Refsgaardsoelberg6045

Thrombolysis for ischemic stroke has been increasing in the United States. We sought to investigate recent trends in thrombolysis use in older adults.

A retrospective, observational analysis of hospitalization data from the Nationwide Inpatient Sample (NIS) in 2005-2010 was performed. Older adults (≥65 years) admitted with a primary diagnosis of acute ischemic stroke were included. Trends in the population-based rates of thrombolysis and outcomes from the NIS were evaluated using the Cochran-Armitage test.

Thrombolysis in older adult stroke patients increased from 1.7% to 5.4% (2005-2010; trend P<0.001). Large increases were observed among urban patients, urban hospitals, and high volume facilities. Individuals ≥85 years were less likely to receive thrombolysis than younger ages throughout the study period, although there was an increase from an odds ratio of 0.50 (95% CI 0.44-0.57) to 0.75 (95% CI 0.69-0.81) from 2005-2006 to 2009-2010 when compared to 65-74 year olds. For those receiving thrombolysis, no change was observed in intracerebral hemorrhage over time. In-hospital mortality rates did not change significantly over the study period for age subgroups and length of stay declined from 2005 to 2010 for the thrombolysis group (7.6 vs 7.0 days; trend P<0.001).

Rates of thrombolysis in older adults progressively increased, especially in the oldest old. Increases were largely driven by urban and high volume hospitals.

Rates of thrombolysis in older adults progressively increased, especially in the oldest old. Increases were largely driven by urban and high volume hospitals.14-3-3 proteins are intracellularly expressed as ubiquitous adaptor proteins. Here, we found localization of 14-3-3δ/ξ on the neuronal cell surface. 14-3-3δ/ξ was identified as a membrane target for 15-deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2). 15d-PGJ2 is a pathological mediator of neurodegenerative diseases including Alzheimer's disease (AD). A causative peptide for AD, amyloid β, is one of binding partner of 14-3-3δ/ξ. Non-permeabilized neurons were used to avoid the intracellular effects of anti-14-3-3δ/ξ antibody in the present study. The plasmalemmal 14-3-3δ/ξ, but not the cytosolic one, was stimulated by its specific antibody, resulting in neuronal cell death. The neurotoxicity of anti-14-3-3δ/ξ antibody was suppressed by an antioxidant, catalase. Catalase prevented neurons from anti-14-3-3δ/ξ antibody-generating neurotoxic H2O2. The neuroprotective effect of catalase was also detected with the post-treatment of neurons after the application of anti-14-3-3δ/ξ antibody. Activation of mitogen-activated protein kinase signaling cascade is a down-stream consequence of H2O2 exposure. A c-Jun N-terminal kinase inhibitor suppressed anti-14-3-3δ/ξ antibody-induced neuronal cell death. To my knowledge, this is the first report that the antibody-stimulated plasmalemmal 14-3-3δ/ξ induced neuronal cell death. Furthermore, H2O2 and JNK contributed to the neurotoxicity of anti-14-3-3δ/ξ antibody as well as those of amyloid β and 15d-PGJ2.β-Catenin signaling plays a pivotal role in the genesis of a variety of malignant tumors, but its role in breast cancer has not been fully elucidated. Here, we examined whether deregulation of β-catenin signaling is related to the aggressive characteristics of certain types of breast cancers. Analysis of cytokine levels in MDA-MB-231 cells overexpressing a constitutively active form of β-catenin (CAβ-catenin) revealed a higher level of CCL5 expression. Cells transfected with CAβ-catenin or stimulated with recombinant CCL5 exhibited increased cell invasion activity and spheroid formation in vitro. Furthermore, CAβ-catenin-transfected MDA-MB-231 cells formed larger tumor masses that contained more Ki-67-positive cells and infiltrating lymphocytes than did the control cells. An inhibitor of CCR5 and a pan-CXCR neutralizing antibody dramatically reduced CAβ-catenin-promoted activities. In addition to CCL5, 6-BIO, a chemical activator of β-catenin, induced cell invasion and spheroid formation in MDA-MB-231 cells. Furthermore, high levels of nuclear β-catenin accumulation were detected in breast cancer in patients with metastasis but not in those without metastasis. Nuclear β-catenin localization is related to increased CCL5 production in breast cancer. These findings suggest that β-catenin expression enhances tumor progression via chemokine production in breast cancers and that β-catenin signaling is a critical regulator of the aggressive traits of breast cancers.Plants synthesize a large number of isoprenoids that are of nutritional, medicinal and industrial importance. 1-Deoxy-d-xylulose 5-phosphate reductoisomerase (DXR) catalyzes the first committed step for plastidial isoprenoid biosynthesis. Here, we identified two DXR isogenes, designated NtDXR1 and NtDXR2, from tetraploid common tobacco (Nicotiana tabacum L.). Southern blotting and genotyping analysis revealed that two NtDXR genes existed in the tetraploid tobacco genome; NtDXR1 and NtDXR2 were separately derived from N. tomentosiformis and N. sylvestris. Both NtDXRs were localized in chloroplasts. Expression patterns indicated that NtDXR1 and NtDXR2 had similar expression profiles. NtDXR genes were highly expressed in leaves with or without trichomes; expression was relatively reduced in flowers and stems, weak in leaf trichomes and marginal in roots and seeds. Overexpressing NtDXR1 under control of the 35S promoter resulted in longer primary roots and enhancement of various photosynthetic pigments and hormones in leaves. In contrast, there were no significant changes in cembrane-related diterpenoids synthesized in glandular trichomes. To elucidate further the function of DXR in the biosynthesis of diterpenoids, overexpression vectors for NtDXR1 under the control of a trichome-specific CYP promoter were transferred to tobacco plants. CYPNtDXR1 tobacco exhibited larger glandular cells and increased cembrane-related diterpenoids in leaf glandular trichomes. Moreover, transcripts of eight MEP (2-C-methyl-d-erythritol 4-phosphate) pathway genes were significantly up-regulated in NtDXR1-overexpressing tobacco plants, indicating that overexpression of NtDXR could boost the expression of downstream genes in the MEP pathway. Our results suggested that overexpression of NtDXR1 could increase the levels of photosynthetic pigments, leaf surface exudates and hormones though the MEP pathway.The role of salicylic acid (SA) and jasmonic acid (JA) signaling in resistance to root pathogens has been poorly documented. We assessed the contribution of SA and JA to basal and partial resistance of Arabidopsis to the biotrophic clubroot agent Plasmodiophora brassicae. SA and JA levels as well as the expression of the SA-responsive genes PR2 and PR5 and the JA-responsive genes ARGAH2 and THI2.1 were monitored in infected roots of the accessions Col-0 (susceptible) and Bur-0 (partially resistant). SA signaling was activated in Bur-0 but not in Col-0. The JA pathway was weakly activated in Bur-0 but was strongly induced in Col-0. The contribution of both pathways to clubroot resistance was then assessed using exogenous phytohormone application and mutants affected in SA or JA signaling. Exogenous SA treatment decreased clubroot symptoms in the two Arabidopsis accessions, whereas JA treatment reduced clubroot symptoms only in Col-0. The cpr5-2 mutant, in which SA responses are constitutively induced, was more resistant to clubroot than the corresponding wild type, and the JA signaling-deficient mutant jar1 was more susceptible. Finally, we showed that the JA-mediated induction of NATA1 drove N(δ)-acetylornithine biosynthesis in infected Col-0 roots. The 35SNATA1 and nata1 lines displayed reduced or enhanced clubroot symptoms, respectively, thus suggesting that in Col-0 this pathway was involved in the JA-mediated basal clubroot resistance. Overall, our data support the idea that, depending on the Arabidopsis accession, both SA and JA signaling can play a role in partial inhibition of clubroot development in compatible interactions with P. brassicae.Body dissatisfaction has been linked to a number of poor health outcomes, including eating disorders. However, very few studies have investigated body dissatisfaction among immigrant adolescents. Using inductive qualitative inquiry, this study recruited a purposeful sample of immigrant adolescents (N=18, 78% female) with an eating disorder (n=8) and without an eating disorder (n=10). All adolescents were between 16 and 19 years of age (M=16.80, SD=0.89) and were recruited from three municipalities in Ontario. Each adolescent participated in a face-to-face, qualitative interview. Content analysis revealed descriptions of body image that were similar across the sample. The main themes emerging from this work include (a) the "moderately slim" and "moderately muscular" ideal, (b) the "slim and curvy paradox," (c) "ideal" privilege, (d) having an "expected" appearance, and (e) wishful comparisons. Findings have implications for reducing appearance-related dissatisfaction among immigrant adolescents in Canada.Experimental studies have demonstrated that exposure to idealized images of women increases state body image disturbance. However, little work has experimentally examined the effects of exposure to images that sexually objectify women, especially as it relates to women and men's state body dissatisfaction and judgments of women. In the current study, 437 women and men were randomly assigned to view advertisements that sexually objectify women and portray appearance ideals, or to view non-appearance-related advertisements. Results indicated that state body dissatisfaction increased for women and men exposed to advertisements that sexually objectified women, although this effect was larger for women. Trait internalization of appearance ideals moderated this effect, indicating that women and men with higher internalization exhibited greater state body dissatisfaction after viewing women sexually objectified in advertisements. Exposure to women sexually objectified in advertisements did not affect women's or men's attractiveness or competence ratings of women in university advertisements.Adrenal crisis is a life-threatening medical emergency, associated with a high mortality unless it is appropriately recognized and early treatment is rendered. Despite it being a treatable condition for almost 70 years, failure of adequate preventive measures or delayed treatment has often led to unnecessary deaths. Gastrointestinal illness is the most common precipitant for an adrenal crisis. Although most patients are educated about "sick day rules," patients, and physicians too, are often reluctant to increase their glucocorticoid doses or switch to parenteral injections, and thereby fail to avert the rapid deterioration of the patients' condition. Therefore, more can be done to prevent an adrenal crisis, as well as to ensure that adequate acute medical care is instituted after a crisis has occurred. There is generally a paucity of studies on adrenal crisis. LY333531 Hence, we will review the current literature, while also focusing on the incidence, presentation, treatment, prevention strategies, and latest recommendations in terms of steroid dosing in stress situations.