Biomedical subjects
Publications and source records attributed to A Denys.
Computed tomography and magnetic resonance imaging are widely used tools to appreciate liver anatomy. Vascular and segmental anatomy are adequately appreciated with CT, while biliary anatomy is mainly seen with MR imaging. Basic principles of techniques and anatomical landmarks will be detailed.
The purpose of this retrospective study was to report 11 cases of severe vascular complications after central venous catheter misplacement. For each patient, data collection included body mass index, the diagnosis at admission, the site of the procedure, the type of catheter, coagulation parameters, the imaging modalities performed and the applied treatment. Eight patients had a lesion of the subclavian artery. Brachiocephalic vein perforations were assessed in three more patients. All patients had a chest roentgenogram after the procedure, six a CT examination, and four an angiographic procedure. Seven patients had a body mass index above 30, and 5 patients had coagulation disorders prior to the procedure. Seven patients were conservatively managed, 2 patients died despite resuscitation, 1 patient was treated with a stent graft, and one by superselective embolization. Subclavian or jugular vein temporary catheter positioning is a practical approach. Identification of any iatrogenic perforation of the subclavian artery or central veins urges obtaining a chest roentgenogram and, when required, a chest CT, selective angiograms or venograms. Body mass index superior to 30, previous unsuccessful catheterization attempts, and coagulation factor depletion seemed to account for risk factors. Recognition of clinical and radiological complications is mandatory.
We report the MRI findings of six unusual lesions of the internal auditory canal: three haemangiomas, one lipoma, one metastasis and one traumatic neuroma. We compare the findings to those of 20 intracanalicular schwannomas. We noted the site and size of the tumour, its signal intensity, borders and the homogeneity of enhancement were studied on T1-weighted images before and after intravenous contrast medium and T2-weighted images. Most schwannomas were homogeneous lesions, isointense on T1- and T2-weighted images, and strongly enhancing. Spontaneous high signal on T1-weighted images, heterogeneous contrast enhancement and extranodular enhancement were helpful for recognising lesions other then schwannomas; site, size and signal on T2-weighted images were not. All the haemangiomas had a specific pattern of contrast enhancement, with an anterior core intensely enhancing portion and a posterior portion which enhanced moderately or not at all.
Phosphorylation of extracellular signal-regulated kinases (ERK1/ERK2) has been implicated in cell proliferation of mammalian cells. In the present study, we investigated the role of docosahexaenoic acid (DHA) in the modulation of ERK1/ERK2 phosphorylation, stimulated either with phorbol 12-myristate 13-acetate (PMA) or transforming growth factor-alpha (TGFalpha) in NIH/3T3 cells. We observed that both PMA and TGFalpha induced ERK1/ERK2 phosphorylation within 5 min of stimulation. PMA acts upstream of MEK and via activation of protein kinase C (PKC), as GF109203X, a potent PKC inhibitor, and U0126, a MEK inhibitor, abolished its actions on ERK1/ERK2 phosphorylation. TGFalpha did not act via PKC because GF109203X failed to curtail the degree of ERK1/ERK2 phosphorylation in these cells. DHA alone failed to induce the phosphorylation of these mitogen-activated protein (MAP) kinases; however, this fatty acid significantly curtailed the PMA- but not TGFalpha-induced MAP kinase enzyme activity and phosphorylation in NIH/3T3 cells. Furthermore, we observed that DHA significantly inhibited PMA-induced translocation of two PKC isoforms, PKC alpha and PKC epsilon, from cytosol to plasma membrane. Interestingly, DHA failed to inhibit the PMA-induced translocation PKC delta isoform in these cells. Furthermore, DHA decreased PMA-induced proliferation of NIH/3T3 cells. In this study, we show for the first time that DHA inhibits MAP kinase ERK1/ERK2) activation and proliferation of NIH/3T3 cells via its inhibitory action on PKC alpha and epsilon isoforms.
Postoperative liver failure is a severe complication of major hepatectomies, in particular in patients with a chronic underlying liver disease. Preoperative interruption of the portal flow in the liver territories planned to be removed, induces their atrophy and the compensatory hypertrophy of the segments spared by the resection. This interruption can be induced by the surgical ligation of the portal branches or by the percutaneous intraportal injection, under ultrasound guidance, of glues or sclerosing agents. Preoperative portal vein embolisation is usually indicated when the remnant liver accounts for less than 25-40% of the total liver volume. Feasibility is close to 100% and the risk comparable to that of a percutaneous liver biopsy. It is well tolerated and the biological impact is minimal in patients without liver failure. Compensatory hypertrophy of the non-embolised segments is maximal during the first 2 weeks and persists, although to a lesser extent during approximately 6 weeks. The magnitude of hypertrophy is correlated with the volume of parenchyma embolised, and is reduced in diabetic or jaundiced patients or when there is an active chronic liver disease. Liver resection is performed 2 to 6 weeks after embolisation. Retrospective studies and one prospective study suggest that patients so prepared have a reduced perioperative risk and that their long term carcinologic results are not impaired.
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After 10 wk of feeding an experimental diet enriched with (n-3) polyunsaturated fatty acids (PUFA), i.e., eicosapentaenoic acid [EPA, 20:5(n-3)] and [DHA, 22:6(n-3)] (EPAX), blood pressure in spontaneously hypertensive rats (SHR), but not in normotensive Wistar-Kyoto (WKY) rats was reduced relative to rats fed an unsupplemented control diet. Concanavalin A-stimulated T-cell proliferation was diminished in both strains of rats fed the PUFA/EPAX diet. The experimental diet lowered secretion of interleukin-2 in SHR, but not in WKY rats compared with rats fed the control diet. To determine whether there was a defect in calcium homeostasis in T cells during hypertension, we employed the following agents: caffeine, which recruits calcium from the cytosolic Ca(2+)-induced Ca(2+)-release pool; ionomycin, which at low concentrations opens calcium channels; and thapsigargin (TG), which mobilizes [Ca(2+)]i from the endoplasmic reticulum (ER) pool. Caffeine-induced increases in [Ca(2+)]i were not modified by the PUFA/EPAX diet. The ionomycin-induced increases in [Ca(2+)]i in T cells from SHR were greater than in those from WKY rats; consumption of the PUFA/EPAX diet did not modify Ca(2+) influx in cells of either strain. The TG-induced increases in [Ca(2+)]i in T cells from SHR were greater than those in cells from WKY rats. Interestingly, consumption of the experimental diet reduced TG-evoked increases in [Ca(2+)]i in T cells from SHR and increased those in T cells from WKY rats, indicating that the PUFA/EPAX diet could reverse the calcium mobilization from the ER pool in T cells. These results suggest that (n-3) PUFA exert antihypertensive effects and modulate T-cell calcium signaling during hypertension in rats.
OBJECTIVE: We evaluate the uniformity and reproducibility of thermal lesion ablation and quantify the volume of tissue destruction and hemorrhage induced with two different commercially available radiofrequency ablation devices. MATERIALS AND METHODS: A four-array anchor expandable needle electrode and a triple-cluster cooled-tip needle electrode were used to induce lesions in three explanted calf livers and in vivo in eight swine livers. The sizes of the radiofrequency-induced lesions were macroscopically evaluated by measuring two perpendicular dimensions immediately after the experiment. Bleeding was evaluated by weighing gauze swabs used to dry the hemorrhage caused by electrode insertions. RESULTS: In explanted liver, the mean diameter of the radiofrequency-induced lesion was 5.3 +/- 0.7 cm for the cooled-tip needle and 3.7 +/- 0.4 cm for the expandable needle (p = 0.042), which correspond to approximate volumes of 65.35 +/- 26.22 cm(3) and 26.67 +/- 9.59 cm(3), respectively (p < 0.002). In vivo, the mean diameter was 3.7 +/- 0.4 cm for the cooled-tip needle and 3 +/- 0.4 cm for the expandable needle (p < 0.0001), which correspond to approximate volumes of 24.18 +/- 7.56 cm(3) and 11.16 +/- 3.65 cm(3), respectively (p < 0.0001). Blood loss attained a median value of 3.5 g for the cooled-tip needle and 2.6 g for the expandable needle; this difference was not statistically significant (p = 0.06). CONCLUSION: The cooled-tip needle induced significantly larger lesions than the expandable needle, but the lesions produced by the expandable needle are more reproducible, uniform, and spheric. The larger size of the lesions produced by the cooled-tip needle may be attributed to the higher maximum power used by the generator and the higher energy deposition, which is due to the cooling of the needle electrode.
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This study was conducted on human Jurkat T cell lines to elucidate the role of EPA and DHA, n-3 PUFA, in the modulation of two mitogen-activated protein (MAP) kinases, that is, extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2). The n-3 PUFA alone failed to induce phosphorylation of ERK1/ERK2. We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. EPA and DHA diminished the PMA- and anti-CD3-induced phosphorylation of ERK1/ERK2 in Jurkat T cells. In the present study, PMA acts mainly via protein kinase C (PKC) whereas anti-CD3 antibodies act via PKC-dependent and -independent mechanisms. Furthermore, DHA and EPA inhibited PMA-stimulated PKC enzyme activity. EPA and DHA also significantly curtailed PMA- and ionomycin-stimulated T cell blastogenesis. Together these results suggest that EPA and DHA modulate ERK1/ERK2 activation upstream of MEK via PKC-dependent and -independent pathways and that these actions may be implicated in n-3 PUFA-induced immunosuppression.
In western European countries most blunt chest traumas are associated with motor vehicle and sport-related accidents. In Switzerland, 39 of 10,000 inhabitants were involved and severely injured in road accidents in 1998. Fifty two percent of them suffered from blunt chest trauma. According to the Swiss Federal Office of Statistics, traumas represented in men the fourth major cause of death (4%) after cardiovascular disease (38%), cancer (28%), and respiratory disease (7%) in 1998. The outcome of chest trauma patients is determined mainly by the severity of the lesions, the prompt appropriate treatment delivered on the scene of the accident, the time needed to transport the patient to a trauma center, and the immediate recognition of the lesions by a trained emergency team. Other determining factors include age as well as coexisting cardiac, pulmonary, and renal diseases. Our purpose was to review the wide spectrum of pathologies related to blunt chest trauma involving the chest wall, pleura, lungs, trachea and bronchi, aorta, aortic arch vessels, and diaphragm. A particular focus on the diagnostic impact of CT is demonstrated.
BACKGROUND: Hepatic arterial chemoembolization (CE) with anthracyclines is an effective treatment for progressive liver metastases of digestive endocrine tumours. Streptozotocin (STZ) is widely used for systemic chemotherapy, but its efficacy by the hepatic arterial route has not been evaluated. PATIENTS AND METHODS: Fifteen consecutive patients, mean age 57.8 years, were prospectively included between July 1993 and January 1997. All patients had progressive liver metastases from either a carcinoid tumour (eight patients) or an islet cell carcinoma (ICC) (seven patients) that had increased in size (> or = 25%) before CE. Five patients had the carcinoid syndrome. STZ was administered, as an emulsion with iodized oil, into the hepatic artery before embolization with gelatin sponge particles. Two to six procedures (median, 3) were performed in 12 patients (one in three patients). Changes in the size of the liver metastases were evaluated by CT scan or MRI according to WHO criteria. The median follow-up was 15 months (1-50). RESULTS: An objective response was achieved in 8/15 patients (53%; median duration of 10.5 months) whatever the primary tumour (carcinoid or ICC). The carcinoid syndrome disappeared in 3/5 patients for 10, 11 and 17 months, respectively. CE effectively controlled hypoglycaemic attacks (decrease of > 50%) in the patient with insulinoma. The biological response was complete in four patients for a median duration of 7 months. CE induced minor side effects, namely nausea, fever and abdominal pain. Acute and reversible tubular necrosis due to CE was observed in one patient who had previously undergone a nephrectomy. CONCLUSION: Hepatic arterial chemoembolization with STZ is an effective treatment for patients with liver metastases caused by digestive endocrine tumours.
Stimulation of the NF-kappaB pathway often causes p65-p50 and p50-p50 dimers to be simultaneously present in the cell nucleus. A natural polymorphism at nucleotide -863 in the human TNF promoter (encoding tumor necrosis factor [TNF]) region provides an opportunity to dissect the functional interaction of p65-p50 and p50-p50 at a single NF-kappaB binding site. We found that this site normally binds both p65-p50 and p50-p50, but a single base change specifically inhibits p50-p50 binding. Reporter gene analysis in COS-7 cells expressing both p65-p50 and p50-p50 shows that the ability to bind p50-p50 reduces the enhancer effect of this NF-kappaB site. Using an adenoviral reporter assay, we found that the variant which binds p50-p50 results in a reduction of lipopolysaccharide-inducible gene expression in primary human monocytes. This finding adds to a growing body of experimental evidence that p50-p50 can inhibit the transactivating effects of p65-p50 and illustrates the potential for genetic modulation of inflammatory gene regulation in humans by subtle nucleotide changes that alter the relative binding affinities of different forms of the NF-kappaB complex.
PURPOSE: To evaluate the accuracy of preoperative computed tomography (CT) in predicting the location and type of ductal involvement and malignant transformation in intraductal papillary mucinous (IPM) pancreatic tumors and to determine the predictive factors for malignancy at CT. MATERIALS AND METHODS: The helical CT scans obtained in 36 operated on patients with a diagnosis of IPM pancreatic tumor were retrospectively assessed. CT-histopathologic correlation was then performed. RESULTS: The final diagnoses of IPM tumor were combined type (n = 26) and branch duct type (n = 10) lesions. Histologic analysis revealed adenocarcinoma (n = 9), hyperplasia (n = 8), low-grade dysplasia (n = 12), and high-grade dysplasia (n = 7). The lesions were located mainly in the head or uncinate process (n = 20) or were diffuse or multifocal (n = 12). In 12 patients (13 cases), CT-histopathologic correlation was poor, including that in the evaluation of ductal involvement (n = 7), evaluation of lesion location (n = 2), and diagnosis of malignant transformation (n = 4). The most specific predictive signs of malignancy were presence of diabetes and, at CT, a solid mass, main pancreatic duct dilatation greater than 10 mm, diffuse or multifocal involvement, and attenuating or calcified intraluminal content. CONCLUSION: The main causes of poor CT-histopathologic correlation were related to evaluation of main pancreatic duct involvement and diagnosis of malignant transformation. The association between diabetes and specific CT criteria was highly suggestive of malignancy.
Viral infections are an important factor in pathogenesis of symptom aggravation in COPD, which is usually accompanied by immunological system insufficiency, i.e. local immunity. Respiratory syncytial viruses are of vital importance. The paper presents possibilities of using active antiviral substances: amantadine, remantadine, ribavirine, zanamivir preparation. Substances isolated from natural resources have also been mentioned.
A new synthesized acridine derivative, 3,6-diamino-10-methyl-9, 10-dihydroacridine (AcrH), was tested for in vitro reverse mutations with Salmonella TA strains, chromosome aberrations and sister chromatid exchanges (SCE) in human lymphocytes, and for in vivo chromosome aberrations in bone marrow of mice. Using the classic plate incorporation method, mutagenicity of AcrH in bacterial cells (TA97a, TA98, TA100 and TA102) was observed in the experiments performed with, and without, rat liver S9 metabolic activation. The reverse mutation assay showed no difference in mutagenic activity between AcrH and acriflavine (Acr(+)) in the test with TA97. The results of in vitro chromosome aberrations assay revealed potential clastogenicity. The test using macroculture of human lymphocytes induced mainly chromatid gaps. The experiments with human lymphocytes revealed SCE-inducing effect of AcrH and Acr(+). In an in vivo study, AcrH given intraperitoneally to Balb/c mice did not cause any significant increase in the percentage of cells with aberrations compared to the negative control.
We have recently reported that cyclophilin B (CyPB), a secreted cyclosporine-binding protein, could bind to T lymphocytes through interactions with two types of binding sites. The first ones, referred to as type I, involve interactions with the conserved domain of CyPB and promote the endocytosis of surface-bound ligand, while the second type of binding sites, termed type II, are represented by glycosaminoglycans (GAG). Here, we further investigated the interactions of CyPB with blood cell populations. In addition to lymphocytes, CyPB was found to interact mainly with platelets. The binding is specific, with a dissociation constant (kd) of 9 +/- 3 nmol/L and the number of sites estimated at 960 +/- 60 per cell. Platelet glycosaminoglycans are not required for the interactions, but the binding is dramatically reduced by active cyclosporine derivatives. We then analyzed the biologic effects of CyPB and found a significant increase in platelet adhesion to collagen. Concurrently, CyPB initiates a transmembranous influx of Ca(2+) and induces the phosphorylation of the P-20 light chains of myosin. Taken together, the present results demonstrate for the first time that extracellular CyPB specifically interacts with platelets through a functional receptor related to the lymphocyte type I binding sites and might act by regulating the activity of a receptor-operated membrane Ca(2+) channel.