Echocardiographic Parameters of Mechanical Synchrony in Healthy Individuals††Conflicts of interest: Fondazione Cardiocentro Ticino has a research contract with GE Healthcare, Milwaukee, Wisconsin. Dr. Conca is a research fellow at Fondazione Cardiocentro Ticino, and her tenure is sponsored by Boston Scientific Corporation. Dr. Faletra received speaker's fees from GE Healthcare. Dr. Sorgente is a research fellow at Fondazione Cardiocentro Ticino, and his tenure is sponsored by Medtronic. Dr. Auricchio is consultant to Sorin and Medtronic, Inc., Minneapolis, Minnesota, and received speaker's fees from Medtronic, Inc., Boston Scientific Corporation, Natick, Massachusetts, Biotronik, Berlin, Germany, GE Healthcare, and Sorin Group, Montrouge, France.

2009 ◽  
Vol 103 (1) ◽  
pp. 136-142 ◽  
Author(s):  
Cristina Conca ◽  
Francesco Fulvio Faletra ◽  
Chinami Miyazaki ◽  
Jae Oh ◽  
Antonio Mantovani ◽  
...  
Keyword(s):  
Conflicts Of Interest ◽  
Boston Scientific ◽  
Healthy Individuals ◽  
Research Fellow ◽  
Scientific Corporation ◽  
Echocardiographic Parameters ◽  
Boston Scientific Corporation ◽  
Mechanical Synchrony ◽  
Research Contract

Frequency, Duration, and Predictors of Newly-Diagnosed Atrial Fibrillation Following Dual-Chamber Pacemaker Implantation in Patients Without a Previous History of Atrial Fibrillation††Conflicts of interest: Dr. Mittal is a consultant for Biotronik and LifeWatch Corporation, Rosemont, Illinois; has received fellowship support from Boston Scientific Corporation, St. Paul, Minnesota, and Medtronic, Minneapolis, Minnesota; and has received speaking honoraria from Boston Scientific Corporation, Medtronic, and St. Jude Medical, St. Paul, Minnesota. Dr. Stein has received speaking honoraria from Boston Scientific Corporation, Medtronic, and St. Jude Medical and is a member of the advisory boards of Boston Scientific Corporation and Medtronic. Dr. Gilliam is a consultant for, has received speaking honoraria from, is a member of the advisory board of, and has received research funding from Boston Scientific Corporation. Stacia Merkel Kraus is a consultant for Boston Scientific Corporation. Drs. Meyer and Christman are employees of Boston Scientific Corporation.

2008 ◽  
Vol 102 (4) ◽  
pp. 450-453 ◽  
Author(s):  
Suneet Mittal ◽  
Kenneth Stein ◽  
F. Roosevelt Gilliam ◽  
Stacia Merkel Kraus ◽  
Timothy Edward Meyer ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Conflicts Of Interest ◽  
Previous History ◽  
Pacemaker Implantation ◽  
Boston Scientific ◽  
Jude Medical ◽  
Advisory Boards ◽  
Scientific Corporation ◽  
Boston Scientific Corporation ◽  
History Of

scholarly journals Esophageal Perforation after Using a Single-Use Disposable Duodenoscope

2021 ◽  
pp. 972-977
Author(s):  
Bakht S. Cheema ◽  
Maged Ghali ◽  
Ron Schey ◽  
Ziad Awad ◽  
Bruno Ribeiro
Keyword(s):  
Esophageal Perforation ◽  
Gastroesophageal Junction ◽  
Unintended Consequences ◽  
Tactile Feedback ◽  
Fistula Formation ◽  
Boston Scientific ◽  
Safety Communication ◽  
Scientific Corporation ◽  
Boston Scientific Corporation ◽  
Single Use

The Food and Drug Administration (FDA) has recently released a safety communication recommending transition to duodenoscopes with innovative designs that facilitate or eliminate the need for reprocessing. Thus, there has been a significant amount of development into disposable duodenoscope components and single-use duodenoscopes, with variable tactile feedback. We describe a case of esophageal perforation after using a single-use disposable duodenoscope (EXALT Model D; Boston Scientific Corporation, Marlborough, MA, USA). To our knowledge, this is the first reported case of an esophageal perforation since FDA approval of this device in December 2019. ERCP was performed with the EXALT Model D single-use duodenoscope (Boston Scientific Corporation) by an experienced gastroenterologist. During the procedure, gentle force applied through the gastroesophageal junction caused a liner perforation in the distal esophagus. An esophageal stent was placed with satisfactory wound healing and no fistula formation. There have been a few reports in the last 2 years showing promising results using this device; however, the differences in the tactile feedback, navigation, and pushability of the device may make it prone to unintended consequences.

HS1 (HCLS1) Protein, a Binding Partner of HAX1, Induces G-CSF-Triggered Granulopoiesis Via LEF-1 Transcription Factor.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 548-548
Author(s):  
Julia Skokowa ◽  
Dan Lan ◽  
Murat Uenalan ◽  
Kshama Gupta ◽  
Karl Welte
Keyword(s):  
Tyrosine Kinases ◽  
Conflicts Of Interest ◽  
Protein A ◽  
Hematopoietic Cells ◽  
Specific Protein ◽  
Actin Assembly ◽  
Healthy Individuals ◽  
Granulocytic Differentiation ◽  
Endogenous Proteins ◽  
First Time

Abstract Abstract 548 Mutations in HS1 (HCLS1) associated protein × 1 (HAX1) have been described in patients with severe congenital neutropenia (CN). HAX1 is a ubiquitously expressed and until now it was unclear how HAX1 mutations cause isolated neutropenia in CN patients. So we were interested in investigating G-CSF-dependent HS1 (HCLS1) protein expression and phosphorylation in CN patients compared to healthy individuals, since HS1 (HCLS1) is a hematopoietic-specific protein and may link HAX1 to the G-CSFR signaling via the tyrosine kinases lyn and syk. Indeed, we found that treatment of CD34+ hematopoietic cells with G-CSF leads to phosphorylation of HS1 (HCLS1) protein and recruitment of receptor thyrosine kinases lyn and syk. In CN patients harboring HAX1 mutations, G-CSF failed to upregulate expression and phosphorylation of HS1 (HCLS1), suggesting that for HS1 phosphorylation functional HAX1 protein is required. Indeed, inhibition of HAX1 in CD34+ hematopoietic cells from healthy individuals significantly abrogated G-CSF-triggered HS1 (HCLS1) phosphorylation. Previously, we found that LEF-1 is a master regulator of granulopoiesis and is severely diminished in myeloid cells of CN patients with HAX1 mutations. Moreover, these cells also exhibited severe defects in F-actin assembly. Using immunoprecipitation assay of endogenous proteins, we found that upon G-CSF stimulation of CD34+ hematopoietic cells, HS1 (HCLS1) protein additional to HAX1, also binds to LEF-1 protein modulating its expression, transcriptional activity and subsequently granulopoietic differentiation. Using CFU, qRT-PCR and reporter gene assays we demonstrated that inhibition of HS1 (HCLS1) severely disturbed G-CSF-triggered granulocytic differentiation in line with downregulation of LEF-1 expression and functions, as well as with pathological redistribution of F-actin. Taken together, in this study we demonstrated for the first time the connection between G-CSF receptor, HAX1 mutations, downregulation of HS1 (HCLS1) and LEF-1, abnormal F-actin assembly and the defective granulocytic differentiation in CN patients. Moreover, we demonstrated for the first time an ultimate direct connection between Wnt signaling and G-CSF cytokine cascade in granulopoiesis. Disclosures: No relevant conflicts of interest to declare.

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