BRIEF REPORT: Incidence, Etiology, Risk Factors, and Outcome of Hospital-acquired Fever: A Systematic, Evidence-based Review

Temperature is universally measured in the hospitalized patient, but the literature on hospital-acquired fever has not been systematically reviewed. This systematic review is intended to provide clinicians with an overview of the incidence, etiology, and outcome of hospital-acquired fever. DATA SOURCES : We searched MEDLINE (1970 to 2005), EMBASE (1988 to 2004), and Web of Knowledge. References of all included articles were reviewed. Articles that focused on children, fever in the developing world, classic fever of unknown origin, or specialized patient populations were excluded. REVIEW METHODS : Articles were reviewed independently by 2 authors before inclusion; a third author acted as arbiter. RESULTS : Of over 1,000 studies reviewed, 7 met the criteria for inclusion. The incidence of hospital-acquired fever ranged from 2% to 17%. The etiology of fever was infection in 37% to 74%. Rates of antibiotic use for patients with a noninfectious cause of fever ranged from 29% to 55% for a mean duration of 6.6 to 9.6 days. Studies varied widely in their methodology and the patient population studied. CONCLUSIONS : Limited information is available to guide an evidence-based approach to hospital-acquired fever. We propose criteria to help standardize future studies of this important clinical situation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71660/1/j.1525-1497.2006.00566.x.pd

Influence of contrast and coherence on the temporal dynamics of binocular motion rivalry

Contains fulltext : 125980.pdf (publisher's version ) (Open Access)Levelt's four propositions (L1-L4), which characterize the relation between changes in "stimulus strength" in the two eyes and percept alternations, are considered benchmark for binocular rivalry models. It was recently demonstrated that adaptation mutual-inhibition models of binocular rivalry capture L4 only in a limited range of input strengths, predicting an increase rather than a decrease in dominance durations with increasing stimulus strength for weak stimuli. This observation challenges the validity of those models, but possibly L4 itself is invalid. So far, L1-L4 have been tested mainly by varying the contrast of static stimuli, but since binocular rivalry breaks down at low contrasts, it has been difficult to study L4. To circumvent this problem, and to test if the recent revision of L2 has more general validity, we studied changes in binocular rivalry evoked by manipulating coherence of oppositely-moving random-dot stimuli in the two eyes, and compared them against the effects of stimulus contrast. Thirteen human observers participated. Both contrast and coherence manipulations in one eye produced robust changes in both eyes; dominance durations of the eye receiving the stronger stimulus increased while those of the other eye decreased, albeit less steeply. This is inconsistent with L2 but supports its revision. When coherence was augmented in both eyes simultaneously, dominance durations first increased at low coherence, and then decreased for further increases in coherence. The same held true for the alternation periods. The initial increase in dominance durations was absent in the contrast experiments, but with coherence manipulations, rivalry could be tested at much lower stimulus strengths. Thus, we found that L4, like L2, is only valid in a limited range of stimulus strengths. Outside that range, the opposite is true. Apparent discrepancies between contrast and coherence experiments could be fully reconciled with adaptation mutual-inhibition models using a simple input transfer-function

Regulation of Granulocyte Colony-Stimulating Factor and Its Receptor in Skeletal Muscle Is Dependent Upon the Type of Inflammatory Stimulus

The cytokine granulocyte colony-stimulating factor (G-CSF) binds to its receptor (G-CSFR) to stimulate hematopoietic stem cell mobilization, myelopoiesis, and the production and activation of neutrophils. In response to exercise-induced muscle damage, G-CSF is increased in circulation and G-CSFR has recently been identified in skeletal muscle cells. While G-CSF/G-CSFR activation mediates pro- and anti-inflammatory responses, our understanding of the role and regulation in the muscle is limited. The aim of this study was to investigate, in vitro and in vivo, the role and regulation of G-CSF and G-CSFR in skeletal muscle under conditions of muscle inflammation and damage. First, C2C12 myotubes were treated with lipopolysaccharide (LPS) with and without G-CSF to determine if G-CSF modulates the inflammatory response. Second, the regulation of G-CSF and its receptor was measured following eccentric exercise-induced muscle damage and the expression levels we investigated for redox sensitivity by administering the antioxidant N-acetylcysteine (NAC). LPS stimulation of C2C12 myotubes resulted in increases in G-CSF, interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-alpha (TNF alpha) messenger RNA (mRNA) and an increase in G-CSF, IL-6, and MCP-1 release from C2C12 myotubes. The addition of G-CSF following LPS stimulation of C2C12 myotubes increased IL-6 mRNA and cytokine release into the media, however it did not affect MCP-1 or TNF alpha. Following eccentric exercise-induced muscle damage in humans, G-CSF levels were either marginally increased in circulation or remain unaltered in skeletal muscle. Similarly, G-CSFR levels remained unchanged in response to damaging exercise and G-CSF/G-CSFR did not change in response to NAC. Collectively, these findings suggest that G-CSF may cooperate with IL-6 and potentially promote muscle regeneration in vitro, whereas in vivo aseptic inflammation induced by exercise did not change G-CSF and G-CSFR responses. These observations suggest that different models of inflammation produce a different G-CSF response