bluuebunny/crossref_metadata_2025_split huggingface dataset:
Patterning the neural crest derivatives during development of the vertebrate head: insights from avian studies
Authors: Creuzet Sophie , Couly Gérard , Le Douarin Nicole M. 
Published: September 2010

AbstractStudies carried out in the avian embryo and based on the construction of quail–chick chimeras have shown that most of the skull and all the facial and visceral skeleton are derived from the cephalic neural crest (NC). Contribution of the mesoderm is limited to its occipital and (partly) to its otic domains. NC cells (NCCs) participating in membrane bones and cartilages of the vertebrate head arise from the diencephalon (posterior half only), the mesencephalon and the rhombencephalon. They can be divided into an anterior domain (extending down to r2 included) in which genes of the Hox clusters are not expressed (Hox‐negative skeletogenic NC) and a posterior domain including r4 to r8 in which Hox genes of the four first paraloguous groups are expressed. The NCCs that form the facial skeleton belong exclusively to the anterior Hox‐negative domain and develop from the first branchial arch (BA1). This rostral domain of the crest is designated as FSNC for facial skeletogenic neural crest. Rhombomere 3 (r3) participates modestly to both BA1 and BA2. Forced expression of Hox genes (Hoxa2, Hoxa3 and Hoxb4) in the neural fold of the anterior domain inhibits facial skeleton development. Similarly, surgical excision of these anterior Hox‐negative NCCs results in the absence of facial skeleton, showing that Hox‐positive NCCs cannot replace the Hox‐negative domain for facial skeletogenesis. We also show that excision of the FSNC results in dramatic down‐regulation of Fgf8 expression in the head, namely in ventral forebrain and in BA1 ectoderm. We have further demonstrated that exogenous FGF8 applied to the presumptive BA1 territory at the 5–6‐somite stage (5–6ss) restores to a large extent facial skeleton development. The source of the cells responsible for this regeneration was shown to be r3, which is at the limit between the Hox‐positive and Hox‐negative domain. NCCs that respond to FGF8 by survival and proliferation are in turn necessary for the expression/maintenance of Fgf8 expression in the ectoderm. These results strongly support the emerging picture according to which the processes underlying morphogenesis of the craniofacial skeleton are regulated by epithelial–mesenchymal bidirectional crosstalk.
Barx1 and evolutionary changes in feeding
Authors: Miletich Isabelle , Buchner Georg , Sharpe Paul T. 
Published: September 2010

AbstractDuring mouse embryonic development, the Barx1 homeobox gene is expressed in the mesenchymal cells of molar teeth and stomach. During early stages of molar development, Barx1 has an instructive role, directing the as yet undetermined ectomesenchymal cells in the proximal region of the jaws to follow a multicuspid tooth developmental pathway. We review here recent results showing an absence of stomach tissue in Barx1 mutant mice. The data strongly suggest that in the presumptive stomach mesenchyme Barx1 acts to attenuate Wnt signalling allowing digestive tract endoderm to differentiate into a highly specialized stomach epithelium. In the light of these new data, we discuss the possibility that evolutionary changes in the Barx1 gene could have simultaneously altered the dentition and the digestive system, therefore positioning Barx1 as a key gene in the evolution of mammals.
Reassessing theDlxcode: the genetic regulation of branchial arch skeletal pattern and development
Authors: Depew Michael J. , Simpson Carol A. , Morasso Maria , Rubenstein John L. R. 
Published: September 2010

AbstractThe branchial arches are meristic vertebrate structures, being metameric both between each other within the rostrocaudal series along the ventrocephalic surface of the embryonic head and within each individual arch: thus, just as each branchial arch must acquire a unique identity along the rostrocaudal axis, each structure within the proximodistal axis of an arch must also acquire a unique identity. It is believed that regional specification of metameric structures is controlled by the nested expression of related genes resulting in a regional code, a principal that is though to be demonstrated by the regulation of rostrocaudal axis development in animals exerted by the nestedHOM‐C/Hoxhomeobox genes. The nested expression pattern of theDlxgenes within the murine branchial arch ectomesenchyme has more recently led to the proposal of aDlxcode for the regional specification along the proximodistal axis of the branchial arches (i.e. it establishes intra‐arch identity). This review re‐examines this hypothesis, and presents new work on an allelic series ofDlxloss‐of‐function mouse mutants that includes various combinations ofDlx1,Dlx2,Dlx3,Dlx5andDlx6. Although we confirm fundamental aspects of the hypothesis, we further report a number of novel findings. First, contrary to initial reports,Dlx1,Dlx2andDlx1/2heterozygotes exhibit alterations of branchial arch structures andDlx2–/–andDlx1/2–/–mutants have slight alterations of structures derived from the distal portions of their branchial arches. Second, we present evidence for a role for murineDlx3in the development of the branchial arches. Third, analysis of compoundDlxmutants reveals four grades of mandibular arch transformations and that the genetic interactions ofcisfirst‐order (e.g.Dlx5andDlx6),transsecond‐order (e.g.Dlx5andDlx2) andtransthird‐order paralogues (e.g.Dlx5andDlx1) result in significant and distinct morphological differences in mandibular arch development. We conclude by integrating functions of theDlxgenes within the context of a hypothesized general mechanism for the establishment of pattern and polarity in the first branchial arch of gnathostomes that includes regionally secreted growth factors such asFgf8andBmpand other transcription factors such asMsx1, and is consistent both with the structure of the conserved gnathostome jaw bauplan and the elaboration of this bauplan to meet organismal end‐point designs.
Changes in the oviducal epithelium during the estrous cycle in the marsupial Monodelphis domestica
Authors: Kress Annetrudi , Morson Gianni 
Published: September 2010

AbstractThe Monodelphis oviduct can be divided into four anatomical segments: preampulla (comprising fimbriae and infundibulum), ampulla, isthmus with crypts and uterotubal junction. Ovaries are enclosed in a periovarial sac, the bursa, and in some specimens tubules of an epoophoron could be identified. In both structures non‐ciliated cells develop small translucent vesicles, which accumulate in the cell apices and presumably produce fluid as often seen in the bursa and in the tubules of the epooophoron. These vesicles do not stain with Alcian blue or PAS. The same applies also to the non‐ciliated cells of the fimbriae. The oviducal epithelium of ampulla and the surface epithelium of the isthmus consisting of ciliated and non‐ciliated, secretory cells undergo considerable changes during the estrous cycle. Proestrus shows low numbers of ciliated cells, some are in the process of neo‐ciliogenesis, non‐ciliated cells carry solitary cilia and few remnant secretory granules from the previous cycle may be found. At estrus the amount of ciliated cells in ampulla and isthmus has increased, most non‐cililated cells lost the solitary cilia, developed longer microvilli and formed numerous secretory granules in their cell apices. At postestrus secretory products, often surrounded by membranes, are extruded into the oviducal lumen and contribute towards egg coat formation. First signs of deciliation processes are apparent. Solitary cilia reappear.At metestrus only few secretory cells are left with some secretory material. The lumen is often filled with shed cilia and cell apices. Proliferation of basal bodies within non‐secretory cells indicate the formation of new ciliated cells.The non‐ciliated epithelial cells of the isthmic crypts form no secretory granules but accumulate a great number of translucent vesicles, which in contrast to the secretory granules do not stain with Alcian blue or PAS.
The functional development of Leydig cells in a marsupial
Authors: Butler Christopher M. , Shaw Geoff , Clark Joan , Renfree Marilyn B. 
Published: September 2010

AbstractLeydig cells are the major source of androgen in the male mammal. We describe here for the first time the development of the Leydig cell in a macropodid marsupial, the tammar wallaby, Macropus eugenii. Leydig cells are first recognized morphologically 2 days after birth with the appearance of lipid droplets in the cytoplasm of certain interstitial cells. Lipid content closely matches the steroid content of the developing testis and marks the maturation of the steroid synthesis pathway in the tammar testis. Morphologically mature Leydig cells, marked by distinct mitochondria with tubular cristae and an extensive anastomosing network of smooth endoplasmic reticulum, are developed by day 10 after birth – the time of peak testosterone content in perinatal tammar testes. The volume percentage of each cell type in the testis does not change over time so the growth of each cellular component keeps pace with growth of the whole testis. There was no morphological or quantitative evidence of a change from one population of Leydig cells to another in the tammar testis as has been reported in several other species including the rat, mouse and human. Maturation of the testis is also marked by the development of tight junctions between the cell membranes of adjacent Sertoli cells. These appear around day 30 after birth and coincide with the onset of mitotic arrest in male germ cells. Overall, the development of the Leydig cell in the tammar wallaby follows a similar pattern to that seen in other mammals, although the start of Leydig cell differentiation is, like many other organ systems in marsupials, post natal, not fetal and there appears to be only a single population of Leydig cells.
The coronary arteries of the C57BL/6 mouse strains: implications for comparison with mutant models
Authors: Fernández B. , Durán A. C. , Fernández M. C. , Fernández‐Gallego T. , Icardo J. M. , Sans‐Coma V. 
Published: September 2010

AbstractThere are few detailed descriptions of the coronary arterial patterns in the mouse. Some recent reports on coronary anomalies in mutant mouse models have uncovered the importance of several genes (i.e. iv and connexin43) in coronary morphogenesis. These mutations spontaneously appeared (iv) or were generated (connexin43) in a C57BL/6 background, which is widely used for the development of mutant mice. We have studied the origin and course of the main coronary arteries of two C57BL/6 mouse strains. Unusual anatomical coronary arterial patterns were found, including: solitary ostium in aorta, accessory ostium, high take‐off, aortic intramural course, slit‐like ostium, sinus‐like ostium and origin of a septal artery from the left coronary artery. In humans, some of these conditions are clinically relevant. Most of these patterns, which differ from those observed in wild mice and Swiss albino mice, coincide with those previously found in iv/iv and connexin43 knockout mice. The results indicate that there is variability in the coronary arterial arrangement of the laboratory mouse. Care should be taken when analysing coronary phenotypes of mutant mouse models.
Maternal diabetes affects specific extracellular matrix components during placentation
Authors: Giachini F. R. C. , Carriel V. , Capelo L. P. , Tostes R. C. , Carvalho M. H. , Fortes Z. B. , Zorn T. M. , San Martin S. 
Published: September 2010

AbstractDuring embryo implantation, invasive trophoblast cells mediate embryo invasion into the decidualized stroma, forming a rich network of lacunae that connect the embryonic tissues to the maternal blood vessels. Placentation is probably guided by the composition and organization of the endometrial extracellular matrix. Certain pathological conditions that occur during pregnancy, including diabetes, have been linked to abnormal placental morphology and consequent fetal morbidity. We used immunoperoxidase techniques to identify members of the collagen, proteoglycan and glycoprotein families in the various compartments of the rat placenta and to determine whether experimentally induced diabetes affects placental morphology and alters the distribution of these molecules during pregnancy. Single injections of alloxan (40 mg kg−1 i.v.) were used to induce diabetes on day 2 of pregnancy in Wistar rats. Placentas were collected on days 14, 17, and 20. Type I and III collagen, as well as the proteoglycans decorin and biglycan, were found to be distributed throughout the placentas of control and diabetic rats. In both groups, laminin expression decreased at the end of pregnancy. In contrast, fibronectin was detected in the labyrinth region of diabetic rats at all gestational stages studied, whereas it was detected only at term pregnancy in the placentas of control rats. These results show for the first time that some extracellular matrix molecules are modulated during placental development. However, as diabetic rats presented increased fibronectin deposition exclusively in the labyrinth region, we speculate that diabetes alters the microenvironment at the maternal–fetal interface, leading to developmental abnormalities in the offspring.
Human sperm anatomy: ultrastructural localization of 1α,25‐dihydroxyvitamin D3 receptor and its possible role in the human male gamete
Authors: Aquila Saveria , Guido Carmela , Perrotta Ida , Tripepi Sandro , Nastro Alfonso , Andò Sebastiano 
Published: September 2010

AbstractPrevious studies have suggested that 1α,25‐dihydroxyvitamin D3[1,25(OH)2D3] has a role in reproductive function. Gonadal insufficiencies were observed as a result of 1,25(OH)2D3 deficiency and in 1,25(OH)2D3 receptor (VDR) null mutant mice. To study human sperm anatomy at the molecular level, we first evaluated the ultrastructural localization of VDR by immunogold electron microscopy using a monoclonal antibody against amino acids 344–424 of human VDR, in normozoospermic samples. Intriguingly, VDR was associated predominantly with the cell nucleus. In fact, it is known that VDR is a transcription factor, and that in vitamin‐D‐depleted animals, VDR is largely localized in the cell nucleus. To assess the significance of VDR in the male gamete, we investigated the role of 1,25(OH)2D3/VDR in sperm survival and capacitation. Our results revealed that the action of 1,25(OH)2D3 depended on its concentration because although lower doses induced cholesterol efflux, protein phosphorylation and sperm survival, a higher concentration seemed to be ineffective or did not show an increased effect. These results increase our knowledge of human sperm anatomy at the molecular level and suggest that 1,25(OH)2D3/VDR may have an important role in sperm survival and the acquisition of fertilizing ability.
Stimulation of natriuretic peptide receptor C attenuates accumulation of reactive oxygen species and nitric oxide synthesis in ammonia‐treated astrocytes
Authors: Skowrońska Marta , Zielińska Magdalena , Albrecht Jan 
Published: September 2010

J. Neurochem.(2010)115, 1068–1076.AbstractOxidative and nitrosative stress contribute to ammonia‐induced astrocytic dysfunction in hepatic encephalopathy. Treatment of cultured astrocytes with 5 mmol/L ammonium chloride (‘ammonia’) increased the production of reactive oxygen species (ROS), including the toxic NADPH oxidase reaction product, •O2−. Atrial natriuretic peptide (ANP), natriuretic peptide C and a selective natriuretic peptide receptor (NPR)‐C ligand, cANP(4–23),each decreased the total ROS content both in control cells and cells treated with ammonia. However, attenuation of •O2−accumulation by ANP and cANP(4–23),was observed in ammonia‐treated cells only and the effect of cANP(4–23)was decreased when the NADPH oxidase‐regulatory protein Giα‐2was blocked with a specific anti‐Giα‐2antibody. Although in contrast to ANP, cANP(4–23)did not elevate the cGMP content in control astrocytes, it decreased cAMP content and reduced the expression of Giα‐2, the NADPH oxidase‐regulatory protein. The results show the presence of functional NPR‐C in astrocytes, activation of which (i) attenuates basal ROS production, and (ii) prevents excessive accumulation of the toxic ROS species, •O2−by ammonia. Ammonia, ANP and cANP(4–23)added separately, each stimulated formation of NOx(nitrates + nitrites) which was associated with up‐regulation of the activity [cANP(4–23)] or/and expression (ammonia) of the endothelial isoform of nitric oxide synthase. However, the ammonia‐induced increase of NOxwas not augmented by co‐addition of ANP, and was reduced to the control level by co‐addition of cANP(4–23), indicating that activation of NPR‐C may also reduce nitrosative stress. Future hepatic encephalopathy therapy might include the use of cANP(4–23)or other NPR‐C agonists to control oxidative/nitrosative stress induced by ammonia.
Ammonium influx pathways into astrocytes and neurones of hippocampal slices
Authors: Kelly Tony , Rose Christine R. 
Published: September 2010

J. Neurochem. (2010) 115, 1123–1136.AbstractAmmonium (NH4+) is required to maintain pathways involved in shuttling metabolic precursors between astrocytes and neurones. Under hyperammonaemic conditions, increases in the cellular influx of NH4+, and accompanying changes in ion concentrations, may contribute to disruptions in metabolism and neurotransmission. We investigated mechanisms of cellular NH4+ influx in hippocampal slices by measuring acute NH4+/NH3‐evoked changes in intracellular pH (pHi) and sodium ([Na+]i). In both astrocytes and neurones, application of 5 mM NH4Cl for 30–45 min decreased pHi by 0.2–0.3 units, consistent with NH4+ influx. In astrocytes, but not neurones, acidifications were accompanied by [Na+]i increases of 25–30 mM. Glial [Na+]i increases were blocked by bumetanide, suggesting that NH4+/NH3 activated Na+‐dependent, K+, Cl− cotransport. Bumetanide also reduced NH4+/NH3‐evoked acidifications in astrocytes. Neuronal acidifications were insensitive to bumetanide and inhibition of Cl−‐dependent transport and K+ channels, but were prevented by inhibition of Na+,K+‐ATPase with ouabain. Furthermore, ouabain reduced astrocyte acidifications. Our results suggest that following rapid elevation of NH4+, Na+,K+‐ATPase is the major influx pathway for NH4+ in neurones, whereas Na+,K+‐ATPase and Na+‐dependent, K+, Cl− cotransport mediate NH4+ transport into astrocytes. The different mechanisms of NH4+ influx in astrocytes and neurones may contribute to the different susceptibility of both cell types to acute hyperammonaemic conditions.
PAPP‐A: a new anti‐aging target?
Authors: Conover Cheryl A. 
Published: September 2010

SummaryThis article focuses on the role of PAPP‐A in mammalian aging. It introduces PAPP‐A and a little of its history, briefly discusses the function of PAPP‐A in the insulin‐like growth factor (IGF) system and the regulators of PAPP‐A expression, and then reviews data concerning PAPP‐A in aging and age‐related diseases especially in regard to the PAPP‐A knockout (KO) mouse. The PAPP‐A KO mouse is a valuable new model to test hypotheses concerning the control of the tissue availability of IGF, independent from systemic levels, on healthspan as well as lifespan.
Acute peritonitis secondary to traumatic breeding in the bitch
Authors: Morey Deborah L. 
Published: September 2010

AbstractObjective:To discuss 2 cases of acute peritonitis caused by traumatic breeding in the bitch.Series summary:Two bitches presented with acute abdominal pain, clinical signs, and laboratory abnormalities compatible with peritonitis. Both bitches were in estrus and had been observed copulating with male dogs prior to the onset of clinical signs. Diagnostic testing revealed bacterial peritonitis in both dogs, and intracellular and extracellular spermatozoa in ascites from 1 of the dogs. Surgical exploration revealed rupture of the uterine body and generalized peritonitis in both animals. Both bitches recovered following surgical and medical treatment.New or unique information provided:This is the first reported series of cases of peritonitis secondary to traumatic breeding. These cases introduce a unique presentation for peritonitis and acute abdominal distress. Peritonitis because of traumatic seeding of the abdominal cavity with bacteria from the urogenital tract, with or without seminoperitoneum, should be considered for bitches presenting with appropriate history, signalment, and clinical signs.
Changes in serum glucose, sodium, and tonicity in cats treated for diabetic ketosis
Authors: Kotas Stephanie , Gerber Lisa , Moore Lisa E. , Schermerhorn Thomas 
Published: September 2010

AbstractObjective –To examine serum sodium, glucose, and tonicity in cats with diabetic ketosis.Design –Retrospective study.Setting –A university‐based referral hospital.Animals –Cats admitted to the ICU during the period 1998 to 2002 with a diagnosis of diabetic ketosis.Interventions –None. Routine clinical management of diabetes and associated conditions.Measurements –Serum biochemistry assessments.Main Results –Abnormalities of glucose, sodium and serum tonicity (ST) were common in the study group. Serum sodium but not glucose correlated closely with ST. A subset of cats treated with intravenous insulin and an isotonic sodium‐containing solution for 72 hours showed a significant decrease in glucose from admission values at 48 and 72 hours (but not at 24 hours). Serum sodium, potassium, and ST were not significantly different from admission values at any time over the 72‐hour period. However, the relative contribution of individual osmolytes varied over the course of treatment. Although glucose decreased >120% from admission values over the 72‐hour treatment period, the approximately 5% rise in serum sodium that occurred offset the osmotic effect of falling glucose and the overall ST change was <3%.Conclusions –The incidence of osmotic‐mediated neurologic complications during treatment of cats with diabetic ketosis is low in part because the minimal fluctuation in ST during treatment likely prevents the development of osmotic gradients between serum and central nervous system tissues. The use of isotonic sodium‐containing fluids in the treatment of feline diabetes acts to minimize large osmotic shifts by adding sodium to the serum compartment as the glucose concentration falls.
A case‐based review of a simplified quantitative approach to acid‐base analysis
Authors: Hopper Kate , Haskins Steve C. 
Published: September 2010

AbstractObjective
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To present a simplified quantitative approach to acid‐base analysis and to demonstrate its clinical utility.Data Sources
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Original research articles and textbooks.Data Synthesis
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A simplified quantitative approach to acid‐base analysis is presented, which is derived from the Fencl‐Stewart approach and calculates the magnitude of the effect on the standardized base excess (SBE) of 5 separate variables: (1) a free water effect (marked by sodium concentration), (2) an effect marked by the chloride concentration, (3) an albumin effect, (4) a lactate effect, and (5) a phosphate effect. Six clinical cases with acid‐base abnormalities are presented in which the quantitative approach provides information that is not apparent from the traditional approach.Conclusion
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This simplified quantitative approach provides a comprehensive evaluation of complex acid‐base disorders, identifies individual processes and their relative influence on SBE, and aids in the development of an appropriate therapeutic plan.