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Biomedical subjects

G L Fricchione

Publications and source records attributed to G L Fricchione.

At least 19 recordsLinked to original sources
PubMed2006

Rapid screening for major depression in post-myocardial infarction patients: an investigation using Beck Depression Inventory II items.

OBJECTIVE: To determine the ability of three questions from the Beck Depression Inventory II (BDI-II) to detect major depressive disorder (MDD) in a cohort of patients hospitalised for acute myocardial infarction (MI). DESIGN: Prospective observational study. SETTING: Coronary care unit and cardiac step-down unit of an urban academic medical centre. PATIENTS: 131 post-MI patients within 72 h of symptom onset. INTERVENTIONS: Patients were administered the BDI-II and participated in a structured diagnostic interview for MDD. Three individual BDI-II items (regarding sadness, loss of interest and loss of pleasure) were examined individually and in two-question combinations to determine their ability to screen for MDD. MAIN OUTCOME MEASURES: Sensitivity, specificity, negative and positive predictive values and proportion of patients with MDD correctly identified. RESULTS: The individual items and two-question combinations had good sensitivity (76-94%), specificity (70-88%) and negative predictive values (97-99%). Item 1 (sadness) performed the best of the individual items (48% with a positive response to the item had MDD; 3% with a negative response had MDD; over 80% of patients with MDD were correctly identified). A combination of questions about sadness and loss of interest performed best among the two-question combinations (37% with positive response had MDD v 1% with a negative response; 94% of patients with MDD were identified). CONCLUSIONS: One to two questions regarding sadness and loss of interest serve as simple and effective screening tools for post-MI depression.

Cohort Studies↗
PubMed2002

Dracunculus medinensis and Schistosoma mansoni contain opiate alkaloids.

The results of analysis, by high-performance liquid chromatography coupled with electrochemical detection and by nano-electrospray-ionization, double quadrupole/orthogonal-acceleration, time-of-flight mass spectrometry, indicate that adult Dracunculus medinensis and Schistosoma mansoni both contain the opiate alkaloid morphine and that D. medinesis also contains the active metabolite of morphine, morphine 6-glucuronide. From these and previous observations, it would appear that many helminths are probably using opiate alkaloids as potent immunosuppressive and antinociceptive signal molecules, to down-regulate immunosurveillance responsiveness and pain signalling in their hosts.

Animals↗
PubMed2001

The relationship of psychiatric illnesses and seizures.

The relationship between epilepsy and behavioral disturbances has been a subject of controversy since the 19th century. Affective changes may occur prior, during, or after the ictal discharge. Depression is the most prevalent comorbidity. Anxiety, panic attacks, and pseudoseizures may resemble complex partial seizures, and their diagnosis and treatment may be confusing, even to experienced clinicians. Epilepsy-related psychosis is less common, manifesting occasionally with symptoms that are indistinguishable from schizophrenia. There is no clear evidence of a distinct "epileptoid" personality, and interictal violence is extremely rare. Pharmacologic treatment with anticonvulsants remains the cornerstone of treatment. In case of psychiatric comorbidities or refractory seizures, the diagnosis should be re-examined.

Humans↗
PubMed2001

The placebo effect and relaxation response: neural processes and their coupling to constitutive nitric oxide.

The placebo effect appears to be a real phenomenon as is the scientifically demonstrated and examined relaxation response. Given this, we attempt to understand how these phenomena work in light of our current understanding of central and peripheral nervous system mechanisms. Central to our hypothesis is the significance of norepinephrine, nitric oxide and opioid signaling both in the central and peripheral nervous system. In this regard, we find that nitric oxide controls norepinephrine processes on many levels, including synthesis, release and actions. In closing, we conclude that enough scientific information exists to support these phenomena as actual physical processes that can be harnessed to provide better patient care.

Animals↗
PubMed2000

The presence of antibacterial and opioid peptides in human plasma during coronary artery bypass surgery.

Antibacterial peptides, found in both invertebrates and vertebrates, represent a potential innate defense mechanism against microbial infections. However, it is unknown whether this process occurs in humans during surgery. We looked for evidence of release of antibacterial peptides during coronary artery bypass grafting (CABG). We used immunological techniques and antibacterial assays combined with high-performance gel-permeation chromatography, reverse-phase HPLC, N-terminal sequencing and comparison with synthetic standards to characterize the peptide B/enkelytin. We show the presence of anionic antibacterial peptide, the peptide B/enkelytin which correspond to the C-terminal part of proenkephalin A, from the plasma of patients undergoing CABG. Our studies show that peptide B/enkelytin is initially present at low levels in plasma and is then released in increased amounts just after skin incision. Antibacterial assays confirmed that the peptides specifically target gram-positive bacteria. We also demonstrate that peptide B/enkelytin is metabolized in vivo to the opioid peptides methionine-enkephalin-Arg-Phe and methionine-enkephalin, peptides that we show have granulocyte chemotactic activity. These findings suggest that in humans, surgical incision leads to the release of antibacterial peptides. Furthermore, these antibacterial peptides can be metabolized into compounds that have immune-activating properties.

Amino Acid Sequence↗
PubMed2000

Functional brain mapping of the relaxation response and meditation.

Meditation is a conscious mental process that induces a set of integrated physiologic changes termed the relaxation response. Functional magnetic resonance imaging (fMRI) was used to identify and characterize the brain regions that are active during a simple form of meditation. Significant (p<10(-7)) signal increases were observed in the group-averaged data in the dorsolateral prefrontal and parietal cortices, hippocampus/parahippocampus, temporal lobe, pregenual anterior cingulate cortex, striatum, and pre- and post-central gyri during meditation. Global fMRI signal decreases were also noted, although these were probably secondary to cardiorespiratory changes that often accompany meditation. The results indicate that the practice of meditation activates neural structures involved in attention and control of the autonomic nervous system.

Adult↗
PubMed2000

Cell-surface estrogen receptors mediate calcium-dependent nitric oxide release in human endothelia.

BACKGROUND: Although estrogen replacement therapy has been associated with reduction of cardiovascular events in postmenopausal women, the mechanism for this benefit remains unclear. Because nitric oxide (NO) is considered an important endothelium-derived relaxing factor and may function to protect blood vessels against atherosclerotic development, we investigated the acute effects of physiological levels of estrogen on NO release from human internal thoracic artery endothelia and human arterial endothelia in culture. METHODS AND RESULTS: We tested the hypothesis that estrogen acutely stimulates constitutive NO synthase activity in human endothelial cells by acting on a cell-surface receptor. NO release was measured in real time with an amperometric probe. 17beta-Estradiol exposure to internal thoracic artery endothelia and human arterial endothelia in culture stimulated NO release within seconds in a concentration-dependent manner. 17beta-Estradiol conjugated to bovine serum albumin also stimulated NO release, suggesting action through a cell-surface receptor. Tamoxifen, an estrogen receptor inhibitor, antagonized this action. We further showed with the use of dual emission microfluorometry that 17beta-estradiol-stimulated release of endothelial NO was dependent on the initial stimulation of intracellular calcium transients. CONCLUSIONS: Physiological doses of estrogen immediately stimulate NO release from human endothelial cells through activation of a cell-surface estrogen receptor that is coupled to increases in intracellular calcium.

Adult↗
PubMed2000

Endogenous morphine.

It is now well accepted that endogenous morphine is present in animals, both in invertebrates and vertebrates. It is a key signaling molecule that plays an important role in downregulating physiological responses, such as those in the immune system, including immune elements in the CNS. It has been demonstrated that a specific mu-opiate-receptor subtype, mu3, mediates these downregulatory effects through release of NO. This article examines morphine as an endogenous signaling molecule, in terms of its role in neural and immune regulation.

Animals↗
PubMed1999

Relation between myocardial infarction, depression, hostility, and death.

OBJECTIVE: To examine the independent impact of major depression and hostility on mortality rate at 6 months and 12 months after discharge from the hospital in patients with a myocardial infarction. METHOD: Three hundred thirty-one patients were prospectively evaluated for depression with a modified version of the National Institute of Mental Health Diagnostic Interview Schedule for major depressive episode. The Cook Medley Hostility Scale data were analyzed by chi(2) procedures for nominal and categoric data, and Student t test was used for continuous data types. RESULTS: Depression was a significant predictor of death at 12 months (P =. 04) but not at 6 months (P =.08). Hostility was not found to be a predictor of death at 6 months or 12 months. CONCLUSIONS: Major depression in patients hospitalized after myocardial infarction is a significant univariable predictor of death at 12 months, although it was not a statistically significant predictor after adjusting for other variables. Hostility is not a predictor of death. Prospective studies are needed to determine the impact of aggressive treatment of depression on post-myocardial infarction survival.

Adult↗
PubMed1999

Estradiol coupling to endothelial nitric oxide stimulates gonadotropin-releasing hormone release from rat median eminence via a membrane receptor.

The median eminence (ME), which is the common termination field for adenohypophysiotropic systems, has been shown to produce nitric oxide (NO), a signaling molecule involved in neuroendocrine secretion. Using an ex vivo technique, 17beta-estradiol exposure to ME fragments, including vascular tissues, stimulated NO release within seconds in a concentration-dependent manner, whereas 17alpha-estradiol or testosterone had no effect. 17Beta-estradiol conjugated to BSA (E2-BSA) also stimulated NO release, suggesting mediation by a membrane surface receptor. Tamoxifen, an estrogen receptor inhibitor, antagonized the action of both 17beta-estradiol and E2-BSA. Furthermore, estradiol-stimulated NO stimulates GnRH release. This was demonstrated by hemoglobin (a NO scavenger), N(omega)-nitro-L-arginine methyl ester, and L-N5-(1-iminoethyl)ornithine (nitric oxide synthase inhibitors) inhibition of estradiol stimulated NO and GnRH release. In this regard, L-N5-(1-iminoethyl)ornithine, specific for endotheliol constitutive nitric oxide synthase, was significantly more potent, suggesting that the estradiol-stimulated NO release arose from vascular endothelial cells. Additionally, the NO-stimulated GnRH release occurs via guanylyl cyclase activation in GnRH nerve terminals, as ODQ, a potent and selective inhibitor of NO-sensitive guanylyl cyclase, abolished the estradiol-stimulated GnRH release. The results suggest that at physiological concentrations, 17beta-estradiol may have immediate actions on ME endothelial cells via nongenomic signaling pathways leading to NO-stimulated GnRH release.

Animals↗
PubMed1998

Aspirin inhibits granulocyte and monocyte adherence to saphenous vein endothelia in a process not mediated by nitric oxide.

We examined the effects of aspirin on human immunocyte adherence to human saphenous vein preparations in vitro. Monocytes and granulocytes were analyzed by phase-contrast microscopy in conjunction with a time-lapse video recording system for cell counting in the medium. Saphenous vein samples taken from five volunteer subjects during their elective coronary artery bypass grafting procedures were used for an in vitro experiment in which each subject's immune cells were added to his/her respective endothelial tissues. In addition, aspirin or morphine was added to the preparations. After 30 min the endothelium and the medium were examined for cell numbers using feature color detection software. The endothelium exposed to a 10 min preincubation with 10 mmol/l aspirin was found to have significantly fewer monocytes and granulocytes attached. The saphenous vein preparations were examined for nitric oxide (NO) release using an NO-selective amperometric microprobe. Aspirin at its immunocyte inhibitory concentrations did not induce NO release from the endothelium, whereas morphine, which is known to stimulate NO production by endothelium, did so. These findings demonstrate that the administration of aspirin in high doses can diminish human granulocyte and monocyte adherence to saphenous vein endothelium in vitro through an NO-independent mechanism.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Cell behavior and signal molecule involvement in a case study of malignant histiocytosis: a negative model of morphine as an immunoregulator.

In a patient diagnosed with histiocytic medullary reticulosis (HM), we examined immunocytes for their responsiveness towards known signaling molecules. Both the granulocytes and monocytes were found to exhibit a high level of spontaneous activation (96% compared to normal cells 7%; P < 0.001). These cells could not be downregulated when exposed to morphine. Following patient treatment with doxorubicin and cyclophosphamide, the immunocytes still exhibited a high spontaneous activation. They responded to morphine exposure in vitro with a cell rounding and becoming immobile for only 20 min whereas normal cells would remain round and immobile for up to 1-2 h. An examination of the plasma from the HM patient revealed that monocyte colony stimulating factor (MCSF) levels were elevated (6.4 and 5.78 compared to a control range of 1-1.75 ng/ml). In the HM patient, the immunocytes did not express the opiate selective and opioid peptide insensitive receptor, mu3, supporting the lack of opiate action. Given this finding, we incubated normal monocytes with MCSF and found that it significantly reduced the mu3 Bmax. Given the role of intracellular calcium in the activation process of immunocytes, we examined the action of various calcium channel blockers for their ability to inhibit the activated HM monocytes. The agents (nimodipine, cardiazem, and verapamil; 10[-9] M) were able to inhibit the HM-associated chemokinesis. Taken together, the data indicate that in the HM patient the immunocytes appear to be overactivated because stimulatory molecules are high and have the ability to downregulate the normal "braking" process. Additionally, the data indicate that MCSF deregulation may be involved as an initiating factor for this disorder.

Aged↗
PubMed1996

Morphine-induced conformational changes in human monocytes, granulocytes, and endothelial cells and in invertebrate immunocytes and microglia are mediated by nitric oxide.

We evaluated the contribution of nitric oxide (NO) to morphine-induced rounding of spontaneously activated (mobile) ameboid human monocytes, granulocytes, or arterial endothelial cells and invertebrate immunocytes and microglia. Morphine induced significant rounding and inactivation of ameboid cells within 20 min except for arterial endothelial cells, which became rounded 24 h after morphine exposure. The effects of morphine on cell conformation were blocked in the presence of N-nitro-L-arginine, a nitric oxide synthase inhibitor. Treatment of cells with the NO donor, sodium nitroprusside, induced cell rounding similar to that observed following morphine exposure, suggesting that NO release may mediate morphine-induced changes in cell conformation. The contribution of NO release to morphine-induced cell rounding was determined by direct evaluation of NO concentration in real-time using a NO-specific amperometric probe. Significant increases in NO concentration were observed 2 min after morphine stimulation, whereas morphine-induced NO release was markedly impaired by pretreatment with N-nitro-L-arginine or the opiate alkaloid antagonist, naloxone. In contrast, opioid peptides failed to induce NO release, consistent with our previous observations that demonstrated the failure of opioid peptides to promote cell rounding. Taken together, these data suggest that morphine-induced NO release may be mediated by activation of the opiate alkaloid-selective, opioid peptide-insensitive micro3 receptor, and that functional coupling of morphine to NO production has been conserved during evolution and may modulate cellular activation.

Animals↗
PubMed1996

Neuroimmunologic implications in coronary artery disease.

In this review, the role of the macrophage in the pathophysiology of coronary artery disease (CAD) is examined. The central interaction of macrophage, endothelial cell and smooth muscle cell in the context of hyperlipidemia is considered. The macrophage appears to be at the beginning of a chain of events that starts with elevated low density lipoprotein (LDL). Stress, particularly in those with a core hostility, may be associated not only with higher catecholamine levels but also with higher serum lipid levels. These lipids will in turn be processed to oxidized LDL by macrophage and endothelial cells. Oxidized LDL molecules will contribute to atherosclerotic plaquing. A side effect of such plaque formation may be a diminished vasodilatory response to the nitric oxide (NO) produced by macrophages and endothelium. Indeed, paradoxical vasoconstriction occurs in atherosclerosis in response to neurotransmitters such as serotonin and acetylcholine, which under normal circumstances cause vasodilation. There also is evidence that both macrophages and endothelial cells can regulate NO production through a specific mu 3 morphine receptor, an effect that can be blocked by naloxone. The clinical effectiveness of morphine and nitroglycerin in CAD patients may relate to these mechanisms. More research will be needed to elucidate the neuroimmunologic basis for atherosclerosis with prospects for better treatment and management in future.

Animals↗
PubMed1996

A novel view of opiate tolerance.

Opiate substances occur as natural compounds in various invertebrate and vertebrate neural tissues. Recently we have discovered a novel opiate alkaloid-selective and opioid peptide-insensitive receptor, designated mu 3, that provides further evidence of the existence of separate morphine processes. Interestingly morphine biosynthesis appears to be linked to the dopamine pathway. Based on studies documenting the presence of morphine after stress, e.g., trauma, it is noted that this signal substance emerges after a timely delay. From this we speculate that this molecule can serve a specific effect to downregulate physiological processes after stress. We conclude that tolerance represents a natural process that terminates its action. In this regard a morphine hypothesis may be essential to a complete picture of motive circuitry. A speculative view of the psychiatric implications in schizophrenia, depression, and autism are presented with this in mind.

Alkaloids↗
PubMed1996

Opioid and opiate immunoregulatory processes.

The discovery of the ability of the nervous system to communicate through "public" circuits with other systems of the body is attributed to Ernst and Berta Scharrer, who described the neurosecretory process in 1928. Indeed, the immune system has been identified as another important neuroendocrine target tissue. Opioid peptides are involved in this communication (i.e., neuroimmune) and with that of autoimmunoregulation (communication between immunocytes). The significance of opioid neuropeptide involvement with the immune system is ascertained from the presence of novel delta, mu, and kappa receptors on inflammatory cells that result in modulation of cellular activity after activation, as well as the presence of specific enzymatic degradation and regulation processes. In contrast to the relatively uniform antinociceptive action of opiate and opioid signal molecules in neural tissues, the presence of naturally occurring morphine in plasma and a novel mu3, opiate-specific receptor on inflammatory cells adds to the growing knowledge that opioid and opiate signal molecules may have antagonistic actions in select tissues. In examining various disorders (e.g., human immunodeficiency virus, substance abuse, parasitism, and the diffuse inflammatory response associated with surgery) evidence has also been found for the involvement of opiate/opioid signaling in prominent mechanisms. In addition, the presence of similar mechanisms in man and organisms 500 million years divergent in evolution bespeaks the importance of this family of signal molecules. The present review provides an overview of recent advances in the field of opiate and opioid immunoregulatory processes and speculates as to their significance in diverse biological systems.

Animals↗
PubMed1995

The biology of deception: the reluctance to accept the cognitive animal.

Cognitive ability did not appear de novo in man. Despite our ability to recognize limited cognitive behavioral characteristics in animals, there has been no outcry to proclaim this phenomenon. Man's image of himself solely possessing cognition has taken advantage of the illusory potential in intersubjectivity and placed him outside of reality. This deception, however, has positive survival value since it is man's self-proclaimed responsibility to excel beyond other simple animal species. However, at this point in evolution, we must allow our cognitive ability to reform itself and, in so doing, evolve with the benefit of the knowledge that this ability is itself creating. By recognizing that animals may have limited cognitive ability, we only enhance our self-esteem, not diminish it.

Animals↗