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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

DNA microsatellites co-segregation of polycystic kidney disease genes (PKD1 & PKD2) in autosomal dominant polycystic kidney disease (ADPKD) families & cell culture models for ADPKD /

Yau, Chung-fai, Forrest. January 1999 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2000. / Includes bibliographical references (leaves 127-144).
2

Investigation of the structure and function of the PKD domain of polycystin-1, the protein product of the PKD1 gene

Case, Ruth January 2002 (has links)
No description available.
3

Effects of green tea and coffee polyphenols on cardiometabolic function in polycystic ovary syndrome

Tomatis, Virginia Beatriz January 2015 (has links)
No description available.
4

Polycystic Disease of the Kidneys with special reference to its Clinical features, Radiological diagnosis and Genetic Nature

de Villiers, Jacquez Charl 15 April 2020 (has links)
This work on polycystic disease of the kidney commenced while the author was engaged in general practice in Swellendam, in the South Western Cape from 1953-1956. Within a period of a year three patients, suffering from this disease, were seen. They were questioned about their family-relationship but they denied any such association. It was regarded as highly unlikely that three patients with a relatively rare disease, should be found in a population existing between those patients. The genealogy of each patient was worked out and when this information was bought together, it was found that they were fairly closely related. This was the first experience that the information obtained from a patient about his family may not be reliable, not even in a small, fairly closed community. As the family become known to the author the members were systematically investigated for polycystic kidney disease and an attempt was made to determine how many individuals were affected and i how many generations.
5

DNA microsatellites co-segregation of polycystic kidney diseasegenes (PKD1 & PKD2) in autosomal dominant polycystic kidney disease(ADPKD) families & cell culture models for ADPKD

游頌輝, Yau, Chung-fai, Forrest. January 1999 (has links)
published_or_final_version / Pathology / Master / Master of Philosophy
6

Dietary management of Polycystic ovary syndrome.

Moran, Lisa Jane January 2007 (has links)
Background Polycystic ovary syndrome (PCOS) is a common endocrine condition in women associated with obesity, reproductive and metabolic abnormalities. It improves with weight loss, however currently no specific dietary recommendations exist and there may be abnormalities in appetite regulation in PCOS that contribute to difficulty in weight management. Aims To assess the effect of 1) short and long-term weight loss and weight maintenance strategies on weight loss, reproductive and metabolic parameters in overweight women with PCOS and to 2) assess the relative effect of weight loss on cardiovascular risk factors and 3) postprandial appetite, appetite hormones (ghrelin, CCK, PYY) and food intake in overweight women with and without PCOS. Results Overweight women with PCOS followed an 8-week weight loss (2 meal replacements/day, 4904.4±127 kJ, n=32) followed by a 6 month carbohydrate (<120 g/day) or fat restricted (<50 g/day) weight maintenance regime (n=23). Reductions in weight (5.6±2.4 kg) and improvements in body composition, insulin, reproductive hormones and menstrual cyclicity occurred and were sustained equivalently for both diet groups. We then assessed the effect of weight loss (4.2±0.7 kg over 8 weeks as described above) in overweight women with (n=15) and without (n=17) PCOS on cardiovascular risk factors. All subjects had similar improvements in body composition, triglycerides, reproductive hormones and fasting and post-prandial insulin. C-reactive protein decreased with weight loss for non-PCOS women (-1.2±0.5 mg/L, P=0.025) but not for PCOS women. We finally assessed appetite regulation in PCOS. Women with (n=20) and without (n=12) PCOS followed a standard protein (55% carbohydrate, 15% protein) or high protein diet (40% carbohydrate, 30% protein) for 16 weeks (~6000 kJ/day). Non-PCOS subjects were more satiated (P=0.001) and less hungry (P=0.007) after the test meals and had a 70% higher fasting baseline ghrelin (P=0.011), a greater increase in fasting ghrelin (57.5 versus 34.0%, P=0.033), a greater post-prandial ghrelin decrease at week 16 (113.5±46.3 versus 49.3±12.2 pg/mL, P=0.05) and a greater maximal decrease in post-prandial ghrelin (-144.1±58.4 versus -28.9±14.2 pg/mL, P=0.02) following weight loss than subjects with PCOS. Lastly, women with (n=14) and without (n=14) PCOS undertook an 8-week weight loss regime (4.2±0.7 kg as described above). At week 0 and 8, women with PCOS again displayed lower ghrelin levels (P=0.01 and P=0.097 respectively) and a lesser post-prandial ghrelin decrease (P=0.048 and P=0.069 respectively) but similar post-prandial appetite, buffet consumption and fasting or post-prandial peptide YY and cholecystokinin compared to women without PCOS. Conclusion Meal replacements and moderate macronutrient restriction are effective strategies for the dietary management of PCOS. Equivalent weight losses improved cardiovascular risk factors similarly for overweight women with and without PCOS with the exception of CRP which did not decrease with weight loss for overweight women with PCOS. PCOS status is associated with altered fasting and post-prandial ghrelin levels but is not consistently associated with other impairments in post-prandial gut peptides or food intake. Further investigation is required to assess if appetite regulation is impaired in PCOS and the optimal strategies and amount of weight loss for improvement of reproductive and metabolic parameters in PCOS. / http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1282329 / Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2007
7

Follicle selection dynamics in the mammalian ovary

Chavez-Ross, Maria Alexandra January 1999 (has links)
No description available.
8

Regulation of sex hormone binding globulin and insulin-like growth factor binding protein-1

Hamilton, Fairley January 1996 (has links)
No description available.
9

Comparative analysis of the PKD1 gene and protein, polycystin-1

Hughes, Jim January 1999 (has links)
No description available.
10

Clinical and molecular characterisation of autosomal recessive polycystic kidney disease (ARPKD) in Afrikaans families

Lambie, Lindsay Ann 24 August 2010 (has links)
MSc (Med)(Genetic Counselling), Faculty of Health Sciences, University of the Witwatersrand / Autosomal recessive polycystic kidney disease (ARPKD; MIM263200) is a severe recessively inherited disease of the kidneys and biliary tract, with an incidence of approximately 1 in 20000 in non-isolated populations. It has a variable clinical spectrum from neonatal demise (in 30-50%) to survival into adulthood. ARPKD is caused by mutations at a single locus, polycystic kidney and hepatic disease 1 (PKHD1), with over 270 pathogenic mutations described to date. The high rate of compound heterozygosity in affected individuals has made genotype-phenotype correlations difficult. A common missense mutation, p.M627K, in exon 20 of PKHD1 was identified previously on the majority of ARPKD disease associated alleles in the Afrikaans population of South Africa suggesting the presence of a founder effect. The aim of this study was to describe the clinical phenotype of ARPKD in Afrikaans speaking individuals found to be homozygous for the common mutation, and to compare this phenotype to previously described cohorts of patients with ARPKD, known to harbour a spectrum of mutations. This descriptive study used retrospective data collected from records of patients with ARPKD at Johannesburg and Pretoria Academic Hospitals. Twenty seven individuals from 24 families were included in the study. Marked clinical variability was demonstrated within this subject group supporting the limitation of genotype-phenotype correlation described worldwide. ARPKD was diagnosed at a median age of 27 days, older than a North American cohort (NAC) born after 1990 (median age of 1 day). The majority (93%) of subjects in this study were diagnosed with chronic renal v insufficiency (CRI) and hypertension (HT), indicating the renal morbidities to be more common than noted in previous studies, but occurring at a later median age (1.4 years vs 13.5 days in the NAC). This may indicate a trend toward milder expression of renal morbidities in the present study. Portal hypertension was also diagnosed more frequently (81%) than in previous studies but at a younger median age (1.3 years vs 2.8 years), although with similar complication rates. Overall statistical correlation was found between the renal and hepatic related morbidities in this study, indicating that progression of the condition is not organ specific. A survival rate of 89% at one year is comparable to previous studies with similar patient ascertainment. This cohort represents the largest series of patients affected by ARPKD with a common mutation, described to date. The findings will provide for more accurate, specific and informative genetic counselling in families with ARPKD and may present a resource for future studies of modifier genes and environmental influences on the phenotypic expression of ARPKD.

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