Tissue-specific reprogramming leads to angiogenic neutrophil specialization and tumor vascularization in colorectal cancer.

Neutrophil (PMN) tissue accumulation is an established feature of ulcerative colitis (UC) lesions and colorectal cancer (CRC). To assess the PMN phenotypic and functional diversification during the transition from inflammatory ulceration to CRC we analyzed the transcriptomic landscape of blood and tissue PMNs. Transcriptional programs effectively separated PMNs based on their proximity to peripheral blood, inflamed colon, and tumors.

Macrophage-endothelial cell crosstalk orchestrates neutrophil recruitment in inflamed mucosa.

Neutrophil (PMN) mobilization to sites of insult is critical for host defense and requires transendothelial migration (TEM). TEM involves several well-studied sequential adhesive interactions with vascular endothelial cells (ECs); however, what initiates or terminates this process is not well-understood. Here, we describe what we believe to be a new mechanism where vessel-associated macrophages through localized interactions primed EC responses to form ICAM-1 "hot spots" to support PMN TEM.

Long-term patency of rescue stenting of an anomalous left circumflex coronary artery after transcatheter aortic valve replacement.

Transcatheter aortic valve replacement (TAVR) in the setting of an anomalous left circumflex coronary artery (LCX) has had a variety of outcomes. Most commonly an anomalous LCX originates as a separate ostium arising from the right coronary sinus or is found branching off of the proximal right coronary artery. The artery courses around the aortic annulus before taking the course seen in typical anatomy.

Iatrogenic ventricular septal defects following transcatheter aortic valve implantation.

Ventricular septal defect (VSD) rarely occurs following transcatheter aortic valve implantation (TAVI). We report two patients who developed VSD following TAVI. One case was a Gerbode defect treated by percutaneous closure, and the second was a restrictive perimembranous VSD managed conservatively.

Kounis syndrome presenting as ST elevation acute myocardial infarction.

Allergic acute coronary syndrome, Kounis syndrome, is a rare cause of ST-segment elevation myocardial infarction triggered by an allergic reaction to a drug or environmental allergen, resulting in atheromatous plaque rupture or coronary artery vasospasm. We report three cases of Kounis syndrome presenting as ST-segment elevation myocardial infarction.

Released Myeloperoxidase Attenuates Neutrophil Migration and Accumulation in Inflamed Tissue.

Neutrophil (PMN) recruitment to sites of insult is critical for host defense, however excessive PMN activity and tissue accumulation can lead to exacerbated inflammation and injury. Myeloperoxidase (MPO) is a PMN azurophilic granule enzyme, which together with HO, forms a powerful antimicrobial system designed to kill ingested bacteria. Intriguingly, in addition to intracellular killing of invading microorganisms and extracellular tissue damage due generation of ROS, soluble MPO has been directly implicated in modulating cellular responses and tissue homeostasis.

Inpatient Mortality and 30-Day Readmission Rates Associated with Troponin Testing in Patients without Acute Myocardial Infarction.

Objective: Troponin values above the threshold established to diagnose acute myocardial infarction (AMI; >99th percentile) are commonly detected in patients with diagnoses other than AMI. The objective of this study was to compare inpatient mortality and 30-day readmission rate in patients with troponin I (TnI) above and below the 99th percentile in those with type 1 AMI and type 2 myocardial injury.

Methods: Between January 1, 2016 and December 31, 2016, there were 56,895 inpatient hospitalizations; of these 14,326 (25.

Pericarditis with Resultant Pulmonary Trunk Compression Secondary to Mycotic Pseudoaneurysm.

Purulent pericarditis is a rare disease in the era of antibiotics, with being a possible, though uncommon etiology. Even more uncommon are mycotic aneurysms secondary to group A strep purulent pericarditis and bacteremia. We report a case of an 18-year-old female with a history of strep pharyngitis develop purulent pericarditis with subsequent ventricular fibrillation (VF).

Rates of Echocardiography, Coronary Angiography, and Coronary Intervention Associated With Troponin Testing in Hospitalized Patients.

Diagnosis of acute myocardial infarction (AMI) often depends on detection of cardiac troponin elevation >99th percentile. However, troponin elevation is commonly found in patients without AMI. We have previously reported an association between troponin elevation and rates of electrocardiogram (ECG), echocardiography (ECHO), and coronary angiography (CAG) in patients with a primary diagnosis of sepsis.

Inhibition of Bacillus anthracis metallo-β-lactamase by compounds with hydroxamic acid functionality.

Metallo-β-lactamases (MBLs) that catalyze hydrolysis of β-lactam antibiotics are an emerging threat due to their rapid spread. A strain of the bacterium Bacillus anthracis has its ability to produce and secrete a MBL, referred to Bla2. To address this challenge, novel hydroxamic acid-containing compounds such as 3-(heptyloxy)-N-hydroxybenzamide (compound 4) and N-hydroxy-3-((6-(hydroxyamino)-6-oxohexyl)oxy)benzamide (compound 7) were synthesized.

New modes of exchanger regulation: physiological implications.

Exchange activity is regulated principally by cytosolic Na+, Ca2+, and PIP2. However, the properties of these modes of regulation that have emerged from excised patch studies appear to be poorly suited to regulating exchange activity on a beat-to-beat basis. Here we summarize recent findings from our lab indicating that (a) allosteric activation by Ca2+ exhibits hysteresis, (b) elevated concentrations of cytosolic Na+ induce a mode of activity that no longer requires regulatory Ca2+ activation, and (c) the requirement for PIP2 is reduced or eliminated after allosteric Ca2+ activation.

Sodium-calcium exchange does not require allosteric calcium activation at high cytosolic sodium concentrations.

The activity of the cardiac Na(+)-Ca(2+) exchanger (NCX1.1) is allosterically regulated by Ca(2+), which binds to two acidic regions in the cytosolically disposed central hydrophilic domain of the NCX protein. A mutation in one of the regulatory Ca(2+) binding regions (D447V) increases the half-activation constant (K(h)) for allosteric Ca(2+) activation from approximately 0.

The peptide beta 43-47 which increases microvascular permeability is released by plasmin during cleavage of fragment Y of fibrinogen.

A synthetic pentapeptide corresponding to sequence 43-47 of human fibrinogen B beta chain elicited, in rabbits, antibodies that during immunoblotting recognized intact fibrinogen, fragments X and Y as well as the B beta chain. Since fragment Y is the last peptide product which reacts with anti-beta 43-47 antibodies, splitting of fragment Y into fragment D and fragment E must be accompanied by plasmin cleavage of the peptide bond beta Lys-47-Ala-48.