Intracranial circulation: pulse-sequence considerations in three- dimensional (volume) MR angiography

The technique and feasibility of magnetic resonance (MR) angiography of intracranial vessels were studied in 35 healthy volunteers. Variations in image orientation, repetition time (TR), and flip angle were evaluated to determine their effects on flow-related enhancement. Gradient modifications--including echo time (TE), motion compensation, bandwidth, and field of view--were also studied in an effort to reduce motion-induced phase shifts. Results indicated that a FISP (fast imaging with steady precession) sequence with a TR of 50 msec, TE of 15 msec, velocity compensation in the read and section-select directions, acceleration compensation in the read direction, anisotropic volume, and a 1.25-mm partition thickness produced three-dimensional angiographic MR images that were accurate and reproducible in the depiction of the major intracranial vessels. Difficulties with field of view, persistent signal void secondary to higher-order motion, and spatial resolution remain major problems requiring additional study.     

AlphaV beta3 (αvβ3) integrin inhibition reduces leukocyte–endothelium interaction in a pressure-induced reperfusion model

The leukocyte-endothelium interaction is known to contribute to reperfusion injury, which is considered to participate in the pathophysiology of pressure ulcers, and integrin alphaV beta3 (alphavbeta3) has been shown to mediate the processes of cellular adhesion in various types of cells. This study aims to clarify leukocyte behavior in our original microcirculatory pressure-induced reperfusion model, which can visualize the microcirculation in vivo. We also estimated the effect of alphavbeta3 integrin inhibition on the reduction of the leukocyte-endothelium interaction. Mice with dorsal skinfold chambers were divided into three groups: the baseline group (n=6), in which animals received no compression; the compression-reperfusion group (n=6), in which animals underwent 2-hour compression of the dorsal skin, followed by release, and the inhibitor-treated group (n=7), in which an alphavbeta3 inhibitor, CP4715, was administered in addition to the compression-release procedure. Staining with rhodamine 6G quantitatively visualized leukocyte behavior under the intravital fluorescent microscope. Compression-reperfusion induced a significant increase in rolling, sticking, and extravasation of the leukocytes. Treatment with the inhibitor strikingly reduced leukocyte sticking and extravasation. The present experiment has provided evidence that alphavbeta3 inhibition reduces leukocyte-endothelium interaction in our original pressure-induced reperfusion model.     

Raf-1 kinase,epidermal growth factor receptors,and mutant ras proteins in colonic carcinomas

Epidermal growth factor receptors (EGFR) andras mutations are known to play a significant role in controlling cell growth and tumor promotion. Both of them transmit mitogenic signals to the nucleus by activation of Raf-1 kinase. In this study, the expression of EGFR and mutant Ras proteins, and, for the first time, the expression, phosphorylation and kinase activity of Raf-1 kinase have been determined in paired samples of colorectal cancer and mucosa. The tumor and mucosa samples did not differ significantly with regard to Raf-1 kinase content and activity. A major difference between tumors and mucosa was found, however, in the phosphorylation of Raf-1. Most of the mucosa samples (13/20), but only 1/20 of the cancer samples, contained hyperphosphorylated Raf-1. EGFR were significantly (p=0.0025) decreased in the tumors. The decreased phosphorylation of Raf-1 in colonic carcinomas could be the result of activation of Raf-1 phosphatases or inactivation of kinases phosphorylating Raf-1. New forms of treatment based on EGFR overexpression do not seem to be suitable for the majority of colonic cancers.This work was supported by the state of Baden-Württemberg (Verbundforschungsprojekt: Aufklärung von Mechanismen der Tumorentstehung und Tumorabwehr).     

Study of some official pharmaceutical preparations in the Sixth Edition of Formule Normales by thin-layer chromatography

Pharmaceutical preparations--containing aminophenazonum, noraminophenazonum sodium mesylicum, acidum acetylsalicylicum and aethylmorphinium chloratum--official in the VI. Edition of Formulae Normales have been investigated. Simple method for studying decomposition products--which can be carried out in pharmacies and can be followed the quality of products with during their usability--has been developed. The method proving and precluding the presence of decomposition products, respectively by means of preparing dilution sets has been capable of semiquantitative determination of decomposition products. DC Alufolien Kieselgel 60 F254 (Merck) layer was used. Temperature of laboratory was 22-26 degrees C and its relative humidity was 30-40%. Developing solvents were: acetone-ether-water (90:15:12) for aminophenazum; benzene-acetone-90% alcohol-wated (35: 33: 26: 11) for noraminophenazonum sodium mesylicum; methenol-glacial acetic acid-ether-benzene (1: 18: 60: 120) for acidum acetylsalicylicum; dichloromethane-methanol-concentrated ammonia (85: 15: 2) for aethylmorphinium chloratum. Detections were carried out under UV light and by using colour reagents (alcoholic ninhydrine solution for aminophenazonum, dimethylamino-benzaldehyde solution for noraminophenazonum sodium mesylicum). Rf-values of intact and decomposed compounds have been given in figures. Interfering effects of other components of preparations were studied too. These components had different Rf-values or did not react with the colour producing reagents in the applied systems.     

Analysis of ischemia-reperfusion injury in a microcirculatory model of pressure ulcers

The aim of this study was to establish a pressure ulcer model that visualizes the microcirculation, and to examine the participation of ischemia-reperfusion injury in the pathophysiology of pressure ulcers. An original system composed of a new skin fold chamber and compression device allowed loading quantitative vertical stress to the skin. An intravital microscopic technique enabled direct visualization of the microcirculation in the physiological condition and in response to pressure application. To estimate the effect of ischemia-reperfusion injury, animals were divided into two groups: the compression-release group (n = 8), in which the animals received four cycles of compression-release which consisted of 2 hours of compression followed by 1 hour of pressure release; and the compression alone group (n = 8) in which the animals underwent continuous compression for 8 hours. Functional capillary density was quantified before the compression procedure and on day 1 (35 hours) after the first evaluation. The cyclic compression-release procedure significantly decreased functional capillary density as compared to continuous compression, indicating that in our experimental setting repetition of ischemia-reperfusion cycle more severely damaged the microcirculation than single prolonged ischemic insult. This finding supports the significant contribution of ischemia-reperfusion injury to the pathophysiology of pressure ulcers at the level of dynamic in vivo microcirculation.     

Detection and enumeration of toxin-producing Pasteurella multocida with a colony-blot assay.

Colonies of toxin-producing Pasteurella multocida were detected with peroxidase-labeled monoclonal antibodies by a membrane assay. Examination of the specificity of the assay with 29 P. multocida cultures representing various geographic origins, hosts, and serotypes indicated that the test was specific for toxin-producing strains. No cross-reactions were observed with Bordetella species that can be associated with P. multocida in producing diseases in animals. A single membrane could be used to assay several isolated strains for toxin production or to enumerate toxin-producing colonies in mixed cultures. Toxin-producing P. multocida colonies were detected in primary cultures; hence, the assay appears to have good potential for widespread application with clinical samples.     

Five-year follow-up pulmonary function studies in patients with anti-trypsin deficient pulmonary emphysema]

Five-year follow-up study was carried out in pulmonary emphysematous patients with intermediate antitrypsin deficiency. The examinations showed no deterioration in the clinical state of the patients but in some parts of the controlled functional parameters a statistically significant worsening was found in this period of study.