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We present a patient with superior vena cava (SVC) obstruction in whom two areas of increased hepatic enhancement within the left lobe were seen on abdominal computed tomography (CT). The significance of this case is that abnormal enhancements of the liver on abdominal CT in the regions described should be suggestive of an SVC obstruction on this basis alone.
Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.
A pilot study on intraoperative radiation therapy (IORT) combined with external beam radiation therapy (EBRT) in nonresectable non-small cell lung cancer (NSCLC) was performed in 31 patients (mean age: 66.2 years, range: 51-80; 10 anatomically and functionally, 21 functionally, nonresectable; 20 squamous-cell, 11 adenocarcinoma). The tumor was exposed by lateral thoracotomy and a staging lymph node dissection was performed (final staging 7 T1, 16 T2, 8 T3; 11 nodal positive). Ten to 20 Gy IORT (energy: 7-20 MeV electrons) were delivered to the tumor. Unilateral continuous positive airway pressure ventilation of the diseased lung was used to reduce the amount of healthy lung tissue in the IORT port and to minimize the ventilatory movement. Secondary collimation and direct shielding of radio-sensitive structures within the IORT port by aluminium sheets were used to further reduce collateral damage. Four weeks after IORT, 46 Gy EBRT (2 Gy/day 5 times a week; 8-23 MeV photons) were administered to the mediastinum and to the tumor-bearing area on an outpatient basis. In nodal positive cases the mediastinal dose was increased to 56 Gy. Twenty-three patients were evaluable. In 13 complete, in 8 partial (50-97% regression) and in 2 minor response has been achieved. Five patients experienced a recurrence (local only: 2; local and distant: 1; distant only: 2). Twelve patients died of underlying cardio-respiratory disorders within 6 to 25 months after IORT; 7 died of cancer. The overall 5-year survival rate including the incidental deaths is 14.7%. The recurrence-free survival rate is 53.2%.
BACKGROUND: It is not known whether pretreatment with nicorandil, an ATP-sensitive K+ channel (K(ATP)channel) opener, induces a preconditioning effect independent of increased collateral recruitment. METHODS: Forty-four patients with angina who underwent percutaneous transluminal coronary angioplasty (PTCA) to proximal left anterior descending artery (LAD) stenosis were randomly allocated for pretreatment with an intravenous injection of 80 g/kg nicorandil 5 min before initial ballooning (n=22) or saline (n=22). 99mTc tetrofosmin was injected during balloon inflation, quantitative analysis of occlusion images by SPECT was conducted, and the defect severity score (SS) was calculated. An ECG was recorded during the 2-min inflation to calculate the sum of ST elevation (sigmaST). RESULTS: SigmaST levels were significantly reduced in patients with nicorandil pretreatment compared with control patients (control:1.89+/-0.85 mV nicorandil:1.24+/-0.57 mV, p=0.0052). However, no difference was observed in defect severity (control: 79.0+/-32.5, nicorandil: 98.7+/-48.9 ns). A close correlation was observed between SS and sigmaST in both groups (nicorandil group R(2)=0.505, control group R(2)=0.599). A multivariate regression model demonstrated that both defect severity (p<0.0001) and pretreatment with nicorandil (p<0.001) were significantly related to the level of sigmaST, suggesting a cellular protective effect against ischaemia by nicorandil, independent of myocardial blood flow. CONCLUSION: Nicorandil pretreatment resulted in the induction of myocardial preconditioning independent of the severity of ischaemia.
Studying the anatomy of lower extremity veins is a tedious and complex task. Although huge efforts have been undertaken to create harmonization, any global description of the venous network is encumbered by the large number of superficial and deep veins, anastomoses and collaterals, and not least by a vastly broad nomenclature. Innumerable anatomic variants contribute to creating a complicated picture. What is needed is a description that correspondingly reflects the reality. Yet, does our description reproduce the actual anatomic and pathologic circumstances? As a rule, a phlebography is performed to localize an acute or chronic venous condition. The examiner must have learn about the "healthy" to What the stethoscope is to a cardiologist, the Doppler sonography transducer was to the phlebologist, an indispensable tool. Nowadays, duplex sonography has to be called the gold standard in that it supplies the most comprehensive information for diagnosing functional disorders of the venous system, thereby enabling a clear therapeutic strategy to be delineated. Most qualitatively average or high-grade ultrasound machines are equipped with duplex sonography, which today's specialists can employ to highly efficiently render a differential diagnosis of deep vein thrombosis. Given the ethic and forensic background and the potentially lethal outcome of a misdiagnosis, the use of this diagnostic tool must be exclusively reserved for physicians with a particularly high level of skill and training. The specialist societies for ultrasonography, angiology and phlebology have published strict guidelines for teaching Doppler sonography in Switzerland.
Increases of individual beta tubulin isotypes in antimicrotubule drug resistant cell lines have been reported by several laboratories. We have previously described elevations in beta(III)and beta(IVa)isotypes in estramustine and paclitaxel resistant human prostate carcinoma cells. To investigate further the function of beta tubulin isotypes in antimicrotubule drug response, human prostate carcinoma cells that normally have very low to undetectable levels of beta(III)were stably transfected with beta(III)cDNA in pZeoSV system. An 18 bp haemagglutinin (HA) epitope tag was added at the 3' end prior to cloning into the vector. Cells were transfected with pZeoSV or pZeoSV-beta(III)plasmids and selected in the presence of Zeocin. Immunofluorescent staining of the transfectant cells have shown significant expression and incorporation of HA-tagged beta(III)tubulin into cellular microtubules. Quantitation of Western blots revealed the HA-tagged beta(III)levels to be approximately 7-fold higher than the vector control cells. RT-PCR analysis confirmed the increase at the transcript level and also revealed a collateral increase of beta(II)and beta(IVb)transcripts. Cell viability assays indicated that sensitivity of beta(III)transfected cells to various antimicrotubule agents was similar to vector transfected cells: IC50 values for estramustine, paclitaxel, colchicine and vinblastine were 4 microM, 4 nM, 22 nM and 2 nM, respectively for both cell lines. Thus, overexpression of beta(III)isotype in human prostate carcinoma cells by stable transfection failed to confer antimicrotubule drug resistance to these cells. Counterregulatory increases of endogenous beta(II)and beta(IVb)tubulin isotypes in these beta(III)transfected cells may be a compensatory mechanism used by the cells to overcome the effects of elevated beta(III)levels on the cellular microtubules. These results highlight the difficulty in isolating the contribution of single tubulin isotypes in drug response studies.
Amaurosis of the right eye occurred in an 18-year-old woman. 17 years later the healthy patient was referred for diagnosis, showing an amaurotic pupil, no protrusion, normal motility and corneal sensitivity, normal morphology of the anterior segment. In ophthalmoscopy optic atrophy with typical retinociliary collateral vessels, calcified and obliterated vessels throughout to the posterior pole and a macular scar. In fluorescein angiography normal choroidal filling, greatly diminished retinal capillary filling, hypofluorescent optical disc with venous shunt to retinociliary collaterals, no preretinal neovascularizations. On cranial CT and nuclear magnetic imaging pathognomonic meningioma of the optic nerve sheaths with tram-tracking lines. Inspite of suprasellar extension no indication to surgical therapy because of normal hormone production.
This study used Interleukin (IL)-stimulated normal human lymphocytes in culture as a model system to examine membrane transport systems and drug cytotoxicity. Normal peripheral blood mononuclear cells were stimulated with either purified IL-1 or phytohemagglutinin (PHA) and maintained for several months in IL-2. Only 'T' lymphocytes grew in culture. Amino acid transport was compared in PHA-stimulated cells and IL-stimulated cells. Both the PHA- and IL-stimulated lymphocyte cell lines had similar generation times and similar uptake and efflux of cisplatin and methotrexate. Yet, PHA-stimulated cells proved 3- to 5-fold more sensitive to the cytotoxic effects of these drugs. The greater drug sensitivity of the PHA-stimulated cell line was associated with enhanced sodium-dependent methionine transport and altered amino acid transport systems. Differences in the nutrient transport systems are comparable to those previously observed between drug sensitive and resistant cells, and may provide the biochemical basis for cisplatin and methotrexate collateral resistance.
OBJECTIVE: We sought to evaluate the anatomy of the posterolateral aspect of the knee with anatomic dissection, MR imaging, MR arthrography, and sectional anatomy. MATERIALS AND METHODS: We assessed the posterolateral corner of the knee during dissection of one gross anatomic specimen. MR imaging and MR arthrography were performed in seven additional knee specimens. T1-weighted spin-echo MR images were obtained in the standard imaging planes as well as in the coronal oblique plane. The specimens underwent T1-weighted spin-echo MR imaging after administration of intraarticular contrast material and were sectioned into planes corresponding to those of the MR images. RESULTS: At anatomic dissection, the following posterolateral structures were identified: the arcuate ligament (medial and lateral limbs), fabellofibular ligament, popliteofibular ligament, popliteus tendon and its two posterior attachments to the lateral meniscus, fibular collateral ligament, direct and anterior arms of the tendon of the long head of the biceps femoris muscle, and direct and anterior arms of the tendon of the short head of the biceps femoris muscle. Correlation of MR imaging and anatomic findings showed that the popliteofibular ligament and oblique popliteal ligament were found in 57% and 100% of specimens, respectively. At least one of the two limbs of the arcuate ligament was identified in 71% of specimens. The fabellofibular ligament was not identified on MR images in any of the specimens. The anteroinferior and posterosuperior popliteomeniscal fascicles were identified in all specimens. CONCLUSION: The posterolateral corner of the knee comprises complex and variable anatomic structures. Recognition of these variations is important in the assessment of MR images of the knee.
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Diagnostic possibilities of various exercise tests (bicycle ergometry, the dipyridamole test, atrial electrostimulation) were demonstrated, as was a relationship between their sensitivity and the number of stenosed coronary arteries, the extent and level of obstruction, collateral circulation specificity and myocardial function.
A clone of a human gastric carcinoma cell line was used to determine whether cells which had survived a treatment with Melphalan would express altered survival responses when treated again with this agent 1 week or more later. Cells were treated for 1 h each week with 2 micrograms/ml (99% lethal dose). After the first Melphalan treatment, the cells exhibited a 10-fold reduction in sensitivity to Melphalan. This was preceded by a 2-fold increase in intracellular glutathione content. By the end of 10 weekly treatments, the cells were 50 times more resistant than controls (based on changes in survival fractions). They also demonstrated collateral resistance to Actinomycin D, 1-(2-chloroethyl)-3-(4-methylcyclohexyl)-1-nitrosourea, galactitol, and X-rays, but showed no change in sensitivity to 5-fluorouracil, bleomycin, and Adriamycin. The resistance to Melphalan was not reversible when treatment was withheld for 4 weeks on two different occasions. The results suggest that treatment with a high dose of Melphalan either selects an existing population of cells with a high GSH content or induces mutations leading to increased GSH content or both, and this results in the expression of greater Melphalan resistance at the time of other treatments. Furthermore, Melphalan treatment stimulates a 50% increase in GSH content in resistant cells in just 6 h, an 85% increase in 36 h, and a 150% increase in 72 h. L-Buthionine sulfoximine partially reversed the expression of resistance to Melphalan by inducing a 60% reduction in intracellular glutathione content.
Some neurons, including cerebellar Purkinje cells, are completely ensheathed by astrocytes. When granule cell neurons and functional glia were eliminated from newborn mouse cerebellar cultures by initial exposure to a DNA synthesis inhibitor, Purkinje cells lacked glial sheaths and there was a tremendous sprouting of Purkinje cell recurrent axon collaterals, terminals of which hyperinnervated Purkinje cell somata, including persistent somatic spines, and formed heterotypical synapses with Purkinje cell dendritic spines, sites usually occupied by parallel fiber (granule cell axon) terminals. Purkinje cells in such preparations failed to develop complex spikes when recorded from intracellularly, and their membrane input resistances were low, making them less sensitive to inhibitory input. If granule cells and oligodendrocytes were eliminated, but astrocytes were not compromised, sprouting of recurrent axon collaterals occurred and their terminals projected to Purkinje cell dendritic spines, but the Purkinje cells had astrocytic sheaths, their somata were not hyperinnervated, the somatic spines had disappeared, complex spike discharges predominated, and membrane input resistance was like that of Purkinje cells in untreated control cultures. When cerebellar cultures without granule cells and glia were transplanted with granule cells and/or glia from another source, a series of changes occurred that included stripping of excess Purkinje cell axosomatic synapses by astrocytic processes, reduction of heterotypical axospinous synapses in the presence of astrocytes, disappearance of Purkinje cell somatic spines with astrocytic ensheathment, and proliferation of Purkinje cell dendritic spines after the introduction of astrocytes. Dendritic spine proliferation was followed by formation of homotypical axospinous synapses when granule cells were present or persistence as unattached spines in the absence of granule cells. The results of these studies indicate that astrocytes regulate the numbers of Purkinje cell axosomatic and axospinous synapses, induce Purkinje cell dendritic spine proliferation, and promote the structural and functional maturation of Purkinje cells.
PURPOSE: Branch retinal vein occlusion (BRVO) induces variable functional deficits depending on the grade of vascular occlusion and its localisation. Theses deficiences are not easily defined by visual acuity measurements. However, microperimetry offers topical mapping of retinal function, allowing precise documentation of the intensity and dimension of retinal functional loss in BRVO. METHODS: Retinal sensitivity was examined using a Rodenstock Scanning Laser Ophthalmoscope (SLO). A standardized grading system of stimuli ranging from 0 to 32 dB was used to document the retinal threshold in three different areas: regions presenting vascular occlusion, the collateral edematous zone and adjacent areas with intact perfusion. Absolute and relative scotomas as well as the fixation behavior were studied. RESULTS: Forty-two patients with isolated BRVO within the vascular arcades were examined with microperimetry and angiography. At initial presentation with BRVO the retinal sensitivity in the area of occlusion on average diminished to 4.1 dB. In the collateral edematous zone retinal threshold was reduced to 21.5 dB; area with intact perfusion demonstrated a threshold of 23.2 dB. Within the occluded area itself defects of significantly differing intensity were found which only partially correlated with the angiographic evidence. Intense scotomas (0 dB) were observed in 59% of the eyes examined: angiographically nonperfused areas or extended intraretinal hemorrhage were present. Relative scotomas (12.1 dB) were seen in 19.1% and minimal, non-significant defects (19.5 dB) were documented in 21.4% of the BRVO. The level of angiographically documented leakage did not correlate with the functional deficits present in these two groups. Measurements performed after 6-8 weeks revealed noticeable spontaneous recovery of retinal sensitivity, unless an additional progressive closure occurred. The average functional improvement in the area of leakage found after laser therapy was less than the results shown in spontaneous resolution of edema. CONCLUSIONS: BRVO may lead to significant reductions of central and paracentral retinal function. Angiographically observed leakage is not always directly correlated to the magnitude of retinal sensitivity loss. As spontenous remission is frequent in one group and intact retinal function can be shown in areas of angiographic leakage, therapeutic interventions, e.g., laser treatment, should be carefully considered. Scanning laser ophthalmoscopy provides additional information for precise evaluation and follow-up of the retinal damage in BRVO.
This article explores the causes and manifestations of obstruction of the inferior vena cava (IVC) with a multiple-modality approach. Caval obstruction may be due to thrombus, extension of a tumor, extrinsic compression, or intrinsic caval disease. Evaluation of the IVC should be tailored to the individual circumstance; no single modality is best in all situations. Although magnetic resonance offers multiplanar imaging, vena cavography or ultrasound are often necessary to exclude intraluminal tumor extension. Computed tomography is sensitive for intracaval thrombus and compression but does not delineate the hepatic IVC well. Nuclear venography demonstrates well the resultant collateral pathways, which can be separated into the deep, intermediate, superficial, and portal systems. Despite the clear visualization of these pathways with this modality, congenital caval anomalies, such as caval interruption with azygos continuation, can be confused with acquired caval disease.
Allergic asthma is an inflammatory lung disease thought to be initiated and directed by type 2 helper T cells responding to environmental Ags. The mechanisms by which allergens induce Th2-adaptive immune responses are not well understood, although it is now clear that innate immune signals are required to promote DC activation and Th2 sensitization to inhaled proteins. However, the effect of ongoing Th2 inflammation, as seen in chronic asthma, on naive lymphocyte activation has not been explored. It has been noted that patients with atopic disorders demonstrate an increased risk of developing sensitivities to new allergens. This suggests that signals from an adaptive immune response may facilitate sensitization to new Ags. We used a Th2-adoptive transfer murine model of asthma to identify a novel mechanism, termed "collateral priming," in which naive CD4(+) T cells are activated by adaptive rather than innate immune signals. Th2 priming to newly encountered Ags was dependent on the production of IL-4 by the transferred Th2 population but was independent of Toll-like receptor 4 signaling and the myeloid differentiation factor 88 Toll-like receptor signaling pathway. These results identify a novel mechanism of T cell priming in which an Ag-specific adaptive immune response initiates distinct Ag-specific T cell responses in the absence of classical innate immune system triggering signals.
Volatile anesthetics are known to depress excitatory synaptic transmission. Inhibition of voltage-dependent Ca2+ channels is speculated to underlie this mechanism, which remains to be clarified in vivo. We examined the sensitivity to halothane in mice lacking the N-type Ca2+ channel, a major contributor of presynaptic neurotransmitter release. Sensitivity to halothane was significantly increased in the knockout mice compared with the wild-type littermates. Halothane also depressed field excitatory postsynaptic potentials recorded from the Schaffer collateral-CA1 hippocampal synapses more greatly in the knockout mice. We further examined sleep time induced by injection of propofol, an intravenous anesthetic that mainly affects inhibitory synaptic transmission. In contrast, sensitivity to propofol was significantly decreased in the knockout mice. We suggest that inhibition of the N-type Ca2+ channel underlies mechanisms of halothane anesthesia but counteracts propofol anesthesia.
PURPOSE: To evaluate the feasibility of a contrast enhanced MR angiography (MRA) technique, using the latest 1.5 T MR tomoscan, to obtain optimal imaging of the portal system and compare the angiographic images with those obtained by color-Doppler and DSA. MATERIAL AND METHODS: Thirty patients (9 women and 21 men: average 53 years old) underwent contrast MRA of the portal vein, after portal hypertension had been diagnosed on the basis of clinical and chemical data and by color-Doppler. We used a dynamic 3D FFE T1-weighted breath - hold sequence during the arterial and venous phase after administering. 0.2 mmol/Kg of gadolinium-DTPA were at the rate of 2 ml/s. The contrast bolus was monitored using a 2D FFE T1-weighted sequence on a coronal plane. A FFE T1-weighted sequence was performed on axial plane before and after the dynamic sequence to obtain evaluate the a hepatic parenchyma. In the post processing phase MIP (maximum intensity projection) were reconstructed. We considered the patency of the portal venous system and the presence of cavernomatous and collateral circles; portal thrombosis was classified as partial or complete and as proximal or distal. RESULTS: Good quality MR angiographic images were obtained in 28 of the 30 cases examined; in 2 patients movement artefacts compromised the image quality. We observed a concordance between MRA and Doppler ultrasound in 79 vessels out of 84 (94%). A 97.5% concordance was found between MRA and DSA (82 vessels out of 84) with a sensitivity of 100% and a specificity of 97.3%. MRA was superior to DSA and Doppler ultrasound for evaluating large collateral shunts, above all gastro-esophageal and paraumbilical shunts, and complex anatomical conditions. CONCLUSIONS: Where available, advanced MRA technology with contrast enhancement should be used as a routine modality to study the anatomy and pathology and the portal system in all patients in whom Doppler ultrasound has yielded doubtful information. MRA is well-suited to obtain good vascular imaging before surgical or interventional procedures.