John Wiley & Sons and the Teratology Society are please to announce a new journal, Birth Defects Research . This new journal is a comprehensive resource of original research and reviews in fields related to embryo-fetal development and reproduction. Birth Defects Research draws from the expertise and reputation of two current Wiley journals, and introduces a new forum for reviews in developmental biology and embryology.     Part C: Embryo Today: Reviews

Birth Defects Research Part C - Embryo Today: Reviews is a new journal announced by John Wiley & Sons and the Teratology Society. This journal serves as a comprehensive resource for original research and reviews in the fields related to embryo-fetal development and reproduction. Birth Defects Research draws from the expertise and reputation of two existing Wiley journals and introduces a new forum for reviews in developmental biology and embryology.

《Birth Defects Research Part C - Embryo Today: Reviews》是由John Wiley & Sons和Teratology Society联合推出的一本新期刊。该期刊是关于胚胎-胎儿发育和生殖领域的原创研究和综述的综合资源。它汇集了两本现有Wiley期刊的专业知识和声誉，并为发育生物学和胚胎学的综述提供了一个新的论坛。

Birth Defects Research Part C - Embryo Today: Reviews

Recent data have revealed new mechanisms that underlie endothelial cell (EC) lumen formation during vascular morphogenic events in development, wound repair, and other disease states. It is apparent that EC interactions with extracellular matrices (ECMs) establish signaling cascades downstream of integrin ligation leading to activation of the Rho GTPases, Cdc42 and Rac1, which are required for lumen formation. In large part, this process is driven by intracellular vacuole formation and coalescence, which rapidly leads to the creation of fluid‐filled matrix‐free spaces that are then interconnected via EC–EC interactions to create multicellular tube structures. EC vacuoles markedly accumulate in a polarized fashion directly adjacent to the centrosome in a region that strongly accumulates Cdc42 protein as indicated by green fluorescent protein (GFP)‐Cdc42 during the lumen formation process. Downstream of Cdc42‐mediated signaling, key molecules that have been identified to be required for EC lumen formation include Pak2, Pak4, Par3, Par6, and the protein kinase C (PKC) isoforms ζ and ε. Together, these molecules coordinately regulate the critical EC lumen formation process in three‐dimensional (3D) collagen matrices. These events also require cell surface proteolysis mediated through membrane type 1 matrix metalloproteinase (MT1‐MMP), which is necessary to create vascular guidance tunnels within the 3D matrix environment. These tunnels represent physical spaces within the ECM that are necessary to regulate vascular morphogenic events, including the establishment of interconnected vascular tube networks as well as the recruitment of pericytes to initiate vascular tube maturation (via basement membrane matrix assembly) and stabilization. Current research continues to analyze how specific molecules integrate signaling information in concert to catalyze EC lumen formation, pericyte recruitment, and stabilization processes to control vascular morphogenesis in 3D extracellular matrices. Birth Defects Research (Part C) 81:270–285, 2007. © 2008 Wiley‐Liss, Inc.

George E. Davis

Wonshill Koh

Amber N. Stratman

Birth Defects Research Part C: Embryo Today: Reviews

Birth Defects Research Pt C

Mechanisms controlling human endothelial lumen formation and tube assembly in three‐dimensional extracellular matrices

控制人类内皮腔形成和三维细胞外基质中管状组装的机制

During endochondral bone development, bone-forming osteoblasts have to colonize the regions of cartilage that will be replaced by bone. In adulthood, bone remodeling and repair require osteogenic cells to reach the sites that need to be rebuilt, as a prerequisite for skeletal health. A failure of osteoblasts to reach the sites in need of bone formation may contribute to impaired fracture repair. Conversely, stimulation of osteogenic cell recruitment may be a promising osteo-anabolic strategy to improve bone formation in low bone mass disorders such as osteoporosis and in bone regeneration applications. Yet, still relatively little is known about the cellular and molecular mechanisms controlling osteogenic cell recruitment to sites of bone formation. In vitro, several secreted growth factors have been shown to induce osteogenic cell migration. Recent studies have started to shed light on the role of such chemotactic signals in the regulation of osteoblast recruitment during bone remodeling. Moreover, trafficking of osteogenic cells during endochondral bone development and repair was visualized in vivo by lineage tracing, revealing that the capacity of osteoblast lineage cells to move into new bone centers is largely confined to undifferentiated osteoprogenitors, and coupled to angiogenic invasion of the bone-modeling cartilage intermediate. It is well known that the presence of blood vessels is absolutely required for bone formation, and that a close spatial and temporal relationship exists between osteogenesis and angiogenesis. Studies using genetically modified mouse models have identified some of the molecular constituents of this osteogenic-angiogenic coupling. This article reviews the current knowledge on the process of osteoblast lineage cell recruitment to sites of active bone formation in skeletal development, remodeling, and repair, considering the role of chemo-attractants for osteogenic cells and the interplay between osteogenesis and angiogenesis in the control of bone formation.

Naomi Dirckx

Matthias Van Hul

Christa Maes

Birth Defect Res C

Osteoblast recruitment to sites of bone formation in skeletal development, homeostasis, and regeneration

骨形成部位的成骨细胞招募在骨骼发育、稳态和再生中的作用

Given the ever-increasing toxic exposure ubiquitously present in our environment as well as emerging evidence that these exposures are hazardous to human health, the current rodent-based regulations are proving inadequate. In the process of overhauling risk assessment methodology, a nonrodent test organism, the zebrafish, is emerging as tractable for medium- and high-throughput assessments, which may help to accelerate the restructuring of standards. Zebrafish have high developmental similarity to mammals in most aspects of embryo development, including early embryonic processes, and on cardiovascular, somite, muscular, skeletal, and neuronal systems. Here, we briefly describe the development of these systems and then chronicle the toxic impacts assessed following chemical exposure. We also compare the available data in zebrafish toxicity assays with two databases containing mammalian toxicity data. Finally, we identify gaps in our collective knowledge that are ripe for future studies.

Catherine W. McCollum

Nicole A. Ducharme

Maria Bondesson

Jan-Ake Gustafsson

Developmental toxicity screening in zebrafish

斑马鱼发育毒性筛选

Skeletogenesis is an exquisitely orchestrated and dynamic process, culminating in the formation of highly variable and complex mineralized structures that are optimized for their function. While cellular and molecular biology studies have provided tremendous recent progress toward understanding how patterns of bone formation are regulated, high resolution imaging techniques such as microcomputed tomography (micro‐CT) can provide complementary quantitative information about the progressive changes in three‐dimensional (3‐D) skeletal morphology and density that occur during early skeletal development and postnatal growth. Furthermore, recently developed in vivo micro‐CT systems promise to be a powerful and efficient tool for noninvasively monitoring normal skeletogenesis, as well as for evaluating the effects of genetic or environmental manipulation. This review focuses on the use of micro‐CT imaging and analysis to better understand normal and abnormal skeletal development and growth. Birth Defects Research (Part C) 72: 250–259, 2004. © 2004 Wiley‐Liss, Inc.

Robert E. Guldberg

Angela S.P. Lin

Rhima Coleman

Galen Robertson

Craig Duvall

Microcomputed tomography imaging of skeletal development and growth

骨骼发育与生长的微型计算机断层扫描成像

Micro-computed tomography (micro-CT) is a high resolution imaging technique that has expanded and strengthened in use since it was last reviewed in this journal in 2004. The technology has expanded to include more detailed analysis of bone, as well as soft tissues, by use of various contrast agents. It is increasingly applied to questions in developmental biology and developmental toxicology. Relatively high-throughput protocols now provide a powerful and efficient means to evaluate embryos and fetuses subjected to genetic manipulations or chemical exposures. This review provides an overview of the technology, including scanning, reconstruction, visualization, segmentation, and analysis of micro-CT generated images. This is followed by a review of more recent applications of the technology in some common laboratory species that highlight the diverse issues that can be addressed.

L. David Wise

Christopher T. Winkelmann

Belma Dogdas

Ansuman Bagchi

Micro-computed tomography imaging and analysis in developmental biology and toxicology

发育生物学与毒理学中的微型计算机断层扫描成像与分析

The human eye is a complex organ whose development requires extraordinary coordination of developmental processes. The conservation of ocular developmental steps in vertebrates suggests possible common genetic mechanisms. Genetic diseases involving the eye represent a leading cause of blindness in children and adults. During the last decades, there has been an exponential increase in genetic studies of ocular disorders. In this review, we summarize current success in identification of genes responsible for microphthalmia, anophthalmia, and coloboma (MAC) phenotypes, which are associated with early defects in embryonic eye development. Studies in animal models for the orthologous genes identified overlapping phenotypes for most factors, confirming the conservation of their function in vertebrate development. These animal models allow for further investigation of the mechanisms of MAC, integration of various identified genes into common developmental pathways and finally, provide an avenue for the development and testing of therapeutic interventions.

Linda M. Reis

Elena V. Semina

Conserved genetic pathways associated with microphthalmia, anophthalmia, and coloboma

与小眼、无眼和缺损相关的保守遗传通路

INTRODUCTION
Pregestational and gestational diabetes mellitus (PGDM; GDM) are significant health concerns because they are associated with an increased rate of malformations and maternal health complications.


METHODS
We reviewed the data that help us to understand the effects of diabetes in pregnancy.


RESULTS
Diabetic embryopathy can affect any developing organ system, but cardiovascular and neural tube defects are among the most frequent anomalies. Other complications include preeclampsia, preterm delivery, fetal growth abnormalities, and perinatal mortality. Neurodevelopmental studies on offspring of mothers with diabetes demonstrated increased rate of Gross and Fine motor abnormalities, of Attention Deficit Hyperactivity Disorder, learning difficulties, and possibly also Autism Spectrum Disorder. The mechanisms underlying the effects of maternal hyperglycemia on the developing fetus may involve increased oxidative stress, hypoxia, apoptosis, and epigenetic changes. Evidence for epigenetic changes are the following: not all progeny are affected and not to the same extent; maternal diet may influence pregnancy outcomes; and maternal diabetes alters embryonic transcriptional profiles and increases the variation between transcriptomic profiles as a result of altered gene regulation. Research in animal models has revealed that maternal hyperglycemia is a teratogen, and has helped uncover potential therapeutic targets which, when blocked, can mitigate or ameliorate the negative effects of diabetes on the developing fetus.


CONCLUSIONS
Tight metabolic control, surveillance, and labor management remain the cornerstone of care for pregnant women with diabetes, but advances in the field indicate that new treatments to protect the mother and baby are not far from becoming clinical realities.

Asher Ornoy

E. Albert Reece

Gabriela Pavlinkova

Claudia Kappen

Richard Kermit Miller

Effect of maternal diabetes on the embryo, fetus, and children: Congenital anomalies, genetic and epigenetic changes and developmental outcomes

母体糖尿病对胚胎、胎儿及儿童的影响：先天性畸形、遗传和表观遗传变化及发育结果

Neural crest cells (NCCs) are unique to vertebrates and emerge from the border of the neural plate and subsequently migrate extensively throughout the embryo after which they differentiate into many types of cells. This multipotency is the main reason why NCCs are regarded as a versatile tool for stem cell biology and have been gathering attention for their potential use in stem cell based therapy. Multiple sets of networks comprised of signaling molecules and transcription factors regulate every developmental phase of NCCs, including maintenance of their multipotency. Pluripotent stem cell lines, such as embryonic stem cells and induced pluripotent stem (iPS) cells, facilitate the induction of NCCs in combination with sophisticated culture systems used for neural stem cells, although at present, clinical experiments for NCC-based cell therapy need to be improved. Unexpectedly, the multipotency of NCCs is maintained after they reach the target tissues as tissue neural crest stem cells (NCSCs) that may contribute to the establishment of NCC-derived multipotential stem cells. In addition, under specific culture conditions, fate-restricted unipotent descendants of NCCs, such as melanoblasts, show multipotency to differentiate into melanocytes, neurons, and glia cells. These properties contribute to the additional versatility of NCCs for therapeutic application and to better understand NCC development.

Takahiro Kunisada

Ken-Ichi Tezulka

Hitomi Aoki

Tsutomu Motohashi

The stemness of neural crest cells and their derivatives

神经嵴细胞及其衍生物的干性

The attachment between tendon and bone occurs across a complex transitional tissue that minimizes stress concentrations and allows for load transfer between muscles and skeleton. This unique tissue cannot be reconstructed following injury, leading to high incidence of recurrent failure and stressing the need for new clinical approaches. This review describes the current understanding of the development and function of the attachment site between tendon and bone. The embryonic attachment unit, namely, the tip of the tendon and the bone eminence into which it is inserted, was recently shown to develop modularly from a unique population of Sox9- and Scx-positive cells, which are distinct from tendon fibroblasts and chondrocytes. The fate and differentiation of these cells is regulated by transforming growth factor beta and bone morphogenetic protein signaling, respectively. Muscle loads are then necessary for the tissue to mature and mineralize. Mineralization of the attachment unit, which occurs postnatally at most sites, is largely controlled by an Indian hedgehog/parathyroid hormone-related protein feedback loop. A number of fundamental questions regarding the development of this remarkable attachment system require further study. These relate to the signaling mechanism that facilitates the formation of an interface with a gradient of cellular and extracellular phenotypes, as well as to the interactions between tendon and bone at the point of attachment.

Elazar Zelzer

Einat Blitz

Megan L. Killian

Stavros Thomopoulos

Tendon-to-bone attachment: From development to maturity

肌腱-骨附着：从发育到成熟

Most of our bones form through the process of endochondral ossification, which is tightly regulated by the activity of the cartilage growth plate. Chondrocyte maturation through the various stages of growth plate physiology ultimately results in hypertrophy. Chondrocyte hypertrophy is an essential contributor to longitudinal bone growth, but recent data suggest that these cells also play fundamental roles in signaling to other skeletal cells, thus coordinating endochondral ossification. On the other hand, ectopic hypertrophy of articular chondrocytes has been implicated in the pathogenesis of osteoarthritis. Thus, a better understanding of the processes that control chondrocyte hypertrophy in the growth plate as well as in articular cartilage is required for improved management of both skeletal growth disorders and osteoarthritis. This review summarizes recent findings on the regulation of hypertrophic chondrocyte differentiation, the cellular mechanisms involved in hypertrophy, and the role of chondrocyte hypertrophy in skeletal physiology and pathophysiology.

Margaret Man-Ger Sun

Frank Beier

Chondrocyte hypertrophy in skeletal development, growth, and disease

骨骼发育、生长与疾病中的软骨细胞肥大

出版信息	出版商: Wiley-Liss Inc.，出版周期: Quarterly，期刊类型: journal，开源期刊: 否
基本数据	创刊年份: 2003，原创研究文献占比: 0.00%，自引率:N.A.， Gold OA占比: 0.00%
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