bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence of cognitive impairment amongst Singapore's elderly Chinese: a community‐based study using the ECAQ and the IQCODE
Authors: Jer Lim Hsien , P'ing Ping Lim Joy , Anthony Philomena , Hong Huang Yeo Donald , Sahadevan Suresh 
Published: February 2003

AbstractObjectivesThis study examined the prevalence of cognitive impairment in the elderly Chinese living in the Queenstown district of Singapore using two locally‐validated cognitive screening instruments: the Elderly Cognitive Assessment Questionnaire (ECAQ), and the Informant Questionnaire on the Cognitive Decline of the Elderly (IQCODE).Methods234 elderly Chinese subjects were randomly selected from the Queenstown district and administered the ECAQ, while their principal relatives were administered the IQCODE. The screening instruments' respective cut‐off scores to identify cognitive impairment indicative of dementia were based on local validation work.ResultsThe prevalence of cognitive impairment was computed based on the percentage of failed scores on the two screening instruments. We found the prevalence of cognitive impairment to be 7.7% by ECAQ (95% Confidence Intervals (CI): 4.6%–10.1%) and 13.2% by IQCODE (95% CI: 9.4%–17.7%). A similar study in 1990 using ECAQ on elderly Chinese from the Henderson district in Singapore showed a cognitive impairment prevalence of 4%. This ECAQ‐based variation between the two studies, likely indicates a true difference in prevalence rates between the two communities. On the other hand, the different ECAQ and IQCODE prevalence rates within our Queenstown study probably reflect spectrum bias, with IQCODE detecting earlier stages of dementia than ECAQ.ConclusionWe have found the prevalence of cognitive impairment amongst Singapore's elderly to be higher than previously reported. These findings imply that current resources may be inadequate for the effective care and management of the cognitively‐impaired elderly in our aging community. Copyright © 2003 John Wiley & Sons, Ltd.
Validation of a Spanish translation of the CLOX for use in Hispanic samples: the Hispanic EPESE study
Authors: Royall Donald R. , Espino David V. , Polk Marsha J. , Verdeja Regina , Vale Sandra , Gonzales Hector , Palmer Raymond R. , Markides Kyriakos P. 
Published: February 2003

AbstractObjectivesClock drawing tests (CDT) appear to be less vulnerable to linguistic, cultural, or educational bias than traditional dementia screening instruments. We investigated a Spanish language translation of CLOX: an executive CDT, in a community sample of Hispanic elders.MethodsIn‐home CLOX evaluations of 1309 Mexican–American elders were reviewed.ResultsBoth CLOX1 (an executive CDT) and CLOX2 (a constructional CDT) showed good internal consistency (Chronbach's alpha; both α = 0.82). Cultural‐demographic variables had little effect on CLOX scores. Although language had a significant effect on CLOX1 failure rates, this was not mediated by age, education, acculturation or income.ConclusionsThese results suggest that the Spanish CLOX can be validly administered to community‐based Hispanic elder samples regardless of education or acculturation. Copyright © 2003 John Wiley & Sons, Ltd.
Reported differences in management strategies by primary care physicians and psychiatrists in older patients who are depressed
Authors: Saarela Tuula , Engeström Ritva 
Published: February 2003

AbstractObjectiveTo compare reported management suggestions by primary care physicians and psychiatry specialists for case vignette examples of old age depression, and to explore further training needs in geriatric depression for both professional groups.DesignQualitative study using case vignettes in focus groups. Single group training sessions were arranged for 25 primary care physicians and 11 psychiatrists. The same two clinical vignettes were presented at all training sessions. Written management suggestions by participants, group discussion field notes and transcripts of group session videotapes were analysed.ResultsDifferences emerged in intended depression management. Primary care physicians tended to assess the symptoms as less serious and the situation as less urgent than psychiatrists. Management suggestions given by the psychiatrists included more recommendations of immediate psychiatric treatment and more precise descriptions of medication. Both groups recognized the somatic issues and were willing to assume responsibility for treatment.ConclusionsIdentifying management differences seems to benefit the professional development of both groups. Exploring and discussing the underlying reasoning leading to management differences may be a productive format for primary care doctors and psychiatric specialists to teach and learn together. It may also promote collaboration in caring for the depressed elderly. Copyright © 2003 John Wiley & Sons, Ltd.
Behavioural disturbances in dementia patients and quality of the marital relationship
Authors: de Vugt Marjolein E. , Stevens Fred , Aalten Pauline , Lousberg Richel , Jaspers Niek , Winkens Ieke , Jolles Jellemer , Verhey Frans R. J. 
Published: February 2003

AbstractObjectivesTo investigate the relationship between behavioural problems in patients with dementia and changes in the marital relationship.MethodsFifty‐three spouse caregivers of patients with dementia participated in the study. Questionnaires and interviews were used to examine caregiver perception of changes in the quality of their relationship. Behavioural disturbances in the patient were measured with the NeuroPsychiatric Inventory (NPI).ResultsCaregivers experienced a deterioration of their relationship, yet at the same time most felt closer to their spouse now than in the past. Regression analysis revealed that patient behavioural problems were, independent of patient cognitive status or functional impairment, associated with deterioration in the quality of the relationship between patient and caregiver. Patient apathy rather than depressive mood was associated with this deterioration. Apathy diminished the amount and reciprocity of interactions between partners.ConclusionsThese results show that passive behaviour rather than excessive behaviour has most impact on the deterioration of the marital relationship. Intervention programmes should target relationship problems when problem behaviour, especially apathy, is present in patients with dementia. Copyright © 2003 John Wiley & Sons, Ltd.
Memory for new information as a cognitive marker of liability to Alzheimer's disease in a high risk group: a research note
Authors: Rice Frances , Abraham Richard , Rudrasingham Varuni , Owen Michael J. , Williams Julie 
Published: February 2003

AbstractBackgroundThe development of Alzheimer's disease (AD) is often insidious and there is evidence that pre‐morbid neuropsychological deficits exist.ObjectivesTo examine aspects of neuropsychological performance as cognitive markers in a group at high risk of developing AD.MethodsMemory for novel information and verbal fluency were examined in 33 unaffected biological siblings of patients who fulfilled criteria for probable AD, and 22 controls who reported no family history of dementia.ResultsComparisons between siblings and controls revealed significant differences on overall memory performance. This was also the case when siblings were grouped according to whether or not they possessed the apoE ε4 allele. There were no significant differences between siblings and controls on verbal fluency measures.ConclusionsDetailed measures of memory performance may be clinically useful in groups at a high risk of developing AD. However, further longitudinal research in such high‐risk groups is needed before conclusions can be made with confidence. Copyright © 2003 John Wiley & Sons, Ltd.
Micro‐bubble emission boiling from horizontal and vertical surfaces to subcooled parallel flow water
Authors: Kumagai Satoshi , Kubo Ryo , Kawasaki Tadashi 
Published: February 2003

AbstractHeat removal of more than 10 MW/m2 in heat flux has been required in high‐heat‐generation equipment in nuclear fusion reactors. In some conditions of water subcooling and velocity, there appears an extraordinary high heat flux boiling in the transition boiling region. This boiling regime is called micro‐bubble emission boiling (MEB) because many micro‐bubbles are spouted from the heat transfer surface accompanying a huge sound. The study intent is to obtain heat transfer performance of MEB in horizontal and vertical heated surfaces to parallel flow of subcooled water, comparing with CHF of this system. Three types of MEB with different heat transfer performance and bubble behavior are observed according to the flow velocity and liquid subcooling. © 2003 Wiley Periodicals, Inc. Heat Trans Asian Res, 32(2): 130–140, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/htj.10077
TGF‐β‐induced protein βig‐h3 is upregulated by high glucose in vascular smooth muscle cells
Authors: Ha Sung‐Woo , Bae Jong‐Sup , Yeo Hye‐Jin , Lee Suk‐Hee , Choi Je‐Yong , Sohn Yoon‐Kyung , Kim Jung‐Guk , Kim In‐San , Kim Bo‐Wan 
Published: February 2003

AbstractTGF‐β‐induced gene‐h3 (βig‐h3) is an adhesive molecule that interacts with integrins. Because TGF‐β plays an important role in diabetic complications and βig‐h3 serves as a cell substrate, we hypothesized that diabetic conditions might increase βig‐h3 synthesis in vascular smooth muscle cells (VSMCs), which may subsequently contribute to the pathogenesis of diabetic angiopathy. The concentrations of βig‐h3 and TGF‐β were measured in conditioned media using an enzyme‐linked immunosorbent assay. An immunohistochemical study showed that βig‐h3 was expressed in the VSMCs and the matrix of rat aortas. TGF‐β stimulated βig‐h3 production, and high glucose induced βig‐h3 as well as TGF‐β production in the VSMCs. The high glucose‐induced βig‐h3 expression was almost entirely blocked by an anti‐TGF‐β antibody. βig‐h3 protein mediated the adhesion, spreading, migration, and proliferation of rat VSMCs. These results suggest that the high glucose‐induced βig‐h3 in VSMCs regulates VSMC functions and may play an important role in diabetic angiopathy. © 2002 Wiley‐Liss, Inc.
Characterization of the neuropilin‐1 promoter; gene expression is mediated by the transcription factor Sp1
Authors: Rossignol Mireille , Pouysségur Jacques , Klagsbrun Michael 
Published: February 2003

AbstractNeuropilin‐1 (NRP1) is a receptor for the vascular endothelial growth factor (VEGF) family of angiogenesis factors and for the semaphorin family of secreted neuronal guidance polypeptides. Very little is known, however, about how NRP1 gene expression is regulated. In this study, it was demonstrated that the tumor promoter, TPA (12‐O‐tetradecanoylphorbol‐13‐acetate) significantly up‐regulated NRP1 mRNA levels by increasing its gene transcription rate in a manner dependent on de novo protein synthesis. To determine which elements regulate functional NRP1 expression, the promoter regions of human and mouse NRP1 genes were cloned and characterized. Promoter‐reporter gene transfection experiments using deletion and point mutations demonstrated that two Sp1 elements are major contributors to both the constitutive and TPA‐induced activity of the NRP1 promoter. Gel shift analysis showed a specific binding of the Sp1 transcription factor to those elements. Further mutational analysis revealed that an AP‐1, and a CCAAT box also contributed to NRP1 constitutive and TPA‐induced promoter activity. It was concluded that NRP1 expression is regulated by the cooperation of several regulatory elements including AP‐1, Sp1, and a CCAAT box. © 2002 Wiley‐Liss, Inc.
A unified model for the action of leptin on bone turnover
Authors: Gordeladze Jan O. , Reseland Janne E. 
Published: February 2003

AbstractLeptin has been advocated as a centrally acting factor responsible for inhibiting accumulation of bone mass. However, recent investigations unequivocally establish leptin as a local (autocrine) factor expressed by osteoblasts. Exogenously added leptin causes osteoblastic cell proliferation and differentiation, while also rendering osteoblasts more efficacious in terms of mineralization. Leptin acts as an anti‐apoptotic agent, and augments messages responsible for the remodelling of bone tissue, i.e., mRNAs for osteoprotegerin (OPG) and the interleukin IL‐6. Furthermore, leptin message is readily expressed in osteoblasts subjected to mechanical strain. In this respect, osteoblasts, which are unilaterally stretched proliferate and differentiate, a phenomenon being potentiated by exposure of the cells to differentiating humoral factors. This article discusses a unified model of dually acting leptin through the central nervous system and the mechanostat principle applied to osteoblasts. The proposed model may account for the finely tuned bone homeostasis maintained within rather narrow limits, depending on exposure to humoral factors and the prevailing mechanostat usage mode. © 2002 Wiley‐Liss, Inc.
Chondrogenesis induced by actin cytoskeleton disruption is regulated via protein kinase C‐dependent p38 mitogen‐activated protein kinase signaling
Authors: Lim Young‐Bin , Kang Shin‐Sung , An Won Gun , Lee Young‐Sup , Chun Jang‐Soo , Sonn Jong Kyung 
Published: February 2003

AbstractDisruption of the actin cytoskeleton in subconfluent mesenchymal cells induces chondrogenic differentiation via protein kinase C (PKC) α signaling. In this study, we investigated the role of p38 mitogen‐activated protein (MAP) kinase in the chondrogenic differentiation of mesenchymal cells that is induced by depolymerization of the actin cytoskeleton. Treatment of mesenchymal cells derived from chick embryonic limb buds with cytochalasin D (CD) disrupted the actin cytoskeleton with concomitant chondrogenic differentiation. The chondrogenesis was accompanied by an increase in p38 MAP kinase activity and inhibition of p38 MAP kinase with SB203580 blocked chondrogenesis. Together these results suggest an essential role for p38 MAP kinase in chondrogenesis. In addition, inhibition of p38 MAP kinase did not alter CD‐induced increased expression and activity of PKCα, whereas down‐regulation of PKC by prolonged exposure of cells to phorbol ester inhibited CD‐induced p38 MAP kinase activation. Our results therefore suggest that PKC is involved in the regulation of chondrogenesis induced by disruption of the actin cytoskeleton via a p38 MAP kinase signaling pathway. © 2002 Wiley‐Liss, Inc.
Role of catenins in the development of gap junctions in rat cardiomyocytes
Authors: Wu Jiahn‐Chun , Tsai Ru‐Yin , Chung Tun‐Hui 
Published: February 2003

AbstractGap junctions are intercellular communicating channels responsible for the synchronized activity of cardiomyocytes. Recent studies have shown that the membrane‐associated guanylate kinase protein, zonula occludens‐1 (ZO‐1) can bind to catenins in epithelial cells and act as an adapter for the transport of the connexin isotype, Cx43 during gap junction formation. The significance of catenins in the development of gap junctions and whether complexes between catenins and ZO‐1 are formed in cardiomyocytes are not clear. In this study, immunofluorescence and confocal microscopy showed sequential redistribution of α‐catenin, β‐catenin, ZO‐1, and Cx43 to the plasma membrane when rat cardiomyocytes were cultured in low Ca2+ (<5 μM) medium, then shifted to 1.8 mM Ca2+ medium (Ca2+ switch). Diffuse cytoplasmic staining of α‐catenin, β‐catenin, ZO‐1, and Cx43 was seen in the cytoplasm when cardiomyocytes were cultured in low Ca2+ medium. Staining of α‐catenin, β‐catenin, and ZO‐1 was detected at the plasma membrane of cell–cell contact sites 10 min after Ca2+ switch, whereas Cx43 staining was first detected, colocalized with ZO‐1 at the plasma membrane, 30 min after Ca2+ switch. Distinct junctional and extensive cytoplasmic staining of α‐catenin, β‐catenin, ZO‐1, and Cx43 was seen 2 h after Ca2+ switch. Immunoprecipitation of Triton X‐100 cardiomyocyte extracts using anti‐β‐catenin antibodies showed that β‐catenin was associated with α‐catenin, ZO‐1, and Cx43 at 2 h after Ca2+ switch. Intracellular application of antisera against α‐catenin, β‐catenin, or ZO‐1 by electroporation of cardiomyocytes cultured in low Ca2+ medium inhibited the redistribution of Cx43 to the plasma membrane following Ca2+ switch. These results suggest the formation of a catenin–ZO‐1–Cx43 complex in rat cardiomyocytes and that binding of catenins to ZO‐1 is required for Cx43 transport to the plasma membrane during the assembly of gap junctions. © 2002 Wiley‐Liss, Inc.
Up‐regulation of cDK5/p35 by oxidative stress in human neuroblastoma IMR‐32 cells
Authors: Strocchi Paola , Pession Annalisa , Dozza Barbara 
Published: February 2003

AbstractCdk5, a member of the cyclin‐dependent kinase (cdk) family, is predominately active in neurons, where its activity is tightly regulated by the binding of its neuronal activators p35 and p39. Cdk5 is implicated in regulating the proper neuronal function; a deregulation of cdk5 has been found associated with Alzheimer's disease and amyotrophic lateral sclerosis. As oxidative stress products have been seen co‐localized with pathological hallmarks of neurodegenerative diseases, we studied the effect of oxidative stress on the cdk5 enzyme in human neuroblastoma IMR‐32 cells. We evaluated the effects of 4‐hydroxynonenal and Ascorbate plus FeSO4 on cdk5 activity and on the expression of cdk5 and p35 proteins. We report here that oxidative stress stimulates cdk5 activity and induces an upregulation of its regulatory and catalytic subunit expression in IMR‐32 vital cells, showing that the cdk5 enzyme is involved in the signaling pathway activated by oxidative stress. © 2002 Wiley‐Liss, Inc.
Biochemical regulation of breast cancer cell expression of S1P2 (Edg‐5) and S1P3 (Edg‐3) G protein‐coupled receptors for sphingosine 1‐phosphate
Authors: Dolezalova Hana , Shankar Geetha , Huang Mei‐Chuan , Bikle Daniel D. , Goetzl Edward J. 
Published: February 2003

AbstractG protein‐coupled receptors (GPCRs) for lysophosphatidic acid (LPA) and sphingosine 1‐phosphate (S1P) transduce signals to many functions of normal cells. Most human cancer cells upregulate S1P and LPA GPCRs, in patterns distinctive for each type of tumor. The findings that 1‐alpha, 25‐dihydroxy‐vitamin D3 (VD3) and all‐trans retinoic acid (RA) differentially alter expression of the predominant S1P3 (Edg‐3) R and S1P2 (Edg‐5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. S1P‐evoked increases in [Ca2+]i in S1P3 R‐predominant BCCs were suppressed by concentrations of VD3 and RA which decreased expression of S1P3 Rs, despite RA‐induced increases in S1P2 Rs. S1P‐elicited chemokinetic migration of S1P3 R‐predominant BCCs across a type IV collagen‐coated micropore filter also was inhibited by concentrations of VD3 and RA which decreased expression of S1P3 Rs. The RA‐induced increase in expression of S1P2 Rs did not prevent suppression by RA of S1P‐elicited chemokinesis, which appears to be mediated by S1P3 Rs, but instead exposed S1P2 R‐mediated inhibition of epidermal growth factor‐stimulated chemotaxis of BCCs. In contrast, expression of the predominant LPA2 Rs, LPA‐evoked increase in [Ca2+]i and LPA‐stimulated chemokinetic migration were suppressed concomitantly by RA but not VD3. Thus two structurally‐homologous S1P Rs of BCCs differ in coupling to [Ca2+]i signaling and have opposite effects on protein growth factor‐stimulated chemotaxis. © 2002 Wiley‐Liss, Inc.
Insulin‐like and non‐insulin‐like selenium actions in 3T3‐L1 adipocytes
Authors: Heart Emma , Sung Chin K. 
Published: February 2003

AbstractIn insulin‐sensitive 3T3‐L1 adipocytes, selenium stimulates glucose transport and antilipolysis and these actions of selenium, like insulin actions, are sensitive to wortmanin, an inhibitor of phosphatidylinositol‐3‐kinase (PI3K). Selenium stimulates PI3K activity that is sustained up to 24 h. Selenium after 5–10 min increases tyrosine phosphorylation of selective cellular proteins, but after 24 h overall tyrosine phosphorylation is increased. Tyrosine phosphorylation of insulin receptor substrate 1 is detected when enriched by immunoprecipitation with anti‐PI3K antibody. Selenium, however, does not stimulate insulin receptor tyrosine kinase activity. Selenium also increases phosphorylation of other insulin signaling proteins, including Akt and extracellular signal regulated kinases. Selenium‐stimulated glucose transport is accompanied by increases in glucose transporter‐1 content in the plasma membrane. These data are consistent with similar selenium action in glucose transport in 3T3‐L1 fibroblasts expressing mainly GLUT1. In chronic insulin‐induced insulin resistant cells, selenium unlike insulin fully stimulates glucose transport. In summary, selenium stimulates glucose transport and antilipolysis in a PI3K‐dependent manner, but independent of insulin receptor activation. Selenium exerts both insulin‐like and non‐insulin‐like actions in cells. © 2002 Wiley‐Liss, Inc.
Chromatin remodeling as a guide to transcriptional regulatory networks in mammals
Authors: Urnov Fyodor D. 
Published: February 2003

AbstractAn important challenge of genome biology is a dissection of transcriptional regulatory networks that operate inside the nucleus during ontogeny and disease (Wyrick and Young [2002] Curr. Opin. Genet. Dev. 12:130). Limitations of existing experimental tools greatly complicate such analysis in the human genome: for example, genome‐wide expression profiling of cells responding to a stimulus fails to reveal a majority of the genes involved in the functional network of responding to that stimulus [Giaver et al., 2002; Birrell et al., 2002]. This article discusses recent advances in analyzing mammalian transcriptional regulatory circuits [Nikiforov et al., 2002; Weinmann et al., 2002; Ren et al., 2000]. As evidenced by these and other data, paucity of information about the location of regulatory DNA elements in the human genome presents an obstacle to comprehensive transcription network analysis. It has been known since the late 1970s that chromatin over active regulatory DNA stretches is stably remodeled into “nuclease hypersensitive sites” [Elgin, 1988; Gross and Garrard 1988]. Massively parallel analysis of such remodeling in cell nuclei identifies regulatory DNA that is difficult to map comprehensively using other approaches, reveals genes poised for rapid activation, and offers a novel perspective on the “epigenome”—the regulatory program being executed by the genome in a given cell type. J. Cell. Biochem. 88: 684–694, 2003. © 2003 Wiley‐Liss, Inc.
Calcyclin (S100A6) regulates pulmonary fibroblast proliferation, morphology, and cytoskeletal organization in vitro
Authors: Breen Ellen C. , Tang Kechun 
Published: February 2003

AbstractCalcyclin (S100A6) is a member of the S100A family of calcium binding proteins. While the precise function of calcyclin is unknown, calcyclin expression is associated with cell proliferation and calcyclin is expressed in several types of cancer phenotypes. In the present study, the functional role of calcyclin was further elucidated in pulmonary fibroblasts. Antisense S100A6 RNA expression inhibited serum and mechanical strain‐induced fibroblast proliferation. This attenuated proliferative response was accompanied by a flattened, spread cell morphology, and disruption of tropomyosin labeled microfilaments. Changes in cytoskeletal organization did not correspond with a decrease in tropomyosin levels. These observations suggest a role for calcyclin in modulating calcium dependent signaling events that regulate progression through the cell cycle. J. Cell. Biochem. 88: 848–854, 2003. © 2003 Wiley‐Liss, Inc.