Evaluation of the influence of the aqueous phase bioconstituent environment on the F-19 T1 of perfluorocarbon blood substitute emulsions

Oxygen-sensitive F-19 magnetic resonance imaging of perfluorocarbon compounds requires that fluorocarbon T1 changes correlate with the local Po₂ and not with the composition of the surrounding aqueous phase. The influence of various bioconstituents and paramagnetic ions within the aqueous phase on the F-19 fluorocarbon phase T1 for PFC emulsions was evaluated at 0.14 and 0.66 T. T1 was measured for FC-43, perflubron, and a fluorinated surfactant. Controlled variables introduced in the aqueous phase included annex solution constituents, blood, pH changes, and Gd-DTPA. For a constant Po₂, the F-19 T1s were independent of the emulsion constituents, blood concentration, and pH. For FC-43 and perflubron, F-19 T1 was independent of the Gd-DTPA concentration, while the aqueous phase T1 decreased by more than an order of magnitude. XMO-10 (smallest emulsion particle size) showed a slight decrease in F-19 T1 with increasing Gd-DTPA concentration at 0.66 T.     

Examination of the effects of hemodynamic and pharmacologic interventions on coronary collateral flow in a patient during cardiac catheterization

The vasomotor response of native human collateral vessels to pharmacologic or hemodynamic vasodilatory stimuli is not well known. We describe a case where retrograde collateral flow velocity was measured both at baseline and following selected hemodynamic and pharmacologic interventions. This index case represents the first in a series of potential human physiologic studies designed to address questions pertaining to control of collateral blood supply in humans. © 1993 Wiley-Liss, Inc.     

Angiodysplasia as the cause of massive lower gastrointestinal hemorrhage in a young adult

PURPOSE: This study was undertaken to clarify the importance of bleeding vascular ectasia of the colon as the etiology of massive lower gastrointestinal hemorrhage in patients 40 years of age or younger. METHODS: An otherwise healthy 21-year-old male was admitted to a tertiary medical center with massive lower gastrointestinal hemorrhage. Technetium-labeled red blood cell scan, selective visceral angiography, and colonoscopy identified the source of bleeding as vascular abnormality of the descending colon. Segmental colonic resection was performed. RESULTS: Histologic review of the specimen demonstrated a vascular ectasia. The patient recovered uneventfully and has had no further stigmata of hemorrhage. A review of the literature was undertaken to make clear the significance of vascular ectasia as the source for massive colonic hemorrhage in the young adult. CONCLUSION: This is the first report that documents histologically a vascular ectasia as the source of massive lower gastrointestinal hemorrhage in an otherwise healthy patient less than 40 years of age. Vascular ectasia is an uncommon cause of lower gastrointestinal hemorrhage in the young adult.The Chief, Bureau of Medicine and Surgery, Navy Department, Washington, DC, Clinical Investigation Program sponsored this report #84-16-1968-532, as required by HSETCINST 6000.41A. The views expressed in this article are those of the authors and do not reflect the official policy or position of the Department of the Navy, Department of Defense, or the United States Government.     

Alpha-melanocyte-stimulating hormone reduces endotoxin-induced liver inflammation.

Alpha-Melanocyte-stimulating hormone (MSH) is a potent anti-inflammatory agent in many models of inflammation, suggesting that it inhibits a critical step common to different forms of inflammation. We showed previously that alpha-MSH inhibits nitric oxide (NO) production in cultured macro-phages. To determine how alpha-MSH acts in vivo, we induced acute hepatic inflammation by administering endotoxin (LPS) to mice pretreated with Corynebacterium parvum, alpha-MSH prevented liver inflammation even when given 30 min after LPS administration. To determine the mechanisms of action of alpha-MSH, we tested its influence on NO, infiltrating inflammatory cells, cytokines, and chemokines. Alpha-MSH inhibited systemic NO production, hepatic neutrophil infiltration, and increased hepatic mRNA abundance for TNF alpha, and the neutrophil and monocyte chemokines (KC/IL-8 and MCP-1). We conclude that alpha-MSH prevents LPS-induced hepatic inflammation by inhibiting production of chemoattractant chemokines which then modulate infiltration of inflammatory cells. Thus, alpha-MSH has an effect very early in the inflammatory cascade.     

The effect of etching on bacterial microleakage of an adhesive composite restoration.

OBJECTIVES: The incidence of bacterial microleakage, pulp inflammation and necrosis associated with dentine etching treatments prior to restoration are not known. Consequently, to resolve some of the controversy surrounding the effects and importance of vital dentine etching, the authors investigated these factors. METHODS: 110 standardised class V cavities were cut into buccal dentine, without exposing the pulp of teeth scheduled for extraction for orthodontic reasons. Cavities were either left unetched, or etched with the non-equivalent treatments of phosphoric acid gel for 60s or Ethylenediaminetetraacetic acid (EDTA) for 30s, prior to placement of composite resin. Teeth were collected and pulp responses were evaluated according to ISO guidelines, using pathohistomorphometric analysis and ANOVA statistics. RESULTS: Etching was found to be correlated to bacterial microleakage (p=0.0001) and tertiary dentine formation (p=0.0023). Bacterial microleakage was correlated to inflammatory activity (p=0.0001). The frequency of bacterial microleakage was: no etching (65%), EDTA (51%) and phosphoric acid (PA) (20%). SIGNIFICANCE: Vital dentine etching treatment is of extreme importance for the placement of RC to minimise bacterial microleakage. PA etching proved to be more effective at preventing bacterial microleakage than non-etching, and etching with EDTA.