bluuebunny/crossref_metadata_2025_split huggingface dataset:
Teratogenic and morphogenetic effects of retinoic acid on the regenerating pectoral fin in zebrafish
Authors: Géraudie Jacqueline , Brulfert Annie , Monnot Marie J. , Ferretti Patrizia 
Published: June 2005

AbstractFollowing amputation, the pectoral fin undergoes a regenerative process which leads to an apparently faithful replacement, both in shape and in size, of the missing part. However, analysis of the fin skeleton in whole mount preparations of normal and regenerated fins has revealed that fin regenerates are not perfect copies of the missing part, and that the distance and the number of ray segments between the amputation plane and the first dichotomy are higher in regenerated than in unamputated fins. This suggests that a respecification of positional values may be induced by amputation. Since retinoic acid (RA) induces duplication of structures in the regenerating amphibian limb, and affects pattern formation in the zebrafish nervous system, we have investigated whether RA could affect regeneration of the pectoral fin in zebrafish. We report that, depending on the concentration and the experimental schedule, RA can have both teratogenic (narrowing of the fin and fusion of rays) and morphogenetic (increased number of ray segments) effects on the regenerating fin, but, unlike in the amphibian limb, these effects often overlap. Furthermore, while the teratogenic effect seems to affect mainly the dorsoventral axis, the morphogenetic effect is observed on the proximodistal axis. Our work suggests that the zebrafish fin may provide another valuable model to study regeneration and pattern formation of animal appendages. © Wiley‐Liss, Inc.
The pseudoblastema in the wound healing process of the leech Hirudo medicinalis L. (Hirudinea): Changes in cell junctions
Authors: Huguet G. , Molinas M. 
Published: June 2005

AbstractThe role of the connective tissue cells and their migratory behavior have been investigated in the formation and evolution of the pseudoblastema during wound healing in the leech Hirudo medicinalis. In H. medicinalis the healing process shows first a flow of cells that effectively seal the wound and form a temporary cellular clump, the pseudoblastema, which contributes to the phagocytotic process and apparently regenerates the extracellular matrix. The migratory cells forming the pseudoblastema are connective tissue cells known as vasocentral cells, which, when in a resting state, are associated with the vasofibrous cells. During the formation and evolution of the pseudoblastema several changes affect vasocentral cell junctions. At rest, vasocentral cells do not show cell to cell junctions but they show adhering junctions in contact with the extracellular matrix. These junctions disrupt during the migratory phase. When vasocentral cells regroup in the pseudoblastema, adhering junctions are formed between them, and adhering junctions making contact with the matrix appear again. As the pseudoblastema evolves, cell to cell adhering junctions become more conspicuous and undergo other changes. During the next stage of retraction, close contacts develop between pseudoblastema cells and neighboring nondamaged muscle fibers, which probably serve as points of anchorage for the approaching movement of the wound edges. Finally, cell to cell and cell to matrix junctions disappear and the pseudoblastema disintegrates. © Wiley‐Liss, Inc.
Pedicle and antler regeneration following antlerogenic tissue removal in red deer (Cervus elaphus)
Authors: Li Chunyi , Suttie James M. 
Published: June 2005

AbstractThe physiological control mechanisms underlying the histogenesis of the pedicle, which precedes antler growth, from the frontal bones of male deer are poorly understood. The aim of this study was to investigate the extent of pedicle/antler regeneration after removal (for histological evaluation) of the antlerogenic region or pedicle tissue during pedicle development to determine whether the subsequent pattern of regeneration could contribute to the understanding of pedicle histogenesis and the mechanism of the transition between permanent pedicles and deciduous antlers. The contralateral pedicles of six stags were not removed and these data serve as controls. All deer were observed frequently and measurements of regeneration were made in March after all antler growth had ceased for that season. The developmental stage of the pedicle was determined by a combination of pedicle height measurements and histological studies. The results showed that pedicle formation histologically covers three stages: a period of intramembranous ossification (when the pedicle is less than 5 mm in height), a period when the ossification pattern changes (when the pedicle is between 5 and 28 mm in height) and a period of modified endochondral ossification (when the pedicle is over 30 mm in height). In all ossification stages some deer regenerated neither antlers nor pedicles. The pedicles which regenerated following the loss of antlerogenic tissue at the intramembranous ossification stage were shorter than the controls (P < 0.01), but longer than the pedicles regenerated after pedicle removal at the transitional stage in the pattern of ossification (P < 0.01). No pedicle tissue was regenerated if the pedicles were removed at the endochondral ossification stage and antlers were directly formed from the deer's head. Thus the final height of the regenerated pedicles was closely linked with the histological ossification stage of the original pedicle at removal. Antler regeneration took place at all stages but two deer grew pedicles only when tissue removal took place during the transition period. Overall the results provide evidence that the potential to regenerate a pedicle diminishes as the pedicle increases in height and the necessity for pedicle growth to precede antler growth also decreases. The fact that some deer, whose tissues were removed at the transition period of ossification change, regenerated pedicles but failed to generate antlers highlights the importance of this stage for the transition between the permanent pedicle and the deciduous antler. The results provide evidence for an hypothesis that it is the transition between ossification types which signals the end of pedicle development and the onset of antler development. © Wiley‐Liss, Inc.
In vivo and in vitro initiation of sperm motility using fresh and cryopreserved gametes from the pacific herring, Clupea pallasi
Authors: Pillai Murali C. , Yanagimachi Ryuzo , Cherr Gary N. 
Published: June 2005

AbstractPacific herring (Clupea pallasi) gametes were cryopreserved in a simple extender (15% dimethyl sulfoxide in herring Ringers). Sperm remained viable for over 7 months when kept at liquid nitrogen temperature. A rapid cooling rate by directly plunging into liquid nitrogen allowed a majority of the cells to remain viable after subsequent thawing at 26°C. Cryopreserved sperm initiated motility (activation) under both in vivo (in the micropyle area of the egg) or in vitro (in the presence of isolated sperm motility initiation factor or low sodium seawater) conditions. In addition to their ability to undergo activation, cryopreserved sperm were capable of fertilizing fresh eggs in a concentration dependent manner resulting in > 90% fertilization and embryonic development. Herring eggs cryopreserved in a similar manner as sperm remained intact in gross morphology. Although cryopreserved eggs were not fertilizable, both fresh and previously frozen sperm were activated in the micropyle areas of the chorions. The method we describe to cryopreserve gametes from this species is simple and is useful for future experimental studies of sperm‐chorion interaction when fresh material is unavailable. © Wiley‐Liss, Inc.
Involvement of the lysosomal system in yolk protein deposit and degradation during vitellogenesis and embryonic development in trout
Authors: Sire Marie‐France , Babin Patrick J. , Vernier Jean‐Marie 
Published: June 2005

AbstractIn adult female rainbow trout (Oncorhynchus mykiss), an immunocytochemical study of the oocyte has shown that a proteolytic enzyme, cathepsin D, is localized in multivesicular bodies (MVB) which begin to differentiate before the phase of vitellogenesis. Estrogens cause the liver to synthesize the protein vitellogenin (VTG), which then enters the systemic circulation. During vitellogenesis, endocytosed VTG is co‐localized with cathepsin D in the MVB. Assays of oocyte cathepsin activities have shown that the only proteolytic activity of note is that of cathepsin D. Along with the yolk proteins derived from VTG, this enzyme will be included in the central coalescent yolk mass.With the installation of the yolk syncytial layer and the surrounding yolk vascular system, embryonic development is characterized by high lysosomal activity, especially in the syncytial layer. At this level, proteolytic activity concerns a cathepsin L, secreted as a proenzyme. We propose the hypothesis that cathepsin D, along with the yolk proteins in the yolk globules that break away from the yolk mass in the vitellolysis zone, activates the proenzyme and leads to protein degradation, which then becomes very rapid. © Wiley‐Liss, Inc.
Occlusion of the parietal eye induces a transient wavelength‐dependent shift in lizard thermoregulatory set points
Authors: Tosini Gianluca , Avery Roger A. 
Published: June 2005

AbstractThermoregulatory set points—i.e., the body temperatures at which heat‐seeking or cooling behavior are initiated—of the lacertid lizard Podarcis muralis were measured by infrared thermography before and after covering the parietal eye with light filters with different cutoff points. The results show that shielding the parietal eye results in a transient alteration of thermoregulatory set points; this effect is wavelength‐dependent. Mean heating rates, bask and forage durations were not affected by the shielding of the parietal eye with any of the filters used. © Wiley‐Liss, Inc.
The effects of neurotransmission on neuronal gene expression
Authors: Mack Kenneth J. 
Published: June 2005

AbstractGene expression is primarily controlled at the level of transcription. Of the 100,000 genes expressed in the human body, 30–50% may be specifically expressed in nervous tissue. Some of this gene expression is genetically determined and is therefore preprogrammed. However, neuronal gene expression can also be affected by environmental factors, mediated through neuronal transmission. It is hypothesized that neurotransmission has a primary role in developmental and adult neuronal plasticity, and that these effects are mediated through alterations in gene expression. Pathological neurotransmission, such as that seen after seizures, may be disruptive to these patterns of gene expression. © 1995 Wiley‐Liss, Inc.
Alterations in synaptic connectivity in cerebral cortex in neuronal storage disorders
Authors: Walkley Steven U. , Wurzelmann Sarah 
Published: June 2005

AbstractNeuronal storage diseases are inborn errors of metabolism characterized by widespread intraneuronal storage and progressive neurological dysfunction, including mental retardation, movement disorders, and seizures. Most of these disorders are associated with specific defects in particular lysosomal enzymes. Moreover, a wide array of genetic defects has been documented. The immense progress made during the past three decades in understanding the primary molecular and enzymatic defects in this family of diseases stands in sharp contrast to the modest advances made in delineating pathogenetic mechanisms and treatment strategies. Although these disorders result from highly selective defects in metabolic pathways, they ultimately are complex conditions characterized by a plethora of seemingly unrelated secondary molecular and cellular abnormalities. Studies of children and animals affected by these diseases have revealed that significant changes in neuronal connectivity occur in the cerebral cortex. These include not only degenerative changes in axons and synapses of inhibitory neurons, but also a regrowth of dendrites and new synapse formation involving pyramidal neurons. The latter finding indicates that neurons in the cerebral cortex undergo significant “rewiring” during the height of the disease process. This regrowth of primary dendrites and formation of new synapses as part of a neurological disease is unprecedented. Understanding the causes and consequences of these changes in cortical synaptic connectivity in neuronal storage diseases may provide insight not only into the precise mechanisms underlying mental retardation in these diseases and their reversibility, but also into processes governing dendritic elaboration and synapse formation in the normal developing nervous system. © 1995 Wiley‐Liss, Inc.
Ischemia and excitotoxins in development
Authors: Johnston Michael V. , Ishiwa Shun 
Published: June 2005

AbstractIschemia in the developing brain triggers a series of events that cause damage after a threshold of severity and duration are reached. Release of glutamate, the major excitatory amino acid neurotransmitter in the brain, is one of the primary events in this cascade of injury. Release of glutamate combined with reversal of glutamate uptake pumps in nerve terminals causes glutamate levels to increase from 10–1000x baseline levels in the brain's extracellular space during ischemia, traumatic brain injury, and hypoglycemia in animal models and in humans. High levels of extracellular glutamate trigger opening of N‐methyl‐D‐asparate (NMDA) and non‐NMDA glutamate channels, allowing calcium and sodium to flood into neurons. Energy failure in mitochondria facilitates opening of NMDA channels by lowering the membrane potential and reducing their blockade by magnesium that resides within the channel at normal membrane potentials. Calcium entry into the cytoplasm triggers several events including activation of lipases, proteases, and nucleases that can destroy the neuron's cellular machinery. Generation of reactive oxygen free radicals including the messenger molecule nitric oxide can have additional destructive effects. Drugs that block glutamate receptors and the “excitotoxic cascade” of downstream events can protect the brain from injury and show promise for clinical application in infants and children. © 1995 Wiley‐Liss, Inc.
Neurotransmitter alterations in congenital hyperammonemia
Authors: Robinson Michael B. , Batshaw Mark L. 
Published: June 2005

AbstractInborn errors of metabolism are associated with a significant risk of mental retardation and other developmental disabilities. Only rarely, is the mechanism of the neural injury clearly understood. This is particularly true for those inborn errors of metabolism associated with hyperammonemia, principally urea cycle disorders and organic acidemias. Previously, it was assumed that elevated ammonia levels alone could account for the brain injury. However, in vitro studies suggest that ammonia is not particularly toxic to intact neurons. Furthermore, there does not appear to be a direct linkage between the peak blood ammonia level during hyperammonemic coma and subsequent neurodevelopmental outcome. There is, however, a correlation between duration of hyperammonemic coma and outcome, suggesting a secondary, time‐influenced mechanism of neural injury. Recent research has focused on excitotoxicity as a possible inducer of neural injury in congenital hyperammonemia. In addition to developmental disabilities, affected children exhibit behavioral abnormalities. An alteration in serotonin metabolism has been proposed as an explanation for these aberrant behaviors during less severe episodes of hyperammonemia. This review focuses on the neurotransmitter abnormalities occuring in congenital hyperammonemia and on new approaches to protecting the brain during hyperammonemic crises. © 1995 Wiley‐Liss, Inc.
Neurotransmitter alterations in the trisomy 16 mouse: A genetic model system for studies of down syndrome
Authors: Oster‐Granite Mary Lou , Lacey‐Casem Merri Lynn 
Published: June 2005

AbstractThis review describes the alterations that occur in a variety of neurotransmitter systems in mouse trisomy 16 and compares those alterations with ones observed in individuals with Down syndrome (Trisomy 21) and Alzheimer's disease. Individuals with Down syndrome who survive into their fourth decade invariably have the neuropathologic and neurochemical features associated with Alzheimer's disease. Thus, comparative studies may provide insight into pathogenetic mechanisms common to all three conditions. These neurotransmitter alterations are accompanied by neuroanatomical as well as neurophysiological alterations in Down syndrome, Alzheimer's disease, and mouse trisomy 16. Because mice with complete trisomy 16 do not survive the perinatal period. Ts 16 neurons placed in culture, as well as primary and secondary chimeras comosed in part of Ts 16 cells, have also been examined for neurotransmitter alterations. Like individuals with Down syndrome, mice with trisomy 16 have triplication of a constellation of genes that have remained together in the same order for roughly 80 million years. As more of these genes have been identified and localized to specific regions of human chromosome 21 and, in some cases, to mouse chromosome 16 as well, effeorts have been made to create mice that are transgenic for these can be studied. Studies of several of these different types of transgenic mice have begun to provide insight inot the mechanisms by which neurotransmitter alterations may arise in Ts 16 mice, and by extrapolation, in DS individuals as well. © 1995 Wiley‐Liss, Inc.
Effect of the uterine environment on the frequency of spontaneous cleft lip in CL/Fr mice
Authors: Bornstein S. , Trasler D. G. , Fraser F. C. 
Published: June 2005

AbstractIt was previously shown (Davidson et al., '69) that the A/J female mouse predisposes her offspring to congenital cleft lip, either by providing a uterine environment or cytoplasmic factors that increase susceptibility, or by not providing a cytoplasmically transmitted factor, present in the C57BL/6J strain, that decreases susceptibility to cleft lip. In the present experiment males of the CL/Fr strain, which has a relatively high frequency of cleft lip, were crossed to females of the C57BL/6J strain, and the F1 offspring were backcrossed to CL/Fr animals. Three second backcrosses were made such that embryos of comparable genotype developed in CL/Fr mothers or in hybrid mothers with or without the postulated cytoplasmic factors. The results showed that the maternal effect on cleft lip susceptibility was present in the CL/Fr strain, and was not mediated through the cytoplasm. Maternal age, parity, litter size, and sex and pigmentation of the offspring showed no consistent associations with frequency of cleft lip. The demonstration of a uterine effect on cleft lip susceptibility suggests that it might be possible to modify the environment in the direction of increased resistance.
An improved apparatus for producing stress‐induced cleft palate in mice
Authors: Rosenzweig Sanford , Blaustein Frances M. , Anderson Clint D. 
Published: June 2005

AbstractA/J mice were restrained for 48 hours beginning on day 14 of pregnancy in an improved cage so constructed that the mouse could drink in its usual manner. This was an improvement over previously used restraining cages in which potato was supplied as a substitute for water. A cleft palate frequency of 15.7% obtained with this new cage was significantly greater than that in the control group and demonstrated that resraint can be teratogenic.
Cysteamine protection against lethal and growth‐inhibiting effects of prenatal X and gamma irradiation
Authors: Roberts Joan M. 
Published: June 2005

AbstractExposure of pregnant rats to gamma radiation on day 16 of gestation produced nearly double the number of neo‐ and postnatal offspring deaths as did X irradiation. Dose level (185 r), dose rate (10–12 r/minute), and distance from the source were the same in both groups. Cysteamine given prenatally prior to either gamma or X irradiation significantly decreased mortality. In the gamma‐irradiated group the mortality rate remained significantly higher than in the control group, but in the X‐irradiated group it was reduced to the control level by pretreatment with cysteamine. Cysteamine given to pregnant rats immediately following gamma irradiation had no effect on offspring mortality.
Trimethadione and human teratogenesis
Authors: German James , Kowal Areta , Ehlers Kathryn H. 
Published: June 2005

AbstractA family is described in which four malformed children were born to a mother while she was taking trimethadione, an antiepileptic drug infrequently prescribed for adults. Following discontinuation of the drug, she had two normal children. This family led to a survey of all 278 epileptic women admitted to one hospital during the 23 years following the introduction of trimethadione for treatment of petit mal. Only eight women had ever taken it or its close congener paramethadione, and only three had taken it early in a pregnancy. Thus the outcomes of 14 pregnancies, during which the mothers took trimethadione or paramethadione early, have become known to the authors, those in the index family and those in three additional families ascertained through the survey. These pregnancies showed a high frequency of abnormality: eight children with developmental defects of various types, only three of whom have survived early infancy; one child with multiple hernias and juvenile, nonfamilial diabetes; and three spontaneous abortions. The survey suggests that neither epileptic women as a group nor those taking antiepileptic drugs usually prescribed for adults have an obviously increased frequency of malformed children but that epileptic women taking trimethadione or paramethadione may constitute a special subgroup whose children do have an increased frequency of birth defects. The small number of observations possible at a single institution, although suggestive, precludes a firm opinion as to the possible role as human teratogens of the oxazolidine‐2,4‐diones.
Early neurovascular abnormalities underlying 6‐aminonicotinamide (6‐AN)‐induced congenital hydrocephalus in rats
Authors: Chamberlain J. G. 
Published: June 2005

AbstractDefects in the rat central nervous system during retarded brain development and congenital hydrocephalus were studied following single maternal injections of the niacinamide antimetabolite 6‐aminonicotinamide (6‐N) late in development. Histological and histochemical analyses indicated CNS hemorrhage and growth retardation of fetal brains 24 hours after treatment; fluid movement into cerebral ventricles was evidenced by secretionlike, circular “blebs” along the ependymal lining. There was transitorily increased glycogen in hypoplastic choroid plexuses with disruption of cerebral layering of neuroblasts. Despite thinned cerebral cortex and increased ventricular surface area, associated with cranial distortion and communicating, compensatory ventricular enlargement, normal intracranial pressure was recorded by day 21 of gestation. During the pathogenetic process macrophagic cells removed cellular debris and RBC's so that by term little evidence of early hemorrhage was apparent.