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Shared Mechanisms (shared + mechanism)

Distribution by Scientific Domains

Medical Sciences	75%
Life Sciences	25%

Selected Abstracts

Shared Mechanisms and Comorbidities in Neurologic and Psychiatric Disorders

HEADACHE, Issue 2001
Stephen D. Silberstein MD
Migraine may be comorbid with several other neurologic and psychiatric conditions, including mood disorders (eg, depression, anxiety, panic disorder), epilepsy, stroke, and essential tremor. Comorbidity presents physicians with opportunities and challenges for both diagnosis and treatment. All diseases must be considered, and therapeutic strategies may need to be modified to avoid potential drug interactions. Comorbidities also may provide clues to the pathophysiologies and any shared mechanisms of the two disorders. Longitudinal studies have demonstrated a bidirectional influence between migraine and major depression, but not between migraine and other severe headache. Migraine is strongly and consistently associated with panic disorder. The risk of migraine in epilepsy is increased particularly in individuals with head trauma, partial seizures, and a positive family history of migraine. The influence is bidirectional. There is also growing evidence of an association between migraine and stroke, particularly among women of childbearing age and individuals who experience migraine with aura. Lastly, a bidirectional association between migraine and essential tremor also exists. These findings suggest that migraine, major depression, epilepsy, and essential tremor share one or more common etiologies. Clinicians should be mindful of them as they design treatment strategies, and also should consider the use of a single pharmacologic agent that is effective for all conditions. [source]

COL5A1 signal peptide mutations interfere with protein secretion and cause classic Ehlers-Danlos syndrome,

HUMAN MUTATION, Issue 2 2009
Sofie Symoens
Abstract Classic Ehlers-Danlos syndrome (EDS) is a heritable connective tissue disease characterized by skin hyperextensibility, atrophic scarring, joint hypermobility and generalized tissue fragility. Mutations in COL5A1 and COL5A2, encoding the type V collagen pro,1- and pro,2-chain, are found in ,50% of patients with classic EDS. The majority of mutations lead to a non-functional COL5A1 allele, as a result of the introduction of a premature stopcodon in one COL5A1 transcript. A minority of mutations affect the structure of the type V collagen central helical domain. We show that mutations in the signal peptide (SP) domain of the preproá1(V)-collagen chain cause classic EDS. The missense mutations (p.L25R and p.L25P) are located in the crucial hydrophobic SP core, which is indispensible for preprotein translocation into the endoplasmic reticulum. As a result, mutant type V procollagen is retained within the cell, leading to a decreased amount of type V collagen in the extracellular matrix and disturbed collagen fibrillogenesis. Our findings further support the observation that decreased availability of type V (pro)collagen is a key factor and a shared mechanism in the pathogenesis of classic EDS. © 2008 Wiley-Liss, Inc. [source]

Individual Differences in Responses to Ethanol and d-Amphetamine: A Within-Subject Study

ALCOHOLISM, Issue 4 2001
Louis Holdstock
Background: In some individuals, ethanol (EtOH) produces marked stimulant-like subjective effects resembling those of stimulant drugs, like d-amphetamine (AMP). In this study, we examined the neurochemical basis of these individual differences by examining the same subjects' responses to both EtOH and AMP. A positive correlation between subjects' responses to the two drugs may suggest that AMP and EtOH produce their stimulant-like subjective effects by a shared mechanism. Methods: Twenty-seven volunteers (17 male, 10 female), aged 21,35, received beverages or capsules containing EtOH 0.8 g/kg, AMP 10 or 20 mg, or placebo on four separate sessions in random order and under double-blind conditions. Various self-reported and objective drug effects were measured, including measures sensitive to subjective and cognitive stimulant-like effects. Results: EtOH and AMP produced their prototypical subjective and behavioral effects, including increased ratings of stimulant-like subjective effects, increased heart rate and blood pressure, and improved vigilance performance after AMP and increased ratings of sedative-like subjective effects, increased heart rate and blood pressure, and impaired vigilance performance after EtOH. Consistent with previous reports, there was substantial intersubject variability in subjective responses to EtOH: some subjects reported primarily stimulant-like effects, whereas others reported primarily sedative-like effects. To examine the relationship between these responses to EtOH and subjects' responses to AMP, correlations were examined between effects of EtOH and AMP. For all subjects together, there was a significant positive correlation between responses to EtOH and 20 mg AMP on the ARCI A scale (a measure of stimulant-like subjective effects;r= 0.41, p < 0.05). Among only those subjects who reported primarily stimulant-like effects from EtOH, the correlation between EtOH and AMP was 0.64 (p < 0.05). Conclusions: Subjects who experience pronounced stimulant-like effects from EtOH also report greater stimulant effects from AMP, suggesting that these effects may be mediated through similar mechanisms. These correlations between the drugs' effects were not observed on other measures, such as DSST or vigilance task performance or heart rate. This may indicate that these other effects are mediated by separate mechanisms. The study illustrates a novel approach to studying the neurochemical basis of drug effects. [source]

A couple with gastrointestinal stromal tumor (GIST)

ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY, Issue 2 2009
Pirooz POURSOLTAN
We present a 70-year old woman with metastatic gastrointestinal stromal tumor (GIST) and her partner, a 79-year old man with multiple gastric GIST tumors. This tumor is considered a rare malignancy with a reported incidence of 6,13 new cases per million. Our patients were found to have different genetic mutations in the C-KIT gene as the cause of their disease but, given the rarity of this tumor, it raises a question about their possible exposure to carcinogens or another shared mechanism that might have been involved in the pathogenesis of this cancer. [source]

Origin and fate of cardiac mesenchyme

DEVELOPMENTAL DYNAMICS, Issue 10 2008
Brian S. Snarr
Abstract The development of the embryonic heart is dependent upon the generation and incorporation of different mesenchymal subpopulations that derive from intra- and extra-cardiac sources, including the endocardium, epicardium, neural crest, and second heart field. Each of these populations plays a crucial role in cardiovascular development, in particular in the formation of the valvuloseptal apparatus. Notwithstanding shared mechanisms by which these cells are generated, their fate and function differ profoundly by their originating source. While most of our early insights into the origin and fate of the cardiac mesenchyme has come from experimental studies in avian model systems, recent advances in transgenic mouse technology has enhanced our ability to study these cell populations in the mammalian heart. In this article, we will review the current understanding of the role of cardiac mesenchyme in cardiac morphogenesis and discuss several new paradigms based on recent studies in the mouse. Developmental Dynamics 237:2804,2819, 2008. © 2008 Wiley-Liss, Inc. [source]

Alzheimer's disease, Parkinson's disease and essential tremor: three common degenerative diseases with shared mechanisms?

EUROPEAN JOURNAL OF NEUROLOGY, Issue 6 2010
E. D. Louis
No abstract is available for this article. [source]

Migraine and Psychiatric Comorbidity: From Theory and Hypotheses to Clinical Application

HEADACHE, Issue 9 2002
Fred D. Sheftell MD
Objective.,To review psychiatric issues that accompany migraine and means of addressing these issues. Background.,Psychiatric factors and migraine may interact in three general ways, etiologically, psychophysiologically or biobehaviorally, and comorbidly (the two disorders coexist), which is the present focus. There are several possible mechanisms of comorbidity. The relation between two disorders may be a result of chance. One disorder can cause another disorder: Diabetes can cause diabetic neuropathy. There might be shared environmental risks: Head trauma can cause both posttraumatic epilepsy and posttraumatic headache. And there may be environmental or genetic risk factors that produce a brain state giving rise to both conditions, that is, there may be some common biology underlying both conditions. This last mechanism seems to be the most likely one underlying comorbidity of migraine and psychiatric disorders. We introduce a possible role for classical paradigms of learned helplessness in regard to psychiatric comorbid depressive and anxiety disorders and migraine. Results.,There appears to be an association between migraine and affective disorders, particularly depression and anxiety. There are a number of formal tools for recognizing depression, but clinical evaluation should not be overlooked. Once diagnosed, depression and anxiety should be treated, both to improve the success of migraine treatment and to improve the patient's quality of life. Patients with recurring headaches are much more likely to overuse and misuse, rather than abuse, pain medications. It is important to be alert for signs that the patient may be misusing medication. Behavioral approaches can surround and support pharmacological therapy. Conclusions.,Migraine is often comorbid with psychiatric disorders, particularly depression and anxiety. The relationship is likely based on shared mechanisms and successful treatment is possible. [source]