PubMed Health⌕ Search

Biomedical subjects

T Lotti

Publications and source records attributed to T Lotti.

At least 19 recordsLinked to original sources
PubMed1995

Scanning electron microscopy of the tunica albuginea of the corpora cavernosa in normal and impotent subjects.

The tunica albuginea (TA) of the penis is thought to play a major role in the erection mechanism. It functions by compressing the subalbugineae venulae, which promotes the slower venous flow during erection, and provides a fibrous frame to give an inextensible support for the vessels and nerves. It acts as the inextensible enclosing structure which contains the erectile tissue and gives the erect penis its shape. The functions of the TA result from its structure, consisting for the most part of collagenic and elastic fibers. This study investigated, with the aid of scanning electron microscopy (SEM), the microarchitecture of the TA and the spatial relation of its fibers in ten impotent patients and in six control subjects with normal erectile function. The arrangement of elastic fibers in the TA seems to account for their function, which is to prevent the overstretching of collagenic fibers during maximum intracavernous pressure. In impotent patients, a reduction in the elastic fibers in the TA appears to produce disorders in the arrangement of the collagenic fibers. These alterations in the architecture of the TA in impotent patients can give rise top erection disorders.

Adult↗
PubMed1995

Neuropeptides in skin.

Neuropeptides are a heterogeneous group of more than 50 molecules that play a role in various cutaneous functions and diseases; they act as neuromodulators, neurotransmitters, neurohormones, and hormones. In the skin, neuropeptides are synthesized locally (i.e., in keratinocytes and in endothelial cells) and are transported by nerve fibers or immune cells (i.e., lymphocytes, monocytes, and polymorphonuclear cells). Specific receptors and binding sites for neuropeptides have been described in different cell lines in the skin (keratinocytes, endothelial cells, immune cells, fibroblasts). Many different biologic actions of neuropeptides have been demonstrated. Depletion of cutaneous neuropeptides (i.e., with capsaicin cream) or therapeutic use of neuropeptide agonists and/or antagonists may aid in the treatment of skin diseases.

Capsaicin↗
PubMed1995

Pharmacologic modulation by cetirizine of some adhesion molecules expression in psoriatic skin lesions.

BACKGROUND: Adhesion molecules play a major role in the pathogenesis of inflammatory skin diseases by regulating lymphocyte trafficking and homing in an inflamed area. METHODS: The expression of the lymphocyte function-associated antigen-1 (LFA-1) and of its ligand, the intercellular adhesion molecule-1 (ICAM-1) has been studied in psoriatic skin lesions of 10 patients with guttate, nummular, and palmoplantar psoriasis. In addition, the peculiar immunophenotype of infiltrating cells (CD3, CD4, CD8, CD25) and their correlation with HLA-DR expression before and after treatment with oral cetirizine, a highly selective, third generation H1-receptor antagonist has been examined using the labeled avidin biotin (LAB) system. RESULTS: Cetirizine treatment modulated in vivo the expression of adhesion molecules LFA-1/CAM-1 as shown in all cases by decreased levels of their expression on keratinocytes and on dermal endothelial cells (P < 0.001). The expression of HLA-DR on keratinocytes and endothelial cells was also inhibited after treatment. The numbers of infiltrating CD3-, CD4-, CD8-positive cells were reduced, whereas there was no significant modification of CD25-positive cells within the epidermis and the dermis. CONCLUSION: This open clinical trial suggests that cetirizine could be effective in treating psoriasis: (1) for its symptomatic control on itching; (2) for its immunopharmacologic modulation of leukocyte integrins and on the immunophenotype pattern of infiltrating and resident cells, and (3) for contributing to the clearing of the lesions clinically.

Administration, Oral↗
PubMed1995

Cell infiltrate in progressive pigmented purpura (Schamberg's disease): immunophenotype, adhesion receptors, and intercellular relationships.

BACKGROUND: Progressive pigmented purpura (Schamberg's disease), a form of purpura pigmentosa chronica, is a lymphocytic capillaritis of unknown etiology and obscure pathogenesis. Our purpose was to assess the expression of cell membrane antigens (CD3, CD4, CD1a, CD36), of adhesion receptors (leukocyte function adhesion 1, LFA-1, endothelial leukocyte adhesion molecule 1, ELAM-1) intercellular adhesion molecule 1, ICAM-1), and the intercellular relationships in the early phase of the disease. METHODS: Quantitative immunohistochemistry and electron-microscopy were performed on specimens of five subjects, aged 45 to 63 years. These studies were repeated in two patients after treatment with topical corticosteroid (betamethasone valerate cream 0.1%) and psoralen-ultraviolet A (PUVA). RESULTS: The infiltrate consisted mainly of CD4+ lymphocytes and CD1a+ dendritic cells. Electron-microscopic investigation showed typical lymphocytes and two distinct types of dendritic cells. In the very early phase of the disease the adhesion receptors LFA-1 and ICAM-1 were expressed intensely by all infiltrating cells; the adhesion receptors ICAM-1 and ELAM-1 were expressed by endothelial cells. Close contact occurred between lymphocytes and dendritic cells. After PUVA (120 J per cm2) and topical steroid therapy the infiltrate disappeared completely. CONCLUSIONS: These data suggest that a cell-mediated immune mechanism may be important in progressive pigmented purpura and that the early endothelial expression of adhesion receptors may determine the pattern of organization of the pericapillary infiltrate.

Administration, Topical↗
PubMed1995

Plasminogen activators, venous leg ulcers and reepithelialization.

BACKGROUND AND OBJECTIVE: The pathogenesis of leg ulcers due to chronic venous hypertension (CVH) seems to be related to perivenular fibrin-film formation due to decreased cutaneous fibrinolytic activity dependent on reduced release of tissue-type plasminogen activator that leads to tissue anoxia and ulcer formation. The purpose of the work is a spectrophotometric evaluation of urokinase (UPA) at the edge, the floor and in the periulcerous skin of leg ulcers. METHODS: We examined a group of 10 patients with chronic leg ulcers caused by CVH. The biopsies from each patient were taken: (1) from the edge of the ulcer; (2) from the perilesional skin and (3) from the floor of the ulcer. Urokinase levels were evaluated in the same areas in 10 control subjects. The UPA activity was determined spectrophotometrically at 405 nm. RESULTS: The results of our study showed that UPA is detectable in the center of the ulcer, on the edge, in the perilesional skin, as well as in the controls. Data are statistically significant. The highest levels of UPA are found at the edge of the ulcer; they were lower in the center and in the periulcerous skin. CONCLUSION: A chemoattracting effect of UPA on human keratinocytes has been documented and this study showed significantly higher levels of UPA at the edge and on the floor of the ulcers, suggesting a possible role of an UPA gradient that could promote mobilization of keratinocytes from the edge to the floor, thus inducing reepithelialization. Moreover, UPA could play some role in neoangiogenesis and fibroblast chemoattraction, thus contributing in various ways to wound healing.

Aged↗
PubMed1995

Elastic fibre concentration in the tunica albuginea of corpora cavernosa and nocturnal tumescence monitoring.

The tunica albuginea of the corpus cavernosum provides the latter with a fibrous framework and plays a significant role in erectile function. Being rich in elastic fibres the tunica albuginea is able to resist overstretching of the corpus at raised levels of intracavernous pressure, compressing the sub-algunineum venous reticulum and promoting the maintenance of erection. Results are reported here on assessment of the concentration of elastic fibres in tunica albuginea in relation to frequency of nocturnal erection, tumescence and penile length and rigidity. Significant correlations were demonstrated between concentration of elastic fibres and duration of nocturnal erection (P< 0.0001), rigidity at TIP(P< 0.001), and rigidity at BASE (P< 0.001). The importance of the structural soundness of the tunica albuginea for achievement of satisfactory erection was thereby underlined.

Adult↗
PubMed1995

Working classification of vasculitis.

Vasculitis is defined as angiocentric segmental inflammation of the blood vessels and fibrinoid necrosis of the vessel wall. Classification of vasculitis is a controversial problem, because of the difficulty in incorporating globally different criteria such as histologic features, size of affected blood vessels, etiology, pathogenesis and other factors in a single classification schema. In this paper we review the principal classifications and make a novel attempt to classify vasculitis on the basis of the size of affected vessels. We hope that a new generation of basic and clinical investigators can achieve a better understanding of the pathogenesis of various vasculitis-related syndromes and that this understanding will facilitate future classification schemas.

Humans↗
PubMed1995

Cellular steps in the pathogenesis of cutaneous necrotizing vasculitis.

Cutaneous necrotizing vasculitis (CNV) have been traditionally divided into "leukocytoclastic" and "lymphomonocytic" forms. The etiology and the pathogenesis of the two forms are not clear. We studied by immunohistochemistry and electronmicroscopy the infiltrate of 5 cases of leukocytoclastic form and 5 cases of lymphomonocytic form of CNV in two phases (early and late). Aim of the study was to evaluate: 1. the immunophenotypical characteristics of the infiltrate; 2. the expression of some adhesion molecules receptors; 3. the ultrastructural characteristic of the infiltrate; 4. the possible sequence of the events. Our results showed, by immunohistochemistry, a rich infiltrate of CD3+, CD4+, CD1a+ cells in both phases of lympho-monocytic vasculitis and a poor infiltrate of CD4+, CD1a+ and CD36+ cells in the early phase of leukocytoclastic vasculitis, while the perivascular infiltrate was rich of these cells in the late phase of this latter form. ICAM-1 and LFA-1 were strongly expressed in lympho-monocytic vasculitis. By electronmicroscopy, most infiltrating cells showing the ultrastructural markers of immature cells of dendritic lineage were in contact with each other and with lymphocytes and perivascular dendritic macrophages in lymphocytic form and in the late phase of leukocytoclastic form. Our results suggest that lymphocytic vasculitis might be related to a cell-mediated immune reaction and that the leukocytoclastic form of CNV, formerly considered a typical neutrophilic disease, is also maintained by a cell-mediated immune response to not yet identified endogenous antigens released in the lesional area.

Adult↗
PubMed1995

Langerhans cells and vasculitis.

Langerhans cells are members of the dendritic cell system, which reside in the skin. These cells have many immunohistochemical and ultrastructural markers (for example, they are CD1a+ and possess Birbeck granules), which consent to identify them in an infiltrate. Langerhans cells have the specific role to present the antigens to T lymphocytes and to induce the cell-mediated immune reaction. Cutaneous necrotizing vasculitis (CNV) can be divided in two major forms: a leukocytoclastic type and a lymphocytic type. The pathogenesis of the first one is presumably immune complex-mediated, while for the second one a cell-mediated immunity has been proposed. Our group investigated on the cell infiltrate of some cases of CNV, both leukocytoclastic and lymphocytic type; and for leukocytoclastic CNV two phases were studied: an early one (at the onset of the lesion) and a later one (more than 24 hours). Special attention was paid to the presence of dendritic cells in the infiltrate and to their relationship to lymphocytes, if present. By immunohistochemistry and electron microscopy we could find many Langerhans cells and T lymphocytes in lymphocytic and in the late phase of leukocytoclastic CNV. The observed pattern of the cell infiltrate suggests that a cell mediated immune response play a major role in the pathogenesis of lymphocytic vasculitis and that dendritic cells and lymphocytes contribute to self-perpetuate leukocytoclastic vasculitis, which cannot be anymore considered as simply due to infiltration of neutrophils.

Animals↗
PubMed1995

Gamma/delta T lymphocytes in cutaneous necrotizing vasculitis.

Sections of lesional skin of 5 patients with leukocytoclastic cutaneous necrotizing vasculitis (CNV) (3 with documented infective etiology and 2 with unknow etiology) and of 5 patients with lymphocytic CNV with unknow etiology were investigated with immunoperoxidase technique. In lymphocytic CNV the dermal infiltrate was mainly constituted of CD3+, CD4+, CD1a+ and CD36+ cells. ICAM-1 and LFA-1 were strongly expressed. In leukocytoclastic CNV the infiltrate was poor of these cells in the early phase of disease, but they increased in the late phase. ICAM-1 and LFA-1 were strongly expressed in the late phase, while gamma/delta T cells and the expression of 72 kD heat shock protein were significantly present only in leukocytoclastic CNV with documented infective etiology. These results seem to suggest the role of a secondary cell-mediated immune response in the late phase of leukocytoclastic CNV, indicating gamma/delta T cells as a possible clue to the infective etiology of CNV.

Adult↗
PubMed1995

Cytokines, fibrinolysis and vasculitis.

Endothelial cells are critical elements in the evolution of all types of cutaneous inflammation. They participate the pathological process through the synthesis and secretion of pro-inflammatory cytokines, including interleukin 1 (IL1), IL6, IL8, and the three colony stimulating factors G-CSF, M-CSF, and GM-CSF and the two chemotactic factors gro-alpha and MCP. They also express a series of cell-surface proteins and glycoproteins known as cell adhesion molecules that allow circulating leukocytes to selectively bind to endothelial cells. In this paper we discuss the role of endothelial cells in the evolution of cutaneous necrotizing vasculitis, an immunologically mediated clinical disorder associated with segmental inflammation and fibrinoid necrosis of the dermal venules, through the release of cytokines or their response to cytokines locally produced from leukocytes themselves primarily involved in the endothelial cells injury. This interaction seems to involve and modulate other biologically active systems including the fibrinolytic system that can act amplifying and self-perpetuating the tissue damage through a non-immunologic mechanism.

Cytokines↗
PubMed1995

The role of regulatory peptides in the pathogenesis of cutaneous necrotizing vasculitis.

Cutaneous necrotizing vasculitides (CNV) are a group of clinical disorders characterized by: 1) angiocentric segmental inflammation, 2) cellular infiltrate, 3) red cell extravasation, 4) fibrinoid necrosis of the blood vessels, and possibly 5) nuclear debris. There are many classifications of vasculitides based or on the diameter of the vessels or on the type of the cellular infiltrate. In this paper we outline the major key role played by the endothelium in this pathological process and the possible role of the regulatory peptides in the pathogenesis of CNV. Despite there are not direct yet clear evidences of the role of neuropeptides in the pathogenesis of cutaneous necrotizing vasculitis, we suggest a possible major role of them, on the basis of the activity of regulatory peptides on microvascular endothelium, on polymorphonuclear chemotaxys and on lymphocytic functions. Thus, neuropeptides and endothelins could act on the tone of the vessel, provoking vasodilation or vasoconstriction, determining a possible stimulus to inflammation and/or venular thrombosis. The release of neuropeptides at the sites of local inflammation could modulate the activity of nearby inflammatory cells and other tissue elements. Organs with neuropeptidergic fibers in high density, such as the skin, could be particularly susceptible to perturbations from inflammation-derived neuropeptides.

Animals↗
PubMed1995

Clinical aspects of cutaneous necrotizing vasculitis.

In this paper we review the clinical manifestations in cutaneous necrotizing vasculitis. Palpable purpura is the most common clinical pattern, while urticarial vasculitis, erythema elevatum diutinum and nodular vasculitis have found less commonly. Clinicopathological lesions may occur in internal locations also, presumably due to circulating immune complex-mediated vessel damage at those sites. In the setting of the disease, it is possible to observe serum sickness-like reactions, distinct clinical patterns, such as Henoch-Schönlein purpura, essential mixed cryoglobulinemia, vasculitis associated with connective tissue diseases and with malignancies.

Connective Tissue Diseases↗
PubMed1994

Treatment of aquagenic pruritus with topical capsaicin cream.

BACKGROUND: Aquagenic pruritus is characterized by pruritus after contact with water; there are no objective cutaneous changes. Capsaicin, which induces the release of neuropeptides from A delta and C cutaneous nerve fibers, has been successfully used in the treatment of several dermatoses associated with pruritus. Among the many different neuropeptides present in human skin, the undecapeptide substance P has been shown to cause pruritus. OBJECTIVE: We evaluated the clinical effect and searched for alterations in cutaneous neuropeptidergic fibers before and after treatment with capsaicin cream. METHODS: Five patients with aquagenic pruritus were treated with capsaicin cream 0.025%, 0.5% or 1.0% three times daily for 4 weeks. Direct immunofluorescence (DIF) was performed before and after treatment to evaluate the storage of neuropeptides in the A delta and C type cutaneous nerve fibers. RESULTS: Before treatment (when by DIF the neuropeptidergic fibers appeared filled with neuropeptides), contact with water consistently provoked itching. After capsaicin treatment (when by DIF the neuropeptidergic fibers were depleted of neuropeptides), contact with water did not evoke pruritus. Areas of skin treated with the vehicle alone showed no clinical improvement or change in neuropeptide content. CONCLUSION: This study suggests that neuropeptides, including substance P, may contribute to mediating the itch in aquagenic pruritus.

Administration, Topical↗