scholarly journals Developmental Biology in Mexico

Author(s):  
Horacio Merchant-Larios

Contemporary scientific endeavor in Mexico emanates from two greatest public institutions: the Universidad Nacional Autónoma de México (UNAM) and the Instituto Politécnico Nacional (IPN), founded in 1929 and 1936, respectively. Here, the first research Institutes and Centers dedicated to various scientific areas were created. Thus, the origin of most laboratories of Developmental Biology in Mexico was like that of other scientific fields. In this article, I have attempted to describe the establishment of a specialized community involved in the understanding of organism development during ontogeny. The use of chick embryos to study heart development was among the first experimental approaches developed in Mexico. Then, a younger group employed chick embryos to study the mechanisms underlying limb development. Various laboratory animal models have been employed, including mouse, rat, rabbit, and recently the naked mole-rat, as well as some wild species, such as sea turtles and bats. Two classical invertebrates, Drosophila melanogaster, and Caenorhadbitis elegans, also form part of the multilayered complex models used by Mexican developmental biologists. My use of animals brought me closer to the pioneer developmental biologists, who worked with animal models. Their academic trajectory was more detailed than that of investigators using plant models. However, the pioneering merit and bright contributions of the two groups are on a par, regardless of the biological model. As current scientific knowledge is the sum of individual contributions throughout human history, here I have attempted to describe my suitable experience as a witness to the birth of the fascinating field of developmental biology in my country.

Development ◽  
1992 ◽  
Vol 115 (2) ◽  
pp. 629-637 ◽  
Author(s):  
C.N. Coelho ◽  
W.B. Upholt ◽  
R.A. Kosher

During early stages of normal chick limb development, the homeobox-containing (HOX) gene GHox-4.6 is expressed throughout the posterior mesoderm of the wing bud from which most of the skeletal elements including the digits will develop, whereas GHox-8 is expressed in the anterior limb bud mesoderm which will not give rise to skeletal elements. In the present study, we have examined the expression of GHox-4.6 and GHox-8 in the wing buds of two polydactylous mutant chick embryos, diplopodia-5 and talpid2, from which supernumerary digits develop from anterior limb mesoderm, and have also examined the expression of these genes in response to polarizing zone grafts and retinoic acid-coated bead implants which induce the formation of supernumerary digits from anterior limb mesoderm. We have found that the formation of supernumerary digits from the anterior mesoderm in mutant and experimentally induced polydactylous limb buds is preceded by the ectopic expression of GHox-4.6 in the anterior mesoderm and the coincident suppression of GHox-8 expression in the anterior mesoderm. These observations suggest that the anterior mesoderm of the polydactylous limb buds is “posteriorized” and support the suggestion that GHox-8 and GHox-4.6, respectively, are involved in specifying the anterior non-skeletal and posterior digit-forming regions of the limb bud. Although the anterior mesodermal domain of GHox-8 expression is severely impaired in the mutant and experimentally induced polydactylous limb buds, this gene is expressed by the prolonged, thickened apical ectodermal ridges of the polydactylous limb buds that extend along the distal anterior as well as the distal posterior mesoderm.(ABSTRACT TRUNCATED AT 250 WORDS)


Development ◽  
1967 ◽  
Vol 17 (2) ◽  
pp. 385-404
Author(s):  
J. R. Hinchliffe ◽  
D. A. Ede

The three groups of abnormal chick embryos known as talpids show a common pattern of remarkably widespread pleiotropic abnormalities, thought to represent the homozygous expression of one or other of three autosomal recessive genes, symbolized respectively as ta1, ta2, ta3. Ede & Kelly (1964 a, b) described in detail the abnormalities of the talpid3 embryos (ta3/ta3), which are essentially similar to those in Cole's talpid (ta1/ta1) (Inman, 1946), while homozygotes for talpid2 (Abbott, Taylor & Abplanalp, 1960) survive longer and, unlike the others, have relatively normal heads. All three possess at 11 days the following trunk abnormalities: (1) a shortening of the vertebral column accompanied by much fusion of adjacent vertebrae; (2) failure of cartilage replacement by bone; (3) substantial subcutaneous oedema and failure of the body wall to close ventrally round the viscera; (4) abnormal feather follicle formation; and (5) polydactyly in the shortened limbs. In the head of ta1/ta1 and ta3/ta3 embryos both the eyes and the maxillary processes are drawn together in the midline.


PEDIATRICS ◽  
1974 ◽  
Vol 53 (5) ◽  
pp. 824-825
Author(s):  
Albert Dorfman

Perhaps some of the comments already made here about developing a theoretical basis for predictive purposes were in disagreement because opportunities vary greatly with the model under discussion. Certainly the general lesson of molecular biology and biochemistry in the last two decades has been surprisingly opposite to that of toxicology in that metabolic pathways are remarkably similar in range, not merely from mouse to man but even from bacteria to man. It is at times hard to accept the claim that animal models are not too useful for studying teratogenesis. Some principles that have been reviewed today are worth summarizing, because if one thinks of certain parameters, such as the final toxic substance (frequently a metabolite of the original pollutant) there is probably not much difference among various species or organisms. At least so it seems from study of enzyme systems. If one considers simpler situations, such as mercury pollution, he can realize the validity of this concept. THREE PARAMETERS OF TOXICITY One could possibly look at the situation as follows: at various stages of the developmental process, starting from the fertilized ovum and progressing to the mature organism or even the aged organism, there are enzymological differences which have become of interest in developmental biology. In particular, in pediatrics we know about programmed processes that go forward inevitably, and others which are subject to control by hormonal influences, by administration of certain substances, or by induction. In the interpretation of any kind of toxic effect, we must consider if our developmental parameter will or will not be toxic at certain stages of development, as I will ifiustrate later.


2020 ◽  
Vol 87 (1) ◽  
pp. 78-81
Author(s):  
Christopher H. Knight

AbstractIn this Research Reflection I shall develop and validate the hypothesis that lactation insufficiency in obese breastfeeding mothers has an endocrine explanation. I shall not present data, but I shall review pertinent literature to show that obesity is associated with a partial or sometimes complete failure to initiate and maintain lactation, and critically examine the belief that this is due to psychosocial factors, a failure of prolactin secretion or both. Since progesterone is inhibitory to lactogenesis and oestrogens are inhibitory to milk secretion, I shall then explore the possibility that these steroids are linked to lactation failure, through sequestration of progesterone and aromatization of oestrogen in mammary adipose tissue. I shall conclude by describing experimental approaches in animal models that could be used to test this hypothesis.


2002 ◽  
Vol 8 (1) ◽  
pp. 87-100 ◽  
Author(s):  
Michael Wheeler ◽  
Seth Bullock ◽  
Ezequiel Di Paolo ◽  
Jason Noble ◽  
Mark Bedau ◽  
...  

Many artificial life researchers stress the interdisciplinary character of the field. Against such a backdrop, this report reviews and discusses artificial life, as it is depicted in, and as it interfaces with, adjacent disciplines (in particular, philosophy, biology, and linguistics), and in the light of a specific historical example of interdisciplinary research (namely cybernetics) with which artificial life shares many features. This report grew out of a workshop held at the Sixth European Conference on Artificial Life in Prague and features individual contributions from the workshop's eight speakers, plus a section designed to reflect the debates that took place during the workshop's discussion sessions. The major theme that emerged during these sessions was the identity and status of artificial life as a scientific endeavor.


2010 ◽  
pp. 633-644 ◽  
Author(s):  
Y Wang ◽  
U Wisloff ◽  
OJ Kemi

Exercise training-induced cardiac hypertrophy occurs following a program of aerobic endurance exercise training and it is considered as a physiologically beneficial adaptation. To investigate the underlying biology of physiological hypertrophy, we rely on robust experimental models of exercise training in laboratory animals that mimic the training response in humans. A number of experimental strategies have been established, such as treadmill and voluntary wheel running and swim training models that all associate with cardiac growth. These approaches have been applied to numerous animal models with various backgrounds. However, important differences exist between these experimental approaches, which may affect the interpretation of the results. Here, we review the various approaches that have been used to experimentally study exercise training-induced cardiac hypertrophy; including the advantages and disadvantages of the various models.


Author(s):  
Lyonna F. Alcantara ◽  
Eric M. Parise ◽  
Carlos A. Bolaños-Guzmán

Animal modeling has advanced our understanding of the underlying pathophysiology of human neuropsychiatric disorders and facilitated development of safer, more efficient medications. Similar to humans with depression, rodents exposed to various stress paradigms exhibit aberrant responses to rewarding stimuli, along with hormonal and immunological dysregulation. Development of more complex models, such as social defeat, has led to a firmer grasp of the mechanisms mediating resilience and susceptibility to stress; and adapted versions of social defeat have yielded insights into how emotional stress influences development of mood disorders. This chapter focuses on stress-induced models of mood disorders and outlines how a depression-like phenotype is induced and tested in rodents.


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