Electron paramagnetic resonance study of Eu2+ centers in melt-grown CsBr single crystals

The structure of Eu2+ monomer centers in CsBr single crystals is investigated using electron paramagnetic resonance (EPR) spectroscopy. These centers are produced by heating the melt-grown crystals above 600 K in vacuum followed by a rapid quench to room temperature (RT) or 77 K. The angular dependence of their EPR spectrum demonstrates that these centers have cubic symmetry. At RT the EPR spectrum decays by aggregation of the Eu2+ ions. This strongly contrasts with the situation for CsBr:Eu needle image plates synthesized by physical vapor deposition, where the Eu2+-related EPR spectrum was observed to exhibit long-term stability at RT

Modulation of nitric oxide synthase activity in macrophages

L-Arginine is converted to the highly reactive and unstable nitric oxide (NO) and L-citrulline by an enzyme named nitric oxide synthase (NOS). NO decomposes into other nitrogen oxides such as nitrite (NO2-) and nitrate (NO2-), and in the presence of superoxide anion to the potent oxidizing agent peroxynitrite (ONOO−). Activated rodent macrophages are capable of expressing an inducible form of this enzyme (iNOS) in response to appropriate stimuli, i.e., lipopolysaccharide (LPS) and interferon-γ (IFNγ). Other cytokines can modulate the induction of NO biosynthesis in macrophages. NO is a major effector molecule of the anti-microbial and cytotoxic activity of rodent macrophages against certain micro-organisms and tumour cells, respectively. The NO synthesizing pathway has been demonstrated in human monocytes and other cells, but its role in host defence seems to be accessory. A delicate functional balance between microbial stimuli, host-derived cytokines and hormones in the microenvironment regulates iNOS expression. This review will focus mainly on the known and proposed mechanisms of the regulation of iNOS induction, and on agents that can modulate NO release once the active enzyme has been expressed in the macrophage

Recent Decisions

Comments on recent decisions by Robert R. Waterson, Hugh E. Wall, Francis W. Matthys, Granville P. Ziegler, Thomas H. Nelson, Stanley A. Rosenstein, and John M. Doyle

Oxidized Lipoproteins Suppress Nitric Oxide Synthase in Macrophages: Study of Glucocorticoid Receptor Involvement

Activated cholesterol-laden macrophages in atherosclerotic lesions are believed to influence the progression of this disease. The induction of nitric oxide synthase (iNOS) activity was investigated in control and cholesterol-laden J774 macrophages, obtained by pre-incubation with oxidized or acetylated low density lipoproteins (oxLDL, acLDL). Loading with oxLDL caused a small induction of NOS activity in unstimulated cells, as indicated by nitrite and citrulline accumulation in the supernatant. However, it suppressed the iNOS activity resulting from stimulation of the cells with lipopolysaccharide with or without interferon-γ. AcLDL had no inhibitory effect, indicating that cholesterol accumulation as such was not responsible. Since the induction of NOS in macrophages is inhibited by glucocorticoids, the possibility that a glucocorticoid-like factor, formed during oxidation of LDL, may cause the inhibition, was investigated. However, addition of the glucocorticoid receptor antagonist mifepristone did not prevent the oxLDL-dependent NOS inhibition, indicating that the glucocorticoid receptor is not involved in the suppressive effect of oxLDL

Traumatic urinary bladder rupture: the usefulness of CT cystography

A 38-year-old male presented at the emergency unit with acute abdominal pain and massive hematuria after a fall in the stairs of his home. At physical examination, tenderness was found in the hypogastric area and in both right and left iliac regions. The first radiological investigation performed was ultrasonography (Fig. A). Free liquid was found in the Morisson pouch, in the perihepatic-space and in the perisplenic fossa. The bladder contained blood clots and there was no liquid in the Douglas pouch. Active bleeding was not excluded. Unenhanced and contrast-enhanced CT of the abdomen in arterial, venous and late phase was performed and large amount of intraperitoneal liquid was confirmed but without evident cause (Fig. B). There were no visceral injuries neither skeletal lesion nor vascular lesion. 60 minutes later, an additional cystography phase was performed and revealed a rupture in the superior aspect of the bladder with intraperitoneal spilling of contrast (Fig. C and D). Consequently, the patient was admitted for surgical repair of the bladder defect

Pseudo-achalasia: a complication of laparoscopic adjustable gastric banding

A 49-year-old woman presented with dyspepsia and nocturnal regurgitation. A laparoscopic adjustable gastric binding (LAGB) had been performed 6 years before presentation. An upper gastrointestinal barium contrast study was performed and revealed a marked dilatation and tortuous course of the esophagus as well as absence of peristalsis and delayed evacuation of the esophagus (Fig. A, B). The findings were compatible with an achalasia-like disorder. An esophageal manometry revealed a constant high LES pressure with aperistalsis, thus confirming the diagnosis of (pseudo-)achalasia. Consequently a complete band deflation was conducted and resulted in a complete resolution of the patient’s symptoms. Two weeks later the control contrast study showed a marked improvement of the delayed evacuation and a small regain of peristaltic function. The dilatation and “sigmoidlike” image of the esophagus remained unchanged (Fig. C)