bluuebunny/crossref_metadata_2025_split huggingface dataset:
Inducible gene deletion in astroglia and radial glia—A valuable tool for functional and lineage analysis
Authors: Mori Tetsuji , Tanaka Kohichi , Buffo Annalisa , Wurst Wolfgang , Kühn Ralf , Götz Magdalena 
Published: May 2006

AbstractAstrocytes are thought to play a variety of key roles in the adult brain, such as their participation in synaptic transmission, in wound healing upon brain injury, and adult neurogenesis. However, to elucidate these functions in vivo has been difficult because of the lack of astrocyte‐specific gene targeting. Here we show that the inducible form of Cre (CreERT2) expressed in the locus of the astrocyte‐specific glutamate transporter (GLAST) allows precisely timed gene deletion in adult astrocytes as well as radial glial cells at earlier developmental stages. Moreover, postnatal and adult neurogenesis can be targeted at different stages with high efficiency as it originates from astroglial cells. Taken together, this mouse line will allow dissecting the molecular pathways regulating the diverse functions of astrocytes as precursors, support cells, repair cells, and cells involved in neuronal information processing. © 2006 Wiley‐Liss, Inc.
Synergetic effects of quetiapine and venlafaxine in preventing the chronic restraint stress‐induced decrease in cell proliferation and BDNF expression in rat hippocampus
Authors: Xu Haiyun , Chen Zhong , He Jue , Haimanot Samson , Li Xiaokun , Dyck Lillian , Li Xin‐Min 
Published: May 2006

AbstractClinical studies show better response rates of patients with depression and schizophrenia to combinations of atypical antipsychotics and antidepressants, compared to responses to either type of drugs alone. Animal studies demonstrate that some antipsychotics and antidepressants increase neurogenesis and BDNF expression in the hippocampus, which is reduced in volume in patients with depression or schizophrenia. We hypothesized that the better therapeutic effects of combined treatment seen in schizophrenia and depression patients are related to the additive or synergistic effects of combined treatment on hippocampal neurogenesis and BDNF expression. To test this hypothesis, we investigated the effects of chronic administration of quetiapine, venlafaxine, and their combination, on hippocampal cell proliferation and BDNF expression in rats, when subjected to chronic restraint stress (CRS) during the last 2 weeks of a 3‐week drug administration period. We found (1) CRS decreased hippocampal cell proliferation and BDNF expression; (2) chronic administration of quetiapine or venlafaxine dose‐dependently prevented these decreases in hippocampal cell proliferation and BDNF expression caused by CRS (6 h/day for 14days); (3) the combination of lower doses of quetiapine (5mg/kg) and venlafaxine (2.5mg/kg) increased hippocampal cell proliferation and prevented BDNF decrease in stressed rats, whereas each of the drugs exerted mild or no effects; (4) individual higher doses of quetiapine (10mg/kg) or venlafaxine (5mg/kg) exerted effects comparable to those produced by their combination. These results support our hypothesis and can lead to future studies to develop new therapeutic approaches for treatment‐resistant depression and the negative symptoms of schizophrenia. © 2006 Wiley‐Liss, Inc.
Minced cartilage without cell culture serves as an effective intraoperative cell source for cartilage repair
Authors: Lu Yiling , Dhanaraj Sridevi , Wang Ziwei , Bradley Dino M. , Bowman Steven M. , Cole Brian J. , Binette Francois 
Published: May 2006

AbstractTraumatic articular cartilage injuries heal poorly and may predispose patients to the early onset of osteoarthritis. One current treatment relies on surgical delivery of autologous chondrocytes that are prepared, prior to implantation, through ex vivo cell expansion of cartilage biopsy cells. The requirement for cell expansion, however, is both complex and expensive and has proven to be a major hurdle in achieving a widespread adoption of the treatment. This study presents evidence that autologous chondrocyte implantation can be delivered without requiring ex vivo cell expansion. The proposed improvement relies on mechanical fragmentation of cartilage tissue sufficient to mobilize embedded chondrocytes via increased tissue surface area. Our outgrowth study, which was used to demonstrate chondrocyte migration and growth, indicated that fragmented cartilage tissue is a rich source for chondrocyte redistribution. The chondrocytes outgrown into 3‐D scaffolds also formed cartilage‐like tissue when implanted in SCID mice. Direct treatment of full‐thickness chondral defects in goats using cartilage fragments on a resorbable scaffold produced hyaline‐like repair tissue at 6 months. Thus, delivery of chondrocytes in the form of cartilage tissue fragments in conjunction with appropriate polymeric scaffolds provides a novel intraoperative approach for cell‐based cartilage repair. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
MRI analysis of in vivo meniscal and tibiofemoral kinematics in ACL‐deficient and normal knees
Authors: Shefelbine Sandra J. , Ma C. Benjamin , Lee Keh‐Yang , Schrumpf Mark A. , Patel Priyesh , Safran Marc R. , Slavinsky John P. , Majumdar Sharmila 
Published: May 2006

AbstractThe objectives of this study were to analyze simultaneously meniscal and tibiofemoral kinematics in healthy volunteers and anterior cruciate ligament (ACL)‐deficient patients under axial load‐bearing conditions using magnetic resonance imaging (MRI). Ten healthy volunteers and eight ACL‐deficient patients were examined with a high‐field, closed MRI system. For each group, both knees were imaged at full extension and partial flexion (∼45°) with a 125N compressive load applied to the foot. Anteroposterior and medial/lateral femoral and meniscal translations were analyzed following three‐dimensional, landmark‐matching registration. Interobserver and intraobserver reproducibilities were less than 0.8 mm for femoral translation for image processing and data analysis. The position of the femur relative to the tibia in the ACL‐deficient knee was 2.6 mm posterior to that of the contralateral, normal knee at extension. During flexion from 0° to 45°, the femur in ACL‐deficient knees translated 4.3 mm anteriorly, whereas no significant translation occurred in uninjured knees. The contact area centroid on the tibia in ACL‐deficient knees at extension was posterior to that of uninjured knees. Consequently, significantly less posterior translation of the contact centroid occurred in the medial tibial condyle in ACL‐deficient knees during flexion. Meniscal translation, however, was nearly the same in both groups. Axial load‐bearing MRI is a noninvasive and reproducible method for evaluating tibiofemoral and meniscal kinematics. The results demonstrated that ACL deficiency led to significant changes in bone kinematics, but negligible changes in the movement of the menisci. These results help explain the increased risk of meniscal tears and osteoarthritis in chronic ACL deficient knees. © 2006 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res
Soluble nickel inhibits HIF‐prolyl‐hydroxylases creating persistent hypoxic signaling in A549 cells
Authors: Davidson Todd L. , Chen Haobin , Di Toro Dominic M. , D'Angelo Gisela , Costa Max 
Published: May 2006

AbstractSoluble nickel compounds are carcinogenic to humans although the mechanism by which they cause cancer remains unclear. One major consequence of exposure to nickel is the stabilization of hypoxia inducible factor‐1α (HIF‐1α), a protein known to be overexpressed in a variety of cancers. In this study, we report a persistent stabilization of HIF‐1α by nickel chloride up to 72 h after the removal of nickel from the culture media. In addition, we show that the HIF‐prolyl hydroxylases (PHD's) are inhibited when cells are exposed to nickel and that they remain repressed for up to 72 h after nickel is removed. We then show that nickel can inhibit purified HIF‐PHD's 2 in vitro, through direct interference with the enzyme. Through theoretical calculations, we also demonstrate that nickel may be able to replace the iron in the active site of this enzyme, providing a plausible mechanism for the persistent inhibition of HIF‐PHD's by nickel. The data presented suggest that nickel can interfere with HIF‐PHD directly and does not inhibit the enzyme by simply depleting cellular factors, such as iron or ascorbic acid. Understanding the mechanisms by which nickel can inhibit HIF‐PHD's and stabilize HIF‐1α may be important in the treatment of cancer and ischemic diseases. © 2006 Wiley‐Liss, Inc.
Persistent infection of hepatitis B virus is involved in high rate of p16 methylation in hepatocellular carcinoma
Authors: Jicai Zhang , Zongtao Yu , Jun Lu , Haiping Li , Jianmin Wu , Lihua Hu 
Published: May 2006

AbstractHigh rate of chronic hepatitis B virus (HBV) infection and p16 promoter methylation were found in the majority of hepatocellular carcinoma (HCC). To investigate the potential linkage between high rate of p16 methylation and HBV infection, p16 methylation was detected with methylation‐specific polymerase chain reaction (PCR), and HBV markers were examined with real‐time PCR and immunologic method. p16 methylation was detected in 5.5% of patients with hepatitis B, 9.1% of noncancerous liver, 36.6% of cirrhotic liver tissue, and 70.5% of cancerous tissue of HCC, primarily in cirrhotic (46.7%) and cancerous tissue (90.6%) with HBV infection. In noncancerous tissue, p16 methylation could only be detected in samples with HBV infection, although no significant difference, the frequency of p16 methylation in noncancerous tissue with HBV infection was higher than those without it. The results showed that, in cancerous, cirrhotic, or noncancerous tissues, the frequency of p16 methylation in samples with HBV infection was higher than those without it, suggesting possible association between HBV infection and p16 methylation. The result of HBV‐DNA analysis showed that 96.1% (49/51) samples with p16 methylation also showed detectable HBV‐DNA; it signifies that replication and/or integration of HBV may contribute to high rate of p16 methylation in hepatocarcinogenesis. Generally, these results indicate that persistent HBV infection may be associated with high rate of p16 methylation, and involved in development of HCC through this way. © 2006 Wiley‐Liss, Inc.
Cross reactivity between many anti‐human antibodies for their hamster homologs provide the tools to study the signal transduction pathway activated by asbestos and SV40 in the malignant mesothelioma model
Authors: Kroczynska Barbara , Carbone Michele 
Published: May 2006

AbstractThe aim of this study was to test the possibility of using human antibodies to study the pathogenic mechanism of SV40 and asbestos in a hamster mesothelioma model. The cellular lysates from human and hamster primary mesothelial cells were tested by Western blot analysis. All of the antibodies we tested (HGF, Notch, VEGF, Sp1, p53, PP2A, p‐ERK1, p‐c‐jun, Fra1, Fra2, MMP1, MMP9, NFκB p65, IκB, GAPDH) cross‐reacted with their hamster counterparts. These data indicate that hamster mesothelioma model and more in general hamster experimental model, can be used for functional studies because many mouse, rabbit, and goat monoclonal antibodies prepared against human antigens cross‐react with their hamster counterparts. © 2006 Wiley‐Liss, Inc.
Thimerosal induces apoptosis and G2/M phase arrest in human leukemia cells
Authors: Woo Kyung Jin , Lee Tae‐Jin , Bae Jae Hoon , Jang Byeong‐Churl , Song Dae‐Kyu , Cho Jae‐We , Suh Seong‐Il , Park Jong‐Wook , Kwon Taeg Kyu 
Published: May 2006

AbstractThimerosal is an organomercury compound with sulfhydryl‐reactive properties. The ability of thimerosal to act as a sulfhydryl group is related to the presence of mercury. Due to its antibacterial effect, thimerosal is widely used as preservatives and has been reported to cause chemically mediated side effects. In the present study, we showed that the molecular mechanism of thimerosal induced apoptosis in U937 cells. Thimerosal was shown to be responsible for the inhibition of U937 cells growth by inducing apoptosis. Treatment with 2.5–5 µM thimerosal but not thiosalicylic acid (structural analog of thimerosal devoid of mercury) for 12 h produced apoptosis, G2/M phase arrest, and DNA fragmentation in a dose‐dependent manner. Treatment with caspase inhibitor significantly reduced thimerosal‐induced caspase 3 activation. In addition, thimerosal‐induced apoptosis was attenuated by antioxidant Mn (III) meso‐tetrakis (4‐benzoic acid) porphyrin (Mn‐TBAP). These data indicate that the cytotoxic effect of thimerosal on U937 cells is attributable to the induced apoptosis and that thimerosal‐induced apoptosis is mediated by reactive oxygen species generation and caspase‐3 activation. © 2006 Wiley‐Liss, Inc.
Molecular targets for the cancer preventive activity of tea polyphenols
Authors: Yang Chung S. , Lambert Joshua D. , Hou Zhe , Ju Jihyeung , Lu Gang , Hao Xinpei 
Published: May 2006

AbstractInhibition of carcinogenesis by tea and tea polyphenols has been demonstrated in many animal models. The mechanisms of action have been extensively investigated mostly in cell culture systems with (‐)‐epigallocatechin‐3‐gallate (EGCG), the most active and major polyphenolic compound from green tea. However, the mechanisms of cancer preventive activity by tea and tea polyphenols are not clearly understood. This article discusses some of the reported mechanisms and possible targets for the action of EGCG. The difficulties and major issues in extrapolating data from studies in cancer cell lines to cancer prevention mechanisms are discussed. Activities observed in cell culture with high concentrations of EGCG may not be relevant because of the limited systemic bioavailability of EGCG. In addition, possible artifacts due to the auto‐oxidation of EGCG may complicate this issue. Some recent studies revealed high‐affinity EGCG binding proteins as possible direct targets for the action of EGCG. Validating the related cancer preventive mechanisms found in in vitro studies in animal models and human samples would be exciting. © 2006 Wiley‐Liss, Inc.
p53 and its downstream proteins as molecular targets of cancer
Authors: Sun Yi 
Published: May 2006

AbstractThe p53 tumor suppressor gene plays a key role in prevention of tumor formation through transcriptional dependent and independent mechanisms. Transcriptional‐dependent mechanisms are mainly mediated by p53 regulation of downstream targets, leading to growth arrest and apoptosis. Mutational inactivation of the p53 gene is detected in more than 50% of human cancers. Mutation of p53 renders cancer cells more resistant to current cancer therapies due to lack of p53‐mediated apoptosis. Extensive studies have been conducted to identify small molecules that manipulate p53, including restoration of mutant p53 conformation to wild‐type, disruption of murine double minute‐2 (Mdm2)‐p53 binding to increase p53 level and inhibition of Mdm2 E3 ubiquitin ligase activity to prevent p53 degradation. Another approach was to identify and validate “drugable” target(s) in p53 signaling pathways that modulate p53‐induced apoptosis. We profiled a p53 temperature‐sensitive lung cancer cell model with the Affymetrix human HG‐U133 GeneChip, covering the entire human transcriptome. We identified thousands of unique genes that were either induced or repressed in response to p53‐induced apoptosis. A follow‐up study characterized a p53‐repressed gene, SAK, a polo‐like kinase (PLK) family member, as an appealing cancer drug target. Snk/Plk‐akin kinase (SAK) silencing via small interfering RNA (siRNA) induced apoptosis, whereas SAK overexpression attenuated p53‐induced apoptosis. Thus, SAK repression by p53 contributes to p53‐induced apoptosis. Future work is directed at determining the normal cell response to SAK silencing. If a therapeutic window is obtained, a SAK inhibitor identified from high throughput screening (HTS) could serve as a lead compound for development of a novel class of apoptosis‐inducing anticancer drugs. © 2006 Wiley‐Liss, Inc.
Congenital dysgranulopoietic neutropenia
Authors: Olcay Lale , Yetgin Sevgi , Erdemli Esra , Germeshausen Manuela , Aktaş Dilek , Büyükaşık Yahya , Okur Hamza 
Published: May 2006

AbstractWe investigated a 15‐year‐old female with congenital dysgranulopoietic neutropenia (CDN) and her non‐neutropenic mother who had recurrent stomatitis. In both patients, cells of the neutrophilic, eosinophilic, monocytic, megakaryocytic, and basophilic series were dysmorphic. Plasmacytoid lymphocytes and mild megaloblastic erythroid precursors were present. Bleeding times of both patients were prolonged. The mother had a secondary aggregation defect; the number of the plasmacytoid lymphocytes, dense granules of platelets, and dysmorphic neutrophils, neutrophil chemotaxis, and myeloperoxidase content fluctuated according to the presence or not of aphthae. The daughter's karyotype revealed 46,XX/46,XX, t(1;8). No ELA2 or G‐CSFR mutation was detected. These findings support stem cell involvement in CDN. Pediatr Blood Cancer 2008;50:115–119. © 2006 Wiley‐Liss, Inc.
Hypertension and prehypertension in long‐term survivors of childhood and adolescent cancer
Authors: Haddy Theresa B. , Mosher Revonda B. , Reaman Gregory H. 
Published: May 2006

AbstractBackgroundHypertension as a late effect following childhood and adolescent cancer has received little attention. Since obesity, a known risk factor for hypertension, is increased following some childhood cancers, it seems likely that significant numbers of survivors would have hypertension.ProceduresThe records of patients seen in the Long Term Follow Up Clinic of Children's National Medical Center were examined for a single institution, retrospective study of blood pressure in survivors of childhood and adolescent cancer. Of 103 consecutive survivors who attended the clinic from January 1 through June 30, 2004, 51 (49.5%) were female and 52 (50.5%) were male. Their mean age was 14.6 years. Systolic and diastolic blood pressures for children and adolescents under 18 years of age were evaluated for hypertension and prehypertensive according to standards for age, sex, and height. Blood pressures for adults 18 years of age and older were evaluated according to standard adult values. Children and adolescents were evaluated for obesity and overweight according to body mass index (BMI) standards for age and sex. Adults were evaluated according to standard adult values.ResultsTwenty‐nine patients (28.2%) were hypertensive or prehypertensive, and 74 (71.8%) were normal. Thirty‐eight patients (36.9%) were obese or overweight, and 65 (63.1%) were non‐obese. Most Wilms tumor patients, 7 of 10 (70.0%), had hypertension or prehypertension, but only 4 of 10 (40.0%) were obese or overweight.ConclusionCareful follow‐up of their blood pressure status is warranted for long‐term survivors of childhood and adolescent cancer, especially for those with an initial diagnosis of Wilms tumor. Pediatr Blood Cancer 2007;49:79–83. © 2006 Wiley‐Liss, Inc.
Maxillary ameloblastic carcinoma in a child
Authors: Yazıcı Nalan , Karagöz Begül , Varan Ali , Yılmaz Taner , Öztürk Arzu , Usubütün Alp , Büyükpamukçu Münevver 
Published: May 2006

AbstractWe report an extremely rare occurrence of ameloblastic carcinoma located in the maxilla of a pediatric patient. Wide surgical resection was done along with adjuvant radiotherapy because of involved surgical margins. Histopathological diagnosis was established with morphological features of both ameloblastoma and carcinoma. Pediatr Blood Cancer 2008;50:175–176. © 2006 Wiley‐Liss, Inc.
Response to rituximab in a child with neuroblastoma and opsoclonus‐myoclonus
Authors: Bell Jessica , Moran Cassandra , Blatt Julie 
Published: May 2006

AbstractOpsoclonus‐myoclonus (OM) is a paraneoplastic syndrome of probable autoimmune origin. Despite current therapies aimed at decreasing autoantibody formation, OM is difficult to control and may impact long‐term neurologic outcome. We present a case of a 19‐month‐old patient who initially presented with OM, neuroblastoma and a constitutional cytogenetic abnormality t(5;12)(q11.2;q15). The patient's OM was recalcitrant to conventional therapies, but showed significant improvement following treatment with rituximab. Pediatr Blood Cancer 2008;50:370–371. © 2006 Wiley‐Liss, Inc.
Radiation effects on SBR–EPDM blends: A correlation with blend morphology
Authors: Dubey K. A. , Bhardwaj Y. K. , Chaudhari C. V. , Bhattacharya Shovit , Gupta S. K. , Sabharwal S. 
Published: May 2006

AbstractThe effect of γ radiation on the morphological and physical properties of Styrene–butadiene rubber (SBR) and Ethylene–propylene–diene monomer (EPDM) blends has been investigated. An attempt has been made to establish a correlation between various parameters like Gordon–Taylor parameter (k), hydrodynamic interaction parameter (Δ[η]mix), chemical shift factor (b), Charlesby–Pinner parameter (p0/q0) and polymer–polymer interaction parameter (χ). The results showed a close dependence of mechanical and physical properties of irradiated blends on these parameters. The probability of spur overlap has been found to increase with the increase in EPDM content in the blends, which in turn results in significant improvement in the mechanical properties of the irradiated SBR–EPDM blends with higher EPDM fraction. The efficiency of four multifunctional acrylates as crosslinking aid for the radiation‐induced vulcanization of SBR–EPDM blend was also studied. The results established lower efficiency of methacrylates over acrylates in the process and indicated that among the crosslinking agents studied trimethylolpropane triacrylate is the most efficient one. © 2006 Wiley Periodicals, Inc. J Polym Sci Part B: Polym Phys 44: 1676–1689, 2006
Urban schools' teachers enacting project‐based science
Authors: Tal Tali , Krajcik Joseph S. , Blumenfeld Phyllis C. 
Published: May 2006

AbstractWhat teaching practices foster inquiry and promote students to learn challenging subject matter in urban schools? Inquiry‐based instruction and successful inquiry learning and teaching in project‐based science (PBS) were described in previous studies (Brown & Campione, 1990; Crawford, 1999; Krajcik, Blumenfeld, Marx, Bass, & Fredricks, 1998; Krajcik, Blumenfeld, Marx, & Solloway, 1994; Minstrell & van Zee, 2000). In this article, we describe the characteristics of inquiry teaching practices that promote student learning in urban schools. Teaching is a major factor that affects both achievement of and attitude of students toward science (Tamir, 1998). Our involvement in reform in a large urban district includes the development of suitable learning materials and providing continuous and practiced‐based professional development (Fishman & Davis, in press; van Es, Reiser, Matese, & Gomez, 2002). Urban schools face particular challenges when enacting inquiry‐based teaching practices like those espoused in PBS. In this article, we describe two case studies of urban teachers whose students achieved high gains on pre‐ and posttests and who demonstrated a great deal of preparedness and commitment to their students. Teachers' attempts to help their students to perform well are described and analyzed. The teachers we discuss work in a school district that strives to bring about reform in mathematics and science through systemic reform. The Center for Learning Technologies in Urban Schools (LeTUS) collaborates with the Detroit Public Schools to bring about reform in middle‐school science. Through this collaboration, diverse populations of urban‐school students learn science through inquiry‐oriented projects and the use of various educational learning technologies. For inquiry‐based science to succeed in urban schools, teachers must play an important role in enacting the curriculum while addressing the unique needs of students. The aim of this article is to describe patterns of good science teaching in urban school. © 2006 Wiley Periodicals, Inc. J Res Sci Teach 43: 722–745, 2006