Cause-and-effect Relationship (cause-and-effect + relationship)

Distribution by Scientific Domains


Selected Abstracts


Does gastroesophageal reflux contribute to the development of chronic sinusitis?

DISEASES OF THE ESOPHAGUS, Issue 6 2006
A review of the evidence
SUMMARY., Although recent studies suggest that gastroesophageal reflux disease (GERD) may contribute to a variety of ear, nose and throat and pulmonary diseases, the cause-and-effect relationship for the vast majority remains far from proven. In this article, the evidence supporting a possible causal association between GERD and chronic sinusitis has been reviewed. The evidence would suggest that: (i) a higher prevalence of GERD and a different esophagopharyngeal distribution of the gastric refluxate occurs in patients with chronic sinusitis unresponsive to conventional medical and surgical therapy compared to the general population; (ii) a biologically plausible pathogenetic mechanism exists whereby GERD may result in chronic sinusitis; and (iii) clinical manifestations of chronic sinusitis respond variably to antireflux therapy. While these findings suggest that GERD may contribute to the pathogenesis of chronic sinusitis in some patients, it is apparent that the quality of the evidence supporting each of these three lines of evidence is low and therefore does not conclusively establish a cause-and-effect relationship. A number of unresolved issues regarding prevalence, pathophysiological mechanism, diagnosis and treatment exist that deserve further investigation in order to solidify the relationship between GERD and chronic sinusitis. In conclusion, given the possible relationship between GERD and chronic sinusitis, until more convincing data are available, it may be prudent to investigate for GERD as a potential cofactor or initiating factor in patients with chronic sinusitis when no other etiology exists, or in those whose symptoms are unresponsive to conventional therapies. [source]


Dopaminergic neurotoxicity by 6-OHDA and MPP+: Differential requirement for neuronal cyclooxygenase activity

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2005
Emilce Carrasco
Abstract Cyclooxygenase (COX), a key enzymatic mediator of inflammation, is present in microglia and surviving dopaminergic neurons in Parkinson's disease (PD), but its role and place in the chain of neurodegenerative events is unclear. Epidemiologic evidence showed that regular use of nonsteroidal antiinflammatory drugs (NSAIDs), specifically non-aspirin COX inhibitors like ibuprofen, lowers the risk for PD; however, the putative cause-and-effect relationship between COX activity in activated microglia and neuronal loss was challenged recently. We examined whether neuronal COX activity is involved directly in dopaminergic cell death after neurotoxic insult. Using low concentrations of 6-hydroxydopamine (6-OHDA) and 1-methyl-4-phenylpyridium ion (MPP+), neurotoxicants used to model selective dopaminergic cell loss in PD, and cultures of embryonic rat mesencephalic neurons essentially devoid of glia, we tested whether the nonselective COX inhibitor ibuprofen attenuated 6-OHDA and MPP+ neurotoxicity. At levels close to its IC50 for both COX isoforms, ibuprofen protected dopaminergic neurons against 6-OHDA but not MPP+ toxicity. Experiments with selective inhibitors of COX-1 (SC-560) and COX-2 (NS-398 and Cayman 10404), indicated that COX-2, but not COX-1, was involved in 6-OHDA toxicity. Accordingly, 6-OHDA, but not MPP+, increased prostaglandin (PG) levels twofold and this increase was blocked by ibuprofen. At concentrations well above its IC50 for COX, ibuprofen also prevented MPP+ toxicity, but had only limited efficacy against loss of structural complexity. Taken together, our data suggest that selective 6-OHDA toxicity to dopaminergic neurons is associated with neuronal COX-2, whereas MPP+ toxicity is COX independent. This difference may be important for understanding and manipulating mechanisms of dopaminergic cell death. © 2005 Wiley-Liss, Inc. [source]


Reversible posterior leukoencephalopathy syndrome in a patient with multiple system atrophy: A possible association with oral midodrine treatment

MOVEMENT DISORDERS, Issue 7 2007
Joong-Seok Kim MD
Abstract We describe a 51-year-old man with a 3-year history of multiple system atrophy, who developed a reversible posterior leukoencephalopathy syndrome (RPLS) after receiving prescription midodrine for therapeutic treatment of orthostatic hypotension. Typical reversible magnetic resonance imaging findings, following treatment with midodrine, suggested a possible relationship between midodrine treatment, supine hypertension, and RPLS, although a cause-and-effect relationship cannot be confirmed. © 2007 Movement Disorder Society [source]


Relationship between stem CO2 efflux, stem sap velocity and xylem CO2 concentration in young loblolly pine trees

PLANT CELL & ENVIRONMENT, Issue 8 2006
CHRIS A. MAIER
ABSTRACT We measured diel patterns of stem surface CO2 efflux (Es, µmol m,2 s,1), sap velocity (vs, mm s,1) and xylem CO2 concetration ([CO2]) (Xs, %) in 8-year-old loblolly pine trees during the spring to determine how vs and Xs influence Es. All trees showed a strong diel hysteresis between Es and stem temperature, where at a given temperature, Es was lower during the day than at night. Diel variations in temperature-independent Es were correlated with vs (R2 = 0.54), such that at maximum vs, Es was reduced between 18 and 40%. However, this correlation may not represent a cause-and-effect relationship. In a subset of trees, vs was artificially reduced by progressively removing the tree canopy. Reducing vs to near zero had no effect on Es and did not change the diel hysteretic response to temperature. Diel Xs tended to decrease with vs and increase with Es, however, in defoliated trees, large increases in Xs, when vs , 0, had no effect on Es. We conclude that at this time of the year, Es is driven primarily by respiration of cambium and phloem tissues and that sap flow and xylem transport of CO2 had no direct influence on Es. [source]


Sporadic inclusion body myositis: Pathogenic considerations,

ANNALS OF NEUROLOGY, Issue 1 2009
FRCP(C), George Karpati OC
Sporadic inclusion body myositis is the commonest acquired disease of skeletal muscles after 50 years of age, and as such it has commanded a great deal of attention of investigators over the past 25 years. As a result, a large amount of information has accumulated concerning its clinical profile, myopathology, and immunopathology. In the myopathology and immunopathology, there is general agreement that the characteristic features could be divided into a degenerative and an inflammatory group. However, there has been controversy about the possible role of these changes in the pathogenesis of muscle fiber damage. In particular, there is no agreement whether a cause-and-effect relationship exists between these two groups of changes, and if so, which is the primary one. In this brief overview, we examine the validity of the various controversial observations and critically review the justification for the two major hypotheses for the primary role of inflammation versus degeneration. Ann Neurol 2009;65:7,11 [source]


Impact of registration procedures on antibiotic policies

CLINICAL MICROBIOLOGY AND INFECTION, Issue 2001
B. Schlemmer
There is increasing concern over antibiotic resistance and its spread in common bacterial species, such as Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae and Escherichia coli. This results in increased morbidity and mortality. Over consumption of antibiotics has been reported in many settings and underlines the need for improving antibiotic policies. Crude measures of both antibiotic use and antibiotic resistance do not share a strong cause-and-effect relationship. However, this relationship is highly suggestive at a country level, at a hospital level, at a cohort level and at an individual level. In addition to overuse, antibiotic misuse has also to be considered, because of its impact on promoting antibiotic resistance, related to choice, dosage, dosing regimen or duration of therapy [1]. [source]