bluuebunny/crossref_metadata_2025_split huggingface dataset:
Delirium Symptoms in Post‐Acute Care: Prevalent, Persistent, and Associated with Poor Functional Recovery
Authors: Marcantonio Edward R. , Simon Samuel E. , Bergmann Margaret A. , Jones Richard N. , Murphy Katharine M. , Morris John N. 
Published: March 2003

OBJECTIVES: To determine the prevalence of delirium symptoms at the time of admission to post‐acute facilities, the persistence of delirium symptoms in this setting, and the association of delirium symptoms with functional recovery.DESIGN: Prospective cohort study.SETTING: Eighty‐five post‐acute care facilities: 55 rehabilitation hospitals and 30 skilled nursing facilities in 29 states.PARTICIPANTS: Five hundred fifty‐one consenting patients aged 65 and older newly admitted to participating facilities from acute care hospitals.MEASUREMENTS: Data were collected as part of a field study effort related to the Minimum Data Set (MDS). Basic demographic data, medical comorbidity, delirium symptoms, and functional status—activities of daily living (ADLs) and instrumental activities of daily living (IADLs)—were obtained from MDS assessments performed within 4 days of admission and again 1 week later by the patient's primary nurse. Six delirium symptoms (easily distracted, periods of altered perception, disorganized speech, periods of restlessness, periods of lethargy, and mental function varies over the course of a day) were assessed after appropriate training.RESULTS: Of the 551 patients (mean age ± standard deviation 78 ± 7, 64% women), 126 had delirium symptoms on post‐acute admission, for an overall prevalence of 23%. In patients with delirium symptoms on the admission assessment, 1 week later, 14% had completely resolved, 22% had fewer delirium symptoms, 52% had the same number of symptoms, and 12% had more symptoms. Of those with no delirium symptoms on admission, 4% had new symptoms 1 week later. Patients who had the same number of or more delirium symptoms at the second assessment had significantly worse ADL and IADL recovery than those with fewer or resolved delirium symptoms or those with no delirium symptoms at either assessment. Persistent delirium symptoms remained significantly associated with worse ADL and IADL recovery after adjusting for age, comorbidity, dementia, and baseline functional status.CONCLUSIONS: The data from this study provide strong preliminary evidence that, in patients newly admitted to post‐acute care facilities from acute care hospitals, delirium symptoms are prevalent, persistent, and associated with poor functional recovery. Educational efforts are warranted to help post‐acute facility staff recognize and manage this common and morbid condition.
Identifying Older People at Risk of Abuse During Routine Screening Practices
Authors: Shugarman Lisa R. , Fries Brant E. , Wolf Rosalie S. , Morris John N. 
Published: March 2003

OBJECTIVES: To examine the association between various characteristics of community‐based older people and a constructed measure of potential elder abuse.DESIGN: Cross‐sectional design.SETTING: Public community‐based long‐term care programs in Michigan.PARTICIPANTS: Individuals aged 60 and older seeking home and community‐based services in Michigan between November 1996 and October 1997 (N = 701).MEASUREMENTS: Data were collected using the Minimum Data Set for Home Care (MDS‐HC) assessment. The dependent variable is a constructed measure of potential elder abuse reflecting physical and emotional abuse and neglect. Independent variables include demographic characteristics; diagnoses; behavioral measures; and cognitive, physical, and social functioning.RESULTS: Several measures of social support and social function were strongly associated with the signs of a potentially abusive environment: brittle support (odds ratio (OR) = 3.5, 90% confidence interval (CI) = 1.5–8.1), older person feels lonely (OR = 2.4, 90% CI = 1.3–4.5), and older person expresses conflict with family/friends (OR = 2.3, 90% CI = 1.2–4.3). Home care participants' alcohol abuse, psychiatric illness, lack of ease interacting with others, and short‐term memory problems were also significantly associated with the signs of potential elder abuse.CONCLUSIONS: The results of this study suggest that the signs of potential elder abuse are associated with a diminishing social network and poor social functioning, although some characteristics of the older person's health are contributing factors. Improved understanding of the link between those characteristics and potential abuse will help healthcare providers, case managers, and others identify older people at high risk of abuse.
Changes in the turnover of Rubisco and levels of mRNAs of rbcL and rbcS in rice leaves from emergence to senescence
Authors: Suzuki Y. , Makino A. , Mae T. 
Published: March 2003

AbstractChanges in the amount of ribulose 1,5‐bisphosphate carboxylase/oxygenase (Rubisco; EC 4·1·1·39) synthesized and degraded and the levels of rbcL and rbcS mRNAs were examined in the eighth leaf blades of rice from emergence to senescence. Synthesis of Rubisco was very active during leaf expansion, became quite low at the time of full expansion and then declined further during senescence. The changes in the levels of rbcL and rbcS mRNAs co‐ordinated approximately with those in the amount of Rubisco synthesized. Thus, it is suggested that the amount of Rubisco synthesized is determined primarily by the levels of rbcL and rbcS mRNAs during the life span of the leaves. Degradation of Rubisco started just before the time of full expansion and became far more active than its synthesis during senescence. Since the synthesis of Rubisco during senescence scarcely contributed to its amount, it can be concluded that the degradation of Rubisco is the major determinant for the amount of Rubisco in senescent leaves. The decline in the level of rbcL mRNA occurred much earlier in the developmental stage and proceeded at a much faster rate than that of rbcL DNA, indicating that the level of rbcL DNA is not a major determinant for the level of rbcL mRNA in senescent leaves of rice.
The relative importance of dispersal limitation of vascular plants in secondary forest succession in Muizen Forest, Belgium
Authors: Verheyen Kris , Hermy Martin 
Published: March 2003

Abstract

Distribution patterns (frequency and percentage cover) of 18 forest plant species were studied in 34 ha of mixed deciduous forest (Muizen Forest, north Belgium). Stands varied in age between 6 and more than 223 years and both slow and fast colonizing species were studied.
Detailed land use history data were combined with the species distribution maps to identify species‐specific colonization sources and calculate colonization distances.
A multiple logistic regression model was constructed with four covariables: pH (which can impose limits on the potential species‐distribution), secondary forest age, distance from nearest colonization source and age–distance interaction, to allow us to account for the gradual completion of colonization over time.
We could distinguish species which are limited by both dispersal and recruitment (Primula elatior, Arum maculatum and Lamium galeobdolon), mainly by dispersal (Anemone nemorosa, Deschampsia cespitosa), mainly by recruitment (Paris quadrifolia and Polygonatum multiflorum) and by neither (Geum urbanum, Ranunculus ficaria, Glechoma hederacea, Aegopodium podagraria, Ajuga reptans, Adoxa moschatellina and Oxalis acetosella).
The low colonizing capacity of ancient forest plants cannot be attributed to a single cause; rather both dispersal and recruitment are limiting but the relative importance varies.
New approach to optical diffraction tomography yielding a vector equation of diffraction tomography and a novel tomographic microscope
Authors: Lauer V. 
Published: March 2003

SummaryWe first obtain a frequency‐space equation of diffraction tomography for the electric field vector, within the first‐order Born approximation, using a simplified formalism resulting from using three‐dimensional spatial frequencies and replacing outgoing waves by linear combinations of homogeneous plane waves. A coherent optical diffraction tomographic microscope is then described, in which a sample is successively illuminated by a series of plane waves having different directions, each scattered wave is recorded by phase‐shifting interferometry, and the object is then reconstructed from these recorded waves. The measurement process in this device is analysed taking into account the illuminating wave, the wave scattered by the sample, the reference wave, and the phase relations between these waves. This analysis yields appropriate equations that take into account the characteristics of the reference wave and compensate random phase shifts. It makes it possible to obtain a high‐resolution three‐dimensional frequency representation in full conformity with theory. The experimentally obtained representations show index and absorptivity with a resolution limit of about a quarter of a wavelength, and have a depth of field of about 40 µm.
Nanosecond fluorescence resonance energy transfer‐fluorescence lifetime imaging microscopy to localize the protein interactions in a single living cell
Authors: Elangovan M. , Day R. N. , Periasamy A. 
Published: March 2003

SummaryVisualizing and quantifying protein–protein interactions is a recent trend in biomedical imaging. The current advances in fluorescence microscopy, coupled with the development of new fluorescent probes such as green fluorescent proteins, allow fluorescence resonance energy transfer (FRET) to be used to study protein interactions in living specimens. Intensity‐based FRET microscopy is limited by spectral bleed‐through and fluorophore concentration. Fluorescence lifetime imaging (FLIM) microscopy and lifetime measurements are independent of change in fluorophore concentration or excitation intensity, and the combination of FRET and FLIM provides high spatial (nanometre) and temporal (nanoseconds) resolution. Because only the donor fluorophore lifetime is measured, spectral bleed‐through is not an issue in FRET–FLIM imaging. In this paper we describe the development of a nanosecond FRET–FLIM microscopy instrumentation to acquire the time‐resolved images of donor in the presence and the absence of the acceptor. Software was developed to process the acquired images for single and double exponential decays. Measurement of donor lifetime in two different conditions allowed us to calculate accurately the distance between the interacting proteins. We used this approach to quantify the dimerization of the transcription factor CAATT/enhancer binding protein alpha in living pituitary cells. The one‐ and two‐component analysis of the donor molecule lifetime in the presence of acceptor demonstrates the distance distribution between interacting proteins.
Hydrogen peroxide‐mediated phosphorylation of ERK1/2,  Akt/PKB and JNK in cortical neurones: dependence  on Ca2+ and PI3‐kinase
Authors: Crossthwaite Andrew J. , Hasan Sumaera , Williams Robert J. 
Published: March 2003

AbstractPrimary cortical neurones exposed to an oxidative insult in the form of hydrogen peroxide (H2O2) for 30 min showed a concentration‐dependent increase in oxidative stress followed by␣a␣delayed NMDA receptor‐dependent cell death measured␣24 h later. Extracellular signal‐regulated protein kinase (ERK1/2), c‐jun N‐terminal kinase (JNK) and the kinase Akt/PKB may regulate neuronal viability in response to oxidative insults. Using phospho‐specific antibodies, a 15‐min stimulation of neurones with H2O2 (100 µm−1 mm) produced a concentration‐dependent phosphorylation of ERK1/2 and Akt/PKB that was partly dependent on extracellular Ca2+ and phosphatidylinositol 3‐kinase (PI3‐K). Higher concentrations of H2O2 (1 mm) also stimulated a phosphorylation of JNK which was totally dependent on extracellular Ca2+ but not PI3‐K. H2O2‐induced phosphorylation of ERK1/2, Akt/PKB or JNK were unaffected by the NMDA channel blocker MK801. Blocking ERK1/2 activation with the upstream inhibitor U0126 (10 µm) enhanced H2O2‐induced (100–300 µm range) neurotoxicity and inhibited H2O2‐mediated phosphorylation of the cyclic AMP regulatory binding protein (CREB), suggesting that ERK1/2 signals to survival under these conditions. At higher concentrations (mm), H2O2‐stimulated a phosphorylation of c‐jun. It is likely, therefore, that subjecting neurones to moderate oxidative‐stress recruits pro‐survival signals to CREB but during severe oxidative stress pro‐death signals through JNK and c‐jun are dominant.
Dietary folate deficiency and elevated homocysteine levels endanger dopaminergic neurons in models of Parkinson's disease
Authors: Duan Wenzhen , Ladenheim Bruce , Cutler Roy G. , Kruman Inna I. , Cadet Jean Lud , Mattson Mark P. 
Published: March 2003

AbstractAlthough the cause of Parkinson's disease (PD) is unknown, data suggest roles for environmental factors that may sensitize dopaminergic neurons to age‐related dysfunction and death. Based upon epidemiological data suggesting roles for dietary factors in PD and other age‐related neurodegenerative disorders, we tested the hypothesis that dietary folate can modify vulnerability of dopaminergic neurons to dysfunction and death in a mouse model of PD. We report that dietary folate deficiency sensitizes mice to MPTP‐induced PD‐like pathology and motor dysfunction. Mice on a folate‐deficient diet exhibit elevated levels of plasma homocysteine. When infused directly into either the substantia nigra or striatum, homocysteine exacerbates MPTP‐induced dopamine depletion, neuronal degeneration and motor dysfunction. Homocysteine exacerbates oxidative stress, mitochondrial dysfunction and apoptosis in human dopaminergic cells exposed to the pesticide rotenone or the pro‐oxidant Fe2+. The adverse effects of homocysteine on dopaminergic cells is ameliorated by administration of the antioxidant uric acid and by an inhibitor of poly (ADP‐ribose) polymerase. The ability of folate deficiency and elevated homocysteine levels to sensitize dopaminergic neurons to environmental toxins suggests a mechanism whereby dietary folate may influence risk for PD.
Cholesterol‐dependent modulation of dendrite outgrowth  and microtubule stability in cultured neurons
Authors: Fan Qi‐Wen , Yu Wei , Gong Jian‐Sheng , Zou Kun , Sawamura Naoya , Senda Takao , Yanagisawa Katsuhiko , Michikawa Makoto 
Published: March 2003

AbstractMicrotubule‐associated protein 2 (MAP2) is a neuron‐specific cytoskeletal protein enriched in dendrites and cell bodies. MAP2 regulates microtubule stability in a phosphorylation‐dependent manner, which has been implicated in dendrite outgrowth and branching. We have previously reported that cholesterol deficiency causes tau phosphorylation and microtubule depolymerization in axons (Fan et al. 2001). To investigate whether cholesterol also modulates microtubule stability in dendrites by modulating MAP2 phosphorylation, we examined the effect of compactin, a 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitor, and TU‐2078 (TU), a squalene epoxidase inhibitor, on these parameters using cultured neurons. We have found that cholesterol deficiency induced by compactin and TU, inhibited dendrite outgrowth, but not of axons, and attenuated axonal branching. Dephosphorylation of MAP2 and microtubule depolymerization accompanied these alterations. The amount of protein phosphatase 2 A (PP2A) and its activity in association with microtubules were decreased, while those unbound to microtubules were increased. The synthesized ceramide levels and the total ceramide content were increased in these cholesterol‐deficient neurons. These alterations caused by compactin were prevented by concurrent treatment of cultured neurons with β‐migrating very‐low‐density lipoproteins (β‐VLDL) or cholesterol. Taken together, we propose that cholesterol‐deficiency causes a selective inhibition of dendrite outgrowth due to the decreased stability of microtubules as a result of inhibition of MAP2 phosphorylation.
Modulation of Aβ peptides by estrogen in mouse models
Authors: Zheng H. , Xu H. , Uljon S. N. , Gross R. , Hardy K. , Gaynor J. , Lafrancois J. , Simpkins J. , Refolo L. M. , Petanceska S. , Wang R. , Duff K. 
Published: March 2003

AbstractClinical studies have shown that estrogen deprivation through menopause is a risk factor in both the initiation and progression of Alzheimer's disease (AD) and that estrogen replacement therapy may be protective. One of the major pathological features in the human AD brain is the senile plaque, a proteinaceous structure composed mainly of heterogeneous peptides collectively known as A‐beta (Aβ). In vitro studies have linked estrogen with Aβ modulation, suggesting that one‐way that estrogen depletion at menopause may exacerbate the features of AD is through Aβ accumulation. To test this, two studies were performed on transgenic models of amyloidosis. Firstly, transgenic mice without detectable amyloid aggregates were subjected to ovariectomy and estradiol supplementation, and Aβ levels were assessed. Secondly, the effects of estrogen modulation were assessed in mice at an age when plaques would be forming initially. Overall, Aβ levels were higher in estrogen‐deprived mice than intact mice, and this effect could be reversed through the administration of estradiol. These data suggest that, in vivo, estrogen depletion leads to the accumulation of Aβ in the CNS, which can be reversed through replacement of estradiol. These results provide evidence that post‐menopausal estrogen depletion may be linked to an increased risk of AD through Aβ modulation.
Overexpression of c‐Fos is sufficient to stimulate tyrosine hydroxylase (TH) gene transcription in rat pheochromocytoma  PC18 cells
Authors: Sun Baoyong , Tank A. William 
Published: March 2003

AbstractThe AP1 site within the tyrosine hydroxylase gene proximal promoter is essential for the response of the gene to numerous stimuli. Stimulation of this gene is often associated with induction of the AP1 transcription factor, c‐Fos. However, many stimuli activate or induce multiple transcription factors that interact with this AP1 site or other sites within the gene's proximal promoter. Hence, it remains unclear whether c‐Fos induction by itself is sufficient to stimulate the tyrosine hydroxylase gene. In this study we produce rat pheochromocytoma PC18 cells that overexpress c‐Fos under control of the tet‐inducible system. We demonstrate that induction of c‐Fos leads to dramatic stimulation of tyrosine hydroxylase gene transcription rate measured using nuclear run‐on assays. This stimulation is closely associated quantitatively with the induction of c‐Fos and does not apparently require phosphorylation of c‐Fos. The response is partially dependent on the AP1 site within the tyrosine hydroxylase proximal promoter. However, the response of the proximal promoter to c‐Fos induction is relatively small compared with that of the endogenous gene. Consequently, our results suggest that c‐Fos exerts its influence on the tyrosine hydroxylase gene via multiple mechanisms that are dependent and independent of the proximal promoter AP1 site.
Dopamine D4 receptors are heterogeneously distributed in the striosomes/matrix compartments of the striatum
Authors: Rivera Alicia , Cuéllar Beatriz , Girón Francisco J. , Grandy David K. , De La Calle Adelaida , Moratalla Rosario 
Published: March 2003

AbstractTwo important aspects of striatal function, exploratory behaviour and motor co‐ordination, require the integrity of the dopamine D4 receptor subtype. These receptors are also implicated in the pathophysiology of certain neuropsychiatric disorders. However, the distribution of D4 receptors in the striatum has not yet been described and this situation impairs our understanding of the anatomical substrate in which D4 receptors function. We developed a D4 receptor‐specific anti‐body that has permitted us to investigate the regional and cellular localization of the receptor in the neostriatum of the rat, mouse, cat and monkey. The subcellular distribution and the synaptic organization of this receptor were also determined in the rat striatum. We found moderate levels of D4 receptor expression in the caudoputamen and lower levels in the nucleus accumbens. These receptors were expressed in cell bodies and in the neuropil and were heterogeneously distributed among different striatal compartments, being more abundant in striosomes than in the matrix. At the subcellular level, the receptor immunoreactivity was mainly localized to dendritic shafts and spines. The prominent immunoreactivity observed in the striosomes indicates that integrative processes involved in D4‐mediated limbic behaviours occurs through the striosomes rather than accumbens, whereas the motor behaviour is based in the striatal matrix.
Essential role of caspase‐11 in activation‐induced cell death of rat astrocytes
Authors: Suk Kyoungho , Kim Sun Yeou , Kim Hocheol 
Published: March 2003

AbstractWe have previously shown that rat astrocytes undergo apoptosis upon inflammatory activation. Nitric oxide (NO) produced by activated astrocytes was the major cytotoxic mediator in this type of autoregulatory apoptosis. However, an inhibitor of nitric oxide synthase did not completely block the apoptosis of activated astrocytes, suggesting the presence of other apoptotic pathways. Here, we present evidence that caspase‐11 is an essential molecule in NO‐independent apoptotic pathway of activated astrocytes. Inflammatory activation (lipopolysaccharide, interferon‐γ, and tumor necrosis factor‐α treatment) of rat astrocyte cultures and C6 glioma cells led to the induction of caspase‐11 followed by activation of caspases‐11, ‐1, and ‐3. In contrast, NO donors induced activation of caspase‐3 only. Inactivation of caspase‐11 by the transfection of dominant negative mutant or treatment with the caspase inhibitors rendered the astrocytes partially resistant to the apoptosis following inflammatory activation, but not NO donor exposure. These results indicate that inflammatory stimuli not only induce the production of cytotoxic NO, but also␣initiate NO‐independent apoptotic pathway through the induction of caspase‐11 expression.
Generation of reactive oxygen species by the mitochondrial electron transport chain
Authors: Liu Yuanbin , Fiskum Gary , Schubert David 
Published: March 2003

AbstractGeneration of reactive oxygen species (ROS) by the mitochondrial electron transport chain (ETC), which is composed of four multiprotein complexes named complex I–IV, is believed to be important in the aging process and in the pathogenesis of neurodegenerative diseases such as Parkinson's disease. Previous studies have identified the ubiquinone of complex III and an unknown component of complex I as the major sites of ROS generation. Here we show that the physiologically relevant ROS generation supported by the complex II substrate succinate occurs at the flavin mononucleotide group (FMN) of complex I through reversed electron transfer, not at the ubiquinone of complex III as commonly believed. Indirect evidence indicates that the unknown ROS‐generating site within complex I is also likely to be the FMN group. It is therefore suggested that the major physiologically and pathologically relevant ROS‐generating site in mitochondria is limited to the FMN group of complex I. These new insights clarify an elusive target for intervening mitochondrial ROS‐related processes or diseases.