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Dean Falk - One of the best experts on this subject based on the ideXlab platform.
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The natural endocast of Taung (Australopithecus africanus): insights from the unpublished papers of Raymond Arthur Dart.
American Journal of Physical Anthropology, 2009Co-Authors: Dean FalkAbstract:Dart's 1925 announcement of Australopithecus africanus (Dart: Nature 115 [1925] 195–199) was highly controversial, partly because of an interpretation of the Taung natural endocast that rested on an erroneous identification of the Lambdoid Suture as the lunate sulcus. Unpublished materials from the University of Witwatersrand Archives (Dart, unpublished material) reveal that Dart reacted to the controversy by: 1) describing and illustrating the entire sulcal pattern on the Taung endocast, in contrast to just two sulcal identifications in 1925, 2) identifying a hypothetical part of the Lambdoid Suture and revising his description of the lunate sulcus, and 3) bolstering his argument that Taung's brain was advanced by detailing expansions in three significant cortical association areas. Four unpublished illustrations of Dart's identifications for sulci and Sutures on the Taung endocast are compared here with those published by Keith (Keith: New discoveries relating to the antiquity of man (1931)), Schepers (Schepers: The endocranial casts of the South African ape-men. In: Broom R, Schepers GWH, editors. The South African fossil ape-men; the Australopithecinae [1946] p 155–272), and Falk (Falk: Am J Phys Anthropol 53 [1980] 525–539), and the thorny issue of the location of the lunate sulcus is revisited in light of new information. Archival materials reveal that Dart believed that Taung's brain was reorganized globally rather than in a mosaic manner, and that the shapes of certain cortical association areas showed that Australopithecus was closer to Pithecanthropus than to the living apes. Although a few of Dart's hitherto-unpublished sulcal identifications, including his revision for the lunate sulcus, were questionable, his claim that the Taung endocast reproduced a shape that was advanced toward a human condition in its prefrontal cortex and caudally protruded occipital lobe was correct. Yrbk Phys Anthropol 52:49–65, 2009. © 2009 Wiley-Liss, Inc.
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The natural endocast of Taung (Australopithecus africanus): insights from the unpublished papers of Raymond Arthur Dart.
American journal of physical anthropology, 2009Co-Authors: Dean FalkAbstract:Dart's 1925 announcement of Australopithecus africanus (Dart: Nature 115 [1925] 195-199) was highly controversial, partly because of an interpretation of the Taung natural endocast that rested on an erroneous identification of the Lambdoid Suture as the lunate sulcus. Unpublished materials from the University of Witwatersrand Archives (Dart, unpublished material) reveal that Dart reacted to the controversy by: 1) describing and illustrating the entire sulcal pattern on the Taung endocast, in contrast to just two sulcal identifications in 1925, 2) identifying a hypothetical part of the Lambdoid Suture and revising his description of the lunate sulcus, and 3) bolstering his argument that Taung's brain was advanced by detailing expansions in three significant cortical association areas. Four unpublished illustrations of Dart's identifications for sulci and Sutures on the Taung endocast are compared here with those published by Keith (Keith: New discoveries relating to the antiquity of man (1931)), Schepers (Schepers: The endocranial casts of the South African ape-men. In: Broom R, Schepers GWH, editors. The South African fossil ape-men; the Australopithecinae [1946] p 155-272), and Falk (Falk: Am J Phys Anthropol 53 [1980] 525-539), and the thorny issue of the location of the lunate sulcus is revisited in light of new information. Archival materials reveal that Dart believed that Taung's brain was reorganized globally rather than in a mosaic manner, and that the shapes of certain cortical association areas showed that Australopithecus was closer to Pithecanthropus than to the living apes. Although a few of Dart's hitherto-unpublished sulcal identifications, including his revision for the lunate sulcus, were questionable, his claim that the Taung endocast reproduced a shape that was advanced toward a human condition in its prefrontal cortex and caudally protruded occipital lobe was correct.
Alessandro Consales - One of the best experts on this subject based on the ideXlab platform.
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Pure Bilateral Lambdoid and Posterior Sagittal Synostosis (Mercedes-Benz Syndrome): Case Report and Literature Review.
World neurosurgery, 2019Co-Authors: Alberto Balestrino, Francesca Secci, Gianluca Piatelli, Giovanni Morana, Marco Pavanello, Mattia Pacetti, Armando Cama, Alessandro ConsalesAbstract:Background Bilateral Lambdoid and posterior sagittal synostosis is a rarely encountered multisutural craniosynostosis accounting for 0.3%−0.7% of all craniosynostoses. It has been named “Mercedes−Benz Syndrome” (MBS) because of the bone ridges that resemble the Mercedes−Benz logo. The typical head shape is usually described as anterior turricephaly combined with mild brachycephaly. We describe a case of pure MBS without involvement of other Sutures. Since we believe that MBS is a different pathology when other Sutures are involved, we will discuss our case with a review of the literature, including all reported cases of bilateral Lambdoid and posterior sagittal synostosis with no other Sutures involved but sagittal and bilateral Lambdoid. Case Description A 3-month-old female baby came to our attention because of a turrycephalic appearance of the head. Findings of the neurologic examination were unremarkable. Computed tomography scan showed premature fusion of posterior third of sagittal Suture and bilateral Lambdoid Suture. Magnetic resonance imaging did not show relevant intracranial abnormalities. She underwent sagittal decompression extended posteriorly below the Lambdoid Suture combined with biparietal decompression to obtain expansion of both parieto-frontal bones and posterior fossa. Post-operative course was uneventful. Follow-up at 3 months showed a good aesthetic result, and results of the neurologic examination were unremarkable. Conclusions Pure MBS is a rare condition that unlike other multisutural complex craniosynostosis is rarely associated with genetic syndromes, has a low rate of associated intracranial anomalies, and has less need for more skull-remodeling surgery. The choice of the most suitable surgical procedure must be tailored on the patient, considering preoperative head appearance and eventually associated anomalies.
Ritva Rice - One of the best experts on this subject based on the ideXlab platform.
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gli3xt j xt j mice exhibit Lambdoid Suture craniosynostosis which results from altered osteoprogenitor proliferation and differentiation
Human Molecular Genetics, 2010Co-Authors: David P.c. Rice, Elaine C. Connor, Jacqueline M. Veltmaat, Lotta Veistinen, Yukiho Tanimoto, Saverio Bellusci, Eva Lanaelola, Ritva RiceAbstract:Gli3 is a zinc-finger transcription factor whose activity is dependent on the level of hedgehog (Hh) ligand. Hh signaling has key roles during endochondral ossification; however, its role in intramembranous ossification is still unclear. In this study, we show that Gli3 performs a dual role in regulating both osteoprogenitor proliferation and osteoblast differentiation during intramembranous ossification. We discovered that Gli3Xt−J/Xt−J mice, which represent a Gli3-null allele, exhibit craniosynostosis of the Lambdoid Sutures and that this is accompanied by increased osteoprogenitor proliferation and differentiation. These cellular changes are preceded by ectopic expression of the Hh receptor Patched1 and reduced expression of the transcription factor Twist1 in the sutural mesenchyme. Twist1 is known to delay osteogenesis by binding to and inhibiting the transcription factor Runx2. We found that Runx2 expression in the Lambdoid Suture was altered in a pattern complimentary to that of Twist1. We therefore propose that loss of Gli3 results in a Twist1-, Runx2-dependent expansion of the sutural osteoprogenitor population as well as enhanced osteoblastic differentiation which results in a bony bridge forming between the parietal and interparietal bones. We show that FGF2 will induce Twist1, normalize osteoprogenitor proliferation and differentiation and rescue the Lambdoid Suture synostosis in Gli3Xt−J/Xt−J mice. Taken together, we define a novel role for Gli3 in osteoblast development; we describe the first mouse model of Lambdoid Suture craniosynostosis and show how craniosynostosis can be rescued in this model.
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Gli3Xt−J/Xt−J mice exhibit Lambdoid Suture craniosynostosis which results from altered osteoprogenitor proliferation and differentiation
Human Molecular Genetics, 2010Co-Authors: David P.c. Rice, Elaine C. Connor, Jacqueline M. Veltmaat, Eva Lana-elola, Lotta Veistinen, Yukiho Tanimoto, Saverio Bellusci, Ritva RiceAbstract:Gli3 is a zinc-finger transcription factor whose activity is dependent on the level of hedgehog (Hh) ligand. Hh signaling has key roles during endochondral ossification; however, its role in intramembranous ossification is still unclear. In this study, we show that Gli3 performs a dual role in regulating both osteoprogenitor proliferation and osteoblast differentiation during intramembranous ossification. We discovered that Gli3Xt−J/Xt−J mice, which represent a Gli3-null allele, exhibit craniosynostosis of the Lambdoid Sutures and that this is accompanied by increased osteoprogenitor proliferation and differentiation. These cellular changes are preceded by ectopic expression of the Hh receptor Patched1 and reduced expression of the transcription factor Twist1 in the sutural mesenchyme. Twist1 is known to delay osteogenesis by binding to and inhibiting the transcription factor Runx2. We found that Runx2 expression in the Lambdoid Suture was altered in a pattern complimentary to that of Twist1. We therefore propose that loss of Gli3 results in a Twist1-, Runx2-dependent expansion of the sutural osteoprogenitor population as well as enhanced osteoblastic differentiation which results in a bony bridge forming between the parietal and interparietal bones. We show that FGF2 will induce Twist1, normalize osteoprogenitor proliferation and differentiation and rescue the Lambdoid Suture synostosis in Gli3Xt−J/Xt−J mice. Taken together, we define a novel role for Gli3 in osteoblast development; we describe the first mouse model of Lambdoid Suture craniosynostosis and show how craniosynostosis can be rescued in this model.
Jacqueline M. Veltmaat - One of the best experts on this subject based on the ideXlab platform.
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gli3xt j xt j mice exhibit Lambdoid Suture craniosynostosis which results from altered osteoprogenitor proliferation and differentiation
Human Molecular Genetics, 2010Co-Authors: David P.c. Rice, Elaine C. Connor, Jacqueline M. Veltmaat, Lotta Veistinen, Yukiho Tanimoto, Saverio Bellusci, Eva Lanaelola, Ritva RiceAbstract:Gli3 is a zinc-finger transcription factor whose activity is dependent on the level of hedgehog (Hh) ligand. Hh signaling has key roles during endochondral ossification; however, its role in intramembranous ossification is still unclear. In this study, we show that Gli3 performs a dual role in regulating both osteoprogenitor proliferation and osteoblast differentiation during intramembranous ossification. We discovered that Gli3Xt−J/Xt−J mice, which represent a Gli3-null allele, exhibit craniosynostosis of the Lambdoid Sutures and that this is accompanied by increased osteoprogenitor proliferation and differentiation. These cellular changes are preceded by ectopic expression of the Hh receptor Patched1 and reduced expression of the transcription factor Twist1 in the sutural mesenchyme. Twist1 is known to delay osteogenesis by binding to and inhibiting the transcription factor Runx2. We found that Runx2 expression in the Lambdoid Suture was altered in a pattern complimentary to that of Twist1. We therefore propose that loss of Gli3 results in a Twist1-, Runx2-dependent expansion of the sutural osteoprogenitor population as well as enhanced osteoblastic differentiation which results in a bony bridge forming between the parietal and interparietal bones. We show that FGF2 will induce Twist1, normalize osteoprogenitor proliferation and differentiation and rescue the Lambdoid Suture synostosis in Gli3Xt−J/Xt−J mice. Taken together, we define a novel role for Gli3 in osteoblast development; we describe the first mouse model of Lambdoid Suture craniosynostosis and show how craniosynostosis can be rescued in this model.
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Gli3Xt−J/Xt−J mice exhibit Lambdoid Suture craniosynostosis which results from altered osteoprogenitor proliferation and differentiation
Human Molecular Genetics, 2010Co-Authors: David P.c. Rice, Elaine C. Connor, Jacqueline M. Veltmaat, Eva Lana-elola, Lotta Veistinen, Yukiho Tanimoto, Saverio Bellusci, Ritva RiceAbstract:Gli3 is a zinc-finger transcription factor whose activity is dependent on the level of hedgehog (Hh) ligand. Hh signaling has key roles during endochondral ossification; however, its role in intramembranous ossification is still unclear. In this study, we show that Gli3 performs a dual role in regulating both osteoprogenitor proliferation and osteoblast differentiation during intramembranous ossification. We discovered that Gli3Xt−J/Xt−J mice, which represent a Gli3-null allele, exhibit craniosynostosis of the Lambdoid Sutures and that this is accompanied by increased osteoprogenitor proliferation and differentiation. These cellular changes are preceded by ectopic expression of the Hh receptor Patched1 and reduced expression of the transcription factor Twist1 in the sutural mesenchyme. Twist1 is known to delay osteogenesis by binding to and inhibiting the transcription factor Runx2. We found that Runx2 expression in the Lambdoid Suture was altered in a pattern complimentary to that of Twist1. We therefore propose that loss of Gli3 results in a Twist1-, Runx2-dependent expansion of the sutural osteoprogenitor population as well as enhanced osteoblastic differentiation which results in a bony bridge forming between the parietal and interparietal bones. We show that FGF2 will induce Twist1, normalize osteoprogenitor proliferation and differentiation and rescue the Lambdoid Suture synostosis in Gli3Xt−J/Xt−J mice. Taken together, we define a novel role for Gli3 in osteoblast development; we describe the first mouse model of Lambdoid Suture craniosynostosis and show how craniosynostosis can be rescued in this model.
Alberto Balestrino - One of the best experts on this subject based on the ideXlab platform.
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Pure Bilateral Lambdoid and Posterior Sagittal Synostosis (Mercedes-Benz Syndrome): Case Report and Literature Review.
World neurosurgery, 2019Co-Authors: Alberto Balestrino, Francesca Secci, Gianluca Piatelli, Giovanni Morana, Marco Pavanello, Mattia Pacetti, Armando Cama, Alessandro ConsalesAbstract:Background Bilateral Lambdoid and posterior sagittal synostosis is a rarely encountered multisutural craniosynostosis accounting for 0.3%−0.7% of all craniosynostoses. It has been named “Mercedes−Benz Syndrome” (MBS) because of the bone ridges that resemble the Mercedes−Benz logo. The typical head shape is usually described as anterior turricephaly combined with mild brachycephaly. We describe a case of pure MBS without involvement of other Sutures. Since we believe that MBS is a different pathology when other Sutures are involved, we will discuss our case with a review of the literature, including all reported cases of bilateral Lambdoid and posterior sagittal synostosis with no other Sutures involved but sagittal and bilateral Lambdoid. Case Description A 3-month-old female baby came to our attention because of a turrycephalic appearance of the head. Findings of the neurologic examination were unremarkable. Computed tomography scan showed premature fusion of posterior third of sagittal Suture and bilateral Lambdoid Suture. Magnetic resonance imaging did not show relevant intracranial abnormalities. She underwent sagittal decompression extended posteriorly below the Lambdoid Suture combined with biparietal decompression to obtain expansion of both parieto-frontal bones and posterior fossa. Post-operative course was uneventful. Follow-up at 3 months showed a good aesthetic result, and results of the neurologic examination were unremarkable. Conclusions Pure MBS is a rare condition that unlike other multisutural complex craniosynostosis is rarely associated with genetic syndromes, has a low rate of associated intracranial anomalies, and has less need for more skull-remodeling surgery. The choice of the most suitable surgical procedure must be tailored on the patient, considering preoperative head appearance and eventually associated anomalies.
