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Biomedical subjects

C Tomasini

Publications and source records attributed to C Tomasini.

At least 55 records · Page 3Linked to original sources
PubMed1992

Clonidine inhibition of norepinephrine release from normal and morphine-tolerant guinea pig cortical slices.

Endogenous norepinephrine (NE) release in cerebral cortex slices taken from normal and morphine-tolerant guinea pigs was measured by HPLC. In normal slices, a linear relationship was found between electrically evoked NE release and the log of the frequency of stimulation in the range of 1-20 Hz. The efficiency of the alpha 2-mediated autofeedback was tested by adding the alpha 2-agonist clonidine and the alpha 2 agonist idazoxan. NE release was dose-dependently reduced by clonidine (1 nmol/L-1 mumol/L) and increased by idazoxan (10-100 nmol/L). The inhibition by clonidine was significantly greater at 1 Hz than at 3 Hz, whereas the absolute increase in NE release induced by idazoxan was greater at 3 Hz than at 1 Hz. Morphine at 1 mumol/L (a concentration per se ineffective) shifted to the left the clonidine concentrations able to inhibit NE release at 3 and 1 Hz (1-10 nmol/L), but at both frequencies, the opiate reduced the maximal inhibition induced by clonidine at 1 mumol/L. In slices taken from morphine-tolerant guinea pigs (in the presence of morphine at 1 mumol/L), clonidine (1 nmol/L-1 mumol/L) was ineffective at the stimulation rate of 3 Hz, but it was more active than in normal slices at 1 Hz. Such a response pattern suggests a reduced availability of alpha 2 receptors and an increase in their sensitivity to clonidine. However, chronic morphine treatment did not influence the physiological autoinhibition because the increase in NE release elicited by idazoxan (10-100 nmol/L) at 1 and 3 Hz was the same in normal and in "morphine-tolerant" slices.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Eccrine angiomatous hamartoma: a multiple variant.

A case of multiple eccrine angiomatous hamartoma present in a boy since birth is reported. Clinically, this condition must be differentiated from other neonatal angiomatoses. Sometimes the clinical findings are nonspecific, whereas histologic examination may exclude angiomatoses with visceral involvement. In our case the hamartomatous nature of this tumor is documented also by the presence of pilar structures intimately related to the eccrine-angiomatous complex in one of two lesions histologically examined. Therefore, the histologic classification of eccrine angiomatous hamartoma into subgroups seems to be excessive.

Child, Preschool↗
PubMed1991

Argyrophilic nucleolar organizer region counts in malignant melanoma associated with benign intradermal nevus.

A silver colloidal technique to demonstrate argyrophilic proteins of the nucleolar organizer regions (AgNORs) was performed on sections of 20 cases of malignant melanoma (MM) associated with underlying benign nevus (BN). In these cases, significant different AgNOR counts were found for MM and BN. In addition, this technique permitted the identification of melanocytic cells located between malignant and benign cells showing AgNOR scores intermediate (5.51) between BN (2.6) and MM (7.71) with a more complex and bizarre morphology than that observed in BN. The AgNOR technique can be suitable in the identification of residual nevus cells in MM, especially when their number is minimal and the common histologic criteria are unsatisfactory; it can also increase the understanding of the natural history of MM.

Diagnosis, Differential↗
PubMed1990

[Eruptive vellus hair cysts: a facial variant].

A case of a 30 year-old man with numerous, pink to whitish, 1-2 mm, cystic lesions, located exclusively on the face and helices in symmetrical distribution is reported. Microscopic examination of serial sections of two biopsies disclosed dermal cystic cavities with vellus hair shafts into the lumen. The cyst wall was connected to rudimentary pilar structures. This picture is typical of eruptive vellus hair cysts (EVHC). Facial variant of this dermatosis is reported only in two cases in the literature. Histogenesis and differential diagnosis are discussed.

Adult↗
PubMed1990

[Maculo-papular juvenile xanthogranuloma. Considerations on a case].

A case of a 6-month-year old child with a yellow, macular and papular, asymptomatic, eruption involving the extremities, upper part of trunk and especially the head is reported. In the early stage histological and immunohistochemical studies were not contributory. Successively, the diagnosis of juvenile xanthogranuloma was made on the basis of the histological, immunohistochemical and ultrastructural findings. Problems of differential diagnosis are discussed.

Arm↗
PubMed1990

[Tricholemmal hamartoma].

A 23-year-old man with a keratotic-nodular lesion localized on the neck since infancy is reported. Histologically, there was a funnel-shaped follicle with central horny material and multiple digitations of the follicular sheath epithelium with some features resembling dilated pore of Winer. In addition, there were pale dyskeratotic epithelial cells in the infundibular portion of the tumor and in the surrounding epidermis. For this unusual tumor the term of tricholemmal hamartoma is proposed.

Adult↗
PubMed1989

Alpha 1-adrenoreceptor-mediated increase in acetylcholine release in brain slices during morphine tolerance.

Norepinephrine, clonidine, and phenylephrine increased the electrically evoked release of endogenous acetylcholine in cortical slices taken from morphine-tolerant guinea pigs. This effect was alpha 1-adrenoreceptor mediated and was opposite to the alpha 2-adrenoreceptor-mediated inhibition of acetylcholine release, normally elicited by norepinephrine and clonidine. In the presence of prazosin, clonidine recovered its normal inhibitory properties, suggesting that morphine tolerance induced the appearance of an alpha 1-adrenoreceptor-mediated response that overshadowed, but did not cancel, the still present alpha 2-adrenoreceptor inhibitory control. The attempt to prove the presence of alpha-adrenoreceptors on the nerve endings by testing the effect of norepinephrine in synaptosomal preparations (preloaded with [3H]choline and depolarized with KCl and veratridine) was unsuccessful. Therefore the problem of the exact location of this excitatory input remains to be solved. These results confirm previous findings reporting the increase in cortical acetylcholine release induced by the alpha-adrenoreceptor agonists in morphine-tolerant, freely moving guinea pigs and demonstrate that opiate tolerance inverts the direction of the noradrenergic modulation even in the isolated intracortical cholinergic structures.

Acetylcholine↗
PubMed1989

Changes in cortical acetylcholine and gamma-aminobutyric acid outflow during morphine withdrawal involve alpha-1 and alpha-2 receptors.

Naloxone (0.3-9 mumol kg-1), electrical stimulation of locus ceruleus or clonidine at low doses (7.5-112 nmol kg-1) increased the release of acetylcholine from the exposed parietal cortex of freely moving, morphine-tolerant guinea pigs. This increase was not additive and was prevented by prazosin (35.8 nmol kg-1), suggesting the involvement of alpha-1 receptors. At high doses (374 nmol kg-1 or more) clonidine inhibited acetylcholine release through alpha-2 receptors, as it did in naive animals at 7.5 nmol kg-1. Clonidine (374 nmol kg-1) and prazosin (35.8 nmol kg-1) reduced the objective signs of naloxone-precipitated withdrawal. Electrical stimulation of the locus ceruleus or naloxone treatment reduced the release of gamma-aminobutyric acid (GABA) from the exposed parietal cortex of morphine-tolerant guinea pigs. This reduction was not additive and was prevented by idazoxan (84 nmol kg-1), suggesting the involvement of alpha-2 receptors. Clonidine (7.5 nmol kg-1), too, reduced the release of GABA in morphine-tolerant animals. However, when tested jointly with naloxone, clonidine (7.5-112 nmol kg-1) induced alpha-1-mediated facilitation of GABA release (like that elicited in naive animals at 112-374 nmol kg-1) leaving the signs of withdrawal unchanged. This points to the stimulation of alpha-1 receptors highly responsive to this agonist (but not to locus ceruleus stimulation) during naloxone-precipitated withdrawal. In conclusion, chronic morphine treatment modifies the alpha-1- and alpha-2-mediated control of GABA and acetylcholine neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1983

Plasma cortisol studies with 0.05% halometasone cream and ointment in patients with psoriasis.

Plasma cortisol levels were determined by a radioimmunological assay in three groups of ten psoriasis patients treated with 0.05% halometasone ointment, 0.05% halometasone cream and 0.025% fluocinolone acetonide ointment, without occlusive dressings, for 7 days. Fourteen grams of the corticoid topical was applied daily (7 g/b.i.d.) to the psoriasis plaques covering an average of 25% of the body surface. No significant differences with respect to plasma cortisol values at 8 a.m. before, during and after treatment were evident in any of the three treatment groups, nor did the treatment groups significantly differ from one another with regard to their effect on the plasma cortisol levels. No side-effects were observed.

Administration, Topical↗