87,177 research outputs found
De vulgari eloquentia
Edizione con Introduzione, traduzione italiana e commento delle poesie provenzali e francesi citate nel 'De vulgari eloquentia' (Appendice I.1 dell'edizione critica a cura di E. Fenzi
Enhanced expression of E-selectin on the vascular endothelium of peripheral nerve in critically ill patients with neuromuscular disorders.
Neuropathic complication often occurs in critically ill patients, and changes in the microcirculation of the peripheral nerve have been suggested to play a role in the pathogenesis of the nerve lesion. We report the results of a pathological and immunohistochemical study of superficial peroneal nerve biopsy specimens in a series of 22 critically ill patients with sepsis and neuromuscular disorders. Eight patients had histopathological features of axonal neuropathy compatible with critical illness polyneuropathy (CIP). The nerve lesions ranged in severity from mildly reduced myelin-fiber density with sporadic axonal degeneration to marked fiber loss with abundant degenerative changes. In no patient did we detect evidence of primary demyelinizatilon or inflammatory infiltrates. We analyzed the immunohistochemical expression of E-selectin, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) and tumor necrosis factor alpha (TNF-α) in nerve microvessels. Expression of E-selectin was significantly increased in endothelium of epineurial and endoneurial vessels, suggesting endothelial cell activation. These findings again confirm axonal degeneration as the major pathological feature of CIP. Our immunohistochemical data provide first evidence that activation of the endothelial cells of the microvessels in the endoneurium of human peripheral nerve does occur during sepsis. This specific activation might have implications with the mechanisms responsible for the axonopathy in critically ill patients
Role of the adenylate cyclase-cAMP system on TSH-stimulated thyroid cell growth
: TSH is a trophic factor for cultured rat thyroid cells (FRTL-5). In the present study we have investigated the mechanism by which TSH promotes cell growth and evaluated the possible role of the adenylate cyclase (AC)-cAMP system in this process. The mitogenic activity of several agents was evaluated by measuring their effect on cell number or 3H-thymidine incorporation into DNA. Forskolin and cholera toxin, two potent and specific activators of the AC, induced a dose dependent increase of 3H-thymidine incorporation. The maximal stimulation, observed at concentrations of 10 microM and 10 ng/ml, respectively, was beta 80% of that obtained with optimal concentrations of TSH. A similar effect was obtained with a Graves' IgG preparation (0.2 mg/ml) able to stimulate the thyroid AC or with 3-isobutyl-1-methyl-xanthine (IBMX, 0.5 mM), a phosphodiesterase inhibitor. 8-bromo cAMP (0.5 mM), a cAMP analog, also stimulated 3H-thymidine incorporation, and its potency was approximately 60% of that of TSH. Similar results were obtained when the mitogenic activity of these compounds was evaluated by cell number. Norepinephrine (NE, 10 microM), although devoid of AC stimulatory activity in these cells, also stimulated 3H-thymidine incorporation, but its potency was only 20-30% of that of TSH. Indomethacin (100 microM), an inhibitor of phospholipid and arachidonic acid metabolism, was able to inhibit the stimulatory effect of NE (84%), and to a lesser extent of TSH (63%) and cholera toxin, had minor effect on forskolin (24%), IBMX (16%) and Graves' IgG (8%), and no effect on 8-bromo cAMP.(ABSTRACT TRUNCATED AT 250 WORDS
Immunoglobulin-binding of thyroid hormones in a case of Waldenström's macroglobulinemia
This paper describes a case of hypothyroidism in a patient with Waldenström's disease in which the evidence of thyroid failure was accompanied by an abnormal binding of thyroid hormones in the gamma-globulin fraction. A 68-yr-old patient with Waldenström's disease appeared to be hypothyroid by clinical and laboratory criteria. Serum TSH was elevated; serum T3 (measured by RIA) was low, while T4 levels were undetectable or very high according to the method used. Serum free thyroid hormones were in the hypothyroid range, and both antithyroglobulin and antimicrosomal thyroid antibodies were undetectable. The thyroid gland was normal at autopsy. Elevated binding of radiolabeled thyroid hormones by the patient's serum gamma-globulins was demonstrated by reverse flow electrophoresis and cellulose acetate electrophoresis. This binding could be inhibited by preincubation of serum samples with unlabeled T4 and T3, but not with human thyroglobulin, rT3, DIT, or MIT. Immunoprecipitation of the patient's serum incubated with [125I]T4 or [125I]T3 showed that 56% of T4 and 30% of T3, respectively, were precipitated using an antihuman immunoglobulin M(IGM) serum; only [125I]T4 was precipitable (22%) by the addition of an antihuman immunoglobulin G(IgG) serum. The binding of the thyroid hormones by IgM and IgG, which reduced T4 and T3 availability for their metabolic action at the tissue level, could have contributed to the clinical picture
Role of the annealing parameters on the resistance of indium tin oxide nanocrystalline films
The optical and electrical properties of films made of nanoparticles of indium tin oxide (ITO) are widely studied because of the significance of this material for transparent electrodes, smart windows, and nonlinear optics components. In this work, a systematic study of the resistance in ITO nanocrystalline films, as a function of post-fabrication parameters, such as the temperature and time of annealing, has been performed. A tunability of the resistance with the annealing parameters, in a range of three orders of magnitude, has been demonstrated. The optical properties of the nanocrystalline films were also evaluated as a function of the same parameters. Results show a different influence of temperature and time on the modification of the absorption properties. Temperature and time can be used synergistically to obtain thin films with desired optical and electrical properties through post-fabrication treatments
Loss of polarity and de novo expression of the beta 1 family of integrins in thyroid tumors.
MRI investigation of liver and myocardium iron overload induced by iron-rich feeding in rats.
The aim of this study was to establish
weather intensive iron introduction by feeding can lead to cardiac iron
overload in addition to the well-established hepatic iron overload in rats. Iron
assessment in both myocardium and liver was performed non-invasively by
MRI, according to previously published methods.
Our results show that intensive iron introduction
by feeding does not implicate significant heart iron accumulation
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