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result(s) for
"Frick, Patricia"
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Outcome assessment in advanced practice nursing
by
Kleinpell, Ruth M
in
Advanced Practice Nursing -- standards
,
Nurse Clinicians -- standards
,
Nurse Practitioners -- standards
2013
Named a 2013 Doody's Core Title!
Named an AJN Book of the Year! \"This is an excellent and timely tool for advanced practice nurses.\" Score: 100, 5 stars -Doody's Medical Reviews Measuring the results of APN care has become increasingly important as a way to demonstrate the significant impact of APN nurses on practice outcomes. The third edition of this award-winning volume has been updated to provide the most current knowledge, perspectives, and research on assessing outcomes of APN care. It addresses not only the health outcomes of APN practice but the economic impact of APN care as well. Chapters discuss outcome measurement in all areas of advance practice nursing, including identifying outcomes in specialty areas and in community and ambulatory settings. The text provides detailed descriptions of how to conduct outcomes assessments, how to locate the most current instruments and measures for APN assessment, and perspectives on international initiatives in APN assessment. Examples of outcomes studies at the DNP level are culled from the most current published projects. Written by expert practitioners, educators, and researchers in APN outcomes assessment, this book will provide the essential information to help all APNs-regardless of specialty area or practice setting-to increase their skill level in designing outcomes-focused clinical research, selecting instruments, and analyzing outcomes data as critical components of their professional practice role. The third edition is completely updated and expanded to include: A new chapter on assessing outcomes at the DNP level through data gained from the most current research An expanded literature review on outcomes measurement research Guidelines for selecting assessment instruments Perspectives on an international initiative for the development of an APN research data collection toolkit New chapter objectives and critical discussion questions Updated web links
Coastal El Niño triggers rapid marine silicate alteration on the seafloor
2023
Marine silicate alteration plays a key role in the global carbon and cation cycles, although the timeframe of this process in response to extreme weather events is poorly understood. Here we investigate surface sediments across the Peruvian margin before and after extreme rainfall and runoff (coastal El Niño) using Ge/Si ratios and laser-ablated solid and pore fluid Si isotopes (δ
30
Si). Pore fluids following the rainfall show elevated Ge/Si ratios (2.87 µmol mol
−1
) and δ
30
Si values (3.72‰), which we relate to rapid authigenic clay formation from reactive terrigenous minerals delivered by continental runoff. This study highlights the direct coupling of terrestrial erosion and associated marine sedimentary processes. We show that marine silicate alteration can be rapid and highly dynamic in response to local weather conditions, with a potential impact on marine alkalinity and CO
2
-cycling on short timescales of weeks to months, and thus element turnover on human time scales.
This study identifies the rapidness of marine mineral reactions, directly after an extreme rainfall event. The reactions have the potential to affect marine cation and CO
2
cycling, impacting element turnover on human time scales
Journal Article
Platelet-derived HMGB1 is a critical mediator of thrombosis
by
Loughran, Patricia
,
Walker, Britta
,
Pagano, Patrick J.
in
Animals
,
Biomedical research
,
Blood clot
2015
Thrombosis and inflammation are intricately linked in several major clinical disorders, including disseminated intravascular coagulation and acute ischemic events. The damage-associated molecular pattern molecule high-mobility group box 1 (HMGB1) is upregulated by activated platelets in multiple inflammatory diseases; however, the contribution of platelet-derived HMGB1 in thrombosis remains unexplored. Here, we generated transgenic mice with platelet-specific ablation of HMGB1 and determined that platelet-derived HMGB1 is a critical mediator of thrombosis. Mice lacking HMGB1 in platelets exhibited increased bleeding times as well as reduced thrombus formation, platelet aggregation, inflammation, and organ damage during experimental trauma/hemorrhagic shock. Platelets were the major source of HMGB1 within thrombi. In trauma patients, HMGB1 expression on the surface of circulating platelets was markedly upregulated. Moreover, evaluation of isolated platelets revealed that HMGB1 is critical for regulating platelet activation, granule secretion, adhesion, and spreading. These effects were mediated via TLR4- and MyD88-dependent recruitment of platelet guanylyl cyclase (GC) toward the plasma membrane, followed by MyD88/GC complex formation and activation of the cGMP-dependent protein kinase I (cGKI). Thus, we establish platelet-derived HMGB1 as an important mediator of thrombosis and identify a HMGB1-driven link between MyD88 and GC/cGKI in platelets. Additionally, these findings suggest a potential therapeutic target for patients sustaining trauma and other inflammatory disorders associated with abnormal coagulation.
Journal Article
Seasonal ecology of a migratory nectar-feeding bat at the edge of its range
by
Heady, Paul A.
,
Arteaga, Maria Clara
,
Earl, Alexis D.
in
Baja California Sur
,
cacti and succulents
,
cactus
2018
Migratory species that cross geopolitical boundaries pose challenges for conservation planning because threats may vary across a species' range and multi-country collaboration is required to implement conservation action plans. The lesser long-nosed bat (Leptonycteris yerbabuenae) is a migratory pollinator bat that was removed from the Endangered Species List in the United States in 2018 and from threatened status in Mexico in 2013. The seasonal ecology and conservation status of the species is well understood in the core part of its range on mainland Mexico and in the southwestern United States, but relatively little is known about the species on the Baja California peninsula in northwestern Mexico, a part of its range range separated by the Gulf of California. We studied the seasonal ecology of lesser long-nosed bats on the Baja peninsula at 8 focal roosts along a 450-km north-to-south transect to test hypotheses about migratory or residential status of the species on the Baja peninsula. We provide evidence of an extensive population of lesser long-nosed bats on the Baja peninsula that is primarily seasonally migratory and includes 2 mating roosts with males on the southern part of the peninsula. Seasonal ecology of lesser long-nosed bats was closely associated with the flowering and fruiting season of the cardón (Pachycereus pringlei), the dominant columnar cactus on the peninsula. However, we discovered that some female lesser long-nosed bats arrive and give birth at southern roosts in mid-February, about 2 months earlier than other migratory populations in more northern Sonoran Desert habitats. We documented the loss of nearly a third of the known maternity roosts during the study, demonstrating that action to protect key roosts remains a high priority. Migratory pollinators are particularly vulnerable to climate and land-use changes and we recommend continued monitoring and research to guide effective range-wide conservation of the species.
Journal Article
Plectin-mediated cytoskeletal crosstalk as a target for inhibition of hepatocellular carcinoma growth and metastasis
by
Kvasnicova, Bibiana
,
Otahal, Martin
,
Jirak, Daniel
in
1-Phosphatidylinositol 3-kinase
,
Ablation
,
AKT protein
2025
The most common primary malignancy of the liver, hepatocellular carcinoma (HCC), is a heterogeneous tumor entity with high metastatic potential and complex pathophysiology. Increasing evidence suggests that tissue mechanics plays a critical role in tumor onset and progression. Here, we show that plectin, a major cytoskeletal crosslinker protein, plays a crucial role in mechanical homeostasis and mechanosensitive oncogenic signaling that drives hepatocarcinogenesis. Our expression analyses revealed elevated plectin levels in liver tumors, which correlated with poor prognosis for HCC patients. Using autochthonous and orthotopic mouse models we demonstrated that genetic and pharmacological inactivation of plectin potently suppressed the initiation and growth of HCC. Moreover, plectin targeting potently inhibited the invasion potential of human HCC cells and reduced their metastatic outgrowth in the lung. Proteomic and phosphoproteomic profiling linked plectin-dependent disruption of cytoskeletal networks to attenuation of oncogenic FAK, MAPK/Erk, and PI3K/Akt signatures. Importantly, by combining cell line-based and murine HCC models, we show that plectin inhibitor plecstatin-1 (PST) is well-tolerated and potently inhibits HCC progression. In conclusion, our study demonstrates that plectin-controlled cytoarchitecture is a key determinant of HCC development and suggests that pharmacologically induced disruption of mechanical homeostasis may represent a new therapeutic strategy for HCC treatment.
Journal Article