Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 7 uppsatser.

No description available.

Christine May Briton-Jones. / "May 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 149-171). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Bovine horns develop primarily after birth and the presence or absence of horns is due to a single gene. It has been reported that the horn bud appears in the bovine embryo at d 60 of gestation. Our hypothesis is that the gene that determines the presence of horns is expressed in osteoprogenitor cells of the early fetus and will affect the expression of RUNX2, MSX1, MSX2, and/or TWIST1. To test this hypothesis, bovine fetal samples were collected from commercial females at the Caviness Packing Company in Hereford, Texas. Fetuses ranged from d 28 to d 80 of gestation. A survey of the expression of genes from the region on bovine chromosome 1 known to contain the locus that causes horns (IFNAR1 to SOD1), was conducted using qualitative and quantitative RT-PCR, and in situ hybridization. Genes with known roles in osteogenesis and chrondrogenesis (MSX1, TWIST1, RUNX2 and SOX9) were included as positive controls. With the exception of OLIG1, which was only expressed in the brain, all of the genes investigated were expressed in fetal frontal and parietal bones by qualitative RT-PCR. The level of expression of C21orf59, C21orf66, IL10RB, and SFRS15 increased in the frontal bone of horned samples from d 55 to d 70 of gestation. At d 60 of gestation, a change in the shape of the frontal bone was observed, which has been reported to be the developmental stage when the horn bud appears. At this time point, MSX1, TWIST1, RUNX2 and SOX9 were detected in frontal bone, in cells from the osteoblast lineage, as expected. Furthermore, C21orf59, C21orf62, C21or66 and SFRS15 from the polled interval were localized to developing mesenchyme, osteoblasts and/or osteoclasts of the frontal bone, suggesting that each of these genes has a role in intramembranous bone formation. In addition, gradients of expressed C21orf66 and SFRS15 were detected in developing endochondral bone. There was evidence of an antisense transcript of C21orf66 expressed in the same cell types as the sense transcript. Further characterization of this antisense transcript demonstrated that it covered the entire sense transcript. Based on observed expression in the mesenchyme, rather than just in mature osteoblasts or osteoclasts, C21orf66 and/or its antisense transcript become the most likely candidates for the polled locus.

OBJECTIVE: Adrenal steroidogenesis is important for maturation of fetal organ systems and plays a role in triggering parturition in ovine pregnancies. Studies have suggested a differential increase in baseline cortisol between twin gestations near term. Our aim was to further delineate the mechanisms responsible for the differences between the hypothalamic- pituitary-adrenal axes of twin fetuses in vivo. STUDY DESIGN: Surgery was performed on pregnant ewes (n = 6) with twin gestations to implant fetal vascular catheters. After recovery but while the subjects were resting, plasma cortisol concentrations were similar in both fetuses. Fetuses received, intravenously, boluses of adrenocorticotropic hormone at 2 doses, and plasma samples were obtained for analysis of the cortisol response. This stimulation by adrenocorticotropic hormone was then repeated in the same fetuses approximately 4 days later, after the increase of resting daily cortisol values in one but not the other fetus. RESULTS: Cortisol responses to adrenocorticotropic hormone before changes in daily resting cortisol concentrations were indistinguishable between twins. However, after separation of daily resting cortisol values, fetuses in group A (elevated resting cortisol concentration) demonstrated a significantly increased response to stimulation by adrenocorticotropic hormone. CONCLUSION: These results suggest a differential development in response to stimulation by adrenocorticotropic hormone between twin fetuses in vivo as the mechanism responsible for the asynchronous elevation of one twin's resting plasma cortisol concentration.

by Lam, Sau Hing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 141-158). / Abstract also in Chinese. / Content / Acknowledgements / Abbreviation / Project Objectives / Abstract / Chapter Chapter One --- Introduction / Chapter 1.1 --- The definition of homeobox genes / Chapter 1.2 --- Homeobox genes as a transcription factor / Chapter 1.3 --- Homeobox in Drosophila / Chapter 1.3.1 --- The development of Drosophila / Chapter 1.3.2 --- Maternal genes / Chapter 1.3.3 --- Segmentation genes / Chapter 1.3.4 --- Homeobox genes / Chapter 1.4 --- Family of Hox genes in the mammalian system / Chapter 1.5 --- Some possible chemical mechanism in the cascade system of the Hox genes in the vertebrate / Chapter 1.6 --- Hox (Antp-Class homeobox gene) in mammal / Chapter 1.6.1 --- Labial Like homeobox genes / Chapter 1.6.2 --- Proboscipedia Like homeobox genes / Chapter 1.7 --- Divergent homeobox genes / Chapter 1.7.1 --- Paired (prd) Class / Chapter 1.7.2 --- Even-Skipped (Eve) Class / Chapter 1.7.3 --- Distal-less (Dll) Class / Chapter 1.7.4 --- Muscle-Specific Homeobox (Msx) Class / Chapter 1.8 --- Orphan homeobox gene / Chapter 1.8.1 --- The characteristic of Hox 11 sequence in human and mouse / Chapter 1.8.2 --- Novel homeobox genes related to hox 11 gene family / Chapter 1.8.3 --- The mechanism of HOX 11 inducing gene regulation and signal transduction pathways / Chapter 1.8.4 --- HOX 11 in human / Chapter 1.8.5 --- Hox11 in mouse / Chapter 1.8.6 --- Hox11 L1 in mouse / Chapter 1.9 --- Homeobox gene involved in haematopoiesis / Chapter 1.10 --- Some translocations of homeobox genes in blood lineage / Chapter 1.11 --- The development of mouse / Chapter 1.11.1 --- Early organogenesis / Chapter 1.11.2 --- Nervous system development / Chapter 1.11.3 --- Somite development / Chapter 1.11.4 --- Eye development / Chapter 1.11.5 --- Neural crest cell migration / Chapter 1.11.6 --- Branchial arches development / Chapter Chapter Two --- Materials and methods / Chapter 2.1 --- Mouse Embryos / Chapter 2.2 --- RNA extraction / Chapter 2.3 --- Large plasmid preparation / Chapter 2.4 --- The synthesis of cDNAs using Reverse Transcription / Polymerase Chain Reaction (RT-PCR) and ligation into Bluescript® II KS / Chapter 2.4.1 --- The synthesis of RT-PCR products / Chapter 2.4.2 --- The formation of blunt ends of cDNA / Chapter 2.4.3 --- The ligation of cDNA with plasmid vectors / Chapter 2.4.4 --- Transformation / Chapter 2.4.5 --- The miniprep plasmid purification / Chapter 2.5 --- T7 sequencing / Chapter 2.6 --- Double stranded DNA cycle sequencing of plasmid / Chapter 2.6.1 --- Gel electrophoresis / Chapter 2.7 --- Northern blot / Chapter 2.7.1 --- Preparation of Northern blot / Chapter 2.7.2 --- Hybridization of Northern blot / Chapter 2.8 --- DIG labeled probes in whole mount in situ hybridization / Chapter 2.8.1. --- Preparation of linear DNA to generate riboprobes / Chapter 2.8.2 --- Preparation of DIG labeled riboprobe / Chapter 2.8.3. --- Preparation of embryo powder / Chapter 2.8.4 --- Absorption of antibody / Chapter 2.8.5 --- Embryo preparation / Chapter 2.8.6 --- Embryos staining / Chapter 2.9 --- Sections from whole mount in situ hybridization / Chapter 2.10 --- The radiolabeled section in situ hybridization / Chapter 2.10.1 --- The preparation of paraffin wax block and sample sections / Chapter 2.10.2 --- Slide pretreatment / Chapter 2.10.3 --- Preparation of probe / Chapter 2.10.4 --- Hybridization / Chapter 2.10.5 --- Washing / Chapter 2.10.6 --- Emulsification and development / Chapter 2.11 --- DIG-label in situ hybridization of frozen / Chapter 2.12 --- H&E staining / Chapter Chapter Three --- Results and Discussion / Chapter 3.1 --- Synthesis of Tlx3 probes for use in the section and whole mount in situ hybridization / Chapter 3.1.1 --- Synthesis of the Tlx cDNA by RT-PCR method / Chapter 3.1.2 --- The Tlx3 genomic clone for detecting the developmental expression of Tlx3 by Northern Blot / Chapter 3.1.3 --- The characterization of Tlx3 cDNAs and the sonic hedgehog cDNA / Chapter 3.2 --- Section in situ hybridization using different probes / Chapter 3.2.1 --- Section in situ hybridization using the transcribed riboprobes of Pax2 cDNA / Chapter 3.2.2 --- The transcribed riboprobes of Tlx genomic clones were used to hybridize the section in situ hybridization / Chapter 3.2.3 --- The in situ hybridization of frozen sections of mouse embryos using the transcribed riboprobes from Tlx3 cDNA subclone / Chapter 3.3 --- Expression pattern of Tlx3 on whole mount embryos using both cDNA and genomic probes / Chapter 3.3.1 --- The expression of Tlx3 on whole mount in situ hybridization of the mouse embryos using the antisense probes from the Tlx3 genomic clone / Chapter 3.3.2 --- Whole mount in situ hybridization of mouse embryo using the transcribed riboprobes of Tlx3 cDNA / Chapter 3.3.3 --- The expression pattern of sonic hedgehog on embryos at 8.5 to9.5 dpc / Conclusion / Future prospective / Appendix / Reference / Acknowledgement

Leung Kim-chuen Andrew. / "August 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 168-200). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

by Tse Kam Wah. / "September 1998." / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 123-145). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

As curvas ponderais, propostas por SIQUEIRA para diagnóstico de desnutrição materna em gestantes normais, foram aplicadas a duas populações de gestantes que frequentaram o Serviço de Obstetrícia (pré-natal e clínica obstétrica) do Hospital das clínicas da Universidade Federal de Goiás (U.F.Go): um grupo foi constituído por gestantes que não apresentaram patologias próprias ou associadas à gestação (Grupo Normais) e o outro foi composto por gestantes que apresentaram processos patológicos (Grupo Patológicas). Foram estudadas variáveis relacionadas à gestação (peso habitual, ganho de peso na gestação, peso ao final da gravidez, estatura da gestante, perímetro cefálico materno, idade da gestante, peso da placenta e idade gestacional pelos métodos de Capurro e Último Período Menstrual Normal (UPMN) e ao recém-nascido (peso, comprimento, perímetro cefálico e perímetro torácico) para ambos os grupos de acordo com o estado nutricional da gestante (desnutridas, nutridas e obesas). Os resultados permitiram concluir que as curvas ponderais propostas por SIQUEIRA são aplicáveis a outros tipos de populações, quer se trate de gestantes normais ou de gestantes patológicas. Foram verificadas as medidas antropométricas (peso, comprimento, perímetro cefálico e perímetro torácico) de 42 crianças que constituíram o grupo Normais e de 23 crianças que formaram o grupo Patológicas, por ocasião do nascimento e ao completarem 1, 3, 6, 9 e 12 meses de idade segundo o estado nutricional materno (desnutridas, nutridas e obesas); foi ainda estudada a idade gestacional dessas 65 crianças pelos métodos de Capurro e do UPMN. Os resultados permitiram concluir que a desnutrição materna contribuiu para o retardo de crescimento da criança no primeiro ano de vida. Verificou-se ainda um retardo no crescimento das crianças cujas mães apresentaram patologias próprias ou associadas à gravidez, mesmo quando classificadas como nutridas ou obesas, mas os filhos de desnutridas patológicas apresentaram ainda um maior déficit no seu crescimento. Concluiu-se que, além da desnutrição materna, também a presença de patologias durante a gestação associou-se com um retardo do crescimento fetal e pós-natal. Além disso, foi possível verificar que a desnutrição e a presença de patologias exerceram um efeito cumulativo sobre o retardo do crescimento fetal e pós-natal. / The weight curves proposed by SIQUEIRA for the diagnosis of maternal malnutrition in normal pregnant women were applied to two pregnant population samples which attended the Obstetric Clinic (Prenatal and Clinical Obstetrics) of the \"Hospital das Clinicas\" of the Federal University of Goiás (U.F.Go) One group (the Normal Group) consisted of expectant women who had no pathological history, either prior to or related to pregnancy, and the other group (the Pathological Group) consisted of expectant mothers who had a history of pathological condition. Several variables related to pregnancy were studied prepregnancy weight, weight-gain during pregnancy weight at and of nregnancy, mother\'s height, maternal cephalic circumference, mother\'s age, weight of placenta and gestational age by Capurro\'s and Last Menstrual Period (LMP) methods as were also some related to thc new-born child (weight, lenght, cephalic and thoracic circumferences) for both of the above groups in accordance with the nutritional status of the mother (undernourished, well-nourished and obese). The results led to the conclusion that the weight curves proposed by SIQUEIRA are applicable to other kinds of populations, whether of nor mal pregnant women or pathological pregnant women. The anthropometric measurements (weight, lenght, cephalic and thoracic circumferences) of the 42 children born to the Normal Group and of the 23 children born to the Pathological Groun were taken at birth and at the end of the 1st·, 6st., gst. and 12th. months, according to the nutritional status of the mother (undernourished, well-nourished and obese). The gestational age of 65 children was also studied, using the Capurro and LMP methods. The results led to the conclusion that maternal malnutrition contributed to the retardation of the child\'s growth in the first year of life. Further, it was discovered that there was a retardation in the growth of children whose mothers presented a pathological history either prior to or associated with pregnancy, even when these were classified as well-nourished or obese. However the children of undernourished mothers wi th a pathological history showed an even greater growth deficiency. The conclusion drawm was that the presence of a pathological condition during pregnancy was associated with retardation of fetal and postnatal growth beyond that caused by maternal malnutrition. It was also possible to establish that malnutrition and the presence of a pathological condition exercised a cumulative effect on the retardation of fetal and postnatal growth.

As curvas ponderais, propostas por SIQUEIRA para diagnóstico de desnutrição materna em gestantes normais, foram aplicadas a duas populações de gestantes que frequentaram o Serviço de Obstetrícia (pré-natal e clínica obstétrica) do Hospital das clínicas da Universidade Federal de Goiás (U.F.Go): um grupo foi constituído por gestantes que não apresentaram patologias próprias ou associadas à gestação (Grupo Normais) e o outro foi composto por gestantes que apresentaram processos patológicos (Grupo Patológicas). Foram estudadas variáveis relacionadas à gestação (peso habitual, ganho de peso na gestação, peso ao final da gravidez, estatura da gestante, perímetro cefálico materno, idade da gestante, peso da placenta e idade gestacional pelos métodos de Capurro e Último Período Menstrual Normal (UPMN) e ao recém-nascido (peso, comprimento, perímetro cefálico e perímetro torácico) para ambos os grupos de acordo com o estado nutricional da gestante (desnutridas, nutridas e obesas). Os resultados permitiram concluir que as curvas ponderais propostas por SIQUEIRA são aplicáveis a outros tipos de populações, quer se trate de gestantes normais ou de gestantes patológicas. Foram verificadas as medidas antropométricas (peso, comprimento, perímetro cefálico e perímetro torácico) de 42 crianças que constituíram o grupo Normais e de 23 crianças que formaram o grupo Patológicas, por ocasião do nascimento e ao completarem 1, 3, 6, 9 e 12 meses de idade segundo o estado nutricional materno (desnutridas, nutridas e obesas); foi ainda estudada a idade gestacional dessas 65 crianças pelos métodos de Capurro e do UPMN. Os resultados permitiram concluir que a desnutrição materna contribuiu para o retardo de crescimento da criança no primeiro ano de vida. Verificou-se ainda um retardo no crescimento das crianças cujas mães apresentaram patologias próprias ou associadas à gravidez, mesmo quando classificadas como nutridas ou obesas, mas os filhos de desnutridas patológicas apresentaram ainda um maior déficit no seu crescimento. Concluiu-se que, além da desnutrição materna, também a presença de patologias durante a gestação associou-se com um retardo do crescimento fetal e pós-natal. Além disso, foi possível verificar que a desnutrição e a presença de patologias exerceram um efeito cumulativo sobre o retardo do crescimento fetal e pós-natal. / The weight curves proposed by SIQUEIRA for the diagnosis of maternal malnutrition in normal pregnant women were applied to two pregnant population samples which attended the Obstetric Clinic (Prenatal and Clinical Obstetrics) of the \"Hospital das Clinicas\" of the Federal University of Goiás (U.F.Go) One group (the Normal Group) consisted of expectant women who had no pathological history, either prior to or related to pregnancy, and the other group (the Pathological Group) consisted of expectant mothers who had a history of pathological condition. Several variables related to pregnancy were studied prepregnancy weight, weight-gain during pregnancy weight at and of nregnancy, mother\'s height, maternal cephalic circumference, mother\'s age, weight of placenta and gestational age by Capurro\'s and Last Menstrual Period (LMP) methods as were also some related to thc new-born child (weight, lenght, cephalic and thoracic circumferences) for both of the above groups in accordance with the nutritional status of the mother (undernourished, well-nourished and obese). The results led to the conclusion that the weight curves proposed by SIQUEIRA are applicable to other kinds of populations, whether of nor mal pregnant women or pathological pregnant women. The anthropometric measurements (weight, lenght, cephalic and thoracic circumferences) of the 42 children born to the Normal Group and of the 23 children born to the Pathological Groun were taken at birth and at the end of the 1st·, 6st., gst. and 12th. months, according to the nutritional status of the mother (undernourished, well-nourished and obese). The gestational age of 65 children was also studied, using the Capurro and LMP methods. The results led to the conclusion that maternal malnutrition contributed to the retardation of the child\'s growth in the first year of life. Further, it was discovered that there was a retardation in the growth of children whose mothers presented a pathological history either prior to or associated with pregnancy, even when these were classified as well-nourished or obese. However the children of undernourished mothers wi th a pathological history showed an even greater growth deficiency. The conclusion drawm was that the presence of a pathological condition during pregnancy was associated with retardation of fetal and postnatal growth beyond that caused by maternal malnutrition. It was also possible to establish that malnutrition and the presence of a pathological condition exercised a cumulative effect on the retardation of fetal and postnatal growth.