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Biomedical subjects

D Schick

Publications and source records attributed to D Schick.

12 recordsLinked to original sources
PubMed2006

[Low-MI-sonography with the contrast-agent SonoVue in the diagnosis of infarction of the spleen, kidney, liver and pancreas].

PURPOSE: The diagnosis of ischemic injury by B-mode-sonography is difficult in many cases. Aim of the pilot-study was to evaluate whether additional examination with the ultrasound contrast agent SonoVue could improve the sonographic diagnosis of ischemic injury. MATERIALS AND METHODS: In a prospective study, intra-abdominal organs (n = 12) with ischemic lesions found by CT-scan were examined. All ischemic organs were examined by native B-mode-sonography and after injection of 1.2 ml SonoVue i. v. The SonoVue-examinations were performed using the CPS-software (Siemens, Erlangen). RESULTS: Native B-mode-sonography detected demarcation of ischemic lesions in only 7 of the 12 organs. In contrast, SonoVue-enhanced sonography diagnosed ischemic lesions in all organs. In one patient with renal infarction, however, the ischemic lesion found by SonoVue-enhanced sonography was smaller compared with the CT-scan. The diagnosis "compatible with ischemia" as cause for the abnormalities in B-mode sonography was described in only 3 out of 12 organs, and none of the organs were classified as "definite diagnosis of ischemia". In contrast, the diagnosis "definite diagnosis of ischemia" was made in 10 of the 12 organs when examined with SonoVue-enhanced sonography. In two further patients, the lesion was classified as "compatible with ischemia". In these patients, the diagnosis of ischemia was verified by CT-scan, due to the accompanying subtotal splenic infarction and a partial thrombosis of the coeliac trunc. CONCLUSION: It became evident that SonoVue-enhanced sonography was more sensitive in the diagnosis of ischemic injury than native B-mode sonography.

Abdomen, Acute↗
PubMed2005

Recommendations for a technical quality control program for diagnostic X-ray equipment.

This position paper was produced by a working party set up by the Radiology Special Interest Group of the ACPSEM in 2001. It is designed to give the consensus view of College members in Australia and New Zealand on the nature and frequency of tests which should be performed on diagnostic x-ray equipment to maintain adequate quality control of imaging performance and radiation safety. Tests on mammographic equipment have been excluded having been covered in a previous ACPSEM position paper (Australas Phys Eng Sci Med, 24(3):107-131, 2001). Detailed descriptions of test procedures are not given but it is intended that a series of workbooks should be produced giving College recommended test methods for each imaging modality. The recommendations are produced here in an easy-to-read, tabular form giving the nature and purpose of each test and the implications of non-compliance with regard to image quality and radiation safety.

Australasia↗
PubMed1999

The zinc finger cluster domain of RanBP2 is a specific docking site for the nuclear export factor, exportin-1.

The Ran-binding protein 2 (RanBP2) is a large scaffold cyclophilin-related protein expressed in photoreceptor cells. Red/green opsin, Ran-GTPase, and the 19 S regulatory complex of the proteasome associate with specific RanBP2 structural modules. Some of these play a role in chaperoning the functional expression of opsin. RanBP2 localization at cytoplasmic fibrils emanating from the nuclear pore complex and interaction with the Ran-GTPase support also its role in nucleocytoplasmic transport processes. The degenerate nucleoporin repeat motifs FXFG, GLFG, and XXFG have been proposed to mediate the movement of nucleocytoplasmic transport factors. In particular, RanBP2 has been implicated in nuclear import processes. Here, we show the zinc fingers of RanBP2 associate with high specificity to the nuclear export factor, exportin-1 (CRM1). The bovine RanBP2 transcript contained only five of the eight zinc fingers reported in the human counterpart and are sufficient for exportin-1 association with RanBP2. In contrast to Ran interaction with RanBP2-exportin-1 complex, exportin-1 binding to the zinc finger cluster domain of RanBP2 is insensitive to leptomycin B and nucleotide-bound state of Ran-GTPase. Our results indicate that the zinc finger-rich domain of RanBP2 constitutes a docking site for exportin-1 during nuclear export. Thus, RanBP2 emerges as a key component of the nuclear export pathway.

Amino Acid Sequence↗
PubMed1998

The cyclophilin-like domain mediates the association of Ran-binding protein 2 with subunits of the 19 S regulatory complex of the proteasome.

The combination of the Ran-binding domain 4 and cyclophilin domains of Ran-binding protein 2 selectively associate with a subset of G protein-coupled receptors, red/green opsins, upon cis-trans prolyl isomerase-dependent and direct modification of opsin followed by association of the modified opsin isoform to Ran-binding domain 4. This effect enhances in vivo the production of functional receptor and generates an opsin isoform with no propensity to self-aggregate in vitro. We now show that another domain of Ran-binding protein 2, cyclophilin-like domain, specifically associates with the 112-kDa subunit, P112, and other subunits of the 19 S regulatory complex of the 26 S proteasome in the neuroretina. This association possibly mediates Ran-binding protein 2 limited proteolysis into a smaller and stable isoform. Also, the interaction of Ran-binding protein 2 with P112 regulatory subunit of the 26 S proteasome involves still another protein, a putative kinesin-like protein. Our results indicate that Ran-binding protein 2 is a key component of a macro-assembly complex selectively linking protein biogenesis with the proteasome pathway and, thus, with potential implications for the presentation of misfolded and ubiquitin-like modified proteins to this proteolytic machinery.

Amino Acid Sequence↗
PubMed1989

[Non-surgical management of an infected ventriculo-atrial shunt].

We report on a 81-year old patient who showed clinical signs of a shunt infection eight months after implantation of a ventriculo-atrial shunt system Heyer-Schulte. The reason was identified to be a massive infection with staphylococcus albus. Elimination of the infection was achieved by intravenous administration of fosfomycine and local instillation of gentamycin into the valve. The follow-up was uneventful for more than two years until the death of the patient in January 1987.

Aged↗
PubMed1988

Increased expression of adhesive proteins on leukocytes by TNF alpha.

To further elucidate the role of tumor necrosis factor alpha (TNF alpha) in cell adhesion, we investigated the effect of TNF alpha on the expression of surface adhesive protein. After treatment with TNF alpha for 1 h, the increased expression of surface adhesive proteins (beta subunit) was observed on granulocytes but not on monocytes or lymphocytes. The expression of Mac-1 (3,4-fold increase) was consistently enhanced more than p 150,95 (1.4-fold increase) and LFA-1 expression was unchanged. Dose-response and time course studies indicated a parallel relationship between TNF alpha-increased expression of surface adhesive proteins and TNF alpha-induced granulocyte adhesion. The anti-inflammatory drug Dexamethasone suppressed both TNF alpha-induced granulocyte adhesion and TNF alpha-induced expression of surface adhesive proteins. The inhibition of granulocyte adhesion correlated with the reduction of surface adhesive protein expression. The data suggest that one contributing factor in the mechanism by which Dexamethasone inhibited TNF alpha-induced granulocyte adhesion may be diminished expression of surface adhesive proteins.

Antigens, Surface↗
PubMed1987

Binding of tumor necrosis factor alpha (TNF-alpha) to high-affinity receptors on polymorphonuclear cells.

The effects of tumor necrosis factor alpha (TNF-alpha) on human polymorphonuclear (PMN) cells were investigated. We found that 125I-TNF-alpha bound specifically to high-affinity receptors on PMN cells. At 4 degrees C, the binding occurred rapidly and reached steady state after 20 min. The Scatchard plot showed a single class of high-affinity receptors with approximately 2200 receptors/cell and a dissociation constant of 2 x 10(-10) M. There was a linear relationship between TNF-alpha binding and TNF-alpha-induced PMN cell adherence. The concentration of TNF-alpha required to achieve approximately 50% of maximum binding was also approximately the concentration required to reach 50% cell adherence. Auranofin was shown to inhibit TNF-alpha-induced PMN cell adherence at a dose of 5-10 micrograms/ml. This inhibitory effect was not due to the inhibition of TNF-alpha binding to PMN cells by the drug. These observations may have clinical implications.

Auranofin↗
PubMedDate not supplied

Bedside terminals and quality of nursing documentation.

In this article, the authors report on part one of a three-part investigation studying the impact of bedside terminals at New York University Medical Center, New York, NY. Using a before-after parallel control-group design, the quality of computerized nursing documentation was studied before and after adding computers to patient rooms. The quality of documentation was defined by timeliness and completeness of data. The study hypothesis, which predicted a positive relationship between the presence of bedside terminals and the quality of nursing documentation, was not supported. Study results showed a minimal use of the computer terminals located in patient rooms. A surprising result was the use of terminals located in rooms other than that of the patient for which documentation was made.

Computer Terminals↗