bluuebunny/crossref_metadata_2025_split huggingface dataset:
Preoperative breast magnetic resonance imaging in early breast cancer
Authors: Tendulkar Rahul D. , Chellman‐Jeffers Melanie , Rybicki Lisa A. , Rim Alice , Kotwal Ashwin , Macklis Roger , Obi Betty B. 
Published: February 2009

AbstractBACKGROUND:Accelerated partial breast irradiation (APBI) of patients with early breast cancer is being investigated on a multi‐institutional protocol National Surgical Adjuvant Breast and Bowel Project (NSABP) B‐39/RTOG 0413. Breast magnetic resonance imaging (MRI) is more sensitive than mammography (MG) and may aid in selection of patients appropriate for PBI.METHODS:Patients with newly diagnosed breast cancer or ductal carcinoma in situ (DCIS) routinely undergo contrast‐enhanced, bilateral breast MRI at the Cleveland Clinic. We retrospectively reviewed the medical records of all early‐stage breast cancer patients who had a breast MRI, MG, and surgical pathology data at our institution between June of 2005 and December of 2006. Any suspicious lesions identified on MRI were further evaluated by targeted ultrasound ± biopsy.RESULTS:A total of 260 patients met eligibility criteria for NSABP B‐39/RTOG 0413 by MG, physical exam, and surgical pathology. The median age was 57 years. DCIS was present in 63 patients, and invasive breast cancer was found in 197 patients. MRI identified suspicious lesions in 35 ipsilateral breasts (13%) and in 16 contralateral breasts (6%). Mammographically occult, synchronous ipsilateral foci were found by MRI in 11 patients (4.2%), and in the contralateral breast in 4 patients (1.5%). By univariate analysis, lobular histology (infiltrating lobular carcinoma [ILC]), pathologic T2, and American Joint Committee on Cancer stage II were significantly associated with additional ipsilateral disease. Of patients with ILC histology, 18% had ipsilateral secondary cancers or DCIS, compared with 3% in the remainder of histologic subtypes (P = .004). No patient older than 70 years had synchronous cancers or DCIS detected by MRI.CONCLUSIONS:Breast MRI identified synchronous mammographically occult foci in 5.8% of early breast cancer patients who would otherwise be candidates for APBI. Cancer 2009. © 2009 American Cancer Society.
Predictors of inactive lifestyle among adult survivors of childhood cancer
Authors: Ness Kirsten K , Leisenring Wendy M. , Huang Sujuan , Hudson Melissa M. , Gurney James G. , Whelan Kimberly , Hobbie Wendy L. , Armstrong Gregory T. , Robison Leslie L. , Oeffinger Kevin C. 
Published: February 2009

AbstractBACKGROUND:Participation in physical activity is important for childhood cancer survivors, because inactivity may compound cancer/treatment‐related late effects. However, some survivors may have difficulty participating in physical activity, and these individuals need to be identified so that risk‐based guidelines for physical activity, tailored to specific needs, can be developed and implemented. The objectives of the current study were to document physical activity patterns in the Childhood Cancer Survivor Study (CCSS) cohort, to compare the physical activity patterns with siblings in the CCSS and with a population‐based sample from the Behavioral Risk Factor Surveillance System, and to evaluate associations between diagnosis, treatment, and personal factors in terms of the risk for an inactive lifestyle.METHODS:Percentages of participation in recommended physical activity were compared among survivors, siblings, and population norms. Generalized linear models were used to evaluate the associations between cancer diagnosis and therapy, sociodemographics, and the risk for an inactive lifestyle.RESULTS:Participants included 9301 adult survivors of childhood cancer and 2886 siblings. Survivors were less likely than siblings (46% vs 52%) to meet physical activity guidelines and were more likely than siblings to report an inactive lifestyle (23% vs 14%). Medulloblastoma (35%) and osteosarcoma (27%) survivors reported the highest levels of inactive lifestyle. Treatments with cranial radiation or amputation were associated with an inactive lifestyle as were being a woman, black race, older age, lower educational attainment, underweight or obese status, smoking, and depression.CONCLUSIONS:Childhood cancer survivors were less active than a sibling comparison group or an age‐ and sex‐matched population sample. Survivors who are at risk for an inactive lifestyle should be considered high priority for developing and testing of intervention approaches. Cancer 2009. © 2009 American Cancer Society.
Clinical significance of the diagnosis of low‐grade squamous intraepithelial lesion, cannot exclude high‐grade squamous intraepithelial lesion
Authors: Alsharif Mariam , Kjeldahl Klint , Curran Colleen , Miller Shelby , Gulbahce H. Evin , Pambuccian Stefan E. 
Published: February 2009

AbstractBACKGROUND:The diagnosis of low‐grade squamous intraepithelial lesion (LSIL), cannot exclude high‐grade squamous intraepithelial lesion (LSIL‐H) was not included in the 2001 Bethesda System. It is used in some institutions to diagnose cases that fulfill criteria for both the diagnosis of LSIL and atypical squamous cells, cannot exclude high‐grade squamous intraepithelial lesion (ASC‐H). In this study, the authors reviewed their experience with cases reported as LSIL‐H during a 4‐year interval.METHODS:Clinical information and histologic follow‐up data were retrieved for Papanicolaou (Pap) tests (PTs) that were diagnosed as LSIL‐H, LSIL, ASC‐H and high‐grade squamous intraepithelial lesion (HSIL) from January 1, 2004 to December 31, 2007.RESULTS:Of 235,645 PTs (97% SurePath) that were processed during the study period, the laboratory diagnosed 0.52% as ASC‐H, 2% as LSIL, 0.30% as LSIL‐H, and 0.39% as HSIL. Biopsy follow‐up was available for 47%, 49%, 56.7% and 74% of these cases, respectively. Cervical intraepithelial neoplasia 2 (CIN‐2) and CIN‐3 or more severe lesions (CIN‐3+) were identified on follow‐up cervical biopsy more often in women who had diagnoses of LSIL‐H and ASC‐H (33.14% and 26.33%, respectively) than in women who had a diagnosis of LSIL (16.11%).CONCLUSIONS:The similarity of histologic follow‐up results between LSIL‐H and ASC‐H suggested that the management of women who have a diagnosis of LSIL‐H should be similar to the management of women who have a diagnosis of ASC‐H. Cancer (Cancer Cytopathol) 2009. © 2009 American Cancer Society.
Schallschutz – Neue Entwicklungen im Ziegelbau1 – Optimierte Ausführungen im Detail
Authors: Meier Andreas , Kuhlemann Clemens 
Published: February 2009

AbstractSchallschutz im Wohnungsbau ist immer wieder ein wichtiges Thema. Leider auch dann, wenn es zu Beschwerden kommt. Ist da der hellhörige Bewohner schuld oder doch das Bauwerk? Als Architekt, Bauträger oder Investor muss man in dieser Situation sicher sein, dass die gewählte Bauweise den geschuldeten Anforderungen des Schallschutzes standhält. Vor diesem Hintergrund werden im vorliegenden Beitrag die aktuellen Entwicklungen im Ziegelbau in Bezug auf den Schallschutz beleuchtet (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Berechnung des sommerlichen Wärmeschutzes
Authors: Schwieger Hartmut 
Published: February 2009

AbstractDie heutige Architektur (auch im Wohnungsbau) mit großen Glasanteilen führt im Winter zu den erwünschten Wärmegewinnen, kann aber zu Problemen im Sommer führen. Die Planung eines wirksamen Hitzeschutzes (sommerlicher Wärmeschutz) ist daher wichtig, damit auch während sommerlicher Hitzeperioden sichergestellt ist, dass in Gebäuden behagliche Raumtemperaturen herrschen. Neben vorhandenen Sonnenschutzeinrichtungen wird das sommerliche Temperaturverhalten eines Gebäudes wesentlich von seiner Bauart beeinflusst. Dabei wirken sich schwere, Wärme speichernde Bauteile positiv aus (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Neue Leitlinien für den Wohnungsbau
Authors: Eichener Volker 
Published: February 2009

AbstractWenn es in der politischen und öffentlichen Diskussion zurzeit ein Thema gibt, dem sämtliche anderen Fragen untergeordnet werden, dann ist es der Klimawandel. Von Regierungen bestellte und bezahlte Klimaforscher malen die globale Apokalypse an die Wand: Die Erde soll sich in Zukunft erwärmen, und als Hauptursache für äußerst komplexe klimatische Prozesse ist der menschenverursachte CO2‐Ausstoß identifiziert (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Die für 2009 geplante Verschärfung der EnEV ist nicht wirtschaftlich verträglich
Authors: Eichener Volker 
Published: February 2009

AbstractUm die äußerst ehrgeizigen CO2‐Minderungsziele erfüllen zu können, zu denen sich die Bundesregierung in verschiedenen internationalen Abkommen selbst verpflichtet hat, ist es unumgänglich, große Teil e des Bestands an Wohngebäuden energetisch zu sanieren. Die Bundesregierung setzt dabei in erster Linie auf Zwangsmaßnahmen, wenn die ohnehin hohen Anforderungen der Energieeinsparverordnung (EnEV) in mehreren Schritten – zunächst 2009, dann 2012, und weitere Schritte sind bereits geplant – weiter verschärft werden sollen (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Erst Weiß, dann Schwarz und vielleicht wieder Weiß – Die Gegensätze in der Wohnungsbaupolitik
Authors: Rast Ronald 
Published: February 2009

AbstractDie Zeit nach der deutschen Wiedervereinigung war ohne Zweifel eine historisch einmalige Phase. Um auch aus Ostdeutschland wieder blühende Landschaften zu machen, stellte die Politik alle Rahmenbedingungen pro Bau, insbesondere pro Wohnungsbau, ein (© 2009 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Experience‐dependent regulation of TrkB isoforms in rodent visual cortex
Authors: Bracken Bethany K. , Turrigiano Gina G. 
Published: February 2009

AbstractWithin primary visual cortex (V1), brain‐derived neurotrophic factor (BDNF) signaling through its high‐affinity receptor TrkB is important for normal development and experience‐dependent plasticity. TrkB is expressed in several alternatively spliced isoforms, including full‐length TrkB (TrkB.FL), and several truncated isoforms (TrkB.T1, TrkB.T2, and TrkB.T4) that lack the intracellular tyrosine kinase domain. These isoforms are important components of BDNF signaling, yet little is known about the developmental or experience‐dependent regulation of their expression. Using immunohistochemistry, we found TrkB.FL and TrkB.T1 expressed in interneurons and pyramidal neurons within V1, but not in cortical astrocytes. We used real‐time PCR to quantify the changes in mRNA expression of BDNF, the four TrkB isoforms, and the low‐affinity receptor P75NTR during normal development, and in response to visual deprivation at two different ages. BDNF expression increased between postnatal days 10 (P10) and P30, and was rapidly down‐regulated by 3 days of visual deprivation during both the pre‐critical period (P14‐P17) and the critical period (P18‐P21). Over the same developmental period, expression of each TrkB isoform was regulated independently; TrkB.T1 increased, TrkB.FL and TrkB.T2 decreased, and TrkB.T4 showed transient changes. Neither brief visual deprivation nor prolonged dark‐rearing induced changes in either TrkB.FL or TrkB.T1 expression. However, TrkB.T4 expression was reduced by brief visual deprivation, whereas TrkB.T4, TrkB.T2 and P75NTR were up‐regulated by prolonged dark‐rearing into the critical period. Our data indicate that TrkB isoform expression can be selectively regulated by visual experience, and may contribute to experience‐dependent cortical plasticity. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009
Increased apoptosis during neonatal brain development underlies the adult behavioral deficits seen in mice lacking a functional paternally expressed gene 3 (Peg3)
Authors: Broad Kevin D. , Curley James P. , Keverne Eric B. 
Published: February 2009

AbstractInactivation of the maternally imprinted, paternally expressed gene 3 (Peg3) induces deficits in olfactory function, sexual and maternal behaviors, oxytocin neuron number, metabolic homeostasis and growth. Peg3 is expressed in a number of developing hypothalamic and basal forebrain structures and is a component of the P53 apoptosis pathway. Peg3 inactivation in neuronal cell culture lines inhibits P53 mediated apoptosis, which is important in the early postnatal development and sexual differentiation of the brain. In this study, we investigated the effect of inactivating the Peg3 gene on the incidence of caspase 3 positive cells (a marker of apoptosis) in 4‐ and 6‐day postpartum mouse brain. Inactivating the Peg3 gene resulted in an increase in the incidence of total forebrain caspase 3 positive cells at 4 and 6 days postpartum. Increases in specific neuroanatomical regions including the bed nucleus of the stria terminalis, nucleus accumbens, caudate putamen, medial pre‐optic area, arcuate nucleus, medial amygdala, anterior cortical and posteriodorsal amygdaloid nuclei, were also observed. In wild‐type mice, sex differences in the incidence of caspase 3 positive cells in the medial amygdala, bed nucleus of the stria terminalis, nucleus accumbens, arcuate nucleus and the M2 motor cortex, were also observed. This neural sex difference was ameliorated in the Peg‐3 mutant. These findings suggest that the neuronal and behavioral deficits seen in mice lacking a functional Peg3 gene are mediated by increases in the incidence of early neonatal apoptosis in neuroanatomical regions important for reproductive behavior, olfactory and pheromonal processing, thermoregulation and reward. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009
Formation of complex AChR aggregates in vitro requires α‐dystrobrevin
Authors: Pawlikowski Bradley T. , Maimone Margaret M. 
Published: February 2009

AbstractEfficient function at the neuromuscular junction requires high‐density aggregates of acetylcholine receptors (AChRs) to be precisely aligned with the motor nerve terminal. A collaborative effort between the motor neuron and muscle intrinsic factors drives the formation and maintenance of these AChR aggregates. α‐Dystrobrevin (αDB), a cytoplasmic protein found at the postsynaptic membrane, has been implicated in the regulation of AChR aggregate density and patterning. To investigate the contribution of αDB to the muscle intrinsic program regulating AChR aggregate development, we analyzed the formation of complex, pretzel‐like AChR aggregates on primary muscle cell cultures derived from αDB knockout (αDB‐KO) mice in the absence of nerve or agrin. In myotubes lacking αDB, complex AChR aggregates failed to form, whereas aggregates formed readily in wildtype myotubes. Five major isoforms of αDB are expressed in skeletal muscle: αDB1, αDB1(−), αDB2, αDB2(−), and αDB3. Expression of αDB1 or αDB1(−) in αDB‐KO myotubes restored formation of complex AChR aggregates similar to those in wildtype myotubes. In contrast, individual expression of αDB2, αDB2(−), αDB3, or an αDB1 phosphorylation mutant resulted in the formation of few, if any, complex AChR aggregates. Collectively, these data suggest that αDB is a significant component of the muscle intrinsic program that mediates the formation of complex AChR aggregates and that αDB's tyrosine phosphorylation sites are of particular functional importance to this program. Although the muscle intrinsic program appears to influence synaptogenesis, the formation of complex mature AChR aggregates in αDB‐KO mice (with the motor neuron present) suggests the motor neuron, not the muscle intrinsic program, is the major stimulus driving the maturation of AChRs from plaque to pretzel in vivo. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2009
Myosin‐II negatively regulates minor process extension and the temporal development of neuronal polarity
Authors: Kollins K.M. , Hu J. , Bridgman P.C. , Huang Y.Q. , Gallo G. 
Published: February 2009

AbstractThe earliest stage in the development of neuronal polarity is characterized by extension of undifferentiated “minor processes” (MPs), which subsequently differentiate into the axon and dendrites. We investigated the role of the myosin II motor protein in MP extension using forebrain and hippocampal neuron cultures. Chronic treatment of neurons with the myosin II ATPase inhibitor blebbistatin increased MP length, which was also seen in myosin IIB knockouts. Through live‐cell imaging, we demonstrate that myosin II inhibition triggers rapid minor process extension to a maximum length range. Myosin II activity is determined by phosphorylation of its regulatory light chains (rMLC) and mediated by myosin light chain kinase (MLCK) or RhoA‐kinase (ROCK). Pharmacological inhibition of MLCK or ROCK increased MP length moderately, with combined inhibition of these kinases resulting in an additive increase in MP length similar to the effect of direct inhibition of myosin II. Selective inhibition of RhoA signaling upstream of ROCK, with cell‐permeable C3 transferase, increased both the length and number of MPs. To determine whether myosin II affected development of neuronal polarity, MP differentiation was examined in cultures treated with direct or indirect myosin II inhibitors. Significantly, inhibition of myosin II, MLCK, or ROCK accelerated the development of neuronal polarity. Increased myosin II activity, through constitutively active MLCK or RhoA, decreased both the length and number of MPs and, consequently, delayed or abolished the development of neuronal polarity. Together, these data indicate that myosin II negatively regulates MP extension, and the developmental time course for axonogenesis. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009
Age‐dependent differential expression of genes involved in steroid signalling pathway in the brain of protandrous black porgy, Acanthopagrus schlegeli
Authors: Tomy Sherly , Wu Guan‐Chung , Huang Horng‐Ru , Chang Ching‐Fong 
Published: February 2009

AbstractThe mechanisms underlying brain sex differentiation in animals are poorly understood. In the present study, using black porgy, Acanthopagrus schlegeli, as primary experimental model, we investigated the temporal expression patterns of receptors for androgen (ar) and estrogen (esr1 and esr2a) in the brain during posthatching ages and analyzed them against the timing of gonadal germ cell development. We hypothesized that endogenous estrogens naturally masculinize the brain of black porgy. The expression of sex steroid receptors was studied in relation to a wider suite of other related genes (nr5a2, nr0b1, star, and cyp19a1b) to provide some insight into the monomale sex differentiation pattern observed in this species. Our results revealed a highly significant increase in esr1 together with the increase in esr2a at 120 dph (days posthatching), suggesting a significant role for esr in sex differentiation in this species. Temporal expression patterns of nr5a2, nr0b1, star, sex steroid receptors, and cyp19a1b in the brain provided evidence for their physiological roles in the monomale sex differentiation in this species. The expression of nr5a2, star, ar, esr1, esr2a, and cyp19a1b increased at 120 dph, a period when brain sex differentiation probably occurs in this species. The study also suggests that neurosteroidogenesis in black porgy may be regulated by both nr5a2‐dependent and nr5a2‐independent mechanisms. The results demonstrated striking differences in the abundance of the gene transcripts in discrete brain region throughout ontogeny. In addition, the sex steroid hormone levels and aromatase activity in brain at different developmental states and the changes in the gene expression patterns in response to aromatase inhibitor treatment are also discussed. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009
MOG35–55 i.v suppresses experimental autoimmune encephalomyelitis partially through modulation of Th17 and JAK/STAT pathways
Authors: Jiang Zhilong , Li Hongmei , Fitzgerald Denise C. , Zhang Guang‐Xian , Rostami Abdolmohamad 
Published: February 2009

AbstractIntravenous (i.v.) administration of encephalitogenic peptide can effectively prevent experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis; however, the underlying cellular and molecular mechanisms are not fully understood. In this study, we induced i.v. tolerance to EAE by administration of MOG35–55 peptide and determined the effect of this approach on intracellular signaling pathways of the IL‐23/IL‐17 system, which is essential for the pathogenesis of MS/EAE. In tolerized mice, phosphorylation of JAK/STAT‐1, ‐4, ERK1/2 and NF‐κBp65 were significantly reduced in splenocytes and the central nervous system. MOG i.v. treatment led to significantly lower production of IL‐17, and administration of exogenous IL‐17 slightly broke immune tolerance, which was associated with reduced activation of STAT4 and NF‐κB. Suppressed phosphorylation of these pathway molecules was primarily evident in CD11b+ and small numbers of CD4+, CD8+ and CD11c+ cells. More importantly, adoptive transfer of CD11b+ splenocytes of tolerized mice effectively delayed onset and reduced clinical severity of actively induced EAE. This study correlates MOG i.v. tolerance with modulation of Jak/STAT signaling pathways and investigates novel therapeutic avenues for the treatment of EAE/MS.
Tumor‐mediated down‐regulation of MHC class II in DC development is attributable to the epigenetic control of the CIITA type I promoter
Authors: Choi Young‐Eun , Yu Ha‐Nul , Yoon Cheol‐Hee , Bae Yong‐Soo 
Published: February 2009

AbstractIn patients with cancer, DC express significantly lower amounts of MHC class II compared with those of normal individuals. However, the underlying mechanisms for this have not yet been fully defined. In the present study, we found that IL‐10 plays a major role in the tumor‐conditioned medium (TCM)‐mediated decrease of MHC class II expression on BM‐derived DC. IL‐10 inhibited the expression of type I CIITA during DC differentiation. GM‐CSF‐mediated histone (H3 and H4) acetylation at the type I promoter (pI) locus of the CIITA gene was markedly increased during DC differentiation and this increase was blocked by IL‐10. We also found that STAT5 bound to the CIITA pI locus during DC differentiation, and the binding was markedly attenuated by TCM or IL‐10. Altogether, these findings suggest that (i) the down‐regulation of MHC class II in tumor microenvironments is most likely attributable to IL‐10 in the TCM and (ii) IL‐10‐mediated MHC class II down‐regulation results from the inhibition of type I CIITA expression. This inhibition is most likely due to blocking of the STAT5‐associated epigenetic modifications of the CIITA pI locus during the entire period of DC differentiation from BM cells, as opposed to a simple inhibition of MHC class II expression at the DC stage.
Regulation of macrophage activation and septic shock susceptibility via p21(WAF1/CIP1)
Authors: Trakala Marianna , Arias Cristina F. , García María I. , Moreno‐Ortiz M. Carmen , Tsilingiri Katerina , Fernández Pablo J. , Mellado Mario , Díaz‐Meco María T. , Moscat Jorge , Serrano Manuel , Martínez‐A Carlos , Balomenos Dimitrios 
Published: February 2009

Abstractp21 is a cell‐cycle inhibitor that is also known to suppress autoimmunity. Here, we provide evidence of a novel role for p21 as an inhibitor of macrophage activation. LPS stimulation of p21‐deficient peritoneal macrophages induced increased activation compared with controls, with elevated production of proinflammatory mediators such as TNF‐α and IL‐1β. The enhanced activity of LPS‐stimulated p21‐deficient macrophages correlated with increased activity of the transcription factor NF‐κB. LPS stimulation of p21‐deficient macrophages led to increased IκBα kinase activity, and increased IκBα phosphorylation and degradation, resulting in elevated NF‐κB activity. The effect of p21 in macrophage activation was independent of its cell‐cycle inhibitory role. p21−/− mice showed greater sensitivity to LPS‐induced septic shock than did WT mice, indicating that p21 contributes to maintenance of a balanced response to inflammatory stimuli and suggesting biological significance for the role of p21 in macrophage activation. Our findings project a role for p21 in the control of NF‐κB‐associated inflammation, and suggest that therapeutic modulation of p21 expression could be beneficial in inflammation‐associated diseases.