Value of digital volume tomography in patients with conductive hearing loss

Digital volume tomography (DVT) is an extension of panoramic tomography. With this diagnostic technique, characterized by high resolution, a narrow section width (0.125 mm) and three-dimensional display, small pathological processes can be well visualized. Twenty-five patients with the history of a progressive hearing loss were examined with DVT (Accu-I-tomo, Morita, Japan). The results were compared with pre- and intraoperative findings to evaluate the diagnostic value of DVT in cases of erosion of the ossicular chain. With high resolution and artifact-free demonstration of the middle ear and the ossicular chain, it was possible to define its continuity preoperatively by DVT in all 25 cases. An intact ossicular chain was found by DVT in 13 cases and was later confirmed by surgery. The predicted erosion of the ossicles was verified in 12 patients, and a tympanoplasty type III was performed. Digital volume tomography is an excellent technique to examine the middle ear cleft and inner ear, and expands the application of diagnostic possibilities in the lateral skull base. Therefore, improvement in preoperative diagnosis is achieved along with more accurate planning of the surgical procedure. Digital volume tomography delivers a small radiation dose with a high resolution and a low purchase price for the equipment.     

Cardiac conduction abnormalities and atrial arrhythmias associated with salicylate toxicity

Cardiac side effects from aspirin are uncommon; however, severe acid-base imbalance, pulmonary edema, ventricular ectopic activity and cardiopulmonary arrest have been reported in patients with toxic serum salicylate concentrations. We saw a patient with salicylate toxicity who developed a variety of sinus and atrioventricular nodal conduction disturbances and atrial arrhythmias with a relatively low toxic serum salicylate concentration. The cardiac rhythm returned to normal as the serum salicylate concentration decreased, and results of subsequent electrophysiologic testing and Holter monitoring were normal. A low serum albumin level may have resulted in altered salicylate binding in this patient, thereby increasing the availability of unbound (active) drug for toxic effects.     

The adrenergic inhibitors

Although most of the centrally and peripherally-acting adrenergic inhibitors have been available for several years, they continue to contribute importantly to antihypertensive therapy. There are remarkably few contraindications to their use. They are useful in hypertension of all grades of severity, and are also valuable in complicated forms of hypertension, such as those associated with renal insufficiency, diabetes mellitus, and chronic obstructive lung disease. They can produce some fairly predictable side effects in patients, but generally do not cause significant metabolic changes. These drugs also seem to be tolerated well by physically active patients. They appear to have desirable effects on cardiac structure. In general, the adrenergic inhibitors cause regression of a left ventricular hypertrophy, which may well be a valuable property, especially in older hypertensive patients.     

Das Jo-1-Syndrom und seine klinischen Manifestationen

Namensgebend für das Jo-1-Syndrom sind Autoantikörper gegen das Jo-1-Antigen, die bei diesem Krankheitsbild im Serum der betroffenen Patienten nachgewiesen werden. Der Name Jo-1 leitet sich von dem ersten Patienten (John P.) ab, bei dem diese Antikörper gefunden wurden. Dieser Patient litt an einer Polymyositis und fibrosierenden Alveolitis. Das Jo-1-Antigen ist identisch mit der Histidyl-Transfer-RNA-Synthetase im Zytosol. Das Jo-1-Syndrom gehört zu einer Familie von Autoimmunerkrankungen, die als Anti-Synthetase- Syndrome bezeichnet werden. Diese Syndrome haben gemeinsam, dass jeweils Autoantikörper gegen unterschiedliche Aminosäure-Transfer-RNASynthetasen nachweisbar sind. Klinisch handelt es sich beim Jo-1-Syndrom um eine Sonderform der Poly- bzw. Dermatomyositis von bisher ungeklärter Ätiologie. Neben einer Muskelbeteiligung kommt es charakteristischerweise zu einer interstitiellen Lungenbeteiligung, die auch prognostisch das Krankheitsbild bestimmt. Zusätzlich können klinisch eine Polyarthritis und weitere Symptome bestehen, die dem klinischen Bild anderer Kollagenosen ähneln. Ebenso wie die Polymyositis und Dermatomyositis kann sich das Jo-1-Syndrom in sog. Myositis-Overlap-Syndromen präsentieren. Zu dieser Diagnose führt ein Symptomenkomplex, der die klare Zuordnung zu einer einzelnen Erkrankung nicht möglich macht. Häufig werden in solchen Fällen U1-RNP-Antikörper nachgewiesen. Therapeutisch spricht das Jo-1-Syndrom auf die Gabe von Kortikosteroiden und—falls notwendig—Azathioprin, Methotrexat und Cyclophosphamid an. Eine Kurzbeschreibung von zwei klinischen Fällen stellt das Krankheitsbild anschaulich dar.     

Characterization of normal and infarcted rat myocardium using a combination of small-animal PET and clinical MRI.

The combination of small-animal PET and MRI data provides quantitative in vivo insights into cardiac pathophysiology, integrating information on biology and morphology. We sought to determine the feasibility of PET and MRI for the quantification of ischemic injury in the rat model. METHODS: Fourteen healthy male Wistar rats were studied with 18F-FDG PET and cine MRI. Myocardial viability was determined in a transmural myocardial infarction model in 12 additional rats, using 18F-FDG PET and delayed-enhancement MRI with gadolinium-diethylenetriaminepentaacetic acid. All PET was acquired with a dedicated small-animal PET system. MRI was performed on a 1.5-T clinical tomograph with a dedicated small-animal electrocardiographic triggering device and a small surface coil. RESULTS: In normal rats, 18F-FDG uptake was homogeneous throughout the left ventricle. The lowest mean uptake of the 18F-FDG was found in the apical regions (79% +/- 6.0% of maximum) and the highest uptake was in the anterior wall (93% +/- 4.3 % of maximum). Myocardial infarct size as determined by histology correlated well with defects of glucose metabolism obtained with 18F-FDG PET (r = 0.89) and also with delayed-enhancement MRI (r = 0.91). Left ventricular ejection fraction in normal rats measured by cine MRI was 57% +/- 5.4% and decreased to 38% +/- 12.9% (P < 0.001) in the myocardial infarction model. CONCLUSION: Integrating information from small-animal PET and clinical MRI instrumentation allows for the quantitative assessment of cardiac function and infarct size in the rat model. The MRI measurements of scar can be complemented by metabolic imaging, addressing the extent and severity of ischemic injury and providing endpoints for therapeutic interventions.     

TGF-beta promotes the establishment of renal cell carcinoma bone metastasis.

Bone metastases develop in approximately 30% of patients with RCC, and the mechanisms responsible for this phenomenon are unknown. We found that TGF-beta1 stimulation of RCC bone metastasis cells promotes tumor growth and bone destruction possibly by stimulating paracrine interactions between tumor cells and the bone. INTRODUCTION: Bone metastasis is a frequent complication and causes marked morbidity in patients with renal cell carcinoma (RCC). Surprisingly, the specific mechanisms of RCC interaction with bone have been scarcely studied despite the inability to prevent or effectively treat bone metastasis. Bone is a reservoir for various growth factors including the pleiotropic cytokine TGF-beta1. TGF-beta1 has been shown to have tumor-supportive effects on advanced cancers and evidence suggests its involvement in promoting the development of breast cancer bone metastasis. Here, we studied the potential role of TGF-beta1 in the growth of RCC bone metastasis (RBM). MATERIALS AND METHODS: To inhibit TGF-beta1 signaling, RBM cells stably expressing a dominant-negative (DN) TGF-betaRII cDNA were generated. The in vivo effect of TGF-beta1 on RBM tumor growth and osteolysis was determined by histological and radiographic analysis, respectively, of athymic nude mice after intratibial injection of parental, empty vector, or DN RBM cells. The in vitro effect of TGF-beta1 on RBM cell growth was determined after TGF-beta1 treatment by MTT assay. RESULTS: TGF-beta1 and the TGF-beta receptors I and II (TGF-betaRI/II) were consistently expressed in both RBM tissues and cell lines. Inhibition of TGF-beta1 signaling in RBM cells significantly reduced tumor establishment and osteolysis observed in vivo after injection into the murine tibia, although no effect on tumor establishment was observed after injection of RBM cells subcutaneously or into the renal subcapsule. Treatment of five RBM cell lines with TGF-beta1 in vitro either had no effect (2/5) or resulted in a significant inhibition (3/5) of cell growth, suggesting that TGF-beta1 may promote RBM tumor growth indirectly in vivo. CONCLUSIONS: TGF-beta1 stimulation of RBM cells plays a role in promoting tumor growth and subsequent osteolysis in vivo, likely through the initiation of tumor-promoting paracrine interactions between tumor cells and the bone microenvironment. These data suggest that inhibition of TGF-beta1 signaling may be useful in the treatment of RBM.     

New surface modification for Ti-6Al-7Nb alloy: oxygen diffusion hardening (ODH)

PVD-TiN coating and N+ implantation of Ti-6Al-7Nb alloy resulted in surface hardening to a depth of less 3 microns. The new oxygen diffusion hardening (ODH) treatment increased the hardness gradually to 50 microns. PUD-TiN showed an improvement in the tribological properties, while N+ implantation increased the PE wear rate. The wear rate of the ultrahigh-molecular-weight as well as the friction coefficient were reduced to one-half of the values achieved with the combination of CoCrMo-alloy when paired against the ODH-treated surface. In pairing with ZrO2-containing bone cement the ODH-treated surface showed only a minimal reaction.     

Nicardipine improves myocardial perfusion in systemic sclerosis

Primary scleroderma myocardial disease may be due in part to myocardial ischemia caused by a disturbance of the coronary microcirculation. We evaluated the effect of the calcium channel blocker nicardipine on myocardial perfusion assessed by thallium-201 scanning in 16 patients with systemic sclerosis. Thallium-201 single photon emission computerized tomography was performed at baseline and 90 min after 40 mg of oral nicardipine. The mean (+/- SD) number of left ventricular segments with perfusion defects significantly decreased from 6.0 +/- 2.0 at baseline to 4.1 +/- 2.3 after nicardipine (p less than 0.01). The mean global perfusion score significantly increased from 10.2 +/- 1.9 at baseline to 11.9 +/- 2.6 after nicardipine (p less than 0.02). Our study demonstrates short-term improvement in thallium-201 myocardial perfusion with nicardipine in patients with systemic sclerosis.