Biomedical subjects

Claudia Weidekamm

Publications and source records attributed to Claudia Weidekamm.

5 recordsLinked to original sources

PubMed2006

[Sports injury of the spine: imaging diagnosis].

Sports injuries, especially those due to trend sports, and overuse resulting from monotonous repetitive movement patterns may cause various spinal abnormalities. Indications for diagnostic imaging should be established more readily in this group of young patients than in adults, as there is a higher probability to find morphologic abnormalities. This diagnostic strategy should also be applied for MRI and CT investigations. Image findings should be interpreted with view on kinetic chains related to distinct sporting activities.

Athletic Injuries↗

PubMed2005

Diffusion weighted imaging of bone marrow pathologies.

Diffusion weighted imaging of non-CNS tissue has attracted much attention during the last years. Its capability of probing the microstructure of a biologic tissue at a sub-millimeter range is used to evaluate its diffusion capacity, which is tissue specific and can be used for tissue characterization. Processes involving bone marrow where the primary target for DWI during the last years. Most experience has been gained for differentiating benign from pathologic vertebral compression fractures, which can be reliably done when quantitative diffusion measurements are available. However, preliminary results exist indicating that this non-invasive technique may be a potential tool for therapy monitoring, which will revise the management of cancer patients. Moreover, this will be the first non-invasive and quantifiable tool for evaluating the effectiveness of modern tumor treatment. In this article, we will give an overview on the current status of DWI in the evaluation of bone marrow alterations; on currently available DWI techniques and a short out-look on future aspects of DWI in bone marrow pathologies.

Bone Marrow Diseases↗

PubMed2005

Effects of TIPS on liver perfusion measured by dynamic CT.

OBJECTIVE: Our aim was to measure the arterial, portal venous, and total perfusion of the liver parenchyma with dynamic, single-section CT in patients with liver cirrhosis before and after transjugular intrahepatic portosystemic shunt (TIPS) placement and to compare the results with normal values. SUBJECTS AND METHODS: Perfusion of the liver parenchyma was measured in 24 healthy volunteers and 41 patients with liver cirrhosis using dynamic single-section CT. Seventeen patients underwent TIPS placement, and CT measurements were repeated within 7 days. CT scans were obtained at a single level comprising the liver, spleen, aorta, and portal vein. Scans were obtained over a period of 88 sec (one baseline scan followed by 16 scans every 2 sec and eight scans every 7 sec) beginning with the injection of a contrast agent bolus (40 mL at 10 mL/sec). Parenchymal and vascular contrast enhancement was measured with regions of interest, and time-density curves were obtained. These data were processed with a pharmaco-dynamic fitting program (TopFit), and the arterial and portal venous component and the total perfusion of the hepatic parenchyma were calculated (milliliters of perfusion per minute per 100 mL of tissue). RESULTS: Mean normal values for hepatic arterial, portal venous, and total perfusion were 20, 102, and 122 mL/min per 100 mL, respectively. In patients with cirrhosis before TIPS, mean hepatic arterial, portal venous, and total perfusion was 28, 63, and 91 mL/min per 100 mL, respectively, which was statistically significant for all values (p <0.05). After TIPS, hepatic perfusion increased to a mean value of 48, 65, 113 mL/min per 100 mL for arterial (p <0.01), portal venous, and total (p=0.011) perfusion, respectively. CONCLUSION: In patients with cirrhosis, the hepatic arterial perfusion increased, whereas portal venous and total perfusion decreased compared with that of healthy volunteers. TIPS placement caused a statistically significant increase of the hepatic arterial and total hepatic perfusion. The portal venous parenchymal perfusion remained unchanged.

Adult↗

PubMed2003

High-dose remifentanil does not impair cerebrovascular carbon dioxide reactivity in healthy male volunteers.

BACKGROUND: Cerebrovascular carbon dioxide reactivity during high-dose remifentanil infusion was investigated in volunteers by measurement of regional cerebral blood flow (rCBF) and mean CBF velocity (CBFv). METHODS: Ten healthy male volunteers with a laryngeal mask for artificial ventilation received remifentanil at an infusion rate of 2 and 4 microg x kg-1 x min-1 under normocapnia, hypocapnia, and hypercapnia. Stable xenon-enhanced computed tomography and transcranial Doppler ultrasonography of the left middle cerebral artery were used to assess rCBF and mean CBFv, respectively. If required, blood pressure was maintained within baseline values with intravenous phenylephrine to avoid confounding effects of altered hemodynamics. RESULTS: Hemodynamic parameters were maintained constant over time. Remifentanil infusion at 2 and 4 microg x kg-1 x min-1 significantly decreased rCBF and mean CBFv. Both rCBF and mean CBFv increased as the arterial carbon dioxide tension increased from hypocapnia to hypercapnia, indicating that cerebrovascular reactivity remained intact. The average slopes of rCBF reactivity were 0.56 +/- 0.27 and 0.49 +/- 0.28 ml. 100 g-1 x min-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.9 +/- 0.8 and 1.6 +/- 0.5, respectively). The average slopes for mean CBFv reactivity were 1.61 +/- 0.95 and 1.54 +/- 0.83 cm x s-1 x mmHg-1 for 2 and 4 microg x kg-1 x min-1 remifentanil, respectively (relative change in percent/mmHg: 1.86 +/- 0.59 and 1.79 +/- 0.59, respectively). Preanesthesia and postanesthesia values of rCBF and mean CBFv did not differ. CONCLUSION: High-dose remifentanil decreases rCBF and mean CBFv without impairing cerebrovascular carbon dioxide reactivity. This, together with its known short duration of action, makes remifentanil a useful agent in the intensive care unit when sedation that can be titrated rapidly is required.

Adult↗

PubMed2002

Effects of AT1 and AT2 receptor blockade on angiotensin II induced apoptosis of human renal proximal tubular epithelial cells.

BACKGROUND: Tubular atrophy is a common histological feature of chronic renal failure, and epithelial cell death by apoptosis might play an important role in its pathogenesis. Angiotensin II contributes to the progressive nature of many kidney diseases and treatment with angiotensin converting enzyme inhibitors preserves the structure of the tubulointerstitial compartment in human and experimental renal diseases. METHODS: Primary cultures of human renal proximal tubular epithelial cells were co-incubated with angiotensin II alone or in combination with the angiotensin II AT1 receptor antagonist losartan or/and the AT2 antagonist PD123319. Apoptosis was determined after 20 hours by TUNEL staining and flow cytometry. RESULTS: Angiotensin II at concentrations of 10(-9) M induced apoptosis (control vs. angiotensin II 4 +/- 3% vs. 73 +/- 11%; p < 0.05). This effect was completely offset by co-incubation with the angiotensin II AT2 receptor blocker at concentrations 10(-7) M (control vs. PD123319 4 +/- 3% vs. 8 +/- 3%; p < 0.05); AT1 blockade was ineffective in apoptosis inhibition. When both angiotensin receptors were blocked, no additional effect on apoptosis inhibition could be detected. CONCLUSION: We provided evidence, that physiological concentrations of angiotensin II can induce apoptosis of human renal proximal tubule epithelial cells. This effect is mediated via AT2 receptors.

Angiotensin II↗