A recombinação cromossômica desempenha um papel vital na diversidade genética. Se estas estruturas são manipuladas de forma incorreta, por meio de processos conhecidos como instabilidade cromossômica e translocação, a célula pode sofrer uma catástrofe mitótica e morrer, ou pode fugir. Inesperadamente apoptose; apoptose, conhecida como "morte celular programada" (a definição correta é "morte celular não seguida de autólise") é um tipo de "autodestruição celular" que ocorre de forma ordenada e demanda energia para a sua execução (diferentemente da necrose). Está relacionada com a manutenção da homeostase e com a regulação fisiológica do tamanho dos tecidos, mas pode também ser causada por um estímulo patológico (como a lesão ao DNA celular). Ao caracterizarmos o sistema dos IGFs, que envolve todo o tipo de detalhes da genética citológica acima resumida, para facilitar a compressão fisiológica sequencial dessas substâncias que irão ter papéis vitais no crescimento de humanos pré-natal, neonatal, criança, infantil, juvenil e adolescente. O receptor de IGF tipo 2 liga-se preferencialmente ao IGF-2 sendo idêntico ao receptor manose 6-fosfato, uma proteína transmembrana de cadeia única. Apesar de a maioria dos efeitos do IGF-2 aparentemente serem mediados por meio de sua interação com o receptor tipo 1, foram descritas ações independentes do IGF-2 via receptor do tipo 2. As concentrações plasmáticas dos IGFs variam de acordo com a idade e a condição fisiológica. As concentrações de IGF-1 são mais baixas ao termo em recém-nascidos e permanecem relativamente baixas na infância até que ocorra um pico durante a puberdade, com os valores elevando-se mais do que em qualquer outro momento da vida. O IGF-1 sérico se reduz a níveis adultos, valores estes maiores que os da infância e menores do que os da puberdade. Com o avançar da idade, os níveis séricos do GH-hormônio de crescimento e IGF-1 diminuem.
As concentrações de IGF-1 são mais precisamente correlacionadas em gêmeos monozigóticos do que em gêmeos dizigóticos do mesmo sexo, indicando um efeito genético na regulação dos níveis de IGF-. A deficiência de GH-hormônio de crescimento leva a concentrações séricas menores de IGF-1 e IGF-2, enquanto o excesso de GH-hormônio de crescimento ocasiona uma elevação de IGF-1, porém sem uma elevação acima do normal de IGF-2. Visto que o IGF-1 sérico é menor nos estados de deficiência nutricional, o IGF-1 não consiste em uma ferramenta perfeita no diagnóstico diferencial das condições de crescimento inadequado, as quais frequentemente incluem um distúrbio do estado nutricional. O IGF-1 inibe a secreção de GH-hormônio de crescimento por meio de um mecanismo de retroalimentação negativa, de modo que os pacientes com deficiência de GH-hormônio de crescimento (síndrome de Laron), ou aqueles incapazes de produzirem IGF-1, apresentam concentrações elevadas de GH-hormônio de crescimento, porém concentrações desprezíveis de IGF-1. Poucos pacientes com deficiência dos receptores de IGF-1 apresentam aumento da concentração de IGF-1 sem atividade biológica.
SIGNIFICANCE OF IGFs SYSTEMS IN PRENATAL, NEWBORN, CHILD, INFANT AND YOUTH, FROM GENETICS; DR.J. S. CAIO.
PLASMA CONCENTRATIONS OF IGF ( INSULIN-LIKE GROWTH FACTORS ) VARY BY AGE ( PRENATAL, NEWBORN, CHILD, INFANT AND YOUTH ) AND PHYSIOLOGICAL CONDITION: PHYSIOLOGY-ENDOCRINOLOGY-NEUROENDOCRINOLOGY-GENETICS-ENDOCRINE-PEDIATRICS (SUBDIVISION OF ENDOCRINOLOGY): DR. JOÃO SANTOS CAIO JR. ET DRA. HENRIQUETA VERLANGIERI CAIO.
The IGF-2 peptide is an amino acid. The gene of prepro-IGF-2 is located on the short arm of chromosome 11, near the gene for preproinsulin. In genetics, a locus (plural loci) is the specific site of a gene or DNA sequence on a chromosome or position.
Each chromosome carries many genes; estimated “haploid” genes encoding human proteins are from 20.000 to 25.000 in 23 different chromosomes. A variant of the DNA sequence located similar to a given locus is called an allele. The ordered list of loci known for a particular genome list is called a genetic map. Genetic mapping is the process of determining the location of a particular biological characteristic. Diploid and polyploidy cells whose chromosomes have the same allele of a given gene somewhere calls are homozygous with respect to this gene, while having different alleles of a given gene in a heterozygous locus are called in respect of that gene. In eukaryotes, nuclear chromosomes are packaged by proteins into a condensed structure called chromatin. This allows long DNA molecules to fit into the cell nucleus. The chromatin structure of chromosomes, and varies through the cell cycle. Chromosomes are further condensed chromatin and are essential for cell division unit. Chromosomes must be replicated, divided, and passed successfully to their daughter cells so as to ensure the genetic diversity and survival of their offspring. Chromosomes may exist as duplicable or non- duplicable. Not duplicated chromosomes are single linear strands, whereas duplicated chromosomes contain two identical copies (called chromatids or sister chromatids) joined by a centromere. Compression of the duplicate chromosomes during mitosis and meiosis results in the classic four-arm structure is located at the centromere of chromosome means a structure or two arms centromere is located near one end. Chromosomal recombination plays a vital role in genetic diversity. If these structures are manipulated incorrectly, through processes known as chromosomal instability and translocation, the cell may undergo mitotic catastrophe and die, or you can run. Unexpectedly apoptosis ; apoptosis, known as "programmed cell death" ( the correct definition is "cell death not followed by autolysis") is a type of "cellular self-destruction" that occurs in an orderly manner and requires energy for its implementation (unlike necrosis).
It is related to the maintenance of homeostasis and the regulation of physiological size of the tissues, but can also be caused by a pathological stimulus (such as damage to cellular DNA). To characterize the system of IGFs, this involves all sorts of details of cytological genetics summarized above, to facilitate sequential physiologic compression of these substances that will have vital roles in the growth of human prenatal, neonatal, newborn, child, infant, youth and adolescent. The type-2 IGF receptor preferentially binds to IGF-2 receptor is identical to the mannose 6-phosphate, a transmembrane protein single chain. Although most of the effects of IGF-2 are apparently mediated through its interaction with the type 1 receptor, independent actions of IGF-2 via the type 2 receptor have been described. Plasma concentrations of IGFs vary with age and physiological condition. Concentrations of IGF-1 are lower at term newborns and remain relatively low in childhood until a peak occurs during puberty, with values rising more than any other time of life. IGF-1 serum reduced to adult levels, values greater than those of children and smaller than puberty. With advancing age, serum levels of GH-Growth Hormone and IGF-1 decrease. Concentrations of IGF-1 are precisely correlated in monozygotic than in dizygotic twins of the same sex, indicating a genetic effect in the regulation of IGF-1. A deficiency in GH-growth hormone leads to lower serum concentrations of IGF-1 and IGF-2, while the excess growth hormone; GH causes an increase of IGF-1, but without an elevation above the normal IGF-2. Whereas, the serum IGF-1 is lower in states of nutritional deficiency, IGF-1 is not a perfect tool in the differential diagnosis of conditions of inadequate growth, which often include a disorder of nutritional status.
IGF-1 inhibits GH secretion, GH-growth hormone through a negative feedback mechanism, so that patients with GH-growth hormone (Laron syndrome) deficiency, or those unable to produce IGF-1, have high concentrations of GH-growth hormone, however negligible concentrations of IGF-1, few patients with deficiency of IGF-1 receptors exhibit increased concentrations of IGF-1 without biological activity.
Dr. João Santos Caio Jr.
Endocrinologia – Neuroendocrinologista
CRM 20611
Dra. Henriqueta V. Caio
Endocrinologista – Medicina Interna
CRM 28930
1. A fisiologia do crescimento pré-natal difere consideravelmente daquela do crescimento pós-natal. O hormônio do crescimento (GH-growth hormone) e o fator de crescimento insulina-símile tipo 1 (IGF-1, insulin-like growth factor 1) compõem o principal sistema endócrino regulador do crescimento linear ou longitudinal durante a fase como criança, infantil, juvenil...
http://hormoniocrescimentoadultos.blogspot.com
2. Nessa fase, o IGF-1, insulin-like growth factor 1e o insulina-like growth factor tipo 2, de maneira independente da secreção de GH-hormônio de crescimento, são os principais fatores endócrinos determinantes do crescimento...
http://longevidadefutura.blogspot.com
3. Este receptor medeia os efeitos do IGF-1, que é um hormônio proteína polipeptídeo semelhante à estrutura molecular da insulina...
http://imcobesidade.blogspot.com
AUTORIZADO O USO DOS DIREITOS AUTORAIS COM CITAÇÃO
DOS AUTORES PROSPECTIVOS ET REFERÊNCIA BIBLIOGRÁFICA.
Referências Bibliográficas:
Caio Jr, João Santos, Dr.; Endocrinologista, Neuroendocrinologista, Caio,H. V., Dra. Endocrinologista, Medicina Interna – Van Der Häägen Brazil, São Paulo, Brasil; "Growth Hormone Deficiency". UK Child Growth Foundation. Retrieved 2009-01-16; "Growth failure (in children) - human growth hormone (HGH)" (pdf). National Institute for Clinical Excellence. 2008-09-25. Retrieved 2009-01-16; James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0; "The Use of Growth Hormone Replacement in Adult Patients with Severe Growth Hormone Deficiency" (pdf). The Society for Endocrinology. 2000-10-01. Retrieved 2009-01-18; "Human Growth Hormone Deficiency". HGH. Retrieved 20 January 2012; "Human growth hormone (somatropin) in adults with growth hormone deficiency". National Institute for Clinical Excellence. 2006-07-01. Retrieved 2009-01-16; Rappold GA, Fukami M, Niesler B, et al. (March 2002). "Deletions of the homeobox gene SHOX (short stature homeobox) are an important cause of growth failure in children with short stature". J. Clin. Endocrinol. Metab. 87 (3): 1402–6. doi:10.1210/jc.87.3.1402. PMID 11889216; Saborio P, Hahn S, Hisano S, Latta K, Scheinman JI, Chan JC (October 1998). "Chronic renal failure: an overview from a pediatric perspective". Nephron 80 (2): 134–48.doi:10.1159/000045157. PMID 9736810; Molitch ME, Clemmons DR, Malozowski S, et al. (May 2006). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline". J. Clin. Endocrinol. Metab. 91 (5): 1621–34. doi:10.1210/jc.2005-2227. PMID 16636129; Aimaretti G, Corneli G, Razzore P, et al. (May 1998). "Comparison between insulin-induced hypoglycemia and growth hormone (GH)-releasing hormone + arginine as provocative tests for the diagnosis of GH deficiency in adults". J. Clin. Endocrinol. Metab. 83 (5): 1615–8. doi:10.1210/jc.83.5.1615. PMID 9589665. Retrieved 2008-07-23; "Guidance on the use of human growth hormone (somatropin) in children with growth failure" (pdf). National Institute for Clinical Excellence. 2002-05-01. Retrieved 2009-01-16; "Consensus Guidelines for Adult Growth Hormone Deficiency 2007".
CONTATO:
Fones: (11) 2371-3337 / 5572-4848 ou 9.8197-4706 tim
Rua Estela, 515 - Bloco D - 12º andar - conj 121 e 122 - Paraiso - São Paulo - SP - CEP 04011-002.
Email: vanderhaagenbrasil@gmail.com
Site Van Der Häägen Brazil
www.vanderhaagenbrazil.com.br
http://drcaiojr.site.med.br
http://dracaio.site.med.br
João Santos Caio Jr
http://google.com/+JoaoSantosCaioJr
Video
http://youtu.be/woonaiFJQwY
Google Maps:
http://maps.google.com.br/maps/place?cid=5099901339000351730&q=Van+Der+Haagen+Brasil&hl=pt&sll=-23.578256,46.645653&sspn=0.005074,0.009645&ie =UTF8&ll=-23.575591,-46.650481&spn=0,0&t = h&z=17
Referências Bibliográficas:
Caio Jr, João Santos, Dr.; Endocrinologista, Neuroendocrinologista, Caio,H. V., Dra. Endocrinologista, Medicina Interna – Van Der Häägen Brazil, São Paulo, Brasil; "Growth Hormone Deficiency". UK Child Growth Foundation. Retrieved 2009-01-16; "Growth failure (in children) - human growth hormone (HGH)" (pdf). National Institute for Clinical Excellence. 2008-09-25. Retrieved 2009-01-16; James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology. (10th ed.). Saunders. ISBN 0-7216-2921-0; "The Use of Growth Hormone Replacement in Adult Patients with Severe Growth Hormone Deficiency" (pdf). The Society for Endocrinology. 2000-10-01. Retrieved 2009-01-18; "Human Growth Hormone Deficiency". HGH. Retrieved 20 January 2012; "Human growth hormone (somatropin) in adults with growth hormone deficiency". National Institute for Clinical Excellence. 2006-07-01. Retrieved 2009-01-16; Rappold GA, Fukami M, Niesler B, et al. (March 2002). "Deletions of the homeobox gene SHOX (short stature homeobox) are an important cause of growth failure in children with short stature". J. Clin. Endocrinol. Metab. 87 (3): 1402–6. doi:10.1210/jc.87.3.1402. PMID 11889216; Saborio P, Hahn S, Hisano S, Latta K, Scheinman JI, Chan JC (October 1998). "Chronic renal failure: an overview from a pediatric perspective". Nephron 80 (2): 134–48.doi:10.1159/000045157. PMID 9736810; Molitch ME, Clemmons DR, Malozowski S, et al. (May 2006). "Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society Clinical Practice Guideline". J. Clin. Endocrinol. Metab. 91 (5): 1621–34. doi:10.1210/jc.2005-2227. PMID 16636129; Aimaretti G, Corneli G, Razzore P, et al. (May 1998). "Comparison between insulin-induced hypoglycemia and growth hormone (GH)-releasing hormone + arginine as provocative tests for the diagnosis of GH deficiency in adults". J. Clin. Endocrinol. Metab. 83 (5): 1615–8. doi:10.1210/jc.83.5.1615. PMID 9589665. Retrieved 2008-07-23; "Guidance on the use of human growth hormone (somatropin) in children with growth failure" (pdf). National Institute for Clinical Excellence. 2002-05-01. Retrieved 2009-01-16; "Consensus Guidelines for Adult Growth Hormone Deficiency 2007".
CONTATO:
Fones: (11) 2371-3337 / 5572-4848 ou 9.8197-4706 tim
Rua Estela, 515 - Bloco D - 12º andar - conj 121 e 122 - Paraiso - São Paulo - SP - CEP 04011-002.
Email: vanderhaagenbrasil@gmail.com
Site Van Der Häägen Brazil
www.vanderhaagenbrazil.com.br
http://drcaiojr.site.med.br
http://dracaio.site.med.br
João Santos Caio Jr
http://google.com/+JoaoSantosCaioJr
Video
http://youtu.be/woonaiFJQwY
Google Maps:
http://maps.google.com.br/maps/place?cid=5099901339000351730&q=Van+Der+Haagen+Brasil&hl=pt&sll=-23.578256,46.645653&sspn=0.005074,0.009645&ie =UTF8&ll=-23.575591,-46.650481&spn=0,0&t = h&z=17





