Practice What We Preach: Beginning a Journey to Embrace Patient-Centered Outcomes Research.

Background: Patient-centered outcomes research seeks to answer patient-centered questions. The process includes varied locations and individuals throughout the care continuum to address individual differences and constraints in implementation and dissemination.

Problem: This paper intends to answer this question: do academic nurses practice what they preach by assisting patient-centered outcomes research and researchers through their engagement with patients, caregivers, and other community stakeholder partners in nursing research?

Approach: This paper provides an overview of how academic nurses in a single institution (the University of Texas Medical Branch at Galveston School of Nursing) began to embrace patient-centered outcomes research.

As Births Diminish and Deaths Increase, Natural Decrease becomes More Widespread in Rural America.

Even before the onset of the Covid-19 pandemic, the U.S. population growth rate last year was the lowest in 100 years.

Metropolitan Reclassification and the Urbanization of Rural America.

We highlight the paradoxical implications of decadal reclassification of U.S. counties (and America's population) from nonmetropolitan to metropolitan status between 1960 and 2017.

The Influence of Human Demography on Land Cover Change in the Great Lakes States, USA.

The Great Lakes region contains productive agricultural and forest lands, but it is also highly urbanized, with 32 of its 52 million residents living in nine large metropolitan areas. Urbanization of undeveloped areas may adversely affect the productivity of agricultural and forest lands, and the provision of ecosystem services. We combine demographic and remote sensing data to evaluate land cover change in the region using a two-phase statistical modeling approach that predicts the incidence and extent of land cover change for each of the region's 10,579 county subdivisions.

Sprawling and diverse: The changing U.S. population and implications for public lands in the 21st Century.

Public lands are typically established in recognition of their unique ecological value, yet both ecological and social values of public lands change over time, along with human distribution and land use. These transformations are evident even in developed countries with long histories of public land management, such as the United States. The 20th Century saw dramatic changes in the American population, in distribution and in racial and ethnic diversity, leading to new challenges and new roles for public lands.

The relocation bump: Memories of middle adulthood are organized around residential moves.

The lifetime temporal distribution of older adults' autobiographical memories peaks during the transitional period of late adolescence and early adulthood, a phenomenon known as the reminiscence bump. This age-specific memory enhancement suggests that transitions may provide a more general organizing structure for autobiographical memory. To test this hypothesis, we examined how older adults' memories of events that occurred between the ages of 40 and 60 were distributed around residential relocations occurring within this same time frame.

Moving Toward Integration? Effects of Migration on Ethnoracial Segregation Across the Rural-Urban Continuum.

This study analyzes the impact of migration on ethnoracial segregation among U.S. counties.

Migration signatures across the decades: Net migration by age in U.S. counties, 1950-2010.

Background: Migration is the primary population redistribution process in the United States. Selective migration by age, race/ethnic group, and spatial location governs population integration, affects community and economic development, contributes to land use change, and structures service needs.

Objective: Delineate historical net migration patterns by age, race/ethnic, and rural-urban dimensions for United States counties.

α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor activation protects against phencyclidine-induced caspase-3 activity by activating voltage-gated calcium channels.

Phencyclidine (PCP) is a noncompetitive, open channel blocker of the N-methyl-D-aspartate (NMDA) receptor-ion channel complex. When administered to immature animals, it is known to cause apoptotic neurodegeneration in several regions, and this is followed by olanzapine-sensitive, schizophrenia-like behaviors in late adolescence and adulthood. Clarification of its mechanism of action could yield data that would help to inform the treatment of schizophrenia.

The role of inflammation in brain cancer.

Malignant brain tumors are among the most lethal of human tumors, with limited treatment options currently available. A complex array of recurrent genetic and epigenetic changes has been observed in gliomas that collectively result in derangements of common cell signaling pathways controlling cell survival, proliferation, and invasion. One important determinant of gene expression is DNA methylation status, and emerging studies have revealed the importance of a recently identified demethylation pathway involving 5-hydroxymethylcytosine (5hmC).

Hispanic Assimilation and Fertility in New Destinations.

This paper evaluates comparative patterns of fertility in new Hispanic destinations and established gateways using pooled cross-sectional data from the 2005-2009 microdata files of the American Community Survey. Changing Hispanic fertility provides a useful indicator of cultural incorporation. Analyses show that high fertility among Hispanics has been driven in part by the Mexican-origin and other new immigrant populations (e.

A combined bioinformatics and chemoinformatics approach for developing asymmetric bivalent AMPA receptor positive allosteric modulators as neuroprotective agents.

PAMs new in town! An effective, combined bioinformatics and chemoinformatics approach was applied to the design of novel asymmetric bivalent α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor positive allosteric modulators (PAMs) with marked potency in vitro and efficacy in vivo for preventing neuroapoptosis. The novel chemotype could provide pharmacological probes and potential therapeutic agents for glutamatergic hypofunction and its related neurological and psychiatric disorders.

Prefrontal dopaminergic and enkephalinergic synaptic accommodation in HIV-associated neurocognitive disorders and encephalitis.

Unlabelled: Changes in synapse structure occur in frontal neocortex with HIV encephalitis (HIVE) and may contribute to HIV-associated neurocognitive disorders (HAND). A postmortem survey was conducted to determine if mRNAs involved in synaptic transmission are perturbed in dorsolateral prefrontal cortex (DLPFC) in subjects with HIVE or HAND. Expression of the opioid neurotransmitter preproenkephalin mRNA (PENK) was significantly decreased in a sampling of 446 brain specimens from HIV-1 infected people compared to 67 HIV negative subjects.

Brain-derived neurotrophic factor prevents phencyclidine-induced apoptosis in developing brain by parallel activation of both the ERK and PI-3K/Akt pathways.

Phencyclidine is an N-methyl d-aspartate receptor (NMDAR) blocker that has been reported to induce neuronal apoptosis during development and schizophrenia-like behaviors in rats later in life. Brain-derived neurotrophic factor (BDNF) has been shown to prevent neuronal death caused by NMDAR blockade, but the precise mechanism is unknown. This study examined the role of the phosphatidylinositol-3 kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK) pathways in BDNF protection of PCP-induced apoptosis in corticostriatal organotypic cultures.

Activation of dopamine D1 receptors blocks phencyclidine-induced neurotoxicity by enhancing N-methyl-D-aspartate receptor-mediated synaptic strength.

Early postnatal blockade of NMDA receptors by phencyclidine (PCP) causes cortical apoptosis in animals. This is associated with the development of schizophrenia-like behaviors in rats later in life. Recent studies show that the mechanism involves a loss of neurotrophic support from the phosphoinositol-3 kinase/Akt pathway, which is normally maintained by synaptic NMDA receptor activation.

Lithium protection of phencyclidine-induced neurotoxicity in developing brain: the role of phosphatidylinositol-3 kinase/Akt and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling pathways.

Phencyclidine (PCP) and other N-methyl-D-aspartate (NMDA) receptor antagonists have been shown to be neurotoxic to developing brains and to result in schizophrenia-like behaviors later in development. Prevention of both effects by antischizophrenic drugs suggests the validity of PCP neurodevelopmental toxicity as a heuristic model of schizophrenia. Lithium is used for the treatment of bipolar and schizoaffective disorders and has recently been shown to have neuroprotective properties.

Atypical anti-schizophrenic drugs prevent changes in cortical N-methyl-D-aspartate receptors and behavior following sub-chronic phencyclidine administration in developing rat pups.

We sought to determine the relationship between phencyclidine (PCP)-induced alterations in behavior and NMDAR expression in the cortex by examining the effect of anti-schizophrenic drug treatment on both. Sprague-Dawley rat pups were pretreated with risperidone or olanzapine prior to treatment with PCP on postnatal day 7 (PN7) or sub-chronically on PN7, 9, and 11. Pre-pulse inhibition (PPI) of acoustic startle was measured on PN24-26 and following a challenge dose of 4 mg/kg PCP, locomotor activity was measured on PN28-35.

Postnatal phencyclidine administration selectively reduces adult cortical parvalbumin-containing interneurons.

Transient postnatal NMDA receptor blockade by phencyclidine (PCP), ketamine, or MK-801 induces developmental neuroapoptosis and adult behavioral deficits, which resemble abnormal human behaviors typically present in schizophrenia. This study tested the hypothesis that PCP-induced developmental apoptosis causes a specific deficit of GABAergic interneurons containing parvalbumin (PV), calretinin (CR), or calbindin (CB). Young adult (PND56) rats that were given a single dose of PCP (10 mg/kg) on PND7 exhibited no densitometric change of either CR or CB neurons in any brain region studied, but demonstrated a selective deficit of PV-containing neurons in the superficial layers (II-IV) of the primary somatosensory (S1), motor (M), and retrosplenial cortices, but not in the striatum (CPu) or hippocampus.

Differential regulation of the NMDA receptor by acute and sub-chronic phencyclidine administration in the developing rat.

Neurodegeneration induced by the NMDA receptor antagonist, phencyclidine (PCP), has been used to model the pathogenesis of schizophrenia in the developing rat. Acute and sub-chronic administration of PCP in perinatal rats results in different patterns of neurodegeneration. The potential role of an alteration in the membrane expression of NMDA receptors in PCP-induced degeneration is unknown.

The role of Akt-GSK-3beta signaling and synaptic strength in phencyclidine-induced neurodegeneration.

N-methyl-D-aspartate (NMDA) receptor antagonists such as phencyclidine (PCP) can induce positive and negative symptoms of schizophrenia in humans and related effects in rodents. PCP treatment of developing rats induces apoptotic neurodegeneration and behavioral deficits later in life that mimic some symptoms of schizophrenia. The precise mechanism of PCP-induced neural degeneration is unknown.

The role of caspase-3 activation in phencyclidine-induced neuronal death in postnatal rats.

This study determined the role of caspase-3 in phencyclidine (PCP)-induced neurodegeneration in postnatal rats. PCP administration to postnatal day 7 rats induced a dose-dependent increase in caspase-3 enzymatic activity in frontal cortex, striatum, and hippocampus. Enzymatic activation was present at 4 h, peaked between 6 and 12 h, and disappeared by 24 h.

Temporal and spatial variation in age-specific net migration in the United States.

As fertility differences in the United States diminish, population redistribution trends are increasingly dependent on migration. This research used newly developed county-level age-specific net migration estimates for the 1990s, supplemented with longitudinal age-specific migration data spanning the prior 40 years, to ascertain whether there are clear longitudinal trends in age-specific net migration and to determine if there is spatial clustering in the migration patterns. The analysis confirmed the continuation into the 1990s of distinct net migration "signature patterns" for most types of counties, although there was temporal variation in the overall volume of migration across the five decades.

Synthesis and structure-activity relationships of 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine analogues as potent, noncompetitive metabotropic glutamate receptor subtype 5 antagonists; search for cocaine medications.

Recent genetic and pharmacological studies have suggested that the metabotropic glutamate receptor subtype 5 (mGluR5) may represent a druggable target in identifying new therapeutics for the treatment of various central nervous system disorders including drug abuse. In particular, considerable attention in the mGluR5 field has been devoted to identifying ligands that bind to the allosteric modulatory site, distinct from the site for the primary agonist glutamate. Both 2-methyl-6-(phenylethynyl)pyridine (MPEP) and its analogue 3-[(2-methyl-4-thiazolyl)ethynyl]pyridine (MTEP) have been shown to be selective and potent noncompetitive antagonists of mGluR5.