bluuebunny/crossref_metadata_2025_split huggingface dataset:
Head regeneration in Hydra
Authors: Bode Hans R. 
Published: January 2003

AbstractHydra, a primitive metazoan, has a simple structure consisting of a head, body column, and foot aligned along a single oral–aboral axis. The body column has a high capacity for regeneration of both the head and foot. Because of the tissue dynamics that take place in adult Hydra, the processes governing axial patterning are continuously active to maintain the form of the animal. Regeneration in hydra is morphallactic and closely related to these axial patterning processes. As might be expected, analysis at the molecular level indicates that the same set of genes are involved in head regeneration and the maintenance of the head in the context of the tissue dynamics of the adult. The genes analyzed so far play roles in axial patterning processes in bilaterians. Developmental Dynamics 226:225–236, 2003. © 2003 Wiley‐Liss, Inc.
Changes in spinal cord regenerative ability through phylogenesis and development: Lessons to be learnt
Authors: Ferretti Patrizia , Zhang Fang , O'Neill Paul 
Published: January 2003

AbstractLower vertebrates, such as fish and amphibians, and developing higher vertebrates can regenerate complex body structures, including significant portions of their central nervous system. It is still poorly understood why this potential is lost with evolution and development and becomes very limited in adult mammals. In this review, we will discuss the current knowledge on the cellular and molecular changes after spinal cord injury in adult tailed amphibians, where regeneration does take place, and in developing chick and mammalian embryos at different developmental stages. We will focus on the recruitment of progenitor cells to repair the damage and discuss possible roles of changes in early response to injury, such as cell death by apoptosis, and of myelin‐associated proteins, such as Nogo, in the transition between regeneration‐competent and regeneration‐incompetent stages of development. A better understanding of the mechanisms underlying spontaneous regeneration of the spinal cord in vivo in amphibians and in the chick embryo will help to devise strategies for restoring function to damaged or diseased nervous tissues in mammals. Developmental Dynamics 226:245–256, 2003.© 2003 Wiley‐Liss, Inc.
Cnidarians: An evolutionarily conserved model system for regeneration?
Authors: Holstein T.W. , Hobmayer E. , Technau U. 
Published: January 2003

AbstractCnidarians are among the simplest metazoan animals and are well known for their remarkable regeneration capacity. They can regenerate any amputated head or foot, and when dissociated into single cells, even intact animals will regenerate from reaggregates. This extensive regeneration capacity is mediated by epithelial stem cells, and it is based on the restoration of a signaling center, i.e., an organizer. Organizers secrete growth factors that act as long‐range regulators in axis formation and cell differentiation. In Hydra, Wnt and TGF‐beta/Bmp signaling pathways are transcriptionally up‐regulated early during head regeneration and also define the Hydra head organizer created by de novo pattern formation in aggregates. The signaling molecules identified in Cnidarian regeneration also act in early embryogenesis of higher animals. We suppose that they represent a core network of molecular interactions, which could explain at least some of the mechanisms underlying regeneration in vertebrates. Developmental Dynamics 226:257–267, 2003.© 2003 Wiley‐Liss, Inc.
Regeneration‐specific expression pattern of three posterior Hox genes
Authors: Christen Bea , Beck Caroline W. , Lombardo Aurora , Slack Jonathan M.W. 
Published: January 2003

AbstractHomeobox genes encode positional information during primary and secondary axis formation during development. For this reason, the Hox genes have attracted attention in regeneration research as well. At early stages of regeneration, Hox genes have been implicated in wound healing and the dedifferentiation process and at later stages in the patterning of the blastema. We studied the expression of three Abdominal B‐type Hox genes in Xenopus: XHoxc10, XHoxa13, and XHoxd13 during normal limb development and during regeneration of limbs and tails. We compared their expression with nonregenerating and with wounded limbs and tails, respectively. We show that the temporal and spatial control of these three Hox genes in blastemas differs from normal development. All three are specific to regeneration, XHoxc10 is up‐regulated at the right time and at the site where cells dedifferentiate and undifferentiated cells are recruited, whereas XHoxa13 is reexpressed slightly later in regeneration, when the blastemal cells proliferate and remains on during patterning of the blastema. XHoxd13 is not expressed until relatively late and appears to be involved only in patterning of the blastema. Developmental Dynamics 226:349–355, 2003.© 2003 Wiley‐Liss, Inc.
Regeneration of the urodele limb: A review
Authors: Nye Holly L.D. , Cameron Jo Ann , Chernoff Ellen A.G. , Stocum David L. 
Published: January 2003

AbstractUrodele amphibians have been widely used for studies of limb regeneration. In this article, we review studies on blastema cell proliferation and propose a model of blastemal self‐organization and patterning. The model is based on local cell interactions that intercalate positional identities within circumferential and proximodistal boundaries that outline the regenerate. The positional identities created by the intercalation process appear to be reflected in the molecular composition of the cell surface. Transcription factors and signaling molecules involved in patterning are discussed within the context of the boundary/intercalation model. Developmental Dynamics 226:280–294, 2003. © 2003 Wiley‐Liss, Inc.
Urodele spinal cord regeneration and related processes
Authors: Chernoff Ellen A.G. , Stocum David L. , Nye Holly L.D. , Cameron Jo Ann 
Published: January 2003

AbstractUrodele amphibians, newts and salamanders, can regenerate lesioned spinal cord at any stage of the life cycle and are the only tetrapod vertebrates that regenerate spinal cord completely as adults. The ependymal cells play a key role in this process in both gap replacement and caudal regeneration. The ependymal response helps to produce a different response to neural injury compared with mammalian neural injury. The regenerating urodele cord produces new neurons as well as supporting axonal regrowth. It is not yet clear to what extent urodele spinal cord regeneration recapitulates embryonic anteroposterior and dorsoventral patterning gene expression to achieve functional reconstruction. The source of axial patterning signals in regeneration would be substantially different from those in developing tissue, perhaps with signals propagated from the stump tissue. Examination of the effects of fibroblast growth factor and epidermal growth factor on ependymal cells in vivo and in vitro suggest a connection with neural stem cell behavior as described in developing and mature mammalian central nervous system. This review coordinates the urodele regeneration literature with axial patterning, stem cell, and neural injury literature from other systems to describe our current understanding and assess the gaps in our knowledge about urodele spinal cord regeneration. Developmental Dynamics 226:295–307, 2003. © 2003 Wiley‐Liss, Inc.
Regeneration of the ear after wounding in different mouse strains is dependent on the severity of wound trauma
Authors: Rajnoch Charissa , Ferguson Sharon , Metcalfe Anthony D. , Herrick Sarah E. , Willis Hayley S. , Ferguson Mark W.J. 
Published: January 2003

AbstractThe replacement and restoration of tissue mass after organ damage or injury in adult higher vertebrates is critical to the architecture and function of the organ. If replacement occurs with scar tissue, this often results in adverse effects on function and growth as well as an undesirable cosmetic appearance. However, certain mammals, such as the MRL/MpJ mouse, have shown a restricted capacity for regeneration, rather than scar tissue formation, after an excisional ear punch wound. To investigate the changes in tissue architecture leading to ear wound closure, initial ear wounding studies with a 2‐mm clinical biopsy punch were performed on MRL/MpJ mice, by using C57BL/6 mice as a nonregenerative control strain. In contrast to previously reported studies on mouse ear regeneration, we observed that C57BL/6 mice in fact showed a limited regenerative capacity. One explanation for this difference could be attributed to the method of wounding used; both previous studies on mouse ear regeneration used a thumb punch, whereas our approach was to use a clinical biopsy punch. This approach led us to further investigate whether the severity of trauma applied influenced the rate of wound healing. We, therefore, compared the effects of the sharp clinical biopsy punch with that of a cruder thumb punch, and introduced a third strain of mouse, Balb/c, known to be a slow‐healing strain. A new method to quantify ear punch hole closure was developed and a histologic investigation conducted up to 4 months after wounding. Image analysis data showed a reduction in original ear wound area of 85% in MRL/MpJ mice at 4 weeks and of 91.7% over 4 months by using a biopsy punch. In contrast, the crude thumb punch methodology resulted in an increase in wound area of up to 58% in Balb/c ears; thought to be due to increased necrosis of the wound site. All biopsy‐punched wound areas plateaued in healing between days 28 and 112. Only 5 of 80 MRL/MpJ mouse ears showed no residual holes macroscopically after 28 days. Histologically, all strains of mice healed their ear wounds in a similar manner involving re‐epithelialization, blastema‐like formation, dermal extension, blood vessel formation, chondrogenesis, folliculogenesis, and skeletal muscle and fat differentiation. However, all regenerative features were more pronounced and accelerated in MRL/MpJ mice when compared with C57BL/6 and Balb/c biopsy‐punched mouse ears. Developmental Dynamics 226:388–397, 2003. © 2003 Wiley‐Liss, Inc.
Matrix metalloproteinase activity correlates with blastema formation in the regenerating MRL mouse ear hole model
Authors: Gourevitch Dmitri , Clark Lise , Chen Pan , Seitz Alexander , Samulewicz Stefan J. , Heber‐Katz Ellen 
Published: January 2003

AbstractThe MRL mouse was proposed as a model of mammalian regeneration because it can close ear holes completely with the restoration of normal tissue. This regeneration process involves the formation of a blastema during healing, the re‐appearance of cartilage and hair follicles, and healing without scarring. Such a process requires extensive tissue remodeling. To characterize differences in ear wounding responses between regenerating and nonregenerating mice, we examined and compared the extracellular matrix remodeling and the matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) response in the MRL and C57BL/6 mouse strains after injury. We found a correlation between the MRL's ability to break down the basement membrane, form a blastema, and close ear hole wounds and an inflammatory response with neutrophils and macrophages seen in the ear after injury. These cells were positive for MMP‐2 and MMP‐9 as well as TIMP‐2 and TIMP‐3. Clear differences between the MRL and B6 response to injury were seen that could explain the differences in healing and blastema formation in the MRL and lack of it in the B6 mice. This finding was further supported by enzyme activity as determined by gelatin zymography. Developmental Dynamics 226:377–387, 2003. © 2003 Wiley‐Liss, Inc.
Role for keratins 6 and 17 during wound closure in embryonic mouse skin
Authors: Mazzalupo Stacy , Wong Pauline , Martin Paul , Coulombe Pierre A. 
Published: January 2003

AbstractInjury to adult skin triggers a response designed to restore its vital barrier function. A conserved aspect of this response is a rapid switch in gene expression whereby the type II keratin 6 (K6) and type I keratins 16 and 17 (K16, K17) are induced in epithelial cells at the wound edge. This induction occurs at the expense of the keratins normally expressed during terminal differentiation and correlates with the activation of epithelial cells at the wound edge, ahead of their migration into the wound site. Here, we show that the capacity to enact this switch is already acquired in E11.5 stage mouse embryos. Such early timing is well ahead of the onset of differentiation‐specific gene expression (∼E13.5) and the acquisition of barrier formation by developing epidermis (∼E16.5). Induction of K6, K16, and K17 correlates with changes in the morphology of epithelial cells at the wound edge. The closure of embryonic wounds is significantly delayed in K17 null embryos, but not embryos null for K6. These observations significantly extend the correlation between K6, K16, and K17 expression and epithelial wound closure, and provide direct evidence that expression of these keratins, K17 in particular, is important for the timeliness of this process. Developmental Dynamics 226:356–365, 2003.© 2003 Wiley‐Liss, Inc.
Chromosome imbalances in thyroid follicular neoplasms: A comparison between follicular adenomas and carcinomas
Authors: Roque Lucia , Rodrigues Raquel , Pinto António , Moura‐Nunes Vasco , Soares Jorge 
Published: January 2003

AbstractThe underlying genetic events associated with follicular thyroid tumorigenesis are still ill defined. In this study, we performed a screening for chromosome imbalances by comparative genomic hybridization (CGH) in a group of 12 follicular adenomas (FAs) and 20 follicular carcinomas (FTCs) previously characterized by conventional cytogenetics and flow cytometry analysis. In general, a great similarity was observed between the CGH profiles of the FAs and FTCs. In both benign and malignant tumors, a combination of gains affecting 5, 7, 12, 17, 19, and 20 was observed. Chromosome 7 was the most frequently affected chromosome, with three regions of consensus gains: 7p11–12, 7q11.3–q21, and 7q31. Recurrent gains of chromosomes 5 and 12 involved 5p11, 5p15, 5q13–q22, 5q21–q23, 12p11, and 12q11–q12. DNA sequence losses were also observed in both tumor groups. Chromosomal arms deleted in at least five of the neoplasms were (in order of frequency): in adenomas, 15q, 2p/2q, 3q, 6p/6q, 11q, and 22q; and in FTCs, 3p, 2p, 8q, 1p, 2q, 3q, 6q, 8p, 9p, 11q, 13q, 6p, and 18q. The statistical evaluation of the CGH data demonstrated that 15q loss was significantly associated with FA. Two regions of minimal common loss were defined by CGH at 15: 15q11–q21 and 15q26‐qter. The identification of these regions provides a basis for further molecular studies. © 2003 Wiley‐Liss, Inc.
Comprehensive molecular cytogenetic characterization of cervical cancer cell lines
Authors: Harris Charles P. , Lu Xin Yan , Narayan Gopeshwar , Singh Bhuvanesh , Murty Vundavalli V. V. S. , Rao Pulivarthi H. 
Published: January 2003

AbstractWe applied a combination of molecular cytogenetic methods, including comparative genomic hybridization (CGH), spectral karyotyping (SKY), and fluorescence in situ hybridization (FISH), to characterize the genetic aberrations in eight widely used cervical cancer (CC) cell lines. CGH identified the most frequent chromosomal losses including 2q, 3p, 4q, 6q, 8p, 9p, 10p, 13q, and 18q; gains including 3q, 5p, 5q, 8q, 9q, 11q, 14q, 16q, 17q, and 20q; and high‐level chromosomal amplification at 3q21, 7p11, 8q23–q24, 10q21, 11q13, 16q23–q24, 20q11.2, and 20q13. Several recurrent structural chromosomal rearrangements, including der(5)t(5;8)(p13;q23) and i(5)(p10); deletions affecting chromosome bands 5p11, 5q11, and 11q23; and breakpoint clusters at 2q31, 3p10, 3q25, 5p13, 5q11, 7q11.2, 7q22, 8p11.2, 8q11.2, 10p11.2, 11p11.2, 14q10, 15q10, 18q21, and 22q11.2 were identified by SKY. We detected integration of HPV16 sequences by FISH on the derivative chromosomes involving bands 18p10 and 18p11 in cell line C‐4I, 2p16, 5q21, 5q23, 6q, 8q24, 10, 11p11, 15q, and 18p11 in Ca Ski, and normal chromosome 17 at 17p13 in ME‐180. FISH analysis was also used further to determine the copy number changes of PIKA3CA and MYC. This comprehensive cytogenetic characterization of eight CC cell lines enhances their utility in experimental studies aimed at gene discovery and functional analysis. © 2003 Wiley‐Liss, Inc.
SIAH1 inactivation correlates with tumor progression in hepatocellular carcinomas
Authors: Matsuo Koichi , Satoh Seiji , Okabe Hiroshi , Nomura Akinari , Maeda Toshiki , Yamaoka Yoshio , Ikai Iwao 
Published: January 2003

AbstractAccumulation of loss of heterozygosity (LOH) on chromosome 16 is frequently observed in human hepatocellular carcinomas (HCCs). To identify tumor‐suppressor genes (TSGs) involved in hepatocarcinogenesis, we performed deletion mapping of chromosome 16 in 59 HCCs. Three commonly deleted regions, located in 16q12.1, 16q22.1, and 16q24.2, were observed. Because there has been no study on LOH at locus 16q12.1 in HCCs, we focused on this region. By searching the Human Genome Database at the National Center for Biotechnology Information web site, we identified 14 known genes in 16q12.1 as TSG candidates. Among these, the expression of SIAH1 was markedly downregulated in HCCs, and inactivation of SIAH1 expression was associated with LOH at 16q12.1. A mutation analysis of SIAH1 revealed no somatic mutations, but one single nucleotide polymorphism was found among the 35 HCCs investigated. Subsequently, we evaluated the relation between SIAH1 expression, confirmed by semiquantitative RT‐PCR, and clinicopathological parameters in HCCs. SIAH1 was significantly downregulated in advanced HCCs, including poorly differentiated tumors, larger tumors, and tumors in advanced stages. These findings suggest that inactivation of SIAH1 plays an important role in HCC progression. © 2003 Wiley‐Liss, Inc.
Genetic markers useful for distinguishing between organ‐confined and locally advanced prostate cancer
Authors: Chu Lisa W. , Troncoso Patricia , Johnston Dennis A. , Liang Jan C. 
Published: January 2003

AbstractProstate cancer is one of the most commonly diagnosed cancers and the second leading cause of cancer deaths among men in the United States. In this study, we performed comparative genomic hybridization (CGH) on 45 primary prostate adenocarcinomas to determine genetic markers that could be useful for distinguishing between organ‐confined and locally advanced prostate cancer. Of these tumors, 24 were pT2 stage, 21 were pT3b; 20 had low Gleason scores (GS), 25 had high GS. The most common chromosomal alterations in all 45 tumors included losses on 8p (57.8%), 10q21→qter (40.0%), 16q (35.6%), 11q21→qter (28.9%), 16p (22.2%), 6q22→24 (22.2%), 10p (20.0%), 5q31→qter (17.8%), 6p (17.8%), 15q22→qter (15.6%), and 17p (15.6%) as well as gains on 7cen→p14 (20.0%), 7cen→q22 (20.0%), and Xcen→q21 (17.8%). Contingency table analysis showed that losses of 8p, 10q25→qter, 6p21, 6q24→qter, and 15q22→qter were significantly increased in frequency (P < 0.05) with increasing stage and/or GS. A model was created following multivariate logistic regression analysis that was predictive of tumor stage in approximately 90% of the tumors studied. This model suggests that loss of 8p is the most valuable predictor of stage. These findings suggest that chromosomal regions identified in this study may be useful for distinguishing between organ‐confined and locally advanced prostate tumors. © 2003 Wiley‐Liss, Inc.
Breakpoints at 1p36.3 in three MDS/AML(M4) patients with t(1;3)(p36;q21) occur in the first intron and in the 5′ region of MEL1
Authors: Xinh Phan Thi , Tri Nguyen Khanh , Nagao Hiromasa , Nakazato Hiroshi , Taketazu Fumitoshi , Fujisawa Shin , Yagasaki Fumiharu , Chen Ying Zhang , Hayashi Yasuhide , Toyoda Atsushi , Hattori Masahira , Sakaki Yoshiyuki , Tokunaga Katsushi , Sato Yuko 
Published: January 2003

AbstractThe recurrent translocation t(1;3)(p36;q21) is associated with myelodysplastic syndrome (MDS)/acute myelogenous leukemia (AML) characterized by trilineage dysplasia, especially dysmegakaryopoiesis and a poor prognosis. Recently, the two genes involved in this translocation have been identified: the MEL1 gene at 1p36.3, and the RPN1 gene at 3q21. The breakpoint in RPN1 is centromeric to the breakpoint cluster region of the inv(3) abnormality. Because the MEL1 transcript is detected only in leukemic cells with t(1;3)(p36;q21), ectopic expression of MEL1 driven by RPN1 at 3q21 is thought to contribute to the pathogenesis of t(1;3)(p36;q21) leukemia. However, the precise breakpoint in the patients has not yet been identified. With fluorescence in situ hybridization analysis by use of BAC/PAC probes, we identified the breakpoint at 1p36.3 in three MDS/AML patients with t(1;3)(p36;q21): within the first intron of the MEL1 gene (one patient) or within a 29‐kb region located in the 5′ region of MEL1 (two other patients). We detected several sizes of MEL1 transcript in two patients including the first patient, although we have not yet clarified whether MEL1 transcripts were different among the patients and whether a truncated MEL1 transcript was expressed in the first patient. This patient showed an unusual clinical profile, repeating progression to overt leukemia and conversion to MDS three times during the 29‐month survival period, which might be related to a different molecular mechanism in this patient. © 2003 Wiley‐Liss, Inc.
Optimal use of high‐resolution topographic data in flood inundation models
Authors: Bates P. D. , Marks K. J. , Horritt M. S. 
Published: January 2003

AbstractIn this paper we explore the optimum assimilation of high‐resolution data into numerical models using the example of topographic data provision for flood inundation simulation. First, we explore problems with current assimilation methods in which numerical grids are generated independent of topography. These include possible loss of significant length scales of topographic information, poor representation of the original surface and data redundancy. These are resolved through the development of a processing chain consisting of: (i) assessment of significant length scales of variation in the input data sets; (ii) determination of significant points within the data set; (iii) translation of these into a conforming model discretization that preserves solution quality for a given numerical solver; and (iv) incorporation of otherwise redundant sub‐grid data into the model in a computationally efficient manner. This processing chain is used to develop an optimal finite element discretization for a 12 km reach of the River Stour in Dorset, UK, for which a high‐resolution topographic data set derived from airborne laser altimetry (LiDAR) was available. For this reach, three simulations of a 1 in 4 year flood event were conducted: a control simulation with a mesh developed independent of topography, a simulation with a topographically optimum mesh, and a further simulation with the topographically optimum mesh incorporating the sub‐grid topographic data within a correction algorithm for dynamic wetting and drying in fixed grid models. The topographically optimum model is shown to represent better the ‘raw’ topographic data set and that differences between this surface and the control are hydraulically significant. Incorporation of sub‐grid topographic data has a less marked impact than getting the explicit hydraulic calculation correct, but still leads to important differences in model behaviour. The paper highlights the need for better validation data capable of discriminating between these competing approaches and begins to indicate what the characteristics of such a data set should be. More generally, the techniques developed here should prove useful for any data set where the resolution exceeds that of the model in which it is to be used. Copyright © 2002 John Wiley & Sons, Ltd.