bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patient centred teaching: a future role for the psychiatric nurse teacher?
Authors: Reynolds William 
Published: December 2006

It was suggested by Reynolds & Cormack (1982), that psychiatric nursing skills could be taught more realistically, if there was a greater concentration of teaching resources in the clinical areas, in order to make fuller use of the learning opportunities to which learners are exposed. They expressed the view that this was essential in order to clarify the psychiatric nurse's role and to shift the emphasis of psychiatric nurse education away from psychomotor skills to inter personal skills.This paper describes a trial teaching programme which was designed to gain access to, and utilize, ‘live’ patient centred teaching opportunities in the clinical area more effectively. It involved the writer and four nurse learners, who were allocated to a long‐term ward during a 12‐week psychiatric nursing module within a comprehensive modular system of nurse training. The main teaching method involved structured interaction with the patients.
Macrophages are comprised of resident brain microglia not infiltrating peripheral monocytes acutely after neonatal stroke
Authors: Denker Sheryl P. , Ji Shaoquan , Dingman Andra , Lee Sarah Y. , Derugin Nikita , Wendland Michael F. , Vexler Zinaida S. 
Published: December 2006

AbstractMacrophages can be both beneficial and detrimental after CNS injury. We previously showed rapid accumulation of macrophages in injured immature brain acutely after ischemia‐reperfusion. To determine whether these macrophages are microglia or invading monocytes, we subjected post‐natal day 7 (P7) rats to transient 3 h middle cerebral artery (MCA) occlusion and used flow cytometry at 24 and 48 h post‐reperfusion to distinguish invading monocytes (CD45high/CD11b+) from microglia (CD45low/medium/CD11b+). Inflammatory cytokines and chemokines were determined in plasma, injured and contralateral tissue 1–24 h post‐reperfusion using ELISA‐based cytokine multiplex assays. At 24 h, the number of CD45+/CD11b+ cells increased 3‐fold in injured compared to uninjured brain tissue and CD45 expression shifted from low to medium with less than 10% of the population expressing CD45high. MCA occlusion induced rapid and transient asynchronous increases in the pro‐inflammatory cytokine IL‐β and chemokines cytokine‐induced neutrophil chemoattractant protein 1 (CINC‐1) and monocyte‐chemoattractant protein 1 (MCP‐1), first in systemic circulation and then in injured brain. Double immunofluorescence with cell‐type specific markers showed that multiple cell types in the injured brain produce MCP‐1. Our findings show that despite profound increases in MCP‐1 in injured regions, monocyte infiltration is low and the majority of macrophages in acutely injured regions are microglia.
Rapid modulation of long‐term depression and spinogenesis via synaptic estrogen receptors in hippocampal principal neurons
Authors: Mukai Hideo , Tsurugizawa Tomokazu , Murakami Gen , Kominami Shiro , Ishii Hirotaka , Ogiue‐Ikeda Mari , Takata Norio , Tanabe Nobuaki , Furukawa Aizo , Hojo Yasushi , Ooishi Yuuki , Morrison John H. , Janssen William G. M. , Rose John A. , Chambon Pierre , Kato Shigeaki , Izumi Shunsuke , Yamazaki Takeshi , Kimoto Tetsuya , Kawato Suguru 
Published: December 2006

AbstractRapid modulation of hippocampal synaptic plasticity by estrogen has long been a hot topic, but analysis of molecular mechanisms via synaptic estrogen receptors has been seriously difficult. Here, two types of independent synaptic plasticity, long‐term depression (LTD) and spinogenesis, were investigated, in response to 17β‐estradiol and agonists of estrogen receptors using hippocampal slices from adult male rats. Multi‐electrode investigations demonstrated that estradiol rapidly enhanced LTD not only in CA1 but also in CA3 and dentate gyrus. Dendritic spine morphology analysis demonstrated that the density of thin type spines was selectively increased in CA1 pyramidal neurons within 2 h after application of 1 nm estradiol. This enhancement of spinogenesis was completely suppressed by mitogen‐activated protein (MAP) kinase inhibitor. Only the estrogen receptor (ER) alpha agonist, (propyl‐pyrazole‐trinyl)tris‐phenol (PPT), induced the same enhancing effect as estradiol on both LTD and spinogenesis in the CA1. The ERbeta agonist, (4‐hydroxyphenyl)‐propionitrile (DPN), suppressed LTD and did not affect spinogenesis. Because the mode of synaptic modulations by estradiol was mostly the same as that by the ERalpha agonist, a search was made for synaptic ERalpha using purified RC‐19 antibody qualified using ERalpha knockout (KO) mice. Localization of ERalpha in spines of principal glutamatergic neurons was demonstrated using immunogold electron microscopy and immunohistochemistry. ERalpha was also located in nuclei, cytoplasm and presynapses.
Hydrogen sulfide attenuates lipopolysaccharide‐induced inflammation by inhibition of p38 mitogen‐activated protein kinase in microglia
Authors: Hu Li‐Fang , Wong Peter T.‐H. , Moore Philip K. , Bian Jin‐Song 
Published: December 2006

AbstractThe present study attempts to investigate the effect of H2S on lipopolysaccharide (LPS)‐induced inflammation in both primary cultured microglia and immortalized murine BV‐2 microglial cells. We found that exogenous application of sodium hydrosulfide (NaHS) (a H2S donor, 10–300 μmol/L) attenuated LPS‐stimulated nitric oxide (NO) in a concentration‐dependent manner. Stimulating endogenous H2S production decreased LPS‐stimulated NO production, whereas lowering endogenous H2S level increased basal NO production. Western blot analysis showed that both exogenous and endogenous H2S significantly attenuated the stimulatory effect of LPS on inducible nitric oxide synthase expression, which is mimicked by SB 203580, a specific p38 mitogen‐activated protein kinase (MAPK) inhibitor. Exogenously applied NaHS significantly attenuated LPS‐induced p38 MAPK phosphorylation in BV‐2 microglial cells. Moreover, both NaHS (300 μmol/L) and SB 203580 (1 μmol/L) significantly attenuated LPS‐induced tumor necrosis factor‐α secretion, another inflammatory indicator. In addition, NaHS (10–300 μmol/L) dose‐dependently decreased LPS‐stimulated NO production in primary cultured astrocytes, suggesting that the anti‐neuroinflammatory effect of H2S is not specific to microglial cells alone. Taken together, H2S produced an anti‐inflammatory effect in LPS‐stimulated microglia and astrocytes, which may be due to inhibition of inducible nitric oxide synthase and p38 MAPK signaling pathways. These findings may have important implications in the treatment of neuroinflammation‐related diseases.
Seventy microsatellite markers from Persea americana Miller (avocado) expressed sequence tags
Authors: BORRONE JAMES W. , SCHNELL RAYMOND J. , VIOLI HELEN A. , PLOETZ RANDY C. 
Published: December 2006

AbstractExpressed sequence tags for Persea americana Mill. were investigated to expand upon the number of informative microsatellite markers available for avocado. Seventy informative loci were discovered using 24 P. americana var. americana Mill. accessions. The number of alleles detected ranged from two to 17 and averaged 7.1 alleles per locus. These primers successfully amplified products in different varieties of P. americana, hybrids and a related species, Persea schiedeana. These primers will be useful for characterizing germplasm, determining genetic relationships of cultivated accessions, and for marker‐assisted development of root rot‐tolerant P. americana var. americana rootstock material.
Transfer of the experimental methodology described in the FDA guidance for corticosteroid bioequivalence testing to pharmacodynamic effects caused by nicotinates
Authors: Remane Yvonne , Leopold Claudia S 
Published: December 2006

SummaryBackground  The measurement of the pharmacodynamic response allows the noninvasive quantification of cutaneous drug penetration.Aims  The objective of this study was to investigate whether the experimental methods described in the US Food and Drug Administration Guidance for Industry “Topical Dermatologic Corticosteroids: In vivo Bioequivalence” may be transferred to other response parameters such as skin redness and surface temperature.Methods  Drug penetration experiments with methyl nicotinate in two different lipophilic vehicles were performed according to the FDA guidance for corticosteroid bioequivalence testing measuring the cutaneous erythema and skin temperature response.Results  The guidance methodology was transferred to the response parameters redness and temperature. Bioequivalence testing was feasible with these response parameters.Conclusions  An open one‐compartment model could only be confirmed for skin redness data by a compartmental analysis of response vs. time profiles. The obtained temperature data can neither be described by an open one‐compartment nor by a two‐compartment model. A correlation between skin color and skin surface temperature could not be found.
Established treatments of skin hypermelanoses
Authors: Nikolaou Vasiliki , Stratigos Alexander J , Katsambas Andreas D 
Published: December 2006

SummaryCutaneous hypermelanoses are frequently encountered conditions that can have severe adverse psychosocial and emotional effects on affected patients. Melasma, postinflammatory hyperpigmentation, drug‐induced pigmentation, and erythema dischromicum perstans are among the most common cutaneous disorders leading to acquired skin hyperpigmentation. The treatment of these disorders is often challenging and requires a great deal of patience from the patient and a wealth of experience and knowledge from the dermatologist. Current treatments include depigmenting agents, chemical peels, and lasers. The ideal bleaching agent has to fulfill certain pharmacologic criteria. It should have a potent bleaching effect with a rapid time of onset, carry no side effects, and lead to a permanent removal of undesired pigment. We review the established treatment approaches of cutaneous hyperpigmentation based on literature review and our personal experience.
Phorbol 12‐myristate 13‐acetate can transform monocyte‐derived dendritic cells to different cell types similar to those found in dermatofibroma
Authors: Aiba Setsuya , Tagami Hachiro 
Published: December 2006

Dermatofibroma is composed largely of interlacing fascicles of slender spindle cells set within a loose collagenous stroma and of scattered foamy histiocytes and multinucleated giant cells. There is clear evidence indicating that factor XIIIa+ dermal dendritic cells (DDCs) are the cells constituting dermatofibromas. However, it is still unknown what stimulation is responsible for trans‐forming DDCs into different cell types, producing different sub‐types of dermatofibromas. Recently, it has become possible to obtain dendritic cells (DCs), that are identical with DDCs in their phenotypic and functional characteristics, from the culture of CD 14+ peripheral blood monocytes to which IL‐4 and GM‐CSF were added. Using these monocyte‐derived DCs, we examined the ability of various cytokines, such as IL‐Iβ, IL‐3, IL‐5, IL‐6, IL‐7, IL‐8, IL‐10, TNFα, TGFβ, M‐CSF, IFNα, and IFNγ, and phorbol 12‐myristate 13‐acetate (PMA), to induce different cell types observed in DFs. Among them, only PMA could induce a variety of cell types such as histiocytic cells, fibroblastic spindle‐shaped cells, and even multinucleated giant cells of Touton or foreign body type. Phenotypically, all the induced cell types expressed CD1a, CD80, CD86, HLA‐DR, and CD68 in a magnitude similar to that of non‐treated monocyte‐derived DCs. The expression of factor XIIIa was strongest in histiocytic cells, moderate in fibroblastic cells, and weakest or negative in giant cells.These data suggest that dermatofibromas are a kind of neoplastic disease which is induced only by the effect of some tumor promoter on DDCs.
Dermal infiltrate of enlarged macrophages in patients receiving chemotherapy
Authors: Valks Ruud , Vargas Erich , Muñoz Elia , Fernández‐Herrera Jesus , Garcia‐Diéz Amaro , Fraga Javier 
Published: December 2006

A histologically distinct maculopapular eruption has heen associated with the use of recombinant forms of granulocyte and gran‐ulocytte‐inacrophage colony‐stimulating factors (GCSF and GMCSF). One of the most distinctive features was an increase in the number and the size of dermal maerophages, which was proposed as a clue to diagnosis of these cytokine‐induced dermatoses.We describe 8 patients who received chemotherapy and who developed a maculopapular eruption, of which histological examination showed an increase in the numher and the size of dermal maerophages. Three patients had also received GM‐CSF or G‐CSF, before the onset of rash, but 5 patients had not.In conclusion, an increase in the number and the size of dermal macrophages is not specific for the reaction to GM‐CSF or G‐CSF, and may also be observed in patients receiving chemotherapy.
Oral lesions in HIV‐positive dental patients – one more argument for tobacco smoking cessation
Authors: Sroussi HY , Villines D , Epstein J , Alves MCF , Alves MEAF 
Published: December 2006

Objective:  To determine the prevalence of oral lesions associated with human immunodeficiency virus (HIV) in a population of dental patients and analyze its association with psycho‐social variables and biological markers.Study design:  The dental charts of 415 dental patients consecutively treated between May and July 2005 in a dedicated HIV dental clinic were reviewed. Oral soft tissue examinations, psycho‐social and medical variables were extracted and recorded for each patient. Ethnicity, gender, HIV treatment, peripheral CD4 counts and tobacco usage were analyzed in correlation with oral lesions associated with HIV.Results:  Fifty‐five percent of all subjects had at least one oral lesion associated with HIV, with oral candidiasis, salivary gland enlargement and oral hairy leukoplakia being the most commonly observed conditions. Gender and ethnicity did not correlate with a higher prevalence in lesions. However, tobacco smoking correlated significantly with a higher prevalence of oral lesions, independent of CD4 counts.Conclusions:  These findings suggest that oral lesions remain commonly observed morbidities among HIV‐infected dental patients independent of gender and ethnicity and that tobacco usage is a major and often underestimated risk factor for those lesions.
Amiodarone Induces Angiotensinogen Gene Expression in Lung Alveolar Epithelial Cells through Activation Protein‐1
Authors: Uhal Bruce D. , Zhang Huiying , Abdul‐Hafez Amal , Shu Ruijie , Li Xiaopeng 
Published: December 2006

Abstract:  Previous work from this laboratory has shown that amiodarone induces alveolar epithelial cell apoptosis that was abrogated by antagonists of angiotensin II. In this study, amiodarone up‐regulated angiotensinogen mRNA and protein in primary cultures of rat type II pneumocytes and in the human A549 cell line. The mechanism of amiodarone‐induced angiotensinogen expression was studied in A549 cells with a human angiotensinogen promoter‐luciferase reporter (angiotensinogen/luciferase). Amiodarone (3 µg/ml) induced both angiotensinogen/luciferase and endogenous angiotensinogen mRNA; the latter was completely blocked by actinomycin‐D. Amiodarone did not affect the half‐life of endogenous angiotensinogen mRNA. Deletion analyses of angiotensinogen/luciferase identified at least two amiodarone‐responsive domains in the angiotensinogen promoter between −350 to −260 bp and −203 to −46 bp. DNA/Protein array and electrophoretic mobility shift assays showed that amiodarone increases DNA binding of both activation protein‐1 and STAT‐5 transcription factors. Site‐directed mutagenesis of three IL‐6‐responsive signal transducer activator of transcription (STAT) binding sites within the amiodarone‐response domains had no effect on amiodarone‐induced angiotensinogen/luciferase expression. In contrast, amiodarone‐induced angiotensinogen/luciferase expression was abrogated by a dominant‐negative fos construct and was stimulated over five times by c‐fos and c‐jun expressed together but not separately. Mutagenesis of the activation protein‐1 binding site at −15 to −12 bp completely eliminated the response to amiodarone. These data show that activation protein‐1 family transcription factors mediate amiodarone‐induced angiotensinogen expression in human alveolar epithelial cells and identify an activation protein‐1 site, located between the TATA (DNA sequence) box and the transcription initiation site, that is required for the response.
N,N‐Diacetyl‐l‐cystine Improves Endothelial Function in Atherosclerotic Watanabe Heritable Hyperlipidaemic Rabbits
Authors: Pettersson Knut S. , Eliasson Ulla Brandt , Abrahamsson Tommy , Wågberg Maria , Carrier Martin , Kengatharan Ken M. 
Published: December 2006

Abstract:N,N‐diacetyl‐l‐cystine (DiNAC), a novel immunomodulator, stimulates contact sensitivity/delayed type hypersensitivity reactions in mice induced by oxazolone and reduces atherosclerosis in Watanabe heritable hyperlipidaemic (WHHL) rabbits. Forty‐week‐old WHHL rabbits were given DiNAC (3 µmol/kg per day) for 8 weeks, and endothelium‐mediated dilatation was investigatedin vivousing pulse wave analysis. A significant improvement in endothelial function was found after 3 weeks of treatment, which was further improved after 8 weeks. For experiments on isolated blood vessels, 40‐week‐old rabbits were treated for 3 weeks. Treatment did not affect plasma lipid levels. At termination, aortic rings from the thoracic and abdominal aorta were contracted with phenylephrinein vitro. Concentration‐effect curves to acetylcholine and the calcium ionophore A 23187 were used to measure endothelium‐mediated vasodilatation, and nitroprusside to elicit endothelium‐independent relaxations. Abdominal aorta relaxations were generally larger than in thoracic aorta. DiNAC improved endothelium‐dependent relaxations in the abdominal but not in the thoracic aorta. This effect was independent of the degree of atherosclerosis. It is concluded that DiNAC improved endothelial function in atherosclerotic rabbit arteriesin vivoandin vitro, and may represent a new treatment modality for atherosclerosis‐related diseases.
Non‐Clinical Pharmacology and Safety Evaluation of TH9507, a Human Growth Hormone‐Releasing Factor Analogue
Authors: Ferdinandi Eckhardt S. , Brazeau Paul , High Kim , Procter Bryan , Fennell Stephen , Dubreuil Pascal 
Published: December 2006

Abstract:  TH9507, an analogue of human growth hormone‐releasing factor (hGRF(1–44)NH2) minimally modified by addition of a trans‐3‐hexenoyl moiety to Tyr1 of the amino acid sequence, was found to be resistant to dipeptidyl aminopeptidase‐IV deactivation. Compared to natural hGRF(1–44)NH2, the modification slowed the in vitro degradation of the peptide in rat, dog and human plasma and prolonged the in vivo plasma elimination kinetics of immunoreactive TH9507. Plasma growth hormone and insulin‐like growth factor‐1 (IGF‐1) markedly increased in pigs, rats and dogs after daily repeat intravenous or subcutaneous injections of TH9507 at doses up to 600 µg/kg. Subchronic toxicity studies in rats and dogs with TH9507 treatment for up to 4 months showed a significant, but not dose‐related, increase in body weight gain associated with increased biomarker response. Although TH9507 was well tolerated by both rats and dogs, a more pronounced anabolic effect and more evident (reversible) adverse effects (liver and kidney findings, anaemia, clinical chemistry changes, organ weight effects) were observed in dogs after repeat daily subcutaneous injections, which were attributed to prolonged exposure to supraphysiological levels of growth hormone and/or IGF‐1. In both rats and dogs, toxicokinetic evaluations indicated that exposure to immunoreactive TH9507 was dose related after both routes of administration. The apparent elimination t1/2 in dogs ranged from 21 to 45 min. In conclusion, TH9507 is a modified hGRF peptide having enhanced potency and duration of action. The adverse treatment‐related effects in dogs appear to be associated with sustained exposure to supraphysiological levels of growth hormone and IGF‐1 induced by prolonged TH9507 treatment.
Early Adolescents Perceptions of Health and Health Literacy*
Authors: Brown Stephen L. , Teufel James A. , Birch David A. 
Published: December 2006

ABSTRACTBackground:  Health illiteracy is a societal issue that, if addressed successfully, may help to reduce health disparities. It has been associated with increased rates of hospital admission, health care expenditures, and poor health outcomes. Because of this, much of the research in the United States has focused on adults in the health care system. This study investigated the effect of aspects of health literacy on the motivation to practice health‐enhancing behaviors among early adolescents.Methods:  Measures were generally based on 3 National Health Education Standards for grades 5‐8. Data were obtained from 1178 9‐ to 13‐year‐old students visiting 11 health education centers in 7 states. Students responded via individual electronic keypads.Results:  Multivariate logistic regression revealed that, in addition to age, difficulty understanding health information and belief that kids can do little to affect their future health, decreased the likelihood for interest in and desire to follow what they were taught about health. Further, low interest independently decreased motivation to follow what was taught. Girls were more likely to turn to school, parents, and medical personnel for health information. Older students were more likely to turn to school and to the Internet.Conclusions:  Programs and curricula should be designed to increase student interest in health issues and their self‐efficacy in controlling their own health destinies. Educators should also teach students to more effectively use nonconventional health information sources such as the Internet, parents, and medical professionals.
Cancer Progression in the Transgenic Adenocarcinoma of Mouse Prostate Mouse Is Related to Energy Balance, Body Mass, and Body Composition, but not Food Intake
Authors: Huffman Derek M. , Johnson Maria S. , Watts Amanda , Elgavish Ada , Eltoum Isam A. , Nagy Tim R. 
Published: December 2006

Abstract
Calorie restriction can inhibit or delay carcinogenesis, reportedly due to a reduction in calorie intake rather than by concurrent changes in body mass and/or composition. Our objective was to test the hypothesis that body mass and/or composition have an important effect, independent of energy intake, on the benefits or hazards associated with calorie restriction or overeating, respectively. In the first experiment, transgenic mice that spontaneously develop prostate cancer [transgenic adenocarcinoma of mouse prostate (TRAMP)] were housed at 27°C or 22°C and pair fed the same diet for 21 weeks (95% of ad libitum intake at 27°C). In the second experiment, TRAMP mice were housed at 27°C or 22°C and fed the same diet ad libitum for 21 weeks. Despite a similar calorie intake, pair-fed mice at 27°C (PF27) were heavier (28.3 ± 3.3 versus 17.6 ± 1.6 g at 21 weeks; P &lt; 0.001; mean ± SD) and had greater fat (6.4 ± 2.1 versus 1.9 ± 0.3 g; P &lt; 0.001) and lean mass (P &lt; 0.001) than pair-fed mice at 22°C. Furthermore, PF27 mice had greater levels of serum leptin (P &lt; 0.001), lower levels of adiponectin (P &lt; 0.05), and a greater frequency of prostatic adenocarcinoma (P &lt; 0.05). In contrast, ad libitum–fed mice housed at 22°C consumed ∼30% more calories than ad libitum–fed mice at 27°C, but there was no difference between groups in body composition or cancer progression. These results imply that the ability of calorie restriction to inhibit or delay cancer incidence and progression is mediated in part by changes in energy balance, body mass, and/or body composition rather than calorie intake per se, suggesting that excess calorie retention, rather than consumption, confers cancer risk. [Cancer Res 2007;67(1):417–24]