UTERO ARCUATO PDF DOWNLOAD

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En estas pacientes, el útero arcuato (56,4%) constituía la malformación más frecuente, seguido del útero subsepto (16,4%), del bicorne unicollis (12,7%), del . DOWNLOAD OR READ: IN UTERO PDF EBOOK EPUB MOBI. Page 1 Rito del Utero in utero UTERO ARCUATO PDF - de falopio. Cervicales. Atresia cervical. Ginecol Obstet Mex ; Artículo de revisión Estado actual de la clasificación, diagnóstico y tratamiento de las malformaciones müllerianas Rosa .


Utero Arcuato Pdf Download

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Download as PDF, TXT or read online from Scribd. Flag for inappropriate A. UTERO BICORNE UNICOLLIS computerescue.info ARCUATO. cuando el tabique se. Download PDF En estas pacientes, el útero arcuato (56,4%) constituía la malformación más frecuente, seguido del útero subsepto (16,4%), del bicorne. erano stati appresi in utero, e da lì inizia a costruirsi nel bambino il riconoscimento viene passato all'area di Broca tramite il fascicolo arcuato. In fine.

Hypothalamic NPY content has been increased by early postnatal nutritional restraint, induced by increasing litter size However, it is less clear to what extent changes in hypothalamic regulators of appetite may persist long term.

Therefore, we hypothesized that uteroplacental insufficiency would impair adult glucose tolerance, insulin secretion and sensitivity, as well as increase adiposity and hypothalamic NPY content in adult offspring, and this would be ameliorated with restoration of postnatal nutrition through cross fostering.

We further hypothesized that exposure to impaired postnatal nutrition only, by cross fostering control pups onto restricted mothers with impaired mammary development or by modestly reducing litter size 17 , would also impair glucose tolerance and insulin sensitivity in adult offspring. Wistar Kyoto rats 9—13 wk of age were obtained from the Australian Resource Centre Murdoch College, Western Australia, Australia , and were provided with a h light, h dark cycle and had access to food and water ad libitum.

On d gestation, pregnant rats were randomly allocated to restricted or control sham surgery groups. The restricted group underwent bilateral uterine artery and vein ligation to induce uteroplacental insufficiency as described previously 16 , 17 , At birth, half the litters from the control sham surgery group litter size nine to 14 pups had their litter size randomly reduced to five to match the restricted group Pups from each of the three groups control, reduced, and restricted were cross fostered the day after birth onto a different control mother or restricted mother as previously described This generated six experimental groups: pup-on-mother control-on-control, control-on-restricted, reduced-on-restricted, reduced-on-control, restricted-on-control, and restricted-on-restricted, with a similar number of male and female pups in each litter.

All pups remained with their mothers and then were weaned at postnatal d 35 as in previous studies Growth measurements and food intake Because individual pups were not identified until postnatal d 3, weights at d 1 were taken as the average of the entire litter for a particular sex.

From postnatal d 14, individual offspring from at least seven different litters per group were studied. Dimensions crown rump length and hind limb length using digital vernier calipers accurate to 0. IAGTTs were performed 2 d after catheterization after an overnight fast as previously described Animals remained conscious and unrestrained in their cage throughout the experiment.

Intra-arterial administration of glucose was chosen rather than ip because it provides a better measure of insulin secretion with an almost instantaneous first-phase response after the glucose bolus is given Arterial blood samples were collected via the catheter 10 and 5 min before, and 1, 3, 5, 10, 20, 30, 40, 60, and min after glucose injection.

Blood removed was replaced with a similar volume of saline. Tail vein blood samples were collected 5 min before, and 20, 40, and 60 min after insulin injection. After decapitation, brains were rapidly removed and dissected on ice into subregions of the hypothalamus containing the paraventricular nucleus PVN , ARC, dorsal medulla, and preoptic area Hind limb soleus and extensor digitorum longus EDL muscles from the left leg, as well as omental, retroperitoneal, and dorsal fat were excised and weighed.

Fasting plasma glucose or insulin was taken as the average of two time points 10 and 5 min before injection for the IAGTT and 5 min before injection for the IC, respectively. Quiubole con Para chavos, Length: Have one to sell?

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Para hombres by Gaby Vargas. Oct 09, Psra De rated it it was amazing. Jul 28, Parx Tenorio rated it really liked it. Nevertheless, changes in local levels of neuropeptides can be most informative about circuit regulation.

Its utility as a marker in developing animals is more doubtful as significant densities of AgRP immunoreactive fibers have been observed in hypothalamic regions prior to their innervation by ARH neurons Bouret S. Given the remarkable plasticity of peptidergic neurons during development, considerable effort will be required to establish patterns of neurotransmitter specific connectivity in the developing hypothalamus.

Development of ARH projections It is remarkable how little information is available about development of hypothalamic pathways. Although a variety of axonal labeling methods have been available for studying development of neural connections, they have only recently been applied to the hypothalamus. The surprising finding is that the projections of this important neuroendocrine nucleus remain immature until well after birth, with the full pattern of projections not represented until the end of the second week of life [ ].

Axons from ARH neurons extend rostally and remain largely confined to the periventricular zone and appear to innervate several key components of feeding circuitry during discrete temporal domains. The DMH is innervated relatively early P6 , followed by the anterior part of the periventricular nucleus, and then ascending fibers finally reach the PVH P The overall pattern of ARH projections does not achieve a distribution resembling that of adult mice until nearly the end of the third postnatal week, and no evidence of regressive events has been reported [ ].

Thus, the ARH does not appear to provide exuberant projectons to inappropriate targets that are then restricted through axon retraction later in development. Rather, the ARH axons appear to achieve their targets through a directed mechanism. This retarded development of ARH projections appears to be unusual among hypothalamic nuclei. AgRP-immunoreactive terminals are observed in neonatal rats in a developmental pattern that generally matches the development of neural projections from the ARH [ ] suggesting that the ability of NPY-containing neurons to regulate the activity of neurons in the DMH and PVH matures along a similar time course.

The sequencial innervation of hypothalamic targets by ARH neurons suggests that the ability of leptin to regulate hypothalamic function may not be mature in neonatal mice.

Indeed, leptin treatment has minimal effects on food intake in neonates [ ]; [ ]. In adult mice, peripheral injections of leptin cause marked increases in cfos expression, however, in neonatal mice, leptin does not induce Fos immunostaining in large numbers of neurons in the PVH and LHA until after innervation by the ARH has occurred [ ].

Both the ARH and DMH contain neurons that express leptin receptors and a substantial number of these cells appear to be directly activated by leptin in neonatal mice. In contrast, most of the leptin dependent activation of neurons in the PVH seems to be transynaptic and dependent on maturation of ARH projections.

Thus, developmental perturbations that disrupt development of ARH projections may contribute to leptin resistance at the level of the PVH. Despite evidence from a variety of sources that neonatal nutrition and maternal factors have long term effects on obesity [ 28 , 29 , — ], we know relatively little about how the neonatal environment influences central mechanisms regulating food intake and energy balance.

Although many of the CNS feeding circuits appear to develop in utero in humans and other primates [ 16 ], these circuits develop during the first postnatal weeks in rodents, facilitating the analysis of their development in rodent models. During gestational diabetes, or in overnourished neonatal rodents, there are significant perturbations in glucose homeostasis that may impact brain development. The elevations in leptin that occur in these conditions can have lasting effects on body weight regulation later in life that correlate with changes in neuropeptide expression in the ARH see [ ]; [ 16 ] for reviews.

Moreover, similar physiological perturbations are observed when insulin is applied directly to the region of the mediobasal hypothalamus during the critical period for development of projections from the ARH to the PVH [ ]. Thus, it is clear that insulin acts on the brain to effect long term changes in body weight regulation. What is considerably less clear is how insulin signaling brings about changes in the organization and function of the hypothalamic circuitry that presumably underlie the observed physiological changes.

Of note is the observation that ARH neurons of rats overfed during postnatal life display altered electrophysiological properties [ 11 ] suggesting direct involvement of ARH neurons in the physiological defects brought about by neonatal overfeeding and the accompanying hyperinsulinemia.

Previous reports that insulin can exert neurotrophic effects on hypothalamic neurons [ ] and can induce cellular differentiation of Y79 cells originally derived from retinoblastoma cells to acquire neuronal-like properties [ ] provide additional support for the notion that insulin functions in hypothalamic development, and may provide a signaling mechanism for translating environmental perturbations into alterations in brain structure.

Developmental Neurobiology of Leptin The discovery of leptin and its activity in regulating specific components of the central nervous system reaffirmed the primacy of the brain in regulating metabolism. An appreciation of the role played by the brain in developmental programming has been slower to emerge, but gained momentum as a result of recent studies of leptin neuroendocrinology in mice.

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The remarkable observation that there is a dramatic surge in circulating leptin levels during this period of apparent leptin insensitivity led Ahima and colleagues to suggest that leptin functions as a developmental cue for brain development [ ]. A more recent report indicates that treatment of neonatal rats with leptin alters expression of hypothalamic neuropeptides in the ARH [ ]. Both the PVH and ARH are known to play important roles in mediating central stress responses and leptin appears to influence glucocorticoid feedback on the hypothalamus in neonatal rodents [ ], which may represent an indirect mechanism through which leptin influences brain development [ , ].

The existence of a discrete leptin surge between P4 and P16 in mice, which is independent of fat mass or food intake unlike the situation in adults , raises the possibility that this adipocyte-derived hormone might regulate the establishment and patterning of ARH projections. As with most important developmental factors, leptin appears to act primarily during a restricted postnatal critical period and this developmental window coincides with the naturally occurring surge in leptin.

The precise limits of this period of maximal sensitivity to the developmental actions of leptin are yet to be defined, and it remains possible that prenatal exposure to leptin may influence development of ARH projections. The projection from the principal nucleus of the bed nuclei of the stria terminalis BSTp to the anteroventral periventricular nucleus of the hypothalamus AVPV is sexually dimorphic in rats and mice and is mature by P14 [ ].

Taken together, these observations suggest that neonatal leptin deficiency does not lead to widespread disruption of hypothalamic circuitry, but may specifically affect development of the ARH. Hypothalamic circuits remain relatively plastic throughout life and a significant action that leptin shares with neurotrophins is the ability to cause synaptic rearrangements.

Collectively, the recent findings on leptin and brain development have renewed interest in the role of perinatal factors as major contributors to obesity. The cellular mechanisms mediating the developmental actions of leptin on brain development are unknown. Direct application of leptin to organotypic explant cultures of the ARH in vitro cause a profound proliferation of neurites extending out from the explants suggesting a direct site of action [ ].

While it remains possible that leptin may function in a target-dependent manner, perhaps by inducing release of diffusible guidance factors from sites such as the PVH or DMH, supportive evidence is lacking for this intriguing notion. Equally unexplored is the possible role of contact-mediated guidance factors that may guide and stabalize ARH axons as they project through the periventricular zone of the hypothalamus. Based on an abundance of both pharmacological and molecular genetic studies in adult animals, a great deal has been learned about how leptin receptors signal in a variety of tissues see [ ] [ ] [ ] for reviews.

Leptin receptors signal in neurons through the action of intracellular kinases.

Binding of leptin to the LRb initiates signaling events mediated by Jak2 resulting in the phosphorylation and transcriptional activation of the latent transcription factor, signal transducer and activator of transcription-3 STAT3. In addition to phosphorylation of STAT3, which appears to be the major mediator of leptin signaling in adult neurons, LRb activation promotes phosphorylation of the extracellular signaling kinase ERK , as well as activation of PI3K signaling pathways.

Bouret and R.

Simerly, unpublished observations. However, how these signals are linked to cellular mechanisms controlling axon outgrowth and targeting remains unknown. Leptin influences synaptic plasticity in the hippocampus. Exposure of hippocampal neurons in vitro to leptin increases synapse density and influences synaptic function [ ]. Interestingly, leptin also alters growth cone morphology of cortical neurons in vitro, an event that appears to involve multiple convergent signaling pathways [ ].

Convergent signaling between leptin receptors and other hormone signaling pathways should also be explored. For example, the neurobiological actions of leptin share certain similarities with those of estrogen see [ ] for review and estrogen can alter leptin signaling events [ ], as well as body weight [ ].

Based on current information, it seems clear that perinatal nutrition has a profound effect on metabolic phenotype. An important priority in the coming years will be to identify signaling pathways for physiological signals that link nutritional status and developmental events impacting energy balance.

A particularly promising avenue of research is to define epigenetic mechanisms that alter gene expression in response to changes in nutritional environments during critical developmental periods [ ]. Central sensitivity to stress hormones appears to be permanantly altered by neonatal events through epigenetic regulation of glucocorticoid receptor gene expression [ ];[ ]. Changes in endocrine profiles permanently alter the structural organization and functional activity of the central nervous system represent an equally powerful mechanism for effecting long term changes in metabolic regulation in response to neonatal events.

In addition to leptin, adrenal steroids may play a role in specifying the organization and sensitivity of a variety of neural pathways controlling energy balance [ ] and possible interactions between the developmental actions of these hormone systems need to be defined.

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Finally, the impact of maternal nutrition and metabolic health on the physiology of pregnancy represents an especially important period of developmental sensitivity that may influence not only prenatal development, but may also affect the impact of postnatal nutrition on brain development. Even though we are just beginning to appreciate the importance of brain development in metabolic dysfunction, it is reasonable to expect that by gaining a better understanding of how developmental events influence the architecture of neural systems that regulate metabolism we may identify new therapeutic approaches for reducing obesity and type 2 diabetes in pediatric populations.

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Bibliography 1. Seasonal hypothermia in a large migrating bird: saving energy for fat deposition? J Exp Biol. Mammalian hibernation: cellular and molecular responses to depressed metabolism and low temperature. Physiol Rev. Ogden CL, et al. Prevalence and trends in overweight among US children and adolescents, — Childhood obesity in Canada: a review of prevalence estimates and risk factors for cardiovascular diseases and type 2 diabetes.

Can J Appl Physiol. Barker DJ. The fetal and infant origins of disease. Eur J Clin Invest. Early programming of glucose-insulin metabolism. Trends Endocrinol Metab.

Gluckman PD, et al. Horm Res.

Rogers I. The influence of birthweight and intrauterine environment on adiposity and fat distribution in later life. Lau C, Rogers JM. Embryonic and fetal programming of physiological disorders in adulthood. Cruz ML, et al. Pediatric obesity and insulin resistance: chronic disease risk and implications for treatment and prevention beyond body weight modification.

Annu Rev Nutr. Davidowa H, Plagemann A. Decreased inhibition by leptin of hypothalamic arcuate neurons in neonatally overfed young rats. Early origins of obesity: programming the appetite regulatory system. J Physiol.

Vickers MH, et al. Neonatal leptin treatment reverses developmental programming. Yura S, et al. Role of premature leptin surge in obesity resulting from intrauterine undernutrition. Cell Metab. Levin BE. Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis.Cianfarani, S. Thus, it is not currently possible to determine if local changes in the density of neuropeptide immunoreactivity are due to alterations in the density of axon terminals, which reflect a true change in the organization of neural circuitry, or simply reflect alterations in neuropeptide synthesis and transport, or changes in local processing and release [ ].

Perinatal nutrition and hormone-dependent programming of food intake. Moreover, local circuits link these two populations of ARH neurons to provide an additional level of coordination and integration [ 58 ]. The ARH has long been associated with obesity [ 48 ], expresses high levels of leptin receptors [ 49 — 51 ], and has high densities of neurons that express Fos protein in response to intravenous injections of leptin [ 52 , 53 ]. La realidad es que seleccionan alimentos ricos en grasas y azucares, lo que produce desequilibrios utero bicorne y suele desembocar en obesidad.

Similarly, variability in the reported outcome of uteroplacental insufficiency for later glucose tolerance and insulin action in the rat may occur in part from differences in early postnatal handling of offspring 4 , 13 — Lepercq J, et al. We understand very little about the molecular mechanisms underlying metabolic imprinting, but it is clear that when an individual is confronted with environmental conditions that differ markedly from those present during perinatal development, disaster can ensue.

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