Biomedical subjects

M Jonas

Publications and source records attributed to M Jonas.

At least 55 records · Page 3Linked to original sources

PubMed1998

In vitro evaluation of a new lithium dilution method of measuring cardiac output and shunt fraction in patients undergoing venovenous extracorporeal membrane oxygenation.

OBJECTIVE: To evaluate, in vitro, a method of measuring cardiac output and shunt fraction during venovenous extracorporeal membrane oxygenation (ECMO). DESIGN: Experimental study using an in vitro model. SETTING: A teaching hospital. MODEL: An ECMO circuit was set up in parallel with a patient circuit consisting of tubing through which saline was circulated from a 50-L reservoir by a pump which was set at 3 L/min to represent cardiac output. A second pump in the ECMO circuit drew saline from the patient circuit and passed it through a membrane oxygenator. The flow from the membrane oxygenator either returned directly to the patient circuit or was diverted, via a third pump, back into the ECMO circuit, thereby producing a shunt. INTERVENTIONS: By adjusting the flow rates of the second (ECMO) and third (shunt) pumps, three shunt fractions of 12%, 25%, and 50% were produced at three different ECMO flow rates. Lithium chloride (0.15 mmol) was injected just downstream of the membrane oxygenator; the lithium ion concentration-time curves were recorded simultaneously in the flow returning to the saline reservoir and in the flow just upstream of the membrane oxygenator using lithium selective electrodes. MEASUREMENTS AND MAIN RESULTS: Nine pairs of curves were recorded, one pair for each combination of ECMO and shunt flow rates. Analysis of these curves allowed shunt flow and "cardiac output" to be calculated and compared with the flow rates delivered by the pumps. Mean "cardiac output" derived from the lithium dilution curves was 2.98 +/- 0.18 (SD) L/min, compared with a delivered pump flow of 3 L/min. Measured shunt flow = 0.008 + 1.09 x actual shunt flow (R = 0.997). CONCLUSIONS: This method would allow cardiac output and shunt flow to be measured in patients undergoing venovenous ECMO. It could result in better patient management and improved cannula design.

Blood Flow Velocity↗

PubMed1998

Characterization of group B streptococcal invasion of human chorion and amnion epithelial cells In vitro.

Group B streptococci (GBS) have been cultured from the chorioamnionic membrane of pregnant women, usually in association with chorioamnionitis and premature labor (K. A. Boggess, D. H. Watts, S. L. Hillier, M. A. Krohn, T. J. Benedetti, and D. A. Eschenbach, Obstet. Gynecol. 87:779-784, 1996). Colonization and infection of placental membranes can be a prelude to neonatal GBS infections even in the presence of intact membranes (R. L. Naeye and E. C. Peters, Pediatrics 61:171-177, 1978), suggesting that GBS cause chorioamnionitis or establish amniotic fluid infections by partial or complete penetration of the placental membranes. We have isolated and grown cultures of primary chorion and amnion cells from human cesarean-section placentas. This has provided a biologically relevant model for investigating GBS adherence to and invasion of the two epithelial barriers of the placental membrane. GBS adhered to chorion cell monolayers to a high degree. Pretreatment of GBS with trypsin reduced adherence up to 10-fold, which suggested that the bacterial ligand(s) was a protein. GBS invaded chorion cells at a high rate in vitro, and invasion was dependent on cellular actin polymerization. GBS could be seen within intracellular vacuoles of chorion cells by transmission electron microscopy. We also demonstrated that GBS were capable of transcytosing through intact chorion cell monolayers without disruption of intracellular junctions. GBS also adhered to amnion cells; in contrast, however, these bacteria failed to invade amnion cells under a variety of assay conditions. GBS interactions with the chorion epithelial cell layer shown here correlate well with epidemiological and pathological studies of GBS chorioamnionitis. Our data also suggest that the amnion cell layer may provide an effective barrier against infection of the amniotic fluid.

Amnion↗

PubMed1998

The locus of tumor necrosis factor-alpha action in lung inflammation.

The pulmonary host response to infection and inflammation appears, at least in part, to be compartmentalized from the systemic host response. Tumor necrosis factor-alpha (TNF-alpha) has been implicated in lung inflammation and injury, but its site(s) of action has not been clearly defined. To investigate this, transgenic mice (surfactant apoprotein C promotor/soluble TNF receptor type II-Fc fusion protein ([SPCTNFRIIFc] mice) were generated in which TNF-alpha was selectively antagonized in the distal lung through tissue-specific expression of sTNFRIIFc, a soluble TNF inhibitor. The lung inflammatory response in these mice to pulmonary challenge with Micropolyspora faeni antigen or lipopolysaccharide (LPS) was compared with the response of wild-type mice, wild-type mice treated with recombinant sTNFRIIFc intravenously, and type I TNF-receptor knockout mice. Recruitment of polymorphonuclear leukocytes (PMN) to the lung after challenge with M. faeni antigen was essentially abolished in the TNFRI knockout mice and markedly reduced in the SPCTNFRIIFc mice. Wild-type mice given sTNFRIIFc intravenously in amounts resulting in lung concentrations similar to those in SPCTNFRIIFc mice also showed significantly reduced lung PMN recruitment, whereas those given doses that achieved such concentrations in the blood but low levels in the lung did not. In contrast, PMN recruitment to the lung following aerosol challenge with LPS was reduced significantly in the TNFRI knockout mice and in mice given high-dose sTNFRIIFc intravenously, but was not reduced significantly in SPCTNFRIIFc mice. Thus, inhibition of PMN recruitment in response to M. faeni antigen correlated largely with the extent of intrapulmonary inhibition of TNF-alpha, whereas the response to LPS correlated best with the extent of extrapulmonary inhibition of TNF-alpha. These studies indicate that TNF-alpha may act at different loci to mediate lung inflammation, with the site of action depending in part on the nature of the inflammatory stimulus, and that SPCTNFRIIFc mice provide a tool by which the locus of TNF action can be addressed.

Administration, Intranasal↗

PubMed1997

Blockade of CD49d (alpha4 integrin) on intrapulmonary but not circulating leukocytes inhibits airway inflammation and hyperresponsiveness in a mouse model of asthma.

Immunized mice after inhalation of specific antigen have the following characteristic features of human asthma: airway eosinophilia, mucus and Th2 cytokine release, and hyperresponsiveness to methacholine. A model of late-phase allergic pulmonary inflammation in ovalbumin-sensitized mice was used to address the role of the alpha4 integrin (CD49d) in mediating the airway inflammation and hyperresponsiveness. Local, intrapulmonary blockade of CD49d by intranasal administration of CD49d mAb inhibited all signs of lung inflammation, IL-4 and IL-5 release, and hyperresponsiveness to methacholine. In contrast, CD49d blockade on circulating leukocytes by intraperitoneal CD49d mAb treatment only prevented the airway eosinophilia. In this asthma model, a CD49d-positive intrapulmonary leukocyte distinct from the eosinophil is the key effector cell of allergen-induced pulmonary inflammation and hyperresponsiveness.

Allergens↗

PubMed1997

Lithium dilution cardiac output measurement: a comparison with thermodilution.

OBJECTIVE: To compare the results of cardiac output measurements obtained by lithium dilution and thermodilution. DESIGN: Case series, observational study. SETTING: High-dependency postoperative unit and intensive care unit of a teaching hospital. PATIENTS: Forty patients were studied. Thirty-four patients had undergoing heart surgery requiring cardiopulmonary bypass within the previous 2 days; the diagnoses in the other patients were myocardial infarct (n = 2), septicemia (n = 2), adult respiratory distress syndrome, and pericardectomy. INTERVENTIONS: Cardiac output was measured five times in each patient, using lithium dilution (single measurement) and bolus thermodilution (series of three to six measurements according to standard clinical practice, taking the average of the closest three). In a subgroup of 14 patients, cardiac output was also measured using "continuous thermodilution." MEASUREMENTS AND MAIN RESULTS: Comparing lithium dilution with bolus thermodilution, the mean of the differences (lithium dilution-thermodilution) was -0.25 +/- 0.46 [SD] L/min. Linear regression analysis gave y = 0.31 + 0.89x (r2 = .94) for lithium dilution vs. thermodilution. CONCLUSIONS: The overall agreement between the two methods was good. The variability of the thermodilution measurements was greater than that of the lithium dilution measurements. The lithium dilution method is at least as accurate as bolus thermodilution and, since pulmonary artery catheterization is not needed, it has the advantages of being safe and quick to perform.

Adult↗

PubMed1997

Invasion of brain microvascular endothelial cells by group B streptococci.

Group B streptococci (GBS) are the leading cause of meningitis in newborns. Although meningitis develops following bacteremia, the precise mechanism or mechanisms whereby GBS leave the bloodstream and gain access to the central nervous system (CNS) are not known. We hypothesized that GBS produce meningitis because of a unique capacity to invade human brain microvascular endothelial cells (BMEC), the single-cell layer which constitutes the blood-brain barrier. In order to test this hypothesis, we developed an in vitro model with BMEC isolated from a human, immortalized by simian virus 40 transformation, and propagated in tissue culture monolayers. GBS invasion of BMEC monolayers was demonstrated by electron microscopy. Intracellular GBS were found within membrane-bound vacuoles, suggesting the organism induced its own endocytic uptake. GBS invasion of BMEC was quantified with a gentamicin protection assay. Serotype III strains, which account for the majority of CNS isolates, invaded BMEC more efficiently than strains from other common GBS serotypes. GBS survived within BMEC for up to 20 h without significant intracellular replication. GBS invasion of BMEC required active bacterial DNA, RNA, and protein synthesis, as well as microfilament and microtubule elements of the eukaryotic cytoskeleton. The polysaccharide capsule of GBS attenuated the invasive ability of the organism. At high bacterial densities, GBS invasion of BMEC was accompanied by evidence of cellular injury; this cytotoxicity was correlated to beta-hemolysin production by the bacterium. Finally, GBS demonstrated transcytosis across intact, polar BMEC monolayers grown on Transwell membranes. GBS invasion of BMEC may be a primary step in the pathogenesis of meningitis, allowing bacteria access to the CNS by transcytosis or by injury and disruption of the endothelial blood-brain barrier.

Brain↗

PubMed1997

Elevated levels of serum creatine kinase induced by hyponatraemia.

Elevated serum creatine kinase levels are one of the major criteria for the diagnosis of myocardial injury. Noncardiac causes such as muscular and brain damage may also be associated with elevated serum creatine kinase levels. Hyponatremia may induce increased serum creatine kinase in association with rhabdomyolysis or with hypothyroidism. A patient is described where three episodes of hyponatraemia not associated with rhabdomyolysis or hypothyroidism induced transient elevations of serum creatine kinase levels. The association between hyponatraemia and elevated creatine kinase levels should be emphasized to prevent erroneous diagnosis of myocardial injury.

Aged↗

PubMed1997

Time course of the human pulmonary vascular response to 8 hours of isocapnic hypoxia.

To examine the hypothesis that the human pulmonary vascular response to hypoxia has a component with a slow time course, we measured pulmonary vascular resistance (PVR) in six healthy adult males during 8 h of isocapnic hypoxia. A balloon-tipped pulmonary artery catheter with thermistor was introduced via a forearm vein and used to derive PVR. The subjects were seated in a chamber in which the oxygen and carbon dioxide concentrations were adjusted to maintain an end-tidal Po2 of 50 Torr and an end-tidal Pco2 equal to the subject's normal prehypoxic value. PVR was measured before and at 0.5-h intervals during 8 h of hypoxia, the following 3 h of isocapnic euoxia (end-tidal Po2 100 Torr), and a subsequent 1-h reexposure to hypoxia. PVR rose from 1.23 +/- 0.26 (SE) Torr-min.1(-1) under euoxia [time (t) = 0] to 1.77 +/- 0.21 Torr.min.1(-1) at t = 0.5 h, reached a maximum at 2 h (2.91 +/- 0.33 Torr.min.1(-1)), and remained fairly constant between 2 and 8 h. Restoration of euoxia at 8 h led to a reduction in PVR with a slow component. Reexposure to hypoxia at 11 h resulted in a greater increase in PVR than at 1 h. Systemic vascular resistance had a similar slow component to its response, falling from 18.6 +/- 1.3 Torr.min.1(-1) at t = 0 to 17.3 +/- 1.4 Torr.min.1(-1) at t = 0.5 h, 14.4 +/- 0.6 Torr.min.1(-1) at t = 4 h, and 13.8 +/- 0.8 Torr.min.1(-1) at t = 8 h. The human pulmonary and systemic vascular responses to hypoxia extend over at least several hours.

Adult↗

PubMed1997

Neutrophil apoptosis in the acute respiratory distress syndrome.

Little is known about neutrophil (PMN) apoptosis in the acute respiratory distress syndrome (ARDS). We uses morphologic criteria to count apoptotic PMN in bronchoalveolar lavage fluid (BAL) of 35 patients on Days 1, 3, 7, 14, and 21 of ARDS and 13 patients on Days 1 and 3 of risk for ARDS. We found that the proportion of apoptotic PMN in BAL was low throughout the course of ARDS. There was no significant difference between the percentage of apoptotic PMN in patients at risk and patients with established ARDS or between patients who lived (2.4%) and patients who died (1.8%). When normal human PMN were incubated in ARDS BAL, a significantly lower proportion became apoptotic (50 +/- 4%), as compared with PMN incubated in lavage fluid from normal volunteers (76 +/- 7%, p < 0.05). This antiapoptotic effect of ARDS BAL was blocked by immunodepleting BAL of G-CSF and GM-CSF. We conclude that the proportion of apoptotic PMN recovered from the lungs of patients with ARDS is low throughout the course of ARD S. Furthermore, BAL from patients with ARDS prolongs survival of normal human PMN in vitro, and this effect is partially mediated by G-CSF and GM-CSF.

Adult↗

PubMed1997

Progressive heterogeneity of myocardial perfusion in heart transplant recipients detected by thallium-201 myocardial SPECT.

UNLABELLED: Progressive graft atherosclerosis is a serious complication in long-term survivors after heart transplantation. Coronary angiography is insensitive with regard to the early and characteristic alterations. We evaluated the progression of these abnormalities and the influence of former rejection episodes. METHODS: Early after transplantation, 43 patients (34 men, mean age 53.7 +/- 10.7 yr) underwent stress and redistribution 201Tl myocardial SPECT after treadmill exercise. Twenty patients were followed-up to the second postoperative year, and 13 patients to the third postoperative year. Thallium-201 distribution and kinetic abnormalities were documented in a scheme enclosing 20 myocardial segments. Additionally, a score was developed that measured the degree of inhomogeneity of 201Tl distribution and the severity of perfusion defects, respectively. RESULTS: Regarding scintigraphy, pathologic results could be found in 40% of segments (redistribution, 25%; reverse redistribution, 30%; persistent defects, 49%). Score values in heart transplant recipients differed significantly from normal controls (p < 0.001) and were comparable to patients with single vessel disease of their native hearts. Thallium-201 inhomogeneity in recipients after treatable rejection episodes did not differ from results in recipients without any biopsy-proven rejection. The follow-up of cardiac transplant patients revealed a significant increase of score values up to the third year after transplantation (p < 0.02), despite reproducible normal angiography. There was no direct correlation between score values and IVUS results, although there was a parallel trend in 10 of 12 follow-ups. CONCLUSION: Despite normal coronary angiography, 201Tl myocardial SPECT frequently revealed pathologic results in heart transplant recipients. Scintigraphic results did not correlate with intimal thickening of epicardial coronary arteries accessible to intravascular ultrasonography in the early phase after transplantation. The presented score of inhomogeneity might reveal progressive disease possibly caused by small vessel alterations.

Case-Control Studies↗

PubMed1997

Is immunosuppressive treatment an option for myocarditis?

Although relatively uncommon among cardiac diseases, myocarditis may often have significant sequelea, including heart failure and death. The development of a murine model and the use of myocardial biopsy and Dallas criteria have broadened our understanding of myocarditis and its manifestations. Regrettably, little can still be done to alter the natural course of the disease. The results of the Myocarditis Treatment Trial do not support routine treatment with immunosuppressive drugs for all patients with myocarditis, however the study did not incorporate methods of viral (DNA or RNA) identification or immunohistochemical techniques. Specific viral myocarditis diagnosis, by polymerase chain reaction or in situ hybridization, together with immunohistochemical markers, may help classify patients according to acute or chronic myocarditis and by etiology, and possibly identify subgroups of patients who would be most likely to benefit from immunosuppression. Some important questions regarding therapy for myocarditis may be answered by the ongoing European Study of the Epidemiology and Treatment of Cardiac Inflammatory Disease, while others still await double-blind controlled confirmation. In the interim, therapy is being directed towards the management of symptoms and complications, using conventional medical regimens for heart failure.

Clinical Trials as Topic↗

PubMed1996

Can Tl-201 myocardial SPECT abnormalities in orthotopic heart recipients be explained by coronary vessel wall alterations assessed by intravascular ultrasound?

UNLABELLED: The aim of this study was to compare findings on coronary intravascular ultrasound and thallium-201 SPECT in patients following orthotopic heart transplantation. BACKGROUND: No data are available on whether pathological thallium scintigraphic findings in heart recipients are based on coronary vessel wall alterations identifiable by intravascular ultrasound. METHODS: 29 patients (mean age: 50.9 +/- 11.5 years; male n = 23) were investigated by means of intravascular ultrasound of selected coronary segments and thallium-201 myocardial SPECT. Patients were investigated 11.6 +/- 5.4 weeks post transplantation, a subgroup of 13 patients was re-investigated 70.2 +/- 18.4 weeks following transplantation. A total of 214 cross-sectional areas of the left coronary artery were examined using a 3.5 French intravascular ultrasound catheter to measure intimal index and the circumferential extension of a three-layer appearance of the vessel wall. Shortly after catheterisation, an ergometric stress-test was performed to examine all recipients by means of thallium-201 SPECT. In each patient, 20 segments of the left ventricle were evaluated using a score system of differentiate between persistent defects, redistribution, and reverse redistribution. A score was developed that measured the degree of inhomogeneity and severity of perfusion defects, respectively. Findings on scintigraphy were correlated to coronary intravascular ultrasound findings. RESULTS: At first investigation, mean intimal index of all evaluated coronary cross-sectional areas was 0.06 +/- 0.1. Sixty-four cross-sectional areas demonstrated a three-layer appearance of the vessel wall, mean circumferential extension was 72 +/- 122 degrees. Thallium scintigraphy demonstrated a total of 336 (40%) pathological left ventricular segments; 168 (20%) were regarded as permanent defects, 67 (8%) demonstrated redistribution and 101 (12%) showed reverse redistribution. The score of inhomogeneity was calculated as 5.8% +/- 2.6%. In the subgroup of patients at the follow-up study, the score was 6.4 +/- 2.8%. There was no correlation between intimal index and the score, nor could any correlation be confirmed between the score and the circumferential extension of a three-layer appearance of the vessel wall. At second investigation, no significant differences of intimal index (0.05 +/- 0.07) or circumferential extension of a three-layer appearance of the vessel wall (74 +/- 118 degrees) could be confirmed. The score was slightly, but significantly increased to 8.1 +/- 4.5% at the second investigation (P < 0.05). CONCLUSION: Early after orthotopic heart transplantation, pathologic thallium distribution patterns of the left ventricle could be observed. These pathological patterns did not correlate with the extent of diffuse coronary vessel wall alterations identifiable by intravascular ultrasound. After more than 1 year, the degree of scintigraphic abnormalities increased significantly, not accompanied by an increase of diffuse coronary vessel wall alterations.

Adult↗

PubMed1996

The importance of leukotrienes in airway inflammation in a mouse model of asthma.

Inhalation of antigen in immunized mice induces an infiltration of eosinophils into the airways and increased bronchial hyperreactivity as are observed in human asthma. We employed a model of late-phase allergic pulmonary inflammation in mice to address the role of leukotrienes (LT) in mediating airway eosinophilia and hyperreactivity to methacholine. Allergen intranasal challenge in OVA-sensitized mice induced LTB4 and LTC4 release into the airspace, widespread mucus occlusion of the airways, leukocytic infiltration of the airway tissue and broncho-alveolar lavage fluid that was predominantly eosinophils, and bronchial hyperreactivity to methacholine. Specific inhibitors of 5-lipoxygenase and 5-lipoxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils indicating a key role for leukotrienes in these features of allergic pulmonary inflammation. The role of leukotrienes or eosinophils in mediating airway hyperresponsiveness to aeroallergen could not be established, however, in this murine model.

5-Lipoxygenase-Activating Proteins↗

PubMed1996

Usefulness of beta-blocker therapy in patients with non-insulin-dependent diabetes mellitus and coronary artery disease. Bezafibrate Infarction Prevention (BIP) Study Group.

The benefit of beta-blocker therapy in patients after myocardial infarction is well established. The use of beta blockers in the high-risk subgroup of patients with combined diabetes mellitus (DM) and coronary artery disease (CAD) remains controversial. From a database of 14,417 patients with chronic CAD who had been screened for participation in the Bezafibrate Infarction Prevention (BIP) study, 2,723 (19%) had non-insulin-dependent DM. Baseline characteristics and 3-year mortality were analyzed in patients with DM receiving (n = 911; 33%) and not receiving (n = 1,812; 67%) beta blockers. Total mortality during a 3-year follow-up was 7.8% in those receiving beta blockers compared with 14.0% in those who were not (a 44% reduction). A reduction in cardiac mortality of 42% between the 2 groups was also noted. Three-year survival curves showed significant differences in mortality with increasing divergence (p = 0.0001). After multiple adjustment, multivariate analysis identified beta-blocker therapy as a significant independent contributor to improved survival (relative risk = 0.58; 90% confidence interval 0.46 to 0.74). Within the diabetic population, the main benefit associated with beta-blocker therapy was observed in older patients, in those with a history of myocardial infarction, those with limited functional capacity, and those at lower risk. Thus, therapy with beta blockers appears to be associated with improved long-term survival in the high-risk subpopulation of patients with DM and CAD.

Actuarial Analysis↗

PubMed1996

Ultrastructural characterization of preosteoclasts derived from bone marrow progenitors stimulated by osteoclast colony stimulating factor.

BACKGROUND: Osteoclast colony stimulating factor (O-CSF) is an osteoclast-specific growth factor that stimulates the clonal growth of primitive osteoclast progenitors from bone marrow cells in culture. To characterize the morphology of immature osteoclasts (preosteoclasts) arising from complex hematopoietic tissues, progenies of O-CSF-responsive progenitors were cocultured with devitalized calvariae, and their cytochemical and ultrastructural features were examined. METHODS: Murine bone marrow cells were cultured in semisolid medium for 14 days in the presence of O-CSF. Colonies derived from osteoclast progenitors were then cocultured with devitalized mouse calvariae for 5 days. Cells attached to the calvariae were stained for tartrate resistant acid phosphatase (TRAPase), and the ultrastructure of these cells was examined by transmission electron microscopy. Bone marrow cells stimulated by macrophage colony stimulating factor (M-CSF) were similarly studied as a control. RESULTS: O-CSF-induced preosteoclasts stained strongly positive for TRAPase when cocultured with calvariae. These cells showed single nuclei, and their cytoplasm contained numerous mitochondria, vacuoles, granules, and coated vesicles. The ruffled cell border consisted of short, blunt, fingerlike projections. The adjacent clear zone contained abundant microtubules, microfilaments, and long narrow channels. M-CSF-induced macrophages were TRAPase negative, with no ruffled borders or clear zones. CONCLUSIONS: All the characteristic features of active osteoclasts were observed in the cells derived from O-CSF-responsive bone marrow progenitors except that these cells were mononucleated, and their ruffled borders were not fully convoluted, indicative of their immature nature. This study documents for the first time the ultrastructural characteristics of preosteoclasts derived from cultured bone marrow progenitors in early stages of development.

Acid Phosphatase↗

PubMed1996

Invasion of respiratory epithelial cells by Burkholderia (Pseudomonas) cepacia.

Pulmonary infections caused by Burkholderia (Pseudomonas) cepacia are an important cause of morbidity and mortality in cystic fibrosis (CF) patients. Several features suggestive of cellular invasion and intracellular sequestration of B. cepacia in CF are persistence of infection in the face of antibiotic therapy to which the organism demonstrates in vitro susceptibility and a propensity to cause bacteremic infections in patients with CF. Epithelial cell invasion was demonstrated in vitro in A549 cells by a modified gentamicin protection assay. The kinetics of invasion appear to be saturable. Electron microscopy of invaded monolayers showed intracytoplasmic bacteria enclosed by membrane-bound vacuoles. No lysosomal fusion with these vacuoles was observed. Intraepithelial cell replication was suggested by electron microscopy and confirmed by both a quantitative assay and a visual assay. Cytochalasin D, but not colchicine, inhibited invasion, suggesting a role for microfilaments but not microtubules. The invasion phenotype in B. cepacia may be an important virulence factor for CF infections.

Burkholderia Infections↗

PubMed1996

[Diagnosis of recurrence of a glomus carotid artery tumor by somatostatin receptor scintigraphy].

Glomus caroticum tumours belong to the non chromaffine paragangliomas. As the incidence is very poor with 1% in the collective of a vascular-surgery department, the correct diagnosis is preoperatively only found in 10-20% of the cases. The early detection of primary- or recurrence-tumour is important for the surgical proceedings. With advanced tumour-stage, i.e. with involvement of the carotid artery in the tumour-process, the perioperative mortality increases. Furthermore nerve lesions following surgical tumour-resection as a complication are more frequent. This case-report point out the importance of the somatostatin-receptor-scintigraphy in the differentiation of glomus caroticum tumour-recurrence and postoperative scar. In our patient the suspicion of tumour-recurrence came up already 2 years ago, but could not be verified by MRT and angiography.

3-Iodobenzylguanidine↗

PubMed1996

Structure distribution relationship of iodine-123-iodobenzamides as tracers for the detection of melanotic melanoma.

UNLABELLED: The influence of systematic structure variations on the biodistribution of positional isomers of N-(N'-dialkylaminoethylene)-[123I]iodobenzamide (ABA) derivatives in melanoma-bearing animals was investigated. METHODS: Radioiodination of six bromo benzamide precursors was achieved by Cu(1)-assisted nonisotopic halogen exchange. Organ distribution, scintigraphic and metabolic studies were performed in nude mice bearing a human melanotic MM (SK-MEL 25). A patient suffering from melanotic melanoma underwent scintigraphy with a [123I]iodobenzamide. RESULTS: High radiochemical yields of 80%-95% and specific activities of > 5 TBq/ mumole were obtained. Animal studies revealed specific tumor uptake of all compounds with longest retention of the most lipophilic derivative p-[123I]ABA 2-2. At shorter times, however, o-[123I]ABA 2-2 exhibited the highest tumor uptake (8.9% ID/g, 1 hr p.i., 10.9% ID/g, 4 hr p.i.). Metabolization of o-[123I]ABA 2-2, mainly to o-[123I]iodohippuric acid (OIH), followed by fast renal excretion of the metabolites lead to tumor/nontumor ratios (T/NT) of > 400 for tumor/blood, and > 70 for tumor/liver at 48 h p.i. Unknown metastases could be localized in a patient using o-[123I]ABA 2-2. CONCLUSION: The effects of the structure variation of iodobenzamides on their lipophilicity, metabolism and thus pharmacokinetics lead to the suggestion of o-[123I]ABA 2-2 as a favorable melanoma imaging agent.

Animals↗