bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the Xenopus Hox 2.4 gene and identification of control elements in its intron
Authors: Bittner Dennis , De Robertis Eddy M. , Cho Ken W. Y. 
Published: February 2005

AbstractWe report on the Xenopus homolog of the Hox 2.4 gene. This gene occupies the next to 5′‐most position in the Xenopus Hox 2 complex. Hox 2.4 RNA is first detected at the early neurula stage, reaching a peak at the early tailbud stage, and is localized in the middle and posterior portions of the embryos Antibodies raised against a fusion protein show expression of Hox 2.4 protein in Xenopus embryos in a band located in the mid spinal cord. Thus, the protein is expressed in a narrower domain than that of Hox 2.4 mRNA. The Xenopus Hox 2.4 antibody cross‐reacts readily with mouse embryonic tissue, where the protein is detected in migrating neural crest cells, the dorsal portion of the spinal cord, somites, lateral plate mesoderm, and in the forelimb bud. The Xenopus Hox 2.4 intron shares considerable sequence identity with the intron in the mouse homolog. A reporter gene containing an element from this intron which can bind homeodomain proteins is activated following microinjection into Xenopus embryos. The short distance between the end of the Hox 2.4 cDNA and the start site of the neighboring gene in the complex raises the possibility that this transcriptional element might be shared by two Hox genes. © 1993 wiley‐Liss, Inc.
Expression of phospholamban mRNA during early avian muscle morphogenesis is distinct from that of α‐actin
Authors: Toyofuku Toshihiko , Doyle Donald D. , Zak Radovan , Kordylewski Leszek 
Published: February 2005

AbstractWe have studied the expression of phospholamban during the early development of chick embryos by in situ hybridization and have compared it to that of α‐cardiac and α‐skeletal actin. In adult cross‐striated muscles there is only one phospholamban gene and it is expressed exclusively in the heart and slow muscles. In the heart phospholamban transcripts were first detected at stage 14 in the region of presumptive ventricle and at stage 20 in the atrium. In the myotomal portion of the somites phospholamban mRNA was first detected at stage 20, which lagged behind the appearance of the α‐actins. In the limb rudiments all three mRNAs were barely detectable through stage 24, but increased by stage 28 +. However, quantitative analysis of signal intensity at stage 28 + indicated that less phospholamban mRNA is present in the limb bud than in the myotome since for phospholamban the ratio of the signal density in the myotome to that in the limb rudiments was about twice the value of the ratio determined for the α‐actins. Northern blot analysis of embryonic day 11 chick fast pectoralis muscle showed that phospholamban mRNA was not detected in vivo while α‐cardiac actin mRNA was. Moreover, no phospholamban mRNA was detected in primary cultures derived from pectoralis muscle of the same age. In concert with previous observations that phospholamban is not detectable at stage 30–32 in wing or thigh muscle, these results suggest that phospholamban mRNA is expressed independently of the α‐actins in the limb buds during early myogenesis. © 1993 wiley‐Liss, Inc.
Evidence for compartmental identity in the development of the rat lateral gastrocnemius muscle
Authors: Gatesy Stephen M. , English Arthur W. 
Published: February 2005

AbstractIn adult rats, each neuromuscular compartment of the lateral gastrocnemius muscle (LG) is exclusively innervated by a primary branch of the LG nerve. In neonates, however, a small percentage of LG cells receives inputs from more than one primary nerve branch; these inputs are known as cross‐compartmental. Cross‐compartmental inputs are normally lost from the medial compartment of LG (LGm) by the 8th postnatal day. To investigate the mechanisms involved in the elimination of cross‐compartmental inputs, muscle fibers in the LGm compartment were denervated by cutting the LGm nerve branch in 1–4 day old rat pups and in adult rats. We then assessed the degree of cross‐compartmental innervation within the “denervated” compartment using intracellular recordings from neonatal muscle fibers or immunohistochemical staining for nerve cell adhesion molecule (N‐CAM) and neurofilament protein in adult muscles. Following LGm axotomy in neonates, cross‐compartmental innervation is more extensive than in controls and is present as late as 20 days after birth. Thus, in the absence of “native” LGm axons, neonatal cross‐compartmental inputs proliferate by axonal sprouting and the formation of new synapses on vacant LGm fibers. In contrast, axotomized adults do not form new cross‐compartmental inputs over the same time period. The differential response of neonates and adults to muscle nerve branch denervation is evidence for the existence of some form of compartment‐specific recognition. We propose that compartmental identity either arises or becomes relatively more potent during ontogeny and normally acts selectively to eliminate foreign axons and deter the formation of new cross‐compartmental inputs. © 1993 wiley‐Liss, Inc.
Ablation of various regions within the avian vagal neural crest has differential effects on ganglion formation in the fore‐, mid‐ and hindgut
Authors: Peters‐Van Der Sanden Marjo J. H. , Kirby Margaret L. , Gittenberger‐De Groot Adriana , Tibboel Dick , Mulder Maarten P. , Meijers Carel 
Published: February 2005

AbstractThe vagal neural crest adjacent to the first seven somites gives rise to both ganglionic and ectomesenchymal derivatives. Ganglionic derivatives are the neurons and supportive cells of the enteric nervous system (ENS), cardiac, and dorsal root ganglia. Ectomesenchymal derivatives are cells in the cardiac outflow tract and the mesenchymal components of thymus and parathyroids. Ectomesenchymal derivatives are formed by a segment of the vagal neural crest, from the level of the otic vesicle down to the caudal boundary of the third somite, called the cardiac neural crest. We performed neural crest ablations to study regional differences within the avian vagal neural crest with regard to the formation of the ENS. Ablation of the entire vagal neural crest from the mid‐otic vesicle down to the seventh somite plus the nodose placode resulted in the absence of ganglia in the midgut (jejunum and ileum) and hindgut (colon). The foregut (esophagus, proventriculus, gizzard, and duodenum) was normally innervated. After ablation of the vagal neural crest adjacent to somites 3–5, ganglia were absent in the hindgut. Ablations of vagal neural crest not including this segment had no effect on the formation of the ENS. We surmise that the innervation of the hindgut in vivo depends specifically on the neural crest adjacent to somites 3–5, whereas innervation of the midgut can be accomplished by all segments within the vagal neural crest. The foregut can also be innervated by a source outside the vagal neural crest.To study intrinsic differences between various vagal neural crest segments regarding ENS formation, we performed chorioallantoic membrane cocultures of segments of quail vagal neural anlage and E4 chicken hindgut. We found that all vagal neural crest segments were able to give rise to enteric ganglia in the hindgut. When the neural crest of somites 6 and 7 was included in the segment, we also found melanocytes in the hindgut, suggesting that this segment is more related to trunk neural crest. Furthermore, we found that the vagal neural anlage from older embryos (>18 somites) showed an increased potential to form enteric ganglia. This suggests that vagal neural crest cells that have been in prolonged contact with the neural tube in vivo, because of either late emigration or delayed migration, have an increased probability to form enteric ganglia. © 1993 wiley‐Liss, Inc.
Colonization of the bowel by neural crest‐derived cells re‐migrating from foregut backtransplanted to vagal or sacral regions of host embryos
Authors: Rothman Taube P. , Le Douarin Nicole M. , Fontaine‐pérus Josiane C. , Gershon Michael D. 
Published: February 2005

AbstractThe enteric nervous system (ENS) in avian embryos is formed by cells that migrate to the bowel from vagal and sacral regions of the neural crest. Experiments were carried out to evaluate the developmental potential of crest‐derived cells at the time they colonize the gut. Backtransplantation of E4 quail foregut (or control aneuronal hindgut) was used to determine whether crest‐derived cells that have previously colonized the bowel are capable of following defined neural crest migration pathways in host embryos. Vagal and sacral, but not truncal, backgrafts provided donor cells for the host's bowel. These cells were immunostained by the neural crest marker, NC‐1, restricted to the ENS, and appeared only when foregut was backgrafted; therefore, they were crest‐derived. In order for cells to migrate to the host's bowel, backgrafts evidently had to be located in the vicinity of the neuraxis at the time crest‐derived cells exited from them. When vagal grafts moved away from the neuraxis, crest‐derived donor cells colonized cephalic ganglia and the vagus nerves near the grafts; however, such cells did not migrate down the vagi to the host's gut. Sacral backgrafts provided crestderived cells for the bowel only if the donor gut was transplanted prior to the formation of somite 28, at the level of the disappearing primitive streak. Cells from vagal backgrafts were capable of reaching the host's cloaca, but backgrafts placed at a sacral level colonized only the postumbilical bowel. In addition, donor cells proliferated extensively within the host's gut. Whenever the host's gut was colonized, donor crest‐derived cells were also found in non‐enteric targets including nerves, cephalic (vagal backgrafts), or sympathetic (sacral backgrafts) ganglia; however, donor cells did not form ectomesenchyme or melanocytes. These data suggest that (i) crest‐derived cells that have colonized the bowel remain capable of remigrating and following defined neural crest migration pathways in host embryos; (ii) remigrating cells must enter these pathways at their start; (iii) the gut stimulates the proliferation of enteric crest‐derived cells; (iv) vagal crest‐derived cells can follow sacral pathways to reach enteric, Remak's, or sympathetic ganglia; and (v) the migration of crest‐derived cells within the gut is determined more by the route they follow to reach the bowel than by their level of origin in the neural crest. © 1993 wiley‐Liss, Inc.
Gene expression of CD24 core peptide molecule in developing brain and developing non‐neural tissues
Authors: Shirasawa Takuji , Akashi Takumi , Sakamoto Kyoichi , Takahashi Hiroshi , Maruyama Naoki , Hirokawa Katsuiku 
Published: February 2005

AbstractCD24 is a signal transducing molecule on the surface of most human B cells, murine immature T cells, myeloid and erythroid lineage cells. We isolated rat CD24 gene from embryonic brain cDNA library and characterized the gene expression during rat embryogenesis. Rat CD24 cDNA is homologous to murine and human CD24 gene with respect to the structure of signal peptide, N‐glycosylation sites, and possible glycosyl phosphatidylinositol (GPI) linker attaching site, suggesting that rat CD24 is a transducing glycorprotein anchoring membrane via GPI linker. In the developing embryo, in situ hybridization analyses revealed that CD24 transcript was detected in primitive ectoderm, mesoderm, and ventral endoderm of day 9 postcoitum (p.c.) embryo. In central nervous systems CD24 transcript was strongly expressed in postmitotic cells of spinal cord, hindbrain, midbrain, and forebrain from day 11 p.c. embryo to day 21 p.c. embryo but was dramatically down regulated in adult brain. Furthermore, expression was also detected in epithelium during development of non‐neural tissues, such as intestinal mucosal epithelium, nasal epithelium, ductal epithelium of salivary gland, bronchial epithelium, renal tubular epithelium, and hair follicles. In tooth development, where correct epithelium requires epithelial‐mesechymal interactions, CD24 mRNA was specifically induced in mesenchymal cells differentiating into odontoblast in dental papilla, suggesting the pivotal role of CD24 molecule in cell differentiations in vivo. We suggest that CD24 gene may encode the core peptide molecule of 31 kDa GPI linked molecule which has been known to be important in the migration of neurons on astroglial processes during development. © 1993 Wiley‐Liss, Inc.
Proportion of proliferative cells in the tadpole retina is increased after embryonic lesion
Authors: Wetts Richard , Kook Ji Hae , Fraser Scott E. 
Published: February 2005

AbstractLittle is known about the cellular mechanisms that cause some cells to stop dividing while leaving neighboring cells free to continue dividing. Such events occur during development of the Xenopus Retina; all cells of the embryonic eyebud are mitotic, but by stage 37 (St 37), only cells at the ciliary margin continue to proliferate as neighboring cells become post‐mitotic. The mechanisms that control these different proliferative fates remain unknown. One possibility is that total cell number regulates the initial number of proliferative cells at the ciliary margin. To test this hypothesis, we reduced the cell number by surgically removing a portion of the embryonic eyebud, including part of the prospective proliferative zone. Cell counts confirmed that the numbers of both the mitotic, undifferentiated cells and the post‐mitotic, differentiated cells were reduced following the partial ablation. A regression analysis suggested that the initial number of undifferentiated cells was a fixed proportion of the total number, but that this proportion was increased by the partial ablation. This increase occurred for all stages that the partial ablation was performed, from early optic vesicle to mid optic cup stages. The proportion of undifferentiated cells was normal in sham‐operated retinas, indicating that the increase in partially ablated retinas was induced by tissue removal and not by wound healing. Analyses of clones derived from single precursors, labeled with a fluorescent lineage tracer, indicated that the rate of proliferation was the same in partially ablated and sham‐operated retinas. Measurements of bromodeoxyuridine incorporation directly confirmed that at the ciliary margin cell division time was unchanged after partial ablation. Our observations are most consistent with the hypothesis that the proportion of undifferentiated cells was increased because cells that would have become post‐mitotic remained proliferative after the partial ablation. Furthermore, cell‐cell interactions most likely play a major role in controlling the initial number of proliferative cells in the tadpole retina. © 1993 Wiley‐Liss, Inc.
Cloning and developmental expression of the chick type II and type III TGFβ receptors
Authors: Barnett Joey V. , Moustakas Aristidis , Lin Wei , Wang Xiao‐Fan , Lin Herbert Y. , Galper Jonas B. , Maas Richard L. 
Published: February 2005

AbstractTo address the role of peptide growth factors in chick organogenesis, we have focused on TGFβ2 and have cloned the chick Type II and Type III TGFβ receptors. The chick Type II receptor is a serine/threonine kinase with a ligand binding profile identical to the human receptor and a divergent N‐terminus when compared to the mammalian receptors. The chick Type III receptor is a betaglycan that demonstrates a binding profile identical to the rat receptor and contains a single transmembrane spanning domain and short cytoplasmic tail that are highly conserved when compared to the mammalian receptors. Both the Type II and Type III TGFβ receptors are coexpressed during chick embryogenesis in the developing heart, lung, and eye, and are developmentally upregulated in parallel in the heart and lung. Levels of both receptor proteins and mRNAs also increase in cardiocytes cultured from different developmental stages, in agreement with the increase in Type II and Type III receptor mRNA levels observed in the developing heart. Although exhibiting different temporal or spatial profiles from the receptors, TGFβ2 is also expressed in the developing heart, lung, and eye. These findings are consistent with recent data indicating that co‐expression of both the Type II and Type III TGFβ receptors is required for high affinity binding of TGFβ2 by the Type II receptor and suggest that TGFβ2 and the Type II and Type III TGFβ receptors participate in heart, lung, and eye development. © 1994 Wiley‐Liss, Inc.
Pattern regulation in the chick autopodium at advanced stages of embryonic development
Authors: Gańan Yolanda , Macias Domingo , Hurle Juan M. 
Published: February 2005

AbstractIn previous studies we have observed that the interdigital tissue of the chick embryo leg bud during the stages previous to interdigital cell death exhibits a considerable chondrogenic potentiality both in vivo and in vitro. In the present investigation we have carried out a variety of experimental manipulations of the chick leg bud at stage 29 to discover possible mechanisms accounting for interdigital ectopic chondrogenesis and extradigit formation. Our results show that the interdigital tissue is capable of forming an extradigit when temporarily isolated microsurgically and regrafted in its original loction and after deletion of one of the adjacent digital primordia, suggesting that developing phalangeal cartilages exercise an inhibitory effect on chondrification in adjoining tissues. Furthermore, and of greater importance, ablation of the primordium of a digit is followed by normal development of the definitive digit if the wound surfaces are suitably apposed. These results reveal a considerable regulatory potentital in the autopodium at advanced stages of development. © 1994 Wiley‐Liss, Inc.
Localization of CRABP‐I and CRABP‐II mRNA in the early mouse embryo by whole‐mount in situ hybridization: Implications for teratogenesis and neural development
Authors: Lyn Sally , Giguère Vincent 
Published: February 2005

AbstractRetinoic acid (RA) has been implicated in vertebrate neural pattern formation. In this paper we analysed the expression patterns of the cellular retinoic acid binding proteins (CRABP‐I and II) during early morphogenesis in normal and RA‐treated mouse embryos by whole‐mount in situ hybridization. This technique allowed a detailed analysis of the spatial and temporal changes in mRNA expression pattern. Both CRABPs were expressed in a rhombomere specific pattern; putative neural crest cells in the branchial arches expressed the CRABPs at levels corresponding to the rhombomere from which they were derived. CRABP‐II, but not CRABP‐I, was expressed in the neural epithelium caudal to the hindbrain. CRABP‐I is strongly expressed in a fine net‐like pattern which extends from the caudal diencephalon to the rostral hindbrain and remains predominantly dorsal to the lateral midline of the neural tube. This network corresponds to the pattern formed by the putative first axons of the embryonic mouse brain which are produced by the developing neurons of the mesencephalic nucleus of the trigeminal nerve. Although the expression of CRABP‐I was unaffected by a teratogenic dose of RA, CRABP‐II expression was increased slightly with no alteration in the normal spatial or temporal boundaries. These results support the suggestion that the CRABPs may play an important role in modulating endogenous RA levels, particularly in the developing nervous system and its neural crest derivatives. Furthermore, the limited ability of CRABP mRNA levels to respond to exogenous retinoids may be a factor in retinoid teratogenicity. © 1994 Wiley‐Liss, Inc.
From gastrulation to neurulation: Transition in retinoic acid sensitivity identifies distinct stages of neural patterning in the rat
Authors: Cunningham Michael L. , Mac Auley Alasdair , Mirkes Philip E. 
Published: February 2005

AbstractEarly neural development is a multistep process with morphologically distinct stages; however, the molecular events that underlie morphologic development are poorly understood. Retinoic acid (RA) was chosen as a teratogen to perturb development because this endogenous molecule is thought to play an integral role in normal neuraxis formation in many vertebrate species. We have examined the effects of RA on early neural patterning in the rat at three morphologically distinct stages: late streak, foregut pocket, and early somite. In this model exogenous RA exposure during mid‐gastrulation (late streak stage) leads to severe disruption of anterior neural development as determined by morphologic and molecular (Engrailed [Eu] gene expression) markers. This disruption in anterior neural development is associated with excessive cell death in the hindbrain posterior to the En expression domain. In contrast, at the time the neural folds begin to elevate (foregut pocket stage) there is a dramatic reduction in the sensitivity of anterior neural development to exogenous RA as reflected by En expression and cell death patterns. These results suggest that we have identified a major transition in the development of the anterior neuraxis that is reflected in a transition in sensitivity to RA. This transition in sensitivity demonstrates that the fundamental patterning mechanisms that separate fore‐ and midbrain from hindbrain occurs very early in neurogenesis. © 1994 Wiley‐Liss, Inc.
The nipple and the areola of the human female breast
Authors: Giacometti Luigi , Montagna William 
Published: February 2005

AbstractThe nipple is covered by an epidermis with a characteristically intricate understructure of ridges. There are numerous, large sebaceous glands in the nipple, some opening inside the milk ducts. The terminal segments of the milk ducts are surrounded by bundles of smooth muscle arranged in sphincter‐like patterns. There are relatively few nerve endings in the epidermis of the nipple and areola; these are Krause‐like endings, and a number of non‐descript nerve endings are found around the epidermal ridges. All of these nerves, and those around the apocrine and eccrine sweat glands in the areola, contain acetylcholinesterase. The tubercles of Montgomery are accessory mammary glands. Though mammary glands are said to be modified apocrine sweat glands, the two have neither gross, nor histological and histochemical resemblances.
Effects of pancreatic homografts on the blood of normal and diabetic hamsters
Authors: House E. L. , Jacobs M. S. , Pansky B. 
Published: February 2005

AbstractPancreatic homografts were placed in the cheek pouches of normal and diabetic hamsters. Blood samples were taken at intervals for the next four weeks. The results were tabulated according to the fate of the implant: whether it was still growing after three weeks or whether it was rejected prior to that time. Among normal animals with good growth, there was an elevation of both the leucocyte and neutrophil counts, the increase being much greater when the grafts were rejected early. In severe diabetics, the increase in both parameters was less than in the controls, regardless of the fate of the graft. The most striking and consistent changes in the serum proteins involved the alpha‐2 and gamma globulins. Among controls the alpha‐2 fraction was as much as three times normal during the first post‐transplant week while the gamma globulin was elevated up to 80% above normal in the third week. In diabetics, the alpha‐2 fraction tended to be below normal while there was no significant increase in the gamma globulin.