Chasm Between Cancer Quality Measures and Electronic Health Record Data Quality.

Purpose: The Medicare Access and CHIP Reauthorization Act of 2015 (MACRA) requires eligible clinicians to report clinical quality measures (CQMs) in the Merit-Based Incentive Payment System (MIPS) to maximize reimbursement. To determine whether structured data in electronic health records (EHRs) were adequate to report MIPS CQMs, EHR data aggregated by ASCO's CancerLinQ platform were analyzed.

Materials And Methods: Using the CancerLinQ health technology platform, 19 Oncology MIPS (oMIPS) CQMs were evaluated to determine the presence of data elements (DEs) necessary to satisfy each CQM and the DE percent population with patient data (fill rates).

Simultaneous electroencephalographic and functional magnetic resonance imaging indicate impaired cortical top-down processing in association with anesthetic-induced unconsciousness.

Background: In imaging functional connectivity (FC) analyses of the resting brain, alterations of FC during unconsciousness have been reported. These results are in accordance with recent electroencephalographic studies observing impaired top-down processing during anesthesia. In this study, simultaneous records of functional magnetic resonance imaging (fMRI) and electroencephalogram were performed to investigate the causality of neural mechanisms during propofol-induced loss of consciousness by correlating FC in fMRI and directional connectivity (DC) in electroencephalogram.

Spatiotemporal reconfiguration of large-scale brain functional networks during propofol-induced loss of consciousness.

Applying graph theoretical analysis of spontaneous BOLD fluctuations in functional magnetic resonance imaging (fMRI), we investigated whole-brain functional connectivity of 11 healthy volunteers during wakefulness and propofol-induced loss of consciousness (PI-LOC). After extraction of regional fMRI time series from 110 cortical and subcortical regions, we applied a maximum overlap discrete wavelet transformation and investigated changes in the brain's intrinsic spatiotemporal organization. During PI-LOC, we observed a breakdown of subcortico-cortical and corticocortical connectivity.

Discordant effects on eicosanoids and fibrin degradation products in two murine models of antiphospholipid antibody.

Two murine models of lupus were employed to challenge an hypothesized mechanism by which antiphospholipid antibodies (APLA) might promote thrombosis: altering prostacyclin (PGI2) and thromboxane (TX) production. PGI2 levels in mouse blood and the ex vivo release of PGI2 and TX from mouse kidney were measured. Since APLA have been reported to alter synthesis or activation of several molecules mediating fibrinolysis, murine plasma levels of the fibrin degradation product, D-dimer were also determined.

Dysfibrinogenemia: a case with thrombosis (fibrinogen Richfield) and an overview of the clinical and laboratory spectrum.

Fibrinogen Richfield exemplifies a dysfibrinogen associated with a life-long thrombotic tendency. The evaluation of this novel case indicates that, like similar thrombotic dysfibrinogenemias, the abnormal protein polymerizes abnormally and demonstrates impaired clot dissolution. A survey of other cases of dysfibrinogenemia indicates that the relatively common abnormalities of Fibrinopeptide A release are generally asymptomatic or associated with bleeding, polymerization abnormalities are likely to be asymptomatic or associated with thrombosis (or occasionally bleeding), and complex abnormalities or additional, independent hemostatic defects are rather common.

Some antiphospholipid antibodies inhibit phospholipase A2 activity.

Certain antiphospholipid antibodies, particularly those associated with arterial thrombosis, reduce vascular prostacyclin production. Studies were conducted to determine whether antibody-mediated inhibition of phospholipase A2 accounts for this effect. In this report we present evidence that purified antiphospholipid antibodies reduce phospholipase A2 activity toward phospholipid substrates, both in vitro and in a defined system.

Lupus anticoagulant inhibition of in vitro prostacyclin release is associated with a thrombosis-prone subset of patients.

Purpose: The effect of lupus anticoagulant-containing sera on endothelial prostacyclin generation (both basal and after thrombin stimulation) was determined. Subsets of patients who had experienced arterial, venous, or no thrombosis were compared with respect to the quantitation of antiphospholipid antibody and effects on prostacyclin production.

Patients And Methods: Serum antiphospholipid antibodies were detected in 26 patients by immunologic (enzyme-linked immunosorbent assay) and kinetic (anticoagulant) assays.

Effects of endothelium-derived relaxing factor and nitric oxide on rat mesangial cells.

We have investigated whether endothelium-derived relaxing factor (EDRF) and nitric oxide (NO), a substance proposed to be one of the EDRFs, could elicit biochemical and biological responses in rat glomerular mesangial cells (MC). In wells with MC alone, guanosine 3',5'-cyclic monophosphate (cGMP) levels were 2.6 +/- 0.

Fish oil supplementation does not lower plasma cholesterol in men with hypercholesterolemia. Results of a randomized, placebo-controlled crossover study.

Study Objective: To determine the effects of fish oil supplementation on plasma cholesterol in middle-aged men with isolated hypercholesterolemia.

Design: Randomized double-blind placebo-controlled (safflower oil) two-period crossover trial with 12-week treatment periods.

Setting: Outpatient general medicine clinic at a university-affiliated Veterans Affairs hospital.

Interleukin 1 enhances arterial thrombogenicity in vitro.

An in vitro model of platelet adhesion, the annular perfusion chamber, was utilized to test the effects of Interleukin 1 on vascular thrombogenicity for platelets. De-endothelialized, everted human umbilical arteries were placed in cell culture media with or without Interleukin 1. The arteries were later perfused with citrated human blood and then fixed.

Lupus anticoagulant induces a selective defect in thrombin-mediated endothelial prostacyclin release and platelet aggregation.

A patient with microvascular thrombosis and thrombocytopenia was found to have a high-titre lupus anticoagulant. The biological effects of the patient's lupus anticoagulant were studied using whole patient serum and plasma. Staph Protein A eluate, and affinity-purified lupus anticoagulant.

Endothelial cell heterogeneity: antioxidant profiles determine vulnerability to oxidant injury.

Human umbilical vein endothelial cells were more sensitive to hydrogen peroxide lysis than cow pulmonary artery endothelial cells. Conversely, activated neutrophils which utilize hydrogen peroxide-mediated cell cytotoxicity cell mechanisms were more toxic to the cow pulmonary artery cells. This discordance was not related to neutrophil adhesion to either cell type or cell passage number.

Interleukin 1 or endotoxin increases the release of von Willebrand factor from human endothelial cells.

von Willebrand factor (vWF), a large adhesive glycoprotein, is synthesized by vascular endothelial cells (EC). Plasma levels of vWF manifest a broad normal range, and are elevated during sepsis and in inflammatory states. Since the inflammatory mediator, interleukin 1 (IL1) and bacterial endotoxin (LPS) both initiate procoagulant changes in vascular endothelium, we investigated the effect of these substances on endothelial cell release and residual endothelial cell content of vWF-antigen (vWFAg).

Interleukin 1 stimulates endothelial cell tissue factor production and expression by a prostaglandin-independent mechanism.

Activation of coagulation occurs at inflammatory sites following the ingress of mononuclear cells, and may result from alterations in the vessel wall. Since the monokine, interleukin 1, initiates diverse responses to inflammation, its ability to enhance vascular procoagulant activity was studied. Interleukin 1-treated cultured human endothelial cells acquired elevated levels of the procoagulant, tissue factor.

Platelet-derived growth factor does not stimulate prostacyclin synthesis by cultured endothelial cells.

We examined the effect of highly purified platelet-derived growth factor (PDGF) on prostacyclin (PGI2) release by cultured human umbilical vein and bovine aortic endothelial cells. PDGF tested at concentrations equal to or exceeding those observed in serum did not increase endothelial cell PGI2 synthesis as measured by radioimmunoassay of its metabolite, 6-keto-PGF1 alpha. In contrast, cells incubated with 20% human whole blood serum (WBS) demonstrated significantly increased PGI2 production (fivefold stimulation).

Structural features of endotoxin required for stimulation of endothelial cell tissue factor production; exposure of preformed tissue factor after oxidant-mediated endothelial cell injury.

Cultured human umbilical vein endothelial cells synthesize the procoagulant, tissue factor, after exposure to bacterial endotoxin. Wild-type lipopolysaccharide from Escherichia coli 0127:B8 stimulates a five- to 20-fold increase in cellular tissue factor. Similarly, rough or incomplete lipopolysaccharide subunits from mutant bacterial strains, or lipid A prepared by mild acid hydrolysis of whole endotoxin, are also stimulatory.

Acute respiratory failure following severe arsenic poisoning.

A 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk.

Oral contraceptive use alters the balance of platelet prostaglandin and thromboxane synthesis.

The ability of platelet microsomes to generate platelet aggregating activity on addition of arachidonic acid was evaluated in women taking oral contraceptives and in controls taking no medication but matched for age, sex, and family history. Oral contraceptive users generated significantly more platelet aggregating activity per 100 ug of platelet microsomal protein than controls. Variation in generation of platelet aggregating activity during the menstrual cycle was also observed with highest activity during the third week.