The effects of a dialogue-based intervention to promote psychosocial well-being after stroke: a randomized controlled trial

Objective: To evaluate the effect of a dialogue-based intervention targeting psychosocial well-being at 12 months post-stroke. Design: Multicenter, prospective, randomized, assessor-blinded, controlled trial with two parallel groups. Setting: Community. Subjects: Three-hundred and twenty-two adults (⩾18 years) with stroke within the last four weeks were randomly allocated into intervention group (n = 166) or control group (n = 156). Interventions: The intervention group received a dialogue-based intervention to promote psychosocial well-being, comprising eight individual 1–1½ hour sessions delivered during the first six months post-stroke. Main measures: The primary outcome measure was the General Health Questionnaire-28 (GHQ-28). Secondary outcome measures included the Stroke and Aphasia Quality of Life Scale-39g, the Sense of Coherence scale, and the Yale Brown single-item questionnaire. Results: The mean (SD) age of the participants was 66.8 (12.1) years in the intervention group and 65.7 (13.3) years in the control group. At 12 months post-stroke, the mean (SE) GHQ-28 score was 20.6 (0.84) in the intervention group and 19.9 (0.85) in the control group. There were no between-group differences in psychosocial well-being at 12 months post-stroke (mean difference: −0.74, 95% confidence interval (CI): −3.08, 1.60). The secondary outcomes showed no statistically significant between-group difference in health-related quality of life, sense of coherence, or depression at 12 months. Conclusion: The results of this trial did not demonstrate lower levels of emotional distress and anxiety or higher levels of health-related quality of life in the intervention group (dialogue-based intervention) as compared to the control group (usual care) at 12 months post-stroke

Genetic diversity and distribution of Peromyscus-borne hantaviruses in North America.

The 1993 outbreak of hantavirus pulmonary syndrome (HPS) in the southwestern United States was associated with Sin Nombre virus, a rodent-borne hantavirus; The virus' primary reservoir is the deer mouse (Peromyscus maniculatus). Hantavirus-infected rodents were identified in various regions of North America. An extensive nucleotide sequence database of an 139 bp fragment amplified from virus M genomic segments was generated. Phylogenetic analysis confirmed that SNV-like hantaviruses are widely distributed in Peromyscus species rodents throughout North America. Classic SNV is the major cause of HPS in North America, but other Peromyscine-borne hantaviruses, e.g., New York and Monongahela viruses, are also associated with HPS cases. Although genetically diverse, SNV-like viruses have slowly coevolved with their rodent hosts. We show that the genetic relationships of hantaviruses in the Americas are complex, most likely as a result of the rapid radiation and speciation of New World sigmodontine rodents and occasional virus-host switching events

Seroepidemiologic studies of hantavirus infection among wild rodents in California.

A total of 4,626 mammals were serologically tested for antibodies to Sin Nombre virus. All nonrodent species were antibody negative. Among wild rodents, antibody prevalence was 8.5% in murids, 1.4% in heteromyids, and < 0.1% in sciurids. Of 1,921 Peromyscus maniculatus (deer mice), 226 (11.8%) were antibody positive, including one collected in 1975. The highest antibody prevalence (71.4% of 35) was found among P. maniculatus on Santa Cruz Island, off the southern California coast. Prevalence of antibodies among deer mice trapped near sites of human cases (26.8% of 164) was significantly higher than that of mice from other sites (odds ratio = 4.5; 95% confidence interval = 1.7, 11.6). Antibody prevalence increased with rising elevation (> 1,200 meters) and correlated with a spatial cluster of hantavirus pulmonary syndrome cases in the Sierra Nevada

Long-term studies of hantavirus reservoir populations in the southwestern United States: rationale, potential, and methods.

Hantaviruses are rodent-borne zoonotic agents that cause hemorrhagic fever with renal syndrome in Asia and Europe and hantavirus pulmonary syndrome (HPS) in North and South America. The epidemiology of human diseases caused by these viruses is tied to the ecology of the rodent hosts, and effective control and prevention relies on a through understanding of host ecology. After the 1993 HPS outbreak in the southwestern United States, the Centers for Disease Control and Prevention initiated long-term studies of the temporal dynamics of hantavirus infection in host populations. These studies, which used mark-recapture techniques on 24 trapping webs at nine sites in the southwestern United States, were designed to monitor changes in reservoir population densities and in the prevalence and incidence of infection; quantify environmental factors associated with these changes; and when linked to surveillance databases for HPS, lead to predictive models of human risk to be used in the design and implementation of control and prevention measures for human hantavirus disease

Climatic and environmental patterns associated with hantavirus pulmonary syndrome, Four Corners region, United States.

To investigate climatic, spatial, temporal, and environmental patterns associated with hantavirus pulmonary syndrome (HPS) cases in the Four Corners region, we collected exposure site data for HPS cases that occurred in 1993 to 1995. Cases clustered seasonally and temporally by biome type and geographic location, and exposure sites were most often found in pinyon-juniper woodlands, grasslands, and Great Basin desert scrub lands, at elevations of 1,800 m to 2,500 m. Environmental factors (e.g., the dramatic increase in precipitation associated with the 1992 to 1993 El Niño) may indirectly increase the risk for Sin Nombre virus exposure and therefore may be of value in designing disease prevention campaigns

The associations between body and knee height measurements and knee joint structure in an asymptomatic cohort

<p>Abstract</p> <p>Background</p> <p>It has been suggested that knee height is a determinant of knee joint load. Nonetheless, no study has directly examined the relationship between anthropometric measures of height and knee joint structures, such as cartilage.</p> <p>Methods</p> <p>89 asymptomatic community-based adults aged 25-62 with no diagnosed history of knee arthropathy were recruited. Anthropometric data (knee height and body height) were obtained by standard protocol, while tibial cartilage volume and defects, as well as bone area were determined from magnetic resonance imaging. Static knee alignment was measured from the joint radiograph.</p> <p>Results</p> <p>All anthropometric height measures were associated with increasing compartmental tibial bone area (<it>p </it>≤ 0.05). Although knee height was associated with tibial cartilage volume (e.g. β = 27 mm³95% CI 7- 48; <it>p </it>= 0.009 for the medial compartment), these relationship no longer remained significant when knee height as a percentage of body height was analysed. Knee height as a percentage of body height was associated with a reduced risk of medial tibial cartilage defects (odds ratio 0.6; 95% confidence interval 0.4 - 1.0; <it>p </it>= 0.05).</p> <p>Conclusion</p> <p>The association between increased anthropometric height measures and increased tibial bone area may reflect inherently larger bony structures. However the beneficial associations demonstrated with cartilage morphology suggest that an increased knee height may confer a beneficial biomechanical environment to the chondrocyte of asymptomatic adults.</p

Specific cellular signal-transduction responses to in vivo combination therapy with ATRA, valproic acid and theophylline in acute myeloid leukemia

Acute myeloid leukemia (AML) frequently comprises mutations in genes that cause perturbation in intracellular signaling pathways, thereby altering normal responses to growth factors and cytokines. Such oncogenic cellular signal transduction may be therapeutic if targeted directly or through epigenetic regulation. We treated 24 selected elderly AML patients with all-trans retinoic acid for 2 days before adding theophylline and the histone deacetylase inhibitor valproic acid (ClinicalTrials.gov NCT00175812; EudraCT no. 2004-001663-22), and sampled 11 patients for peripheral blood at day 0, 2 and 7 for single-cell analysis of basal level and signal-transduction responses to relevant myeloid growth factors (granulocyte-colony-stimulating factor, granulocyte/macrophage-colony-stimulating factor, interleukin-3, Flt3L, stem cell factor, erythropoietin, CXCL-12) on 10 signaling molecules (CREB, STAT1/3/5, p38, Erk1/2, Akt, c-Cbl, ZAP70/Syk and rpS6). Pretreatment analysis by unsupervised clustering and principal component analysis divided the patients into three distinguishable signaling clusters (non-potentiated, potentiated basal and potentiated signaling). Signal-transduction pathways were modulated during therapy and patients moved between the clusters. Patients with multiple leukemic clones demonstrated distinct stimulation responses and therapy-induced modulation. Individual signaling profiles together with clinical and hematological information may be used to early identify AML patients in whom epigenetic and signal-transduction targeted therapy is beneficial

Hantavirus and Arenavirus Antibodies in Persons with Occupational Rodent Exposure, North America

Risk for infection was low among those who handled neotomine or sigmodontine rodents on the job

Tick-, mosquito-, and rodent-borne parasite sampling designs for the National Ecological Observatory Network

Parasites and pathogens are increasingly recognized as significant drivers of ecological and evolutionary change in natural ecosystems. Concurrently, transmission of infectious agents among human, livestock, and wildlife populations represents a growing threat to veterinary and human health. In light of these trends and the scarcity of long-term time series data on infection rates among vectors and reservoirs, the National Ecological Observatory Network (NEON) will collect measurements and samples of a suite of tick-, mosquito-, and rodent-borne parasites through a continental-scale surveillance program. Here, we describe the sampling designs for these efforts, highlighting sampling priorities, field and analytical methods, and the data as well as archived samples to be made available to the research community. Insights generated by this sampling will advance current understanding of and ability to predict changes in infection and disease dynamics in novel, interdisciplinary, and collaborative ways. (Résumé d'auteur