Lymphoid cell rich fine-needle aspirations of the salivary gland: What is the risk of malignancy?

Objectives: Lymphoid cell rich fine-needle aspirations (FNAs) of the salivary glands pose a diagnostic dilemma, with a wide range of differential diagnoses that include several benign and malignant entities. There is limited literature regarding the entities that are commonly encountered in this situation. Our goal was to characterize the surgical outcome in these cases and to evaluate the risk of malignancy.

Macrophage angiotensin-converting enzyme reduces atherosclerosis by increasing peroxisome proliferator-activated receptor α and fundamentally changing lipid metabolism.

Aims: The metabolic failure of macrophages to adequately process lipid is central to the aetiology of atherosclerosis. Here, we examine the role of macrophage angiotensin-converting enzyme (ACE) in a mouse model of PCSK9-induced atherosclerosis.

Methods And Results: Atherosclerosis in mice was induced with AAV-PCSK9 and a high-fat diet.

The Tox Gene Encodes Two Proteins with Distinct and Shared Roles in Gene Regulation.

Here we report that the murine Tox gene encodes two proteins from a single mRNA, and we investigate the mechanism of production and function of these proteoforms. The annotated thymocyte selection-associated HMG-box protein (TOX) coding sequence is predicted to produce a 526-aa protein (TOXFL). However, Western blots reveal two bands.

RASAL3 Is a Putative RasGAP Modulating Inflammatory Response by Neutrophils.

As first responder cells in host defense, neutrophils must be carefully regulated to prevent collateral tissue injury. However, the intracellular events that titrate the neutrophil's response to inflammatory stimuli remain poorly understood. As a molecular switch, Ras activity is tightly regulated by Ras GTPase activating proteins (RasGAP) to maintain cellular active-inactive states.

Tumors exploit CXCR4CD62L aged neutrophils to facilitate metastatic spread.

Granulocytes are key players in cancer metastasis. While tumor-induced expansion of immunosuppressive myeloid-derived suppressor cells (MDSCs) is well-described, the fate and contribution of terminally differentiated mature neutrophils to the metastatic process remain poorly understood. Here, we show that in experimental metastatic cancer models, CXCR4CD62L aged neutrophils accumulate via disruption of neutrophil circadian homeostasis and direct stimulation of neutrophil aging mediated by angiotensin II.

Epigenetic and Posttranscriptional Regulation of CD16 Expression during Human NK Cell Development.

The surface receptor FcγRIIIA (CD16a) is encoded by the gene and is acquired by human NK cells during maturation. NK cells bind the Fc portion of IgG via CD16a and execute Ab-dependent cell-mediated cytotoxicity, which is critical for the effectiveness of several antitumor mAb therapies. The role of epigenetic regulatory mechanisms controlling transcriptional and posttranscriptional CD16 expression in NK cells is unknown.

IL-18 Drives ILC3 Proliferation and Promotes IL-22 Production via NF-κB.

Group 3 innate lymphoid cells (ILC3s) are important regulators of the immune system, maintaining homeostasis in the presence of commensal bacteria, but activating immune defenses in response to microbial pathogens. ILC3s are a robust source of IL-22, a cytokine critical for stimulating the antimicrobial response. We sought to identify cytokines that can promote proliferation and induce or maintain IL-22 production by ILC3s and determine a molecular mechanism for this process.

CAR-Engineered NK Cells Targeting Wild-Type EGFR and EGFRvIII Enhance Killing of Glioblastoma and Patient-Derived Glioblastoma Stem Cells.

Glioblastoma (GB) remains the most aggressive primary brain malignancy. Adoptive transfer of chimeric antigen receptor (CAR)-modified immune cells has emerged as a promising anti-cancer approach, yet the potential utility of CAR-engineered natural killer (NK) cells to treat GB has not been explored. Tumors from approximately 50% of GB patients express wild-type EGFR (wtEGFR) and in fewer cases express both wtEGFR and the mutant form EGFRvIII; however, previously reported CAR T cell studies only focus on targeting EGFRvIII.

Variables associated with discordance between emergency physician and neurologist diagnoses of transient ischemic attacks in the emergency department.

Study Objective: Transient ischemic attack is a common clinical diagnosis in emergency department (ED) patients with acute neurologic complaints. Accurate diagnosis of transient ischemic attack is essential to help guide evaluation and avoid treatment delays. We seek to determine the prevalence of discordant diagnosis for patients receiving an ED diagnosis of transient ischemic attack compared with neurologist final diagnosis.

Can the ABCD2 risk score predict positive diagnostic testing for emergency department patients admitted for transient ischemic attack?

Background And Purpose: We sought to determine if the ABCD2 score, typically used for risk stratification, could predict having a positive diagnostic test in patients evaluated acutely for transient ischemic attack.

Methods: We performed a retrospective cohort study for patients admitted from our emergency department with a new diagnosis of transient ischemic attack confirmed by a neurologist. ABCD2 scores were calculated and patients with a score of > or = 4 were placed in the high-risk cohort.