106 research outputs found

    Estudo anatomico do ligamento popliteo obliquo

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    OBJECTIVE:To study the anatomy of the oblique popliteal ligament, as regards its dimensions, expansion and anatomical relationships.METHODS:Eleven cadaver knees were dissected in order to study the anatomy and take mea-surements of anatomical structures and relationships of the oblique popliteal ligament. The dissection was for posterior access to the proper exposure of the oblique popliteal ligament, the semimembranosus muscle and its expansions. For measurement of dimensions, 40 × 12 needles were used for marking the specific points and a caliper. The angles were calculated using the software ImagePro Plus(r) .RESULTS:The distance from the origin of the oblique popliteal ligament to the tibial plateau was 7.4 mm, the thickness at its origin was 7.3 mm, length was 33.6 mm and the tibial plateau angle 34.8°. The length of the expansion of the proximal oblique popliteal ligament was 39.2 mm, thickness 7.8 mm and angle of the oblique popliteal ligament with its expansion 32.2°.CONCLUSION:The oblique popliteal ligament is thick, rises in the semimembranosus and protrudes proximally forming an acute angle with the joint interline, crossing the popliteal fossa. In some cases it has a proximal expansion.OBJETIVO:Estudar a anatomia do ligamento poplíteo oblíquo no que se refere às suas dimensões, expansões e relações anatômicas.MÉTODOS:Onze joelhos de cadáveres foram dissecados com o intuito de se estudar a anatomia e fazer medições das estruturas e das relações anatômicas do ligamento poplíteo oblíquo. A dissecção foi por acesso posterior até a exposição adequada do ligamento poplíteo oblíquo, do músculo semimembranoso e de suas expansões. Para aferição das medidas, foram usados agulhas 40x12 na marcação dos pontos específicos e um paquímetro. Os ângulos foram calculados com o auxílio do software ImagePro Plus(r).RESULTADOS:A distância da origem do ligamento poplíteo oblíquo ao platô tibial foi de 7,4 mm, a espessura na sua origem foi de 7,3 mm, o comprimento foi de 33,6 mm e o ângulo com o platô tibial foi de 34,8°. O comprimento da expansão proximal do ligamento poplíteo oblíquo foi de 39,2 mm, a espessura foi de 7,8 mm e o ângulo do ligamento poplíteo oblíquo com sua expansão foi de 32,2°.CONCLUSÃO:O ligamento poplíteo oblíquo é espesso, nasce no músculo semimembranoso, projeta-se proximalmente, forma um ângulo agudo com a interlinha articular e cruza a fossa poplítea. Em alguns casos apresenta uma expansão proximal.Universidade Federal do ParanaUniversidade Federal de São Paulo (UNIFESP)Universidade Federal de São Paulo (UNIFESP) Escola Paulista de MedicinaPontificia Universidade Catolica do ParanaUNIFESP, EPMSciEL

    Genetic parameters for faecal egg count, packed-cell volume and body-weight in Santa Inês lambs

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    Worm infection is one of the main factors responsible for economic losses in sheep breeding in Brazil. Random regression analysis was used to estimate genetic parameters for the factors faecal egg-count (FEC), packed-cell volume (PCV) and body weight (BW) in Santa Inês lambs. Data from 119 female, offspring of nine rams, were collected between December, 2005 and December, 2006, from the experimental flock of Embrapa Tabuleiros Costeiros, the Brazilian Agricultural Research Corporation located in Frei Paulo, SE, Brazil. After weaning, females were drenched until the faecal egg count had dropped to zero. Two natural challenges were undertaken. FEC heritability was extremely variable, this increasing from 0.04 to 0.27 in the first challenge and from 0.01 to 0.52 during the second. PCV heritability peaks were 0.31 and 0.12 in the first and second challenges, respectively. In the second challenge, BW heritability was close to 0.90. The genetic correlations among these traits did not differ from zero. There is the possibility of increasing parasite resistance in Santa Inês by selecting those animals with lower FEC. Selection to increase resistance will not adversely affect lamb-growth, although lambs with a slow growth-rate may be more susceptible to infection

    Analysis of Medaka sox9 Orthologue Reveals a Conserved Role in Germ Cell Maintenance

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    The sex determining gene is divergent among different animal species. However, sox9 is up-regulated in the male gonads in a number of species in which it is the essential regulator of testis determination. It is therefore often discussed that the sex determining gene-sox9 axis functions in several vertebrates. In our current study, we show that sox9b in the medaka (Oryzias latipes) is one of the orthologues of mammalian Sox9 at syntenic and expression levels. Medaka sox9b affects the organization of extracellular matrices, which represents a conserved role of sox9, but does not directly regulate testis determination. We made this determination via gene expression and phenotype analyses of medaka with different copy numbers of sox9b. Sox9b is involved in promoting cellular associations and is indispensible for the proper proliferation and survival of germ cells in both female and male medaka gonads. Medaka mutants that lack sox9b function exhibit a seemingly paradoxical phenotype of sex reversal to male. This is explained by a reduction in the germ cell number associated with aberrant extracellular matrices. Together with its identified roles in other vertebrate gonads, a testis-determining role for Sox9 in mammals is likely to have been neofunctionalized and appended to its conserved role in germ cell maintenance

    Oestrogen blocks the nuclear entry of SOX9 in the developing gonad of a marsupial mammal

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    <p>Abstract</p> <p>Background</p> <p>Hormones are critical for early gonadal development in nonmammalian vertebrates, and oestrogen is required for normal ovarian development. In contrast, mammals determine sex by the presence or absence of the <it>SRY </it>gene, and hormones are not thought to play a role in early gonadal development. Despite an XY sex-determining system in marsupial mammals, exposure to oestrogen can override <it>SRY </it>and induce ovarian development of XY gonads if administered early enough. Here we assess the effect of exogenous oestrogen on the molecular pathways of mammalian gonadal development.</p> <p>Results</p> <p>We examined the expression of key testicular (<it>SRY</it>, <it>SOX9</it>, <it>AMH </it>and <it>FGF9</it>) and ovarian (<it>WNT4</it>, <it>RSPO1</it>, <it>FOXL2 </it>and <it>FST</it>) markers during gonadal development in the marsupial tammar wallaby (<it>Macropus eugenii</it>) and used these data to determine the effect of oestrogen exposure on gonadal fate. During normal development, we observed male specific upregulation of <it>AMH </it>and <it>SOX9 </it>as in the mouse and human testis, but this upregulation was initiated before the peak in <it>SRY </it>expression and 4 days before testicular cord formation. Similarly, key genes for ovarian development in mouse and human were also upregulated during ovarian differentiation in the tammar. In particular, there was early sexually dimorphic expression of <it>FOXL2 </it>and <it>WNT4</it>, suggesting that these genes are key regulators of ovarian development in all therian mammals. We next examined the effect of exogenous oestrogen on the development of the mammalian XY gonad. Despite the presence of <it>SRY</it>, exogenous oestrogen blocked the key male transcription factor SOX9 from entering the nuclei of male somatic cells, preventing activation of the testicular pathway and permitting upregulation of key female genes, resulting in ovarian development of the XY gonad.</p> <p>Conclusions</p> <p>We have uncovered a mechanism by which oestrogen can regulate gonadal development through the nucleocytoplasmic shuttling of SOX9. This may represent an underlying ancestral mechanism by which oestrogen promotes ovarian development in the gonads of nonmammalian vertebrates. Furthermore, oestrogen may retain this function in adult female mammals to maintain granulosa cell fate in the differentiated ovary by suppressing nuclear translocation of the SOX9 protein.</p> <p>See commentary: http://www.biomedcentral.com/1741-7007/8/110</p
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