bluuebunny/crossref_metadata_2025_split huggingface dataset:
Work environments of different types of nursing subunits*
Authors: Leatt Peggy , Schneck Rodney 
Published: December 2006

Based upon organizational theory, the purpose of this research was to identify and describe similarities and differences in the work environments of nine different types of nursing subunits (intensive care, medical, surgical, psychiatric, auxiliary, rehabilitation, rural, paediatric and obstetrical) in hospitals. Six measures of nursing subunit environment were developed: these included measures of nursing subunit autonomy, and the complexity and pervasiveness of other medical and hospital groups interacting with the nursing subunit. Data were collected by questionnaire from headnurses in 157 nursing subunits located in 24 hospitals in Alberta, Canada.The results indicated that the types of nursing subunits were similar in their degree of autonomy from both physicians and administration in the larger context in which they were located but were significantly different in terms of number and heterogeneity of groups outside nurses with which they interacted and the extent to which such groups pervaded the subunits. For example, intensive care units appeared as the type of nursing subunit with the greatest need for interaction with physicians, paramedicals, hotel services and so on, whereas, psychiatric subunits appeared to be the least dependent on groups outside nursing in the hospital. These findings have implications for the management practices and educational programme for nursing.
Serotonin and epilepsy
Authors: Bagdy Gyorgy , Kecskemeti Valeria , Riba Pal , Jakus Rita 
Published: December 2006

AbstractIn recent years, there has been increasing evidence that serotonergic neurotransmission modulates a wide variety of experimentally induced seizures. Generally, agents that elevate extracellular serotonin (5‐HT) levels, such as 5‐hydroxytryptophan and serotonin reuptake blockers, inhibit both focal and generalized seizures, although exceptions have been described, too. Conversely, depletion of brain 5‐HT lowers the threshold to audiogenically, chemically and electrically evoked convulsions. Furthermore, it has been shown that several anti‐epileptic drugs increase endogenous extracellular 5‐HT concentration. 5‐HT receptors are expressed in almost all networks involved in epilepsies. Currently, the role of at least 5‐HT1A, 5‐HT2C, 5‐HT3and 5‐HT7receptor subtypes in epileptogenesis and/or propagation has been described. Mutant mice lacking 5‐HT1Aor 5‐HT2Creceptors show increased seizure activity and/or lower threshold. In general, hyperpolarization of glutamatergic neurons by 5‐HT1Areceptors and depolarization of GABAergic neurons by 5‐HT2Creceptors as well as antagonists of 5‐HT3and 5‐HT7receptors decrease the excitability in most, but not all, networks involved in epilepsies. Imaging data and analysis of resected tissue of epileptic patients, and studies in animal models all provide evidence that endogenous 5‐HT, the activity of its receptors, and pharmaceuticals with serotonin agonist and/or antagonist properties play a significant role in the pathogenesis of epilepsies.
In vivo regulation of an Aplysia glutamate transporter, ApGT1, during long‐term memory formation
Authors: Collado Maria Sol , Lyons Lisa C. , Levenson Jonathan M. , Khabour Omar , Pita‐Almenar Juan D. , Schrader Laura , Eskin Arnold 
Published: December 2006

AbstractRegulation of glutamate transporters often accompanies glutamatergic synaptic plasticity. We investigated the mechanisms responsible for the increase in glutamate uptake associated with increased glutamate release at the Aplysia sensorimotor synapse during long‐term sensitization (LTS) and long‐term facilitation. An increase in the Vmax of transport, produced by LTS training, suggested that the increased glutamate uptake was due to an increase in the number of transporters in the membrane. We cloned a high‐affinity, Na+‐dependent glutamate transporter, ApGT1, from Aplysia central nervous system that is highly enriched in pleural sensory neurons, and in pleural‐pedal synaptosome and cell/glial fractions. ApGT1, expressed in Xenopus oocytes, demonstrated a similar pharmacological profile to glutamate uptake in Aplysia synaptosome and cell/glial fractions (strong inhibition by threo‐beta‐benzyloxyaspartate and weak inhibition by dihydrokainate) suggesting that ApGT1 may be the primary glutamate transporter in pleural‐pedal ganglia. Levels of ApGT1 and glutamate uptake were increased in synaptosomes 24 h after induction of LTS by electrical stimulation or serotonin. Regulation of ApGT1 during LTS appears to occur post‐transcriptionally and results in an increased number of transporters in synaptic membranes. These results suggest that an increase in levels of ApGT1 is responsible, at least in part, for the long‐term increase in glutamate uptake associated with long‐term memory.
GAP‐43 regulates NCAM‐180‐mediated neurite outgrowth
Authors: Korshunova Irina , Novitskaya Vera , Kiryushko Darya , Pedersen Nina , Kolkova Kateryna , Kropotova Ekaterina , Mosevitsky Mark , Rayko Mikhail , Morrow John S. , Ginzburg Irith , Berezin Vladimir , Bock Elisabeth 
Published: December 2006

AbstractThe neural cell adhesion molecule (NCAM), and the growth‐associated protein (GAP‐43), play pivotal roles in neuronal development and plasticity and possess interdependent functions. However, the mechanisms underlying the functional association of GAP‐43 and NCAM have not been elucidated. In this study we show that (over)expression of GAP‐43 in PC12E2 cells and hippocampal neurons strongly potentiates neurite extension, both in the absence and in the presence of homophilic NCAM binding. This potentiation is crucially dependent on the membrane association of GAP‐43. We demonstrate that phosphorylation of GAP‐43 by protein kinase C (PKC) as well as by casein kinase II (CKII) is important for the NCAM‐induced neurite outgrowth. Moreover, our results indicate that in the presence of GAP‐43, NCAM‐induced neurite outgrowth requires functional association of NCAM‐180/spectrin/GAP‐43, whereas in the absence of GAP‐43, the NCAM‐140/non‐receptor tyrosine kinase (Fyn)‐associated signaling pathway is pivotal. Thus, expression of GAP‐43 presumably acts as a functional switch for NCAM‐180‐induced signaling. This suggests that under physiological conditions, spatial and/or temporal changes of the localization of GAP‐43 and NCAM on the cell membrane may determine the predominant signaling mechanism triggered by homophilic NCAM binding: NCAM‐180/spectrin‐mediated modulation of the actin cytoskeleton, NCAM‐140‐mediated activation of Fyn, or both.
Activation of GABAA receptors facilitates astroglial differentiation induced by ciliary neurotrophic factor in neural progenitors isolated from fetal rat brain
Authors: Yoneyama Masanori , Fukui Masaki , Nakamichi Noritaka , Kitayama Tomoya , Taniura Hideo , Yoneda Yukio 
Published: December 2006

AbstractImmunocytochemical analysis confirmed the validity of isolation procedures of neural progenitors capable of self‐replication and differentiation from discrete fetal rat brain structures. A reverse transcription‐polymerase chain reaction analysis revealed the expression of particular GABAA receptor (GABAAR), GABABR‐1 and GABACR, but not GABABR‐2, subunits in neocortical cells before commitment. Sustained exposure to the GABAAR agonist muscimol at 100 μmol/L led to significant increases in the mitochondrial activity and the total areas of neocortical neurospheres formed during the cultivation for 12 days in a manner sensitive to a GABAAR antagonist, with lactate dehydrogenase release being unchanged. Moreover, prior sustained exposure to muscimol significantly facilitated the subsequent expression of an astroglial marker protein in cells differentiated by ciliary neurotrophic factor (CNTF) toward an astroglial lineage, with a concomitant decrease in the neuronal marker protein expression, in an antagonist‐sensitive manner on Western blotting analysis. However, muscimol failed to significantly affect the expression of both marker proteins in cells differentiated in either the presence or absence of all‐trans‐retinoic acid. These results suggest that prior activation of GABAAR may preferentially facilitate the commitment by CNTF of neural progenitor cells toward an astroglial lineage after simulation of the self‐replication activity in the developing rat brain.
Calnuc binds to Alzheimer’s β‐amyloid precursor protein and affects its biogenesis
Authors: Lin Ping , Li Feng , Zhang Yun‐wu , Huang Haining , Tong Gary , Farquhar Marilyn Gist , Xu Huaxi 
Published: December 2006

AbstractCalnuc, a Golgi calcium binding protein, plays a key role in the constitution of calcium storage. Abnormal calcium homeostasis has been linked to Alzheimer’s disease (AD). Excessive production and/or accumulation of β‐amyloid (Aβ) peptides that are proteolytically derived from the β‐amyloid precursor protein (APP) have been linked to the pathogenesis of AD. APP has also been indicated to play multiple physiological functions. In this study, we demonstrate that calnuc interacts with APP through direct binding to the carboxyl‐terminal region of APP, possibly in a calcium‐sensitive manner. Immunofluorescence study revealed that the two proteins co‐localize in the Golgi in both cultured cells and mouse brains. Over‐expression of calnuc in neuroblastoma cells significantly reduces the level of endogenous APP. Conversely, down‐regulation of calnuc by siRNA increases cellular levels of APP. Additionally, we show that over‐expression of calnuc down‐regulates the APP mRNA level and inhibits APP biosynthesis, which in turn results in a parallel reduction of APP proteolytic metabolites, sAPP, CTFs and Aβ. Furthermore, we found that the level of calnuc was significantly decreased in the brain of AD patients as compared with that of age‐matched non‐AD controls. Our results suggest a novel function of calnuc in modulating the levels of APP and its proteolytic metabolites, which may further affect the patho/physiological functions of APP including AD pathogenesis.
Excessive hippocampal acetylcholine levels in acetylcholinesterase‐deficient mice are moderated by butyrylcholinesterase activity
Authors: Hartmann Joachim , Kiewert Cornelia , Duysen Ellen G. , Lockridge Oksana , Greig Nigel H. , Klein Jochen 
Published: December 2006

AbstractCentral cholinergic systems are involved in a plethora of brain functions and are severely and selectively damaged in neurodegenerative diseases such as Alzheimer’s disease and dementia with Lewy bodies. Cholinergic dysfunction is treated with inhibitors of acetylcholinesterase (AChE) while the role of butyrylcholinesterase (BChE) for brain cholinergic function is unclear. We have usedin vivomicrodialysis to investigate the regulation of hippocampal acetylcholine (ACh) levels in mice that are devoid of AChE (AChE‐/‐ mice). Extracellular ACh levels in the hippocampus were 60‐fold elevated in AChE‐/‐ mice compared with wild‐type (AChE+/+) animals. In AChE‐/‐ mice, calcium‐free conditions reduced hippocampal ACh levels by 50%, and infusion of tetrodotoxin by more than 90%, indicating continuous ACh release. Infusion of a selective AChE inhibitor (BW284c51) caused a dose‐dependent, up to 16‐fold increase of extracellular ACh levels in AChE+/+ mice but did not change ACh levels in AChE‐/‐ mice. In contrast, infusion of a selective inhibitor of BChE (bambuterol) caused up to fivefold elevation of ACh levels in AChE‐/‐ mice, but was without effect in AChE+/+ animals. These results were corroborated with two other specific inhibitors of AChE and BChE, tolserine and bis‐norcymserine, respectively. We conclude that lack of AChE causes dramatically increased levels of extracellular ACh in the brain. Importantly, in the absence of AChE, the levels of extracellular ACh in the brain are controlled by the activity of BChE. These results point to a potential usefulness of BChE inhibitors in the treatment of central cholinergic dysfunction in which brain AChE activity is typically reduced.
Paradoxical effects of hair removal systems: a review
Authors: Lolis Margarita S , Marmur Ellen S 
Published: December 2006

SummaryAlthough a variety of lasers have proven to be clinically effective for long‐term hair removal, the use of these lasers has also been associated with undesirable side effects, such as hyper‐ and hypopigmentation, crusting, erythema, and edema. One notable side effect that seems to be underreported in the literature is the growth of fine dark hair in untreated areas close to the treated ones. This contradictory hypertrichosis is known as the paradoxical effect. In this paper, we review the published reports of the paradoxical effect and offer some possible explanations for this effect. The paradoxical effect has been documented most commonly after the use of induced pulse light and alexandrite lasers. One possible explanation is the activation of dormant hair follicles by suboptimal fluences. Another mechanism may be the synchronization of hair growth cycles by direct light stimulation.
Cutaneous epithelioid schwannomas: a rare variant of a benign peripheral nerve sheath tumor
Authors: Smith Kathleen , Mezebish David , Williams John P. , Menon Padman , Rolfe Aian , Cobb Mark , Skelton Henry 
Published: December 2006

Although benign epithelioid peripheral nerve sheath tumors have been described, they are rare, and benign epithelioid schwannomas have not yet been established as a specific histologic variant.We present four cases of tumors which we believe would meet criteria to be classified as benign epithelioid schwannomas. Biopsy specimens obtained from four different patients were examined with routine and immunohistochemical staining. All the tumors were well‐circumscribed lesions that were surrounded by a capsule containing EMA‐positive cells. The cellular component was composed of epithelioid cells, in which there was a lack of mitotic activity. Immunohistochemical studies showed the tumor cells were S‐100 protein and Leu 7 positive and HMB‐45 negative. In addition, type IV collagen encircled individual cells within the tumor, indicating a continuous basal lamina. We report a group of cutaneous epithelioid schwannomas. Although the presence of such tumors is not unexpected, this diagnosis may not be initially considered because of this rare cytoiogic feature.
Utility of deeper sections and special stains for dermatopathology specimens
Authors: Maingi Chetan P. , Helm Kiaus F. 
Published: December 2006

Special (non‐hematoxylin and eosin) stains and deeper sections are routinely used in dermathopathology, although their utility has not been well established. All cases requiring special stains or deeper sections over a three‐month period were reviewed to see how often these additional studies contributed to accurate diagnosis.In our series, deeper sections provided diagnostic information to the pathologist in 37.3% [95% confidence interval (CI) 28‐46%] of the cases in which they were performed. Deeper sections are more likely to provide a more accurate diagnosis (23.6%, 95% CI 16‐32%) rather than establish a new diagnosis not seen on the original sections (13.6%, 95% CI 7‐20%). Their use is especially helpful in assessing the presence or absence of cutaneous malignancy rather than in diagnosing inflammatory skin processes. Special stains contributed to the diagnosis in 21.1% (95% CI 11‐32%) of cases. When special stains were performed to diagnose an infection they were effective in 14,7% (95% CI 6‐24%) of the cases When special stains were performed to diagnose any other pathologic processes (neoplasm, inflammation, collagen vascular disease, and amyloid) they were effective in 31.8% (95% CI 24‐44%) of the cases.
Increased Expression Ratio of Bcl‐2/Bax Is Associated with Crocin‐Mediated Apoptosis in Bovine Aortic Endothelial Cells
Authors: Xu Guanglin , Gong Zhunan , Yu Weiping , Gao Lei , He Shuying , Qian Zhiyu 
Published: December 2006

Abstract:  Crocin, extracted and purified from Gardenia jasminoids Ellis in our laboratory, has been reported to have antioxidative, hypolipidaemic and anti‐atherosclerorotic effects. However, the underlying molecular mechanisms by which crocin acts as a cytoprotective agent remain to be elucidated. In the present study, we examined the mechanisms of crocin, the digentiobiosyl ester of crocetin, on bovine aortic endothelial cell apoptosis induced by hydrogen peroxide (H2O2). The cells were obtained from the thoracic aorta of newborn calves, and apoptosis was induced by 200 µM H2O2. Before addition of H2O2, the cells were pretreated with different concentrations of crocin for 6 hr. After incubation of the cells with H2O2, a comparative reverse transcriptase–polymerase chain reaction‐based repeated amplification protocol assay was used to determine the ratio of bcl‐2/bax mRNA expression, and cells loaded with fluo‐3/AM were subjected to laser scanning confocal microscopy for detection of intracellular calcium ([Ca2+]i) levels. Treatment of the cells with H2O2 alone decreased the ratio of bcl‐2/bax expression to almost twice of those of untreated cells (from 0.33 ± 0.05 to 0.16 ± 0.02). In the presence of 1 and 10 µM crocin, the ratios were enhanced when compared with H2O2 alone respectively (from 0.16 ± 0.02 to 0.58 ± 0.04, 1.18 ± 0.13). The treatment of cells with crocin alone had little effect on the value of this ratio. In the presence or absence of extracellular Ca2+, H2O2 could induce intracellular calcium elevation not only in the elevation presence of extracellular Ca2+ (Hanks), but also without extracellular calcium present (D‐Hanks). But the extent of [Ca2+]i under conditions lacking extracellular calcium is less. Crocin concentration dependently inhibited the [Ca2+]i elevation induced by H2O2 under these two conditions. Our data suggest that crocin may exert anti‐atherosclerotic effects by increasing the expression ratio of bcl‐2/bax, as a result, inhibiting the bovine aortic endothelial cell apoptosis that plays an important role in the initiation and progression of atherosclerosis.
Not Just Pushing and Shoving: School Bullying Among African American Adolescents
Authors: Fitzpatrick Kevin M. , Dulin Akilah J. , Piko Bettina F. 
Published: December 2006

ABSTRACTBackground:  The primary purpose of this study was to examine the prevalence of bullying among a sample of African American adolescents and the risk factors associated with odds that a student engages in bullying behavior.Methods:  Using a self‐report school‐based survey, 1542 African American adolescents from a single school district (grades 5‐12) living in a midsized, Southern metropolitan region, were asked questions regarding bullying behavior and risk behaviors. A response rate of nearly 80% was obtained.Results:  Our results indicate that bullying behavior was higher among this group of African American adolescents than reported for other general student populations (8‐12%). In addition, age, family violence, negative peer relationships, and behavioral risks all contributed to increased odds of students reporting bullying behavior.Conclusions:  Our findings underscore the importance of intervention at an early age. Whether the intervention is in a formal or nonformal setting, specialists along with teachers, parents, and siblings need to begin a multipronged approach (data collection, training/education of school personnel, curriculum development, etc) to address the causes and consequences of bullying among adolescents.
Aberrant Promoter Methylation Profile and Association with Survival in Patients with Non–Small Cell Lung Cancer
Authors: Gu Jian , Berman David , Lu Charles , Wistuba Ignacio I. , Roth Jack A. , Frazier Marsha , Spitz Margaret R. , Wu Xifeng 
Published: December 2006

Abstract
Purpose: The aim of this study was to investigate the prognostic value of hypermethylation of tumor suppressor genes in patients with non-small cell lung cancer (NSCLC).
Experimental Design: We examined the methylation status of nine genes in 155 tumors from patients with NSCLC using quantitative methylation-specific PCR. We analyzed the associations between gene methylation status and overall patient survival.
Results: The methylation index, defined as the ratio between the number of methylated genes and the number of genes tested, was significantly higher in adenocarcinomas (0.38 ± 0.20) than in squamous cell carcinomas (0.30 ± 0.22; P = 0.027), in tumors from older patients (0.37 ± 0.20) than younger patients (0.30 ± 0.22; P = 0.040), and in tumors from heavier smokers (0.39 ± 0.21) than lighter smokers (0.29 ± 0.20; P = 0.042). In the Cox proportional hazards model, p16 methylation was associated with significantly poorer survival [hazard ratio, 1.95; 95% confidence interval (95% CI), 1.21-3.39]. Kaplan-Meier survival curves showed that patients with hypermethylated p16 had significantly shorter survival (median = 21.7 months) than patients without p16 hypermethylation (median = 62.5 months; P = 0.0001, log-rank test). Hypermethylation of CDH1 or TIMP3 gene was associated with significantly better survival with hazard ratios of 0.51 (95% CI, 0.29-0.90) and 0.59 (95% CI, 0.36-0.97), respectively. Joint analysis of these three genes showed a significant trend for poorer survival as the number of unfavorable events increased (P = 0.0007).
Conclusion: Hypermethylation of multiple genes exhibited significant differential effect on NSCLC patient survival. Assessment of the effect of each methylated gene on survival is needed to provide optimal prognostic value.
Identification of a Highly Immunogenic HLA-A*01-Binding T Cell Epitope of WT1
Authors: Asemissen Anne Marie , Keilholz Ulrich , Tenzer Stefan , Müller Margret , Walter Steffen , Stevanovic Stefan , Schild Hansjörg , Letsch Anne , Thiel Eckhard , Rammensee Hans-Georg , Scheibenbogen Carmen 
Published: December 2006

AbstractPurpose: The transcription factor Wilms tumor protein 1 (WT1) belongs to a new generation of tumor antigens, as it is essential for tumor cell proliferation and is highly expressed in various hematologic and solid malignancies. The aim of this study was to apply a modified reverse immunology strategy to identify immunogenic epitopes of WT1 which could be useful for immunotherapy.Experimental Design: Potential HLA-A*01 epitopes predicted by a MHC binding algorithm were screened for recognition by peripheral blood mononuclear cells (PBMC) from patients with spontaneous T cell responses using intracellular cytokine cytometry. Epitope processing was shown by proteasomal cleavage. Epitope-specific T cells were generated from CD4+CD25+ regulatory T cell–depleted PBMC.Results: One of five predicted HLA-A*01-binding candidate epitopes showed high immunogenicity as 5 of 14 patients with hematologic malignancies had WT1.317-327–reactive T cells ranging from 0.4% to 1.5% of CD3+CD8+ T cells. Proteasomal degradation assays indicated the cleavage of WT1.317-327. The depletion of regulatory T cells from PBMCs enabled the rapid expansion of WT1.317-327–specific CTL, whereas no CTL could be generated from unfractionated PBMC. WT1.317-327–specific CTL efficiently lysed an autologous WT1-expressing tumor cell line but not HLA-A*01–negative WT1-expressing tumor cells. Immunogenicity of the epitope across histologies was verified by the demonstration of spontaneous ex vivo WT1.317-327–specific T cell responses in two of six patients with HLA-A*01–positive melanoma or lung cancer.Conclusion: In this study, a modified reverse immunology strategy was employed to identify a first immunogenic HLA-A*01–restricted T cell epitope of the tumor antigen WT1, which is of considerable interest for use in vaccination trials.