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Biomedical subjects

M Geraci

Publications and source records attributed to M Geraci.

At least 19 recordsLinked to original sources
PubMed2003

[Influence of obesity on postural capacities of teenagers. Preliminary study].

OBJECTIVE: The purpose of this work was to define the influence of obesity on static postural control of teenagers. SUBJECTS AND METHOD: Nine obese subjects and seven non-obese subjects were characterised with stabilometric data of surface, of lengths and spontaneous sway in the lateral (X) and antero-posterior (Y) axis with open eyes and closed eyes in two conditions on firm floor and foam floor condition. RESULTS: For length data, significative differences were observed between the two groups for the opened eyes condition (p < 0.02) and eyes closed (p < 0.03) during foam floor condition. CONCLUSION: During experimental solicitations, obesity influences significatively the postural control of teenagers. Instead of systematic statistic differences, we observed a decrease in balance capacities of obese subjects. The effects of fat tissue distributions were not verified.

Adolescent↗
PubMed2001

Regional cerebral blood flow correlated with flashback intensity in patients with posttraumatic stress disorder.

BACKGROUND: Nuclear imaging studies have examined cerebral blood flow (rCBF) in subjects with posttraumatic stress disorder (PTSD) using symptom evocation paradigms. To date, no such studies have investigated rCBF as related to subjects' reports of flashback intensity. METHODS: Subjects with varying traumatic histories and longstanding PTSD were studied using [15O]-H2O positron emission tomography with an auditory script of their traumatic event. Eight subjects had three resting scans followed by their script and additional scans. Heart rate responses as well as the presence of flashbacks and their intensity were recorded. rCBF was correlated with flashback intensity in each subject's scan. Combined analysis of all subjects' data yielded common regions related to the flashback experience. RESULTS: rCBF correlated directly with flashback intensity in the brainstem, lingula, bilateral insula, right putamen and left hippocampal and perihippocampal, somatosensory and cerebellar regions. Inverse correlations with rCBF were found in bilateral dorsolateral prefrontal, right fusiform and right medial temporal cortices. CONCLUSIONS: This study correlated flashback intensity and rCBF in a group of patients with chronic PTSD suggesting involvement of brainstem, and areas associated with motor control, complex visual/spatial cues and memory.

Adult↗
PubMed2001

Expression of angiogenesis-related molecules in plexiform lesions in severe pulmonary hypertension: evidence for a process of disordered angiogenesis.

Pulmonary arteries of patients with severe pulmonary hypertension (SPH) presenting in an idiopathic form (primary PH-PPH) or associated with congenital heart malformations or collagen vascular diseases show plexiform lesions. It is postulated that in lungs with SPH, endothelial cells in plexiform lesions express genes encoding for proteins involved in angiogenesis, in particular, vascular endothelial growth factor (VEGF) and those involved in VEGF receptor-2 (VEGFR-2) signalling. On immunohistochemistry and in situ hybridization, endothelial cells in the plexiform lesions expressed VEGF mRNA and protein and overexpressed the mRNA and protein of VEGFR-2, and the transcription factor subunits HIF-1alpha and HIF-1beta of hypoxia inducible factor, which are responsible for the hypoxia-dependent induction of VEGF. When compared with normal lungs, SPH lungs showed decreased expression of the kinases PI3 kinase and src, which, together with Akt, relay the signal transduction downstream of VEGFR-2. Because markers of angiogenesis are expressed in plexiform lesions in SPH, it is proposed that these lesions may form by a process of disordered angiogenesis.

Aryl Hydrocarbon Receptor Nuclear Translocator↗
PubMed2001

Effects of chronic estrogen-receptor blockade on ovine perinatal pulmonary circulation.

Prolonged infusions of 17beta-estradiol reduce fetal pulmonary vascular resistance (PVR), but the effects of endogenous estrogens in the fetal pulmonary circulation are unknown. To test the hypothesis that endogenous estrogen promotes pulmonary vasodilation at birth, we studied the hemodynamic effects of prolonged estrogen-receptor blockade during late gestation and at birth in fetal lambs. We treated chronically prepared fetal lambs with ICI-182,780 (ICI, a specific estrogen-receptor blocker, n = 5) or 1% DMSO (CTRL, n = 5) for 7 days and then measured pulmonary hemodynamic responses to ventilation with low- and high-fraction inspired oxygen (FI(O(2))). Treatment with ICI did not change basal fetal PVR or arterial blood gas tensions. However, treatment with ICI abolished the vasodilator response to ventilation with low FI(O(2)) [change in PVR -30 +/- 6% (CTRL) vs. +10 +/- 13%, (ICI), P < 0.05] without reducing the vasodilator response to ventilation with high FI(O(2)) [change in PVR, -73 +/- 3% (CTRL) vs. -77 +/- 4%, (ICI); P = not significant]. ICI treatment reduced prostacyclin synthase (PGIS) expression by 33% (P < 0.05) without altering expression of endothelial nitric oxide synthase or cyclooxygenase-1 and -2. In situ hybridization and immunohistochemistry revealed that PGIS is predominantly expressed in the airway epithelium of late gestation fetal lambs. We conclude that prolonged estrogen-receptor blockade inhibits the pulmonary vasodilator response at birth and that this effect may be mediated by downregulation of PGIS. We speculate that estrogen exposure during late gestation prepares the pulmonary circulation for postnatal adaptation.

Animals↗
PubMed2001

Severe pulmonary hypertension after the discovery of the familial primary pulmonary hypertension gene.

The recent discoveries of the familial primary pulmonary hypertension gene and somatic mutations in key cell growth and cell death regulatory genes in primary pulmonary hypertension have added a new dimension to severe pulmonary hypertension research. These findings have already impacted on how the disease is viewed, and ultimately, how severe pulmonary hypertension is diagnosed and treated. However, this new information raises several fundamental questions related to the role of bone morphogenetic protein receptor signalling in the control of lung vascular cell function. Furthermore, additional genes and gene products may also be involved in the pathogenesis of the disease. The way severe pulmonary hypertension is viewed and studied is on the verge of shifting from a vasoconstrictive to a cell growth paradigm.

Bone Morphogenetic Protein Receptors, Type II↗
PubMed1998

Anti-growth factor therapy for lung cancer.

Lung cancers are the leading cause of cancer death in developed countries. In the USA, lung cancer accounts for 29% of all cancer deaths. The cure rate for lung cancer is low (14%) because the cancer spreads early and because chemotherapy cannot cure metastatic disease. In small cell lung cancer (SCLC) two-thirds of patients present with metastatic disease in a distant organ (stage IV). In non-small cell lung cancers (adenocarcinoma, squamous carcinoma, large cell carcinoma) one-third present with metastatic disease. Initial chemotherapy produces high response rates in both SCLC (85%-90% response rate) and NSCLC (50% response rate) but response duration is short and drug resistance develops rapidly. Growth factors play an important role in the pathogenesis and the progression of lung cancers. Knowledge of the role of these growth factors, their receptors and their signal pathways has produced new therapeutic targets. Compounds developed toward these targets have completed preclinical testing and are now in clinical trials. Some of these compounds are active in both drug sensitive and drug resistant lung cancers. They also produce synergistic growth inhibition when combined with cytotoxic chemotherapeutic agents. Thus, these compounds may provide a new way to overcome drug resistance in lung cancer.

Journal Article↗
PubMed1997

A comparison of the effects of intravenous pentagastrin on patients with social phobia, panic disorder and healthy controls.

The present study sought to determine whether social phobics, like patients with panic disorder, have increased sensitivity to the panicogenic effects of pentagastrin. Intravenous pentagastrin and placebo were administered in a double-blind fashion to 19 social phobics, 11 patients with panic disorder, and 19 healthy controls while they participated in a structured social interaction task. Behavioral, cardiovascular, and neuroendocrine responses were obtained. Pentagastrin led to panic attacks in 47% of the social phobics, 64% of the panic disorder patients, and 11% of the healthy controls. The social interaction itself increased anxiety, blood pressure, and pulse in all three groups. These findings suggest that the panicogenic effects of pentagastrin are not limited to patients with panic disorder and provide further evidence for shared neurobiology in social phobia and panic disorder.

Adolescent↗
PubMed1997

Effects of the 5-HT3 antagonist, ondansetron, on the behavioral and physiological effects of pentagastrin in patients with panic disorder and social phobia.

Pentagastrin, a cholecystokinin (CCK) agonist, produces anxiety and panic in patients with panic disorder and social phobia. Preclinical data suggests that pentagastrin-induced anxiogenesis may be mediated via 5-HT3 receptors. In the present study, 14 patients with panic disorder or social phobia underwent pharmacological challenge in three conditions: (1) pretreatment with saline followed by pentagastrin infusion; (2) pretreatment with ondansetron followed by pentagastrin infusion; and (3) pretreatment with saline followed by saline infusion. As expected, pentagastrin administration led to increased anxiety, physical symptoms of panic attacks, pulse, plasma adrenocorticotropic hormone (ACTH), and cortisol. Pentagastrin's behavioral effects were not blocked by ondansetron, and in fact, tended to be exaggerated. Ondansetron pretreatment did not alter the pentagastrin-induced cortisol increase but significantly prolonged the pentagastrin-induced increase in ACTH. These findings suggest that pentagastrin's behavioral effects are not mediated by 5HT3 receptors. Mechanisms by which peripherally administered CCK agonists lead to anxiety remain to be elucidated.

Adult↗
PubMed1992

Evidence for hypothalamo-growth hormone dysfunction in panic disorder: profile of growth hormone (GH) responses to clonidine, yohimbine, caffeine, glucose, GRF and TRH in panic disorder patients versus healthy volunteers.

Given the abrupt and time-limited nature of daytime-awake and nocturnal-sleep panic attacks, several chemical and neuroendocrine challenge tests have been employed to investigate the neurobiology of "spontaneous" panic attacks. Previously we demonstrated that panic disorder patients have blunted growth hormone (GH) responses to clonidine, an alpha 2-adrenergic agonist. However, the mechanism of this blunted response and the role of hypothalamic-GH dysfunction, if any, remains unclear. To further delineate the status of hypothalamic-GH function in panic disorder, we review the literature and present original data on the GH responses to a number of different chemical and neuroendocrine challenge paradigms. Although stress-mediated increases in GH are thought to be a common correlate of stress in humans, our findings indicate that panic disorder patients have significantly blunted GH responses to clonidine, yohimbine, growth-hormone releasing factor, and caffeine compared to normal control subjects. A similar trend was noted in the delayed rise in GH after glucose challenge. There was no difference in the rate of abnormal GH responses to thyrotropin-releasing hormone in panic disorder compared to normal control subjects. No drug or neuroendocrine challenge, even if associated with marked increases in anxiety, produced a significantly enhanced GH response compared to normal control subjects. These findings provide support for a hyporesponsive hypothalamic-GH system in panic disorder. These observations, combined with preliminary observations from our clinic of short stature in several cases of prepubescent children with anxiety disorders, also underscore the need for assessing early growth patterns in individuals with panic disorder. Strategies for investigating the site(s) of possible neurotransmitter or hypothalamic-GH-somatomedin dysfunction are discussed.

Caffeine↗
PubMed1990

Inefficacy of single-dose nifedipine in the treatment of phobic anxiety.

Single-dose nifedipine was given to 13 phobic patients with increased generalized anxiety. Nifedipine failed to demonstrate anxiety-reducing effects on baseline anxiety ratings. Furthermore, in a subset of four patients, the drug failed to show an anxiolytic effect in exposure-related anxiety.

Arousal↗
PubMed1986

Life events and the onset of panic disorder.

The authors examined the number, type, and effect of life events during the year before the onset of panic attacks in 44 patients with a Research Diagnostic Criteria diagnosis of panic disorder and 44 healthy control subjects matched for age, sex, and time of retrospection. The patients had significantly more life events, and these events had a more adverse impact on them. Furthermore, the types of events experienced by the patients were more typically distressing than those experienced by the control subjects. The patients reported events involving moves to other neighborhoods and/or cities far more frequently than did the control subjects.

Adult↗