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NCT ID: NCT00396773 Not yet recruiting - Epilepsy Clinical Trials

Neonatal Brain Waves After Electrocoagulation

Start date: February 2007
Phase: Phase 0
Study type: Observational

Electrocoagulation effect of neonatal brain waves after cesarean section

NCT ID: NCT00396734 Suspended - Clinical trials for Opioid-Related Disorders

The Effects of Pharmacotherapy on Brain Mechanisms Underlying Cocaine Dependence.

Start date: April 2007
Phase: N/A
Study type: Interventional

The overall aim of this project is to use an advanced brain imaging technique, PET, in order to monitor the progress of pharmacotherapy with modafinil or topiramate for cocaine dependence in methadone-maintained patients who use cocaine in addition. Comparisons will be made within the cocaine dependent methadone maintained subjects, between the start and end of treatment, and between the two medications. This is the first systematic research study of pharmacological treatment for cocaine dependence in Israel. This study is of major clinical use, with implications for the treatment of cocaine dependence in poly-drug abusers in Israel. Successful pharmacotherapy for cocaine dependence is expected in reduction in cue-induced subjective craving and in glucose metabolism in brain areas elicited by cocaine craving. Metabolic activity in regions that are activated by craving should be correlated with dopamine DRD2 receptor occupancy in all patients.

NCT ID: NCT00396695 Recruiting - Clinical trials for Stress Disorders, Post-Traumatic

Neuroimmunological Model of Traumatic Memory

Start date: October 2006
Phase: N/A
Study type: Observational

Traumatic events may lead to strong emotional episodic memories common in Post- Traumatic Stress Disorder(PTSD). Intense affect may inhibit efficacy of glutamatergic neurotransmission in two particular areas of the limbic system that have been implicated in the processing of emotionally charged memories: the amygdala and the hippocampus(1,2). Dysfunction of glutamatergic neurotransmission is associated with disbalance of long-term potentiation (LTP) and long-term depression (LTD)- two underlying mechanisms that cooperate to achieve synaptic plasticity and its expressations- learning and memory(3). LTP- the long lasting enhancement of synaptic function includes changes in the amount of neurotransmitter glutamate released into a synapse, changes in the levels of key proteins in synapses, protein phosphorylation and changes the density of receptors on their synaptic membranes. LTD is the inverse of LTP, a long lasting reduction in synaptic transmission (4). Interactions among the different forms of plasticity underlie different forms of memories. Normally these mechanisms are balanced. In the current literature there is data that a class I major histocompatibility complex (MHC class I) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependence, long-term structural and synaptic modifications (5). The brain produces its own immune molecules, the proteins MHC class I and CD3-zeta (a component of receptors for MHC class I). In the immune system, the two proteins act as part of a lock and key system to recognize and get rid of the body’s foreign invaders. The CD3-zeta polypeptide is component of the T cell antigen receptor (TCR) which contribute to its efficient cell surface expression and account for part of its transducing capability (6). In the brain, they may be part of a signaling system that recognizes and eliminates inappropriate neural connections. Expression of MHC class I is regulated by the naturally occurring electrical activity, and sensitive to both natural and pathological changes in the activity. Electrical activity of neurons drives to an establishment of the final pattern of connection. Changes in the strength of individual synapses such as potention and depression leads to stabilization and withdrawal, respectively, of the affected connections. There are data, that in mice with deficiency of MHC class I and CD3-zeta the LTP in the hippocampus is enhanced significantly and LTD is absent. Thus, MHC class I is crucial for translating activity into changes in synaptic strength and neuronal connectivity in vivo. He required for normal activity dependent potentiation, depression, removal of inappropriate connection and responding to injury in the CNS (6). Glutamate receptors play critical roles in LTP/LTD mechanisms. Some researchers consider that a key role in pathogenesis of PTSD is being played by excessive excitation of NMDA-receptors in limbic system structures (1). The existing data allows to assume, that equation of plasticity mechanisms depends on mutual relations between the MHC class I and glutamate receptors. T-cells, like neurons, express high levels of glutamate receptors that are identical to the brain glutamate receptors. Presence of ionotropic and metabotropic glutamate receptors in membranes of lymphocytes makes them sensitive to the same alarm molecules which operate neuronal activity. Glutamate by itself triggers several T-cell activation which differs quantitatively or qualitatively from that ones triggered by “classical’ T-cell activators like antigens(7). There are data about influence of T cell receptor-CD3 complex- on the expression of T-cells glutamate receptors (8). It is possible, that the key roles in this function play CD3-zeta.

NCT ID: NCT00396669 Recruiting - Clinical trials for Tobacco Use Disorder

A Brain Imaging Study Into Nicotine Induced Dopamine Release in Cigarette Smokers.

Start date: July 2007
Phase: N/A
Study type: Interventional

Dopamine (DA) plays a critical role in nicotine (and other) addiction and this drug is known to release DA in brain areas mediating reward and motivational processes. Although imaging studies show that release of DA follows smoking, little is known regarding how common genetic polymorphisms for three genes associated in some studies with smoking (dopamine D2 receptor, dopamine and serotonin transporter) interact with smoking status and modulate individual differences in nicotine-induced DA release and dopamine receptor occupancy, in vivo. The current proposal combines brain imaging and genomics ('imaging genomics') towards partially unraveling the complex relationship between smoking phenotype and common polymorphisms. Understanding whether genetic factors contribute to inter-individual variability in smoking is crucial for interpreting imaging results in the context of disease pathology. We hypothesize that a model of vulnerability to addiction based on interactions between genotype, receptor and transporter availability and in vivo nicotine-induced DA release will elucidate some of the fundamental neurochemical and neurogenetic circuits underlying addiction.

NCT ID: NCT00396539 Completed - Clinical trials for Oral Malodor (Halitosis)

Hydrogen Sulfide Production by Oral Microflora

Start date: January 2007
Phase: N/A
Study type: Observational

Oral malodor is a common condition. In most cases this condition results from the proteolytic activity of anaerobic oral bacteria. These bacteria produce volatile sulfide compounds which are fowl smelling and are felt during exhalation and speech. the aim of the present study is to examine a simple method of detecting these bacteria in samples taken from the oral cavity of oral malodor patients.

NCT ID: NCT00395772 Completed - Clinical trials for Venous Thromboembolism

Once-daily Oral Direct Factor Xa Inhibitor BAY59-7939 in Patients With Acute Symptomatic Deep-vein Thrombosis

Start date: December 2004
Phase: Phase 2
Study type: Interventional

The purpose of this study is to determine the optimal dose of BAY 59-7939 and to compare the safety and effectiveness of this new drug with the standard way of treatment of deep vein thrombosis (heparin infusion plus one of the vitamin K antagonists), taking into account new events of thrombosis and pulmonary embolism and bleeding risk.

NCT ID: NCT00395512 Completed - Diabetes Mellitus Clinical Trials

Efficacy of Alogliptin With Pioglitazone (Actos®) in Subjects With Type 2 Diabetes Mellitus

Start date: November 2006
Phase: Phase 3
Study type: Interventional

The purpose of this study is to evaluate the combination of alogliptin, once daily (QD), and pioglitazone in patients with type 2 diabetes mellitus who are inadequately controlled with diet and exercise alone.

NCT ID: NCT00395369 Not yet recruiting - Cardiac Surgery Clinical Trials

Effect of Intraoperative Aprotinin Administration on Post Cardiac Surgery Optic Nerve and Retinal Thickness.

Start date: December 2007
Phase: N/A
Study type: Interventional

Cognitive and neurological dysfunction after coronary artery bypass surgery (CABG) is common and multi-factorial in origin. Several previous studies have shown that intraoperative aprotinin administration may be neuroprotective.in the current prospective randomized study, the effect of intraoperative aprotinin administration on the integrity of the optic nerve and retinal nerve fiber layer will be examined. Optical coherance tomography will be used to examin the optic nerve and retinal nerve fiber layer.

NCT ID: NCT00395070 Completed - Metastatic Melanoma Clinical Trials

A Phase 3 Pivotal Trial Comparing Allovectin-7® Alone vs Chemotherapy Alone in Patients With Stage 3 or Stage 4 Melanoma

Start date: October 2006
Phase: Phase 3
Study type: Interventional

To compare the safety and efficacy of Allovectin-7® versus Dacarbazine (DTIC)or Temozolomide (TMZ) in subjects with recurrent stage 3 or stage 4 melanoma.

NCT ID: NCT00394797 Completed - Clinical trials for Moderate Ischemic Mitral Regurgitation

Surgical Correction of Moderate Ischemic Mitral Regurgitation

Start date: n/a
Phase: N/A
Study type: Observational

The purpose of this study is to try and determine whether repair of moderate ischemic mitral regurgitation at the time of coronary bypass graft surgery (CABG) has an impact on survival.We will compare patients undergoing CABG + mitral repair or CABG only groups. Primary endpoints include late survival. Secondary endpoints include event free survival, symptoms, and echocardiographic outcomes.