractory to conventional ventilator therapy. We present a case series of three non-H1N1 Influenza patients with ARDS, who completely recovered after VV-ECMO. Case Presentation: In January and February 2013, we experienced three cases of Influenza A induced ARDS that failed conventional ARDS ventilator therapy. All three patients presented with typical flu-like symptoms, which deteriorated over several days, requiring intubation. They were all treated with oseltamivir. They had bilateral chest infiltrates on chest x-rays. After a few days of failing conventional treatment these patients were placed on VV-ECMO using Avalon Dual Lumen catheters. Presented 24th Annual ELSO Conference

The impact of a new ECMO program on clinical outcomes of patients with acute myocardial infarction complicated by cardiogenic shock.

Objective: To investigate if a new ECMO program will improve the outcome of patients who had acute myocardial infarction complicated with cardiogenic shock. Presented 24th Annual ELSO Conference. Philadelphia, PA. Sep 19-21, 2013

MRSA sepsis and acute respiratory distress syndrome during veno-arterial extracorporeal membrane oxygenation (ECMO).

Presentation: A 39 year old female African American presented with respiratory distress two days after ERCP for pancreatitis. The patient quickly deteriorated, required intubation, and developed severe hypotension requiring vasopressors. VA-ECMO was initiated for ARDS and SIRS due to on-going pancreatitis. Pre ECMO ABG: PH 7.01, PaCO2 70, PaO2 70 with FiO2 100% with PEEP 15 Profound hypotension, required 2 pressors Preliminary results of cultures were negative at the time of ECMO placement. Presented 24th Annual ELSO Conference. Philadelphia, PA. Sep 19-21, 2013

Lysophosphatidic Acid Acyltransferase β (LPAATβ) Promotes the Tumor Growth of Human Osteosarcoma

Osteosarcoma is the most common primary malignancy of bone with poorly characterized molecular pathways important in its pathogenesis. Increasing evidence indicates that elevated lipid biosynthesis is a characteristic feature of cancer. We sought to investigate the role of lysophosphatidic acid acyltransferase β (LPAATβ, aka, AGPAT2) in regulating the proliferation and growth of human osteosarcoma cells. LPAATβ can generate phosphatidic acid, which plays a key role in lipid biosynthesis as well as in cell proliferation and survival. Although elevated expression of LPAATβ has been reported in several types of human tumors, the role of LPAATβ in osteosarcoma progression has yet to be elucidated.Endogenous expression of LPAATβ in osteosarcoma cell lines is analyzed by using semi-quantitative PCR and immunohistochemical staining. Adenovirus-mediated overexpression of LPAATβ and silencing LPAATβ expression is employed to determine the effect of LPAATβ on osteosarcoma cell proliferation and migration in vitro and osteosarcoma tumor growth in vivo. We have found that expression of LPAATβ is readily detected in 8 of the 10 analyzed human osteosarcoma lines. Exogenous expression of LPAATβ promotes osteosarcoma cell proliferation and migration, while silencing LPAATβ expression inhibits these cellular characteristics. We further demonstrate that exogenous expression of LPAATβ effectively promotes tumor growth, while knockdown of LPAATβ expression inhibits tumor growth in an orthotopic xenograft model of human osteosarcoma.Our results strongly suggest that LPAATβ expression may be associated with the aggressive phenotypes of human osteosarcoma and that LPAATβ may play an important role in regulating osteosarcoma cell proliferation and tumor growth. Thus, targeting LPAATβ may be exploited as a novel therapeutic strategy for the clinical management of osteosarcoma. This is especially attractive given the availability of selective pharmacological inhibitors

Does skin pigmentation effect readings of cerebral oximeter devices while on cardiopulmonary support?

Introduction: Cerebral oximetry is utilized as a non-invasive method to ensure adequate cerebral perfusion. In a review of our clinical experience, it was noted that there were consistent inaccurate values from normal utilizing relative (INVOS, Covidien, Mansfield, MA) cerebral oximetry as opposed to absolute (FORESIGHT, CAS medical, Branford, CT) cerebral oximetry in darker skin patients. Presented 24th Annual ELSO Conference. Philadelphia, PA. Sep 19-21, 2013

Antithrombin III deficiency in a patient requiring extracorporeal membrane oxygenation.

Introduction: Antithrombin or antithrombin III (ATIII) is a vitamin K-independent, natural anticoagulant that is the major inhibitor of thrombin. With the binding of heparin, a conformational change in antithrombin occurs that increases the inactivation of thrombin by antithrombin by 4000-fold. Antithrombin deficiency can be hereditary or acquired; the acquired form is frequently encountered in patients requiring mechanical circulatory support. Formulation of clots within the circuit of extracorporeal membrane oxygenation (ECMO) is a life-threatening emergency and requires emergent intervention. Decreased ATIII is associated with a hypercoagulable state, which can lead to dangerous complications for patients requiring mechanical circulatory support

MicroRNA-592 Inhibits the Growth of Ovarian Cancer Cells by Targeting ERBB3

Objectives: Ovarian cancer is the most lethal gynecologic malignancy, and targeted therapy for different pathological types and molecular phenotypes is urgent to be studied. Studies have shown that MicroRNA-592 (miR-592) plays an important negative regulatory role in the occurrence of gastrointestinal malignancies, breast cancer, non-small cell lung cancer, and glioma, but the expression of miR-592 in ovarian cancer and the mechanism of action are still unclear. Methods: The expressions of miR-592 were examined by RT-PCR and Western Blot. Cell viability and migratory capacity were detected by CCK-8 and transwell assay. TargetScan ( http://www.targetscan.org ) was analyzed to predict potential targets of miR-592. Then Dual-luciferase reporter gene assay was performed to verify the targeting relationship between miR-592 and ERBB3. A mouse xenograft model was applied to confirm the effect of miR-592. Results: In our study, we found that the expression of miR-592 is reduced in epithelial ovarian cancer tissues. The exogenous expression of miR-592 inhibits the proliferation, migration, and invasion in epithelial ovarian cancer tumor cells. Furthermore, the exogenous expression of miR-592 inhibits tumor growth in the nude mouse xenograft model. Therefore, miR-592 may play a role of tumor suppressor miRNA in the occurrence and development of ovarian cancer. Further experiments demonstrated that tumor-related ERBB3 is a target gene mediated by miRNA-592. The dual-luciferase reporter system was used to identify miRNA-592 target genes; qPCR and Western Blot were used to detect the expression of ERBB3. Mechanical experiments confirmed that miRNA-592 negatively regulated ERBB3. Conclusion: Together, these findings identify a heretofore unrecognized link between miR-592 and ERBB3 and suggest that targeting on miR-592 warrants attention as a novel and potential therapeutic strategy for ovarian cancer

Phylogenetic Tree Construction and “Truncal Loss” Analysis Reveal Hidden Associations Between Loss of Protein Expression in SWI/SNF Complex Components and Tumor Stage and Survival in Clear Cell Renal Cell Carcinoma (CCRCC)

Background Polybromo-1 (PBRM1), a targeting subunit of the SWI/SNF chromatin remodeling complex, is mutated at a rate of ~40% in clear cell Renal Cell Carcinoma (ccRCC), second only to VHL. Whether its mutation is correlated with tumor stage is controversial. As other components of the SWI/SNF complex were also reported to be mutated in ccRCC, we aim to examine the protein expression patterns of PBRM1, ARID1A, BRG1, and BRM in ccRCC, and to investigate possible association between their loss of expression and tumor stage, as well as survival. We also included a histone modifier, SETD2, which is recently discovered to be mutated in ~15% of ccRCC