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PubMed1996

Role of catecholamines in platelet function: pathophysiological and clinical significance.

Platelets are involved in the pathogenesis of vascular damage in both atherosclerosis and arterial hypertension. Their reactivity in vivo is influenced by different factors, including sympathoadrenal activation, plasma levels of atherogenic lipoproteins and haemorrheological changes. In the present review, we examine the modulation of platelet function by the sympathoadrenal system and concentrate on the role of circulating catecholamines in the control of platelet responses. Human platelets exhibit both adrenergic and dopaminergic receptors that are influenced by different catecholamines. alpha(2)-Adrenoceptors of alpha(2A) subtype prevail on platelet membrane; through their stimulation, catecholamines potentiate the effects of other agonists and, at higher concentrations, initiate platelet responses, including aggregation, secretion and arachidonate pathway activation. Physiological and pathological conditions causing sympathoadrenal activation in vivo, i.e. physical activity, mental stress, insulin-induced hypoglycaemia, acute coronary ischaemia and heart failure, modify the circulating platelet populations and modulate platelet reactivity through an increase in circulating catecholamines. A sympathoadrenal hyperactivation modifies the function of circulating platelets through direct catecholamine effects, catecholamine-induced changes of haemodynamic factors and lipid pattern and inhibition of the vascular eicosanoid synthesis. The catecholamine effects on platelet function can be involved in the interplay among stress, adrenomedullary system activation and cardiovascular diseases.

Adrenal Glands↗
PubMed1997

Lesions of 13q may occur independently of deletion of 16q in spindle cell/pleomorphic lipomas.

AIMS: Very recent multidisciplinary investigations have allowed for the definition among lipomas of a clinical and histological subtype called spindle cell and/or pleomorphic lipoma, possibly associated with partial monosomy 16 and anomalies of chromosome 13. In order to get nearer to the underlying critical molecular changes further multidisciplinary pathological and genetic research is indicated, to identify which chromosome(s) anomalies are crucial in the development of these tumours. METHODS AND RESULTS: In an ongoing multidisciplinary study of lipomatous tumours, including clinical findings, morphology, histochemistry and cytogenetics, two instances were found of spindle cell lipoma with clonal chromosome changes. In both cases chromosome 13 was involved, whereas only one showed a partial monosomy 16. CONCLUSIONS: Partial monosomy 16 is a characteristic lesion in spindle cell lipoma, usually associated with anomalies of chromosome 13. The present report confirming a previous single observation indicates, however, that lesions of 13 may occur independently from lesions of 16, suggesting different underlying molecular lesions in these otherwise very similar lipomas.

Chromosome Deletion↗
PubMedDate not supplied

Bladder instability: a re-appraisal of classical experimental approaches and development of new therapeutic strategies.

1 Despite the growing social interest in human urinary tract disorders, the aetiology of detrusor instability remains poorly understood. Myogenic and neural impairment of detrusor activity caused by CNS or autonomic injuries can results in dysfunctions of normal voiding of the bladder such as urinary incontinence. 2 The contractility of human detrusor smooth muscle is critically dependent on acetylcholine-induced muscarinic receptor activation. Biochemical and functional in vivo and in vitro studies suggest the presence of an heterogeneous population of muscarinic receptor subtypes (M1-M4) localized at muscular and neutral sites. There is increasing evidence on the prejunctional auto- and hetero-regulation of acetylcholine release from parasympathetic nerve endings in modulating detrusor muscle contraction during micturition. 3 Activation of P2X purinoreceptors closely associated with the parasympathetic varicosities seems to be implicated to varying extent in the contractility in normal or instable human detrusor. Interestingly, P2X(1) subtype expression on smooth muscle increases considerably in the symptomatically obstructed bladder. A striking absence of P2X(3) and P2X(5) subtypes was observed in the cholinergic innervation of detrusor from patients with urgent incontinence. Thus, it is likely that alteration of the neural acetylcholine control can play a critical role in pathological states. 4 If the failures in storage and voiding can be recognized urodynamically, considerable difficulties remain in investigating the underlying functional changes especially because the study of the pathophysiology requires techniques that can be justified in animals but not in humans. 5 Recently, to solve this problem an alternative technique using human smooth muscle cells in culture has been developed. Human cell lines may be relevant in investigating the molecular pathways in physiological and pathological conditions. 6 The potential development of novel molecular therapeutic strategies such as gene therapy and tissue engineering is also discussed.

Acetylcholine↗
PubMedDate not supplied

Differential patterns of sympathetic responses to selective stimulation of nucleus tractus solitarius purinergic receptor subtypes.

1. Studies are described that indicate that stimulation of different purinergic receptor subtypes (A1, A2A and P2X) located in the sub-postremal nucleus tractus solitarius (NTS) evokes qualitatively and quantitatively different regional haemodynamic and efferent sympathetic responses. 2. Stimulation of A2A receptors evoked the most diverse pattern of regional sympathetic responses: preganglionic adrenal nerve activity (pre-ASNA) was increased, lumbar sympathetic nerve activity (LSNA) did not change, while renal (RSNA) and post-ganglionic adrenal (post-ASNA) sympathetic nerve activity was decreased. Stimulation of A1 receptors evoked qualitatively uniform, although quantitatively different, sympathoactivation: pre-ASNA > RSNA > LSNA. Stimulation of P2X receptors evoked qualitatively uniform, although quantitatively different, sympathoinhibition: RSNA=post-ASNA > LSNA = pre-ASNA. 3. These qualitatively and quantitatively different patterns of regional sympathetic responses strongly suggest that purinergic receptor subtypes may be specifically located and differentially expressed on NTS neurons/neural terminals that control different sympathetic outputs. Different NTS purinoceptors may contribute to patterned autonomic responses observed in specific physiological or pathological situations.

Adrenal Medulla↗
PubMed1998

P2X7 receptor activation-induced contraction and lysis in human saphenous vein smooth muscle.

In cutaneous veins where purinergic neurotransmission is more prominent compared with in deep vessels, physiological and pathological roles of nerve-released ATP have been described. Neuronally released ATP has been reported to act through activation of unidentified ionotropic P2X receptor(s). This study analyzed P2X receptor subtypes expressed in human saphenous vein smooth muscle and their physiological functions. Transcripts for both hP2X1 receptors, already identified in other smooth muscles, and, surprisingly, hP2X7 receptors known to be responsible for the cytotoxic effect of ATP in macrophages were detected by Northern blot analysis in total RNA from saphenous vein smooth muscle. ATP and other P2X receptor agonists [alphabeta-methylene-ATP, 2-methylthio-ATP, and 2',3'-(4-benzoyl)benzoyl-ATP] dose-dependently contracted venous rings, but the contraction induced by 2-methylthio-ATP was more transient than that evoked by the other P2X agonists. The effect of hP2X1 agonists involved the activation of a rapidly desensitizing cation current recorded in freshly isolated myocytes. The action of hP2X7 receptor agonists was related to a maintained nondesensitizing cation current. In addition, hP2X7 receptor activation formed membrane pores that were permeable to large molecules. hP2X1 and hP2X7 receptors coexpressed in COS cells did not associate to form heteromultimers. Our data indicate that both hP2X1 and hP2X7 receptors are expressed as 2 separated populations of channels in human saphenous vein myocytes and are involved in ATP-induced tension. We suggest that cell lysis consequent to hP2X7 receptor-induced pore formation contributes to the disorganization and decrease in the amount of contractile myocytes in the media of varicose veins.

Adenosine Triphosphate↗
PubMed2001

Neuropeptides and anxiety-related behavior.

Behavior is shaped by a variety of genetic and epigenetic mechanisms, including those underlying anxiety and fear. Neuropeptides are ideal candidates to be involved in the regulation of emotional facets as they are released within the brain and act as neuromodulators/neurotransmitters; furthermore, their large number is prone to direct changes by mutations. A variety of approaches have been used to reveal the physiological involvement of neuropeptides in anxiety-related behavior, including those focused on behavioral effects of neuropeptides and, vice versa, the influence of behavioral phenomena on intracerebral neuropeptides. In concert with other neuropeptides and classical transmitters, particularly CRH and vasopressin are promising candidate neuropeptides to determine not only the activity of the hypothalamopituitary-adrenocortical axis, but also anxiety-related behavior including its cognitive components. CRH and vasopressin interactions with specific receptor subtypes have been shown to induce consequences on emotionality, and CRH and vasopressin responses to both anxiogenic stimuli and extreme levels of inborn anxiety confirm their critical involvement in normal and pathological anxiety. Based on behavioral and neuroendocrine data obtained from proper animal models, the neurobiological and genetic analyses of anxiety and fear will provide the prerequisites to develop novel and more causal therapeutic strategies for anxiety disorders.

Animals↗
PubMed1991

[A case of metastasis of lung cancer to renal cell carcinoma].

A 62-year-old male was admitted with abnormal shadow in chest X-P. CT and other examinations were done, and he was diagnosed left renal cell carcinoma with metastatic lung cancer. He rejected operation and was discharged. We gave him alpha-interferon injection every day. About 5 months later, he complained of fever and dyspnea, and was admitted. On the 10th day after admission, he died suddenly with massive hemoptysis. This hemoptysis was from the pulmonary artery, which was surrounded by tumors and ruptured into the trachea. Pathological diagnosis was double cancer, such a case is very rare with a primary lung cancer (oat cell carcinoma) which has metastasized into a renal cell carcinoma (common type, clear cell subtype).

Carcinoma, Renal Cell↗
PubMedDate not supplied

Prognostic factors in well-differentiated thyroid cancer.

The differentiated thyroid carcinomas are malignant neoplasms most of them following an indolent course with infrequent metastases and long survival. However, a few cases behave in an aggressive fashion and, despite every attempt to treat, cause the death of the patient. Numerous investigations have been carried out to define the markers which affect the prognostic course of these tumors. There are three types of prognostic markers: clinicopathological, pathological (morphological) and biological. The first group include: age, sex, size of the tumor, multifocality, vascular and extrathyroidal invasion, grading and metastases. The second category collects some morphological features like tumor subtype, association with autoimmune thyroid diseases and ploidy. The last group features the oncogenes (RET and RET/PTC rearrangements). The accurate evaluation of all the previous prognostic markers is the basis of the treatment schemes discussed in the last section.

Biomarkers, Tumor↗
PubMed1991

[Familial background of patients with Gilles de la Tourette's disease].

A study was made of hereditary loading of probands with Gilles de la Tourette's syndrome (GTS) and of the degree of genetic homogeneity of the clinical varieties of the disturbance. Among 131 relatives of the patients, GTS was encountered in 1.52% of cases, whereas tics in 8.3% on the whole. It turned out as a result of a genetico-statistical analysis of different varieties of GTS that the excitable and inhibited subtypes of the typical Tourette's syndrome are homogeneous in terms of their hereditary loading and significantly differ (p greater than 0.05) from schizophrenia with Tourette-like disorders in the pathology of the schizophrenic spectrum (schizophrenia, schizoid psychopathy). Schizophrenia with Tourette-like disorders is genetically similar to sluggish schizophrenia of childhood (p = 0.95). In homogeneous hereditary predisposition to hyperkineses, their clinical diversity is determined both by the ground which gives rise to their development and by contribution of environmental factors.

Adult↗
PubMed1997

Endothelin-1-induced circulatory response in the rat: the role of ETA and ETB receptors.

Production of the powerful vasoconstrictor endothelin-1 (ET1) is increased in a number of pathological conditions. This study was performed 1. to assess the effects of a twofold elevation of circulating ET1 on global hemodynamics and cardiac function, and 2. to determine the ET receptor subtypes that are responsible for this action. We have used the ETA receptor-selective antagonist BQ 610, the novel ETA receptor antagonist ETR-Pl/fl peptide and the specific ETB receptor antagonist IRL 1038 to investigate the role of these receptor subtypes in mediating circulatory changes induced by ET1 in anesthetized Wistar rats. ET1 infusion produced a significant rise in mean arterial pressure (MAP), elevated total peripheral resistance (TPR), and decreased cardiac output (CO). BQ 610 and ETR-Pl/fl pretreatment significantly attenuated the ET1-induced hemodynamic changes. Pretreatment with IRL 1038 had no effect on CO, but significantly reduced MAP and TPR elevation 20 min after ET1 infusion. These results suggest that ET1 may contribute to circulatory failure in conditions with increased ET1 production via a mechanism involving ETA receptors. ETB receptors, albeit to a lesser extent than ETA receptors, are also involved in mediating ET1-induced peripheral vasoconstriction in the rat.

Animals↗
PubMedDate not supplied

Receptor biology of the melanocortins, a family of neuroimmunomodulatory peptides.

Melanocortins, melanocyte-stimulating hormones (MSH) and adrenocorticotropic hormone (ACTH) are homologous natural peptides derived from pro-opiomelanocortin (POMC). Recent breakthroughs in melanocortin receptor (MCR) biology are relevant to neuroimmunomodulation because melanocortins are known to modulate fever, inflammation and immunity, by acting both on peripheral targets and within the brain. During fever, endogenous melanocortins exert antipyretic effects by acting on MCR located within the brain, suggesting a protective counterregulatory role of the central melanocortin system. MCR are also found in melanocytic cells and adrenal cortical cells, the classical targets for alpha-MSH and ACTH, respectively, in myelogenous and lymphoid tissues, and in various endocrine and exocrine glands, adipocytes, and in autonomic ganglia. In the CNS, MCR are prominently distributed in close proximity to the terminal fields of melanocortinergic neurons that innervate neuroendocrine and autonomic motor nuclei as well as other subcortical brain regions important in neuroendocrine and autonomic regulation, sensory processing and various aspects of behavior. Furthermore, the presence of MCR in circumventricular organs of the brain provides direct access of systemic melanocortin hormones to central MCR. Together, these attributes provide an anatomical basis for bidirectional MCR-mediated communication between brain and periphery. A group of five G-protein-associated MCR subtypes, each of which is positively coupled to adenylate cyclase, has been identified. Among these, the adrenal ACTH receptor (MC2-R) is selectively activated by ACTH. In contrast, the other MCR subtypes (MC1-R, MC3-R, MC4-R, MC5-R) recognize a common group of ligands that includes various forms of MSH as well as ACTH; nevertheless they do exhibit important differences in ligand selectivity. MCR concentrations and MCR mRNA levels are influenced by availability of cognate ligands, by drugs, and by pathological stimuli. Two types of endogenous MCR antagonist proteins have been discovered: agouti protein and the corticostatins. Agouti protein dramatically alters coat color in mammals by antagonizing melanocytic MC1-R. Moreover, spontaneous dominant mutations of the agouti gene in several strains of mice lead to its ubiquitous overexpression and produces not only yellow coat color, but also obesity and insulin resistance, perhaps as a result of its antagonism of other MCR subtypes. The recent emergence of synthetic MCR antagonists, and the feasibility of molecular approaches for targeted inactivation of individual MCR subtypes, should facilitate elucidation of the roles and mechanisms of neuroimmunomodulation by endogenous melanocortins, and the determination of whether selective pharmacological targeting of MCR may ultimately have therapeutic utility.

Adjuvants, Immunologic↗
PubMed2000

Pathology of small-cell lung cancer.

The morphological differentiation between small-cell and non-small-cell lung cancer has great prognostic and therapeutic significance for the patient. Malignant lung tumors are now classified according to the new 1999 WHO/IASLC classification of lung and pleural tumors. The variant of heterogeneously differentiated "combined small-cell carcinoma" can be distinguished from classical small-cell carcinoma, whereas the subtype of "intermediate cell carcinoma" is no longer used. Together with "large-cell neuroendocrine carcinomas" and typical or atypical carcinoid tumors, small-cell lung cancers are currently histogenetically categorized as neuroendocrine lung tumors. In contrast to large-cell neuroendocrine carcinoma, the immunohistochemical demonstration of neuroendocrine differentiation is not a prerequisite for the diagnosis of small-cell lung cancer. Although electron-microscopical, immunohistochemical, and molecular-biological findings have considerably increased our understanding of the pathogenesis and progression of malignant lung tumors, routine pathological-anatomical diagnostics are still decisively based on light-microscopical evaluation of tissue samples.

Carcinoma, Small Cell↗
PubMed2006

Marked genomic differences characterize primary and secondary glioblastoma subtypes and identify two distinct molecular and clinical secondary glioblastoma entities.

Glioblastoma is classified into two subtypes on the basis of clinical history: "primary glioblastoma" arising de novo without detectable antecedent disease and "secondary glioblastoma" evolving from a low-grade astrocytoma. Despite their distinctive clinical courses, they arrive at an indistinguishable clinical and pathologic end point highlighted by widespread invasion and resistance to therapy and, as such, are managed clinically as if they are one disease entity. Because the life history of a cancer cell is often reflected in the pattern of genomic alterations, we sought to determine whether primary and secondary glioblastomas evolve through similar or different molecular pathogenetic routes. Clinically annotated primary and secondary glioblastoma samples were subjected to high-resolution copy number analysis using oligonucleotide-based array comparative genomic hybridization. Unsupervised classification using genomic nonnegative matrix factorization methods identified three distinct genomic subclasses. Whereas one corresponded to clinically defined primary glioblastomas, the remaining two stratified secondary glioblastoma into two genetically distinct cohorts. Thus, this global genomic analysis showed wide-scale differences between primary and secondary glioblastomas that were previously unappreciated, and has shown for the first time that secondary glioblastoma is heterogeneous in its molecular pathogenesis. Consistent with these findings, analysis of regional recurrent copy number alterations revealed many more events unique to these subclasses than shared. The pathobiological significance of these shared and subtype-specific copy number alterations is reinforced by their frequent occurrence, resident genes with clear links to cancer, recurrence in diverse cancer types, and apparent association with clinical outcome. We conclude that glioblastoma is composed of at least three distinct molecular subtypes, including novel subgroups of secondary glioblastoma, which may benefit from different therapeutic strategies.

Astrocytoma↗
PubMed1998

Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris.

Acne affects between 40 to 50 million individuals in the United States. Recent findings regarding the multifactorial pathogenesis of acne have facilitated a reexamination of the classification of acne and acne-related disorders. Disorders without a microcomedo as the initial pathologic condition are no longer classified as "acne." Research has also identified that the clinical characteristics of acne vary with age, pubertal status, gender, and race. These findings may have implications for the clinical management of acne and acne-related disorders.

Acne Vulgaris↗
PubMed1996

Expression of intercellular adhesion molecule-3 (ICAM-3/CD50) in malignant lymphoproliferative disorders and solid tumors.

ICAM-3/CD50 is a recently described LFA-1 counter receptor that seems to play an important role in the initiation of immune responses. In this study we have examined the expression of ICAM-3/CD50 in a large series of human neoplasms including 101 Non-Hodgkin's lymphomas (NHL), 26 Hodgkin's disease, and 38 solid tumors to define the distribution patterns of this molecule in malignant neoplasms and their possible correlation with clinical and pathological characteristics of the patients. In NHL, ICAM-3/CD50 was expressed in almost all the tumors with a tendency to be lost in high grade lymphomas. Reed-Sternberg cells and their variants in Hodgkin's disease were always negative independently of the histological subtype of the disease. No expression was observed in tumor epithelial cells of the 38 solid tumors examined. Strong endothelial cell staining was observed in 31% of the NHL and 31% of Hodgkin's disease. ICAM-3 expression in these cases was restricted to small tumor vessels. ICAM-3 expression in endothelial cells of NHL was significantly more frequent in high grade (40%) than in low grade lymphomas (14%) (p = 0.012). In addition, tumor vessels were also positive in 29% of solid tumors independently of the histological type. No correlation was observed between ICAM-3 expression in tumor or endothelial cells and other clinical and pathological characteristics of the patients. These findings indicate that ICAM-3 expression in human tumors is restricted to hematological neoplasms with a tendency to be lost in high grade lymphomas and Hodgkin's disease. ICAM-3 is also expressed by endothelial cells from tumor-associated neovascularization in both lymphoid and solid tumors.

Animals↗
PubMed2005

Molecular pathology of ovarian cancer.

Ovarian cancer is the leading cause of death among women with gynecologic malignancies. Epithelial tumors typically constitute 80-90% of ovarian malignancies and are classified primarily as serous, mucinous, endometrioid or clear cell. Current data indicate that each of these histologic subtypes is associated with distinct morphologic and molecular genetic alterations. We describe such genetic alterations with specific reference to histologic subtypes.

Adenocarcinoma, Clear Cell↗
PubMed2006

An outbreak of avian influenza subtype H9N8 among chickens in South Korea.

Low pathogenic avian influenza subtype H9N8 was diagnosed on a Korean native chicken farm in Gyeonggi province, South Korea, in late April 2004. Clinical signs included moderate respiratory distress, depression, mild diarrhoea, loss of appetite and a slightly elevated mortality (1.4% in 5 days). Pathologically, mucopurulent tracheitis and air sacculitis were prominently found with urate renal deposition. The isolated A/chicken/Kr/164/04 (H9N8) had an Ala-Ser-Gly-Arg (A/S/G/R) motif at the cleavage site of haemagglutinin, which has been commonly found in H9N2 isolated from Korean poultry. Phylogenetic analysis of the haemagglutinin and neuraminidase genes of the H9N8 avian influenza virus (AIV) isolate showed that reassortment had occurred. Its haemagglutinin gene was similar to that of Korean H9N2 AIVs, but its neuraminidase gene was closely related to that of A/WBF/Kr/KCA16/03 (H3N8) isolated from the faeces of wild birds in Korea. The pathogenicity of the isolate was tested on 6-week-old specific pathogen free chickens. The inoculated virus (H9N8) was recovered from most tested organs, including the trachea, lung, kidney, spleen, and caecal tonsil. This is the first report of an outbreak of low pathogenic avian influenza in chickens caused by AIV subtype H9N8.

Animals↗