bluuebunny/crossref_metadata_2025_split huggingface dataset:
How does winter pruning affect peach tree–Myzus persicae interactions?
Authors: Grechi Isabelle , Sauge Marie‐Hélène , Sauphanor Benoît , Hilgert Nadine , Senoussi Rachid , Lescourret Françoise 
Published: May 2008

AbstractWinter tree pruning is a cultural practice known to modify vegetative growth, which is likely to affect the development of pests. However, it has been poorly addressed as a cultural control method for diminishing the population levels of the green peach aphid, Myzus persicae (Sulzer) (Homoptera: Aphididae), in peach [Prunus persica (L.) Batsch (Rosaceae)] orchards. In this study, we conducted a 2‐year, on‐station experiment to evaluate how winter pruning affects peach–M. persicae interactions, by examining tree vegetative growth, aphid population dynamics, and crop yield and fruit quality. We collected data under an insect‐proof shelter on adult peach trees submitted to various levels of pruning and artificially infested with aphids. Our results showed that pruning enhanced shoot growth due to the proportion of growing shoots, which increased exponentially (10–60%), whereas the growth rate of growing shoots was not affected. The degree of infestation of peach trees increased with increasing pruning intensity. This effect was mainly due to the increase of the proportion of growing shoots, on which aphids developed better than on rosettes. In turn, the higher the aphid infestation, the higher the aphid‐induced shoot‐tip damage, leaf curling, and leaf fall that disturbed the growth of growing shoots. However, aphids did not considerably reduce fruit quality at harvest. They did not affect fresh fruit weight, and the refractometric index (indicator of sugar content) was reduced by only 3–4%. The relevance of winter pruning as a cultural method for pest control in orchards conducted under integrated fruit production guidelines is discussed.
Role of prey–host plant associations on Harmonia axyridis and Episyrphus balteatus reproduction and predatory efficiency
Authors: Alhmedi Ammar , Haubruge Eric , Francis Frédéric 
Published: May 2008

AbstractIn order to predict possible locations of Harmonia axyridis Pallas (Coleoptera: Coccinellidae) and Episyrphus balteatus DeGeer (Diptera: Syrphidae) in the field, we studied their oviposition and prey preferences in relation to several host plant–prey associations under laboratory conditions. Oviposition preference of H. axyridis and E. balteatus females was determined for three aphid (Homoptera: Aphididae)–host plant associations: Microlophium carnosum Buckton on stinging nettle [Urtica dioica L. (Urticaceae)], Acyrthosiphon pisum Harris on green pea [Pisum sativum L. (Fabaceae)], and Sitobion avenae F. on wheat [Triticum aestivum L. (Poaceae)]. Prey preference of H. axyridis and E. balteatus larvae was determined with the aphids M. carnosum, A. pisum, and S. avenae. Harmonia axyridis females showed a strong oviposition preference for the stinging nettle–M. carnosum association. The preferred association for ovipostion by E. balteatus was pea‐hosting A. pisum, on which fecundity was also highest. Feeding behaviour was less restricted in H. axyridis, in which the preferred preys were M. carnosum and S. avenae. A lower specificity of predation was observed in E. balteatus larvae with respect to A. pisum. These laboratory experiments may help us to understand the spatial distribution of H. axyridis and E. balteatus in the field.
The induction of endochondral bone formation by transforming growth factor‐β3: experimental studies in the non‐human primate Papio ursinus
Authors: Ripamonti Ugo , Nathaniel Ramoshebi L. , Teare June , Renton Louise , Ferretti Carlo 
Published: May 2008

AbstractTransforming growth factor‐β3 (TGF‐β3), a multi‐functional growth modulator of embryonic development, tissue repair and morphogenesis, immunoregulation, fibrosis, angiogenesis and carcinogenesis, is the third mammalian isoform of the TGF‐β subfamily of proteins. The pleiotropism of the signalling proteins of the TGF‐β superfamily, including the TGF‐β proteins per se, are highlighted by the apparent redundancy of soluble molecular signals initiating de novo endochondral bone induction in the primate only. In the heterotopic bioassay for bone induction in the subcutaneous site of rodents, the TGF‐β3 isoform does not initiate endochondral bone formation. Strikingly and in marked contrast to the rodent bioassay, recombinant human (h)TGF‐β3, when implanted in the rectus abdominis muscle of adult non‐human primates Papio ursinus at doses of 5, 25 and 125 μg per 100 mg of insoluble collagenous matrix as carrier, induces rapid endochondral bone formation resulting in large corticalized ossicles by day 30 and 90. In the same animals, the delivery of identical or higher doses of theTGF‐β3 protein results in minimal repair of calvarial defects on day 30 with limited bone regeneration across the pericranial aspect of the defects on day 90. Partial restoration of the bone induction cascade by the hTGF‐β3 protein is obtained by mixing the hTGF‐β3 device with minced fragments of autogenous rectus abdominis muscle thus adding responding stem cells for further bone induction by the hTGF‐β3 protein. The observed limited bone induction in hTGF‐β3/treated and untreated calvarial defects in Papio ursinus and therefore by extension to Homo sapiens, is due to the influence of Smad‐6 and Smad‐7 down‐stream antagonists of the TGF‐β signalling pathway. RT‐PCR, Western and Northern blot analyses of tissue specimens generated by the TGF‐β3 isoform demonstrate robust expression of Smad‐6 and Smad‐7 in orthotopic calvarial sites with limited expression in heterotopic rectus abdominis sites. Smad‐6 and ‐7 overexpression in hTGF‐β3/treated and untreated calvarial defects may be due to the vascular endothelial tissue of the arachnoids expressing signalling proteins modulating the expression of the inhibitory Smads in pre‐osteoblastic and osteoblastic calvarial cell lines controlling the induction of bone in the primate calvarium.
Farnesyl diphosphate synthase is involved in the resistance to zoledronic acid of osteosarcoma cells
Authors: Ory B. , Moriceau G. , Trichet V. , Blanchard F. , Berreur M. , Rédini F. , Rogers M. , Heymann D. 
Published: May 2008

AbstractWe recently demonstrated original anti‐tumor effects of zoledronic acid (Zol) on osteosarcoma cell lines independently of their p53 and Rb status. The present study investigated the potential Zol‐resistance acquired by osteosarcoma cells after prolonged treatment. After 12 weeks of culture in the presence of 1 μm Zol, the effects of high doses of Zol (10–100 μm) were compared between the untreated rat (OSRGA, ROS) and human (MG63, SAOS2) osteosarcoma cells and Zol‐pretreated cells in terms of cell proliferation, cell cycle analysis, migration assay and cytoskeleton organization. Long‐term treatment with 1 μm Zol reduced the sensitivity of osteosarcoma cells to high concentrations of Zol. Furthermore, the Zol‐resistant cells were sensitive to conventional anti‐cancer agents demonstrating that this resistance process is independent of the multidrug resistance phenotype. However, as similar experiments performed in the presence of clodronate and pamidronate evidenced that this drug resistance was restricted to the nitrogen‐containing bisphosphonates, we then hypothesized that this resistance could be associated with a differential expression of farnesyl diphos‐phate synthase (FPPS) also observed in human osteosarcoma samples. The transfection of Zol‐resistant cells with FPPS siRNA strongly increased their sensitivity to Zol. This study demonstrates for the first time the induction of metabolic resistance after prolonged Zol treatment of osteosarcoma cells confirming the therapeutic potential of Zol for the treatment of bone malignant pathologies, but points out the importance of the treatment regimen may be important in terms of duration and dose to avoid the development of drug metabolic resistance.
Type I IFN induced IL1‐Ra expression in hepatocytes is mediated by activating STAT6 through the formation of STAT2: STAT6 heterodimer
Authors: Wan Lei , Lin Cheng‐Wen , Lin Ying‐Ju , Sheu Jim J.C. , Chen Bing‐Hung , Liao Chiu‐Chu , Tsai Yuhsin , Lin Wei‐Yong , Lai Chih‐Ho , Tsai Fuu Jen 
Published: May 2008

AbstractThe biological activities of type I interferons (IFNs) are mediated by their binding to a heterodimer receptor complex (IFNAR1 and IFNAR2), resulting in the activation of the JAK (JAK1 and TYK2)‐STAT (1, 2, 3, 5 isotypes) signalling pathway. Although several studies have indicated that IFN‐α and IFN‐β can activate complexes containing STAT6, the biological role of this activation is still unknown. We found that exposure of hepatoma cells (HuH7 and Hep3B) to IFN‐α or IFN‐β led to the activation of STAT6. Activated STAT6 in turn induced the formation of STAT2: STAT6 complexes, which led to the secretion of IL‐1Ra. The activation of STAT6 by type I IFN in hepatocytes was mediated by JAK1 and Tyk2. In addition, IFN‐α or IFN‐β significantly enhanced the stimulatory effect of IL‐1β on production of IL‐1Ra. The present study suggests a novel function of IFN‐α and IFN‐β signalling in human hepatocytes. Our results provide evidence for the mechanism how IFN‐α and IFN‐β modulate inflammatory responses through activation of STAT6 and production of secreted IL‐1Ra.
S100B induces tau protein hyperphosphorylation via Dickopff‐1 up‐regulation and disrupts the Wnt pathway in human neural stem cells
Authors: Esposito Giuseppe , Scuderi Caterina , Lu Jie , Savani Claudia , De Filippis Daniele , Iuvone Teresa , Steardo Jr Luca , Sheen Volney , Steardo Luca 
Published: May 2008

AbstractPrevious studies suggest that levels of the astrocyte‐derived S100B protein, such as those occurring in brain extra‐cellular spaces consequent to persistent astroglial activation, may have a pathogenetic role in Alzheimer's disease (AD). Although S100B was reported to promote β amyloid precursor protein overexpression, no clear mechanistic relationship between S100B and formation of neurofibrillary tangles (NFTs) is established. This in vitro study has been aimed at investigating whether S100B is able to disrupt Wnt pathway and lead to tau protein hyperphosphorylation. Utilizing Western blot, electrophoretic mobility shift assay, supershift and reverse transcriptase‐polymerase chain reaction techniques, it has been demonstrated that micromolar S100B concentrations stimulate c‐Jun N‐terminal kinase (JNK) phosphorylation through the receptor for advanced glycation ending products, and subsequently activate nuclear AP‐1/cJun transcription, in cultured human neural stem cells. In addition, as revealed by Western blot, small interfering RNA and immunofluorescence analysis, S100B‐induced JNK activation increased expression of Dickopff‐1 that, in turn, promoted glycogen synthase kinase 3β phosphorylation and β‐catenin degradation, causing canonical Wnt pathway disruption and tau protein hyperphosphorylation. These findings propose a previously unrecognized link between S100B and tau hyperphosphorylation, suggesting S100B can contribute to NFT formation in AD and in all other conditions in which neuroinflammation may have a crucial role.
Thrombin bound to a fibrin clot confers angiogenic and haemostatic properties on endothelial progenitor cells
Authors: Smadja David M. , Basire Agnès , Amelot Aymeric , Conte Aurélie , Bièche Ivan , Le Bonniec Bernard F. , Aiach Martine , Gaussem Pascale 
Published: May 2008

AbstractRecent data suggest that endothelial progenitor cells (EPCs) are involved in recanalizing venous thrombi. We examined the impact of a fibrin network, and particularly of adsorbed thrombin, on EPCs derived from cord blood CD34+ cells. Fibrin networks generated in microplates by adding CaCl2 to platelet‐depleted plasma retained adsorbed thrombin at the average concentration of 4.2 nM per well. EPCs expressed high levels of endothelial cell protein C receptor and thrombomodulin, allowing the generation of activated protein C on the fibrin matrix in the presence of exogenous human protein C. The fibrin matrix induced significant EPC proliferation and, when placed in the lower chamber of a Boyden device, strongly enhanced EPC migration. These effects were partly inhibited by hirudin by 41% and 66%, respectively), which suggests that fibrin‐adsorbed thrombin interacts with EPCs via the thrombin receptor PAR‐1. Finally, spontaneous lysis of the fibrin network, studied by measuring D‐dimer release into the supernatant, was inhibited by EPCs but not by control mononuclear cells. Such an effect was associated with a 10‐fold increase in plasminogen activator inhibitor‐1 (PAI‐1) secretion by EPCs cultivated in fibrin matrix. Overall, our data show that EPCs, in addition to their angiogenic potential, have both anticoagulant and antifibrinolytic properties. Thrombin may modulate these properties and contribute to thrombus recanalization by EPCs.
Elevated levels of pro‐apoptotic p53 and its oxidative modification by the lipid peroxidation product, HNE,in brain from subjects with amnestic mild cognitive impairment and Alzheimer's disease
Authors: Cenini Giovanna , Sultana Rukhsana , Memo Maurizio , Butterfield D. Allan 
Published: May 2008

AbstractOxidative stress has been implicated in the pathogenesis of Alzheimer's disease (AD). Both AD and arguably its earlier form, mild cognitive impairment (MCI), have elevated membrane oxidative damage in brain. The tumor suppressor and transcription factor p53 plays a pivotal function in neuronal apoptosis triggered by oxidative stress. Apoptosis contributes to neuronal death in many neurological disorders, including AD. In this study, we investigated p53 expression in a specific region of the cerebral cortex, namely the inferior parietal lobule (IPL), in MCI and AD brain, to test the hypothesis that alterations of this pro‐apoptotic protein may be involved in neuronal death in the progression of AD. By immunoprecipitation assay, we also investigated whether 4‐hydroxy‐2‐transnonenal (HNE), an aldehydic product of lipid peroxidation, was bound in excess to p53 in IPL from subjects with MCI and AD compared to control. Overall, the data provide evidence that p53 is involved in the neuronal death in both MCI and AD, suggesting that the observed alterations are early events in the progression of AD. In addition, HNE may be a novel non‐protein mediator of oxidative stress‐induced neuronal apoptosis.
Unfavourable clinical implications for HLA‐G expression in acute myeloid leukaemia
Authors: Yan W.‐H. , Lin A. , Chen B.‐G. , Luo W.‐D. , Dai M.‐Z. , Chen X.‐J. , Xu H.‐H. , Li B.‐L. 
Published: May 2008

AbstractHuman leukocyte antigen‐G (HLA‐G) molecule exerts multiple immunoregulatory functions that have been suggested to contribute to the immune evasion of tumour cells. Studies on HLA‐G expression in malignant haematopoietic diseases are controversial, and the functions of HLA‐G on this context are limited. In the current study, HLA‐G expression was analysed in different types of patients: de novo acute myeloid leukaemia (AML, n = 54), B cell acute lymphoblastic leukaemia (B‐ALL, n= 13), chronic myeloid leukaemia (CML, n= 9) and myelodysplastic syndrome (MDS, n= 11). HLA‐G expression was observed in 18.5% cases of AML, 22.2% in CML and 18.2% in MDS, but not in B‐ALL patients. In AML, HLA‐G‐positive patients had a significant higher bone marrow leukaemic blast cell percentage when compared with that of HLA‐G‐negative patients (P < 0.01). Total T‐cell percentage was dramatically decreased in HLA‐G‐positive patients (P < 0.05). Cytogenetic karyotyping results showed that all HLA‐G‐positive AML patients (n= 5) were cytogenetically abnormal, which was markedly different from that of HLA‐G‐negative patients (P < 0.01). Ex vivo cytotoxicity analysis revealed that HLA‐G expression in AML leukaemic cells could directly inhibit NK cell cytolysis (P < 0.01). These findings indicated that HLA‐G expression in AML is of unfavourable clinical implications, and that HLA‐G could be a potential target for therapy.
Modeling and remodeling of human extraction sockets
Authors: Trombelli Leonardo , Farina Roberto , Marzola Andrea , Bozzi Leopoldo , Liljenberg Birgitta , Lindhe Jan 
Published: May 2008

AbstractIntroduction: The available studies on extraction wound repair in humans are affected by significant limitations and have failed to evaluate tissue alterations occurring in all compartments of the hard tissue defect.Aim: To monitor during a 6‐month period the healing of human extraction sockets and include a semi‐quantitative analysis of tissues and cell populations involved in various stages of the processes of modeling/remodeling.Material and Methods: Twenty‐seven biopsies, representative of the early (2–4 weeks, n=10), intermediate (6–8 weeks, n=6), and late phase (12–24 weeks, n=11) of healing, were collected and analysed.Results: Granulation tissue that was present in comparatively large amounts in the early healing phase of socket healing, was in the interval between the early and intermediate observation phase replaced with provisional matrix and woven bone. The density of vascular structures and macrophages slowly decreased from 2 to 4 weeks over time. The presence of osteoblasts peaked at 6–8 weeks and remained almost stable thereafter; a small number of osteoclasts were present in a few specimens at each observation interval.Conclusions: The present findings demonstrated that great variability exists in man with respect to hard tissue formation within extraction sockets. Thus, whereas a provisional connective tissue consistently forms within the first weeks of healing, the interval during which mineralized bone is laid down is much less predictable.
CD4‐negative variant of CD4+/CD56+ hematodermic neoplasm: description of three cases
Authors: Ascani Stefano , Massone Cesare , Ferrara Gerardo , Rongioletti Franco , Papini Manuela , Pileri Stefano , Cerroni Lorenzo 
Published: May 2008

Background:  CD4+/CD56+ hematodermic neoplasm (HN) (blastic natural killer (NK)‐cell lymphoma) is a rare entity characterized by dense, monomorphous infiltrates of medium‐sized cells with blastic appearance and a characteristic immunophenotype (positivity for CD4, CD56 and CD123). The combination of CD4 and CD56 positivity is thought to be so striking that it has been used to name this entity.Methods:  Three cases of HN with ambiguous phenotypic profile were included in this study. In all cases, phenotypic, molecular and in situ hybridization studies were carried out.Results:  All three cases showed an aberrant phenotype with negativity for CD4.Conclusions:  CD4‐negative or CD56‐negative cases of HN have been rarely reported in the literature and represent a diagnostic problem. Our three cases confirm that CD4 is not always expressed in these neoplasms. The term ‘CD4+/CD56+ hematodermic neoplasm’ adopted in the World Health Organization–European Organization for Research and Treatment of Cancer classification of cutaneous lymphomas may be misleading and should probably be revised in the light of all data published in the literature.
An fMRI study of face encoding and recognition in first-episode schizophrenia
Authors: Anilkumar Anantha P. P. , Kumari Veena , Mehrotra Ravi , Aasen Ingrid , Mitterschiffthaler Martina T. , Sharma Tonmoy 
Published: May 2008

Background:Schizophrenia has been associated with limited abilities to interact effectively in social situations. Face perception and ability to recognise familiar faces are critical for social interaction. Patients with chronic schizophrenia are known to show impaired face recognition. Studying first-episode (FE) patients allows the exclusion of confounding effects of chronicity, medication and institutionalisation in this deficit.Objective:To determine brain (dys)functions during a face encoding and recognition paradigm in FE schizophrenia.Methods:Thirteen antipsychotic-naïve FE schizophrenia patients and 13 age- and sex-matched healthy controls underwent functional magnetic resonance imaging during a face encoding and recognition paradigm. Behavioural responses were recorded on line.Results:Patients recognised significantly fewer of previously presented faces than the controls (p = 0.008). At the neural level, both groups activated a network of regions including the fusiform area, occipital, temporal and frontal regions. In brain activity, the two groups did not differ in any region during encoding or recognition conditions (p > 0.05, corrected or uncorrected).Conclusions:Our findings show impaired face recognition without a significant alteration of related brain activity in FE schizophrenia patients. It is possible that neural changes become more strongly evident with progression of the illness, and manifest themselves as behavioural impairments during the early course.
An uncommon zoonosis
Authors: Mairhofer Daniela , Schmidt Peter , Kitzwögerer Melitta , Müller Simone , Bruns Ute , Gebhart Walter , Trautinger Franz 
Published: May 2008

SummaryIn a patient with foreign‐body granulomas, dog hairs were identified as the causative agent by combing history, histopathology and highly sensitive detection of species‐specific canine mitochondrial DNA. Granulomas from human hair are well known in hairdressers. Animal hair granulomas have so far been only described in dog groomers, milkers, and shearers. To the best of our knowledge this patient represents the first described case of dog hair granulomas in a pet owner.
Indoor versus outdoor childhood submersion injury in a densely populated city
Authors: Hon Kam‐Lun Ellis , Leung Ting‐Fan , Chan Sze‐yan Jennette , Cheung Kam‐Lau , Ng Pak‐Cheung 
Published: May 2008

AbstractAim: To review the outcome of childhood submersion injury (SI).Methods: We reviewed discharge data of all children with SI who were hospitalized in a university teaching hospital between January 2002 and January 2008.Results: There were 15 admissions (8 males and 7 females). Outdoor SI (n = 10) were more common than indoor SI (n = 5) and 7 cases occurred in public swimming pools with life guard service. There were significant differences between the two types of SI. Indoor SI more likely occurred in the Chinese mainland. The victims were generally younger, more likely to have low Glasgow Coma Scale (GCS), asystole and intubation at the emergency department (ED). They were more likely to require intensive care, ventilatory support, neurological imaging and had worse neurological sequlae of death or hypoxic‐ischaemic encephalopathy (HIE).Conclusion: Indoor SI was associated with worse prognosis. All patients with GCS of 3 at ED and required intensive care support were either dead or incapacitated. Low GCS, pulselessness and intubation at the ED and seizures are also associated with adverse outcomes. Describing the mode of paediatric SI in a city where SI rarely occurs serves to heighten public awareness especially of home safety in the prevention of SI.
Newer forms of conventional ventilation for preterm newborns
Authors: Sinha Sunil K , Donn Steven M 
Published: May 2008

AbstractAlthough life saving, mechanical ventilation can cause complications such as ventilator‐induced lung injury and bronchopulmonary dysplasia in very preterm babies. The ventilator‐induced lung injury is multi‐factorial. There has been an introduction of a number of newer forms of mechanical ventilation, which are aimed to reduce such complications. These are based on sound physiologic principles and clinicians should familiarize themselves with these advances.