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Detection of Y Mosaicism in Blood and Gonad of Patients with Gonadal Dysgenesis (성선 이형성 환자 혈액 및 성선 조직에서 Y 염색체 모자이시즘의 진단)

  • Kim, Jin-Yeong;Lee, Sang-Joon;Park, Ki-Hyun;Kim, Jung-Yeon;Bai, Sang-Wook;Lee, Byung-Seok;Kim, Se-Kwang;Kim, In-Kyu;Cho, Dong-Je;Song, Chan-Ho;Kim, Jae-Wook;Lee, Ho-Joon
    • Clinical and Experimental Reproductive Medicine
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    • v.26 no.3
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    • pp.457-465
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    • 1999

  • Objective: The presence of Y chromosome in patients with gonadal dysgenesis is related to the risk of gonadoblastoma. Since the patients with abnormal sexual differentiation may have cryptic Y mosaicism, it is important to detect the presence of Y material in these patients. But sometimes it is difficult to detect Y material only with karyotyping. This study was performed to evaluate the usefulness of the SRY gene screening in blood and gonad by using PCR in detecting the presence of Y material and possible tissue mosaicism in patients with gonadal dysgenesis as Turner syndrome and 46,XY pure gonadal dysgenesis (PGD, Swyer syndrome). Method: In 26 patients with gonadal dysgenesis, we screened for Y material by using PCR for SRY gene in peripheral leukocytes and in gonadal tissues of some patients. They were 22 cases of Turner syndrome (7 45,XO, 2 46,Xi(Xq), 3 45,XO/46,XX, 5 45,XO/46,Xi(Xq), 1 45, XO/46,XY, 1 45,XO/46,Xi(Yq), 1 45,XO/47,XYY, 1 46,XX,del(X)(q24) and 1 46,X,+mar) and 4 cases of 46,XY pure gonadal dysgenesis. PCR for SRY gene in the gonadal tissue was performed in 5 Turner syndrome and 2 PGD to determine the cryptic Y mosaicism between blood and gonad. Results: By using PCR analysis for SRY, Y chromosome material was detected in the blood of 4 of 22 Turner syndrome patients (45,XO/46,Xi(Xq), 45,XO/46,Xi(Yq), 45,XO/46,XY, and 45, XO/47,XYY), 3 of 4 46,XY pure gonadal dysgenesis. Discrepancy between karyotyping and blood PCR for SRY was noted in 1 Turner syndrome (45,XO/46,Xi(Xq)) and 1 PGD. Laparoscopic gonadectomy was performed in Y containing or SRY positive cases. In addition, PCR analysis for SRY in the gonads of 5 Turner syndrome and 2 PGD showed discrepancy between blood and gonad or between both gonads in 3 Turner syndrome (45,XO/46,Xi(Xq), 45,XO/46,Xi(Y q), 45,XO/46,XY) and 2 PGD patients. Conclusion: In gonadal dysgenesis, PCR analysis for SRY gene is useful to detect the cryptic Y mosaicism that is sometimes undetected by karyotyping. And since there may be tissue mosaicism, it is necessary to evaluate Y mosaicism in various tissues even in the case without Y chromosome on karyotyping.

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Effects of Dietary Protein and Lipid Levels on the Growth Performance, Feed Utilization and Innate Immunity of Juvenile Red Seabream Pagrus major (사료 내 단백질과 지방 수준이 참돔(Pagrus major) 치어의 성장, 사료효율 및 비특이적 면역력에 미치는 영향)

  • Kim, Sung-Sam;Oh, Dae-Han;Choi, Se-Min;Kim, Kang-Woong;Kim, Kyoung-Duck;Lee, Bong-Joo;Han, Hyon-Sob;Lee, Kyeong-Jun
    • Korean Journal of Fisheries and Aquatic Sciences
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    • v.48 no.3
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    • pp.308-313
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    • 2015

  • A $3{\times}3$ factorial study was conducted to investigate the effects of dietary protein and lipid levels on the growth, feed utilization and innate immunity of red seabream Pagrus major. Nine diets consisting of three protein levels (42%, 46% and 50% crude protein) and three lipid levels (10%, 14% and 18% crude lipid) were formulated. Triplicate groups of red seabream were fed the experimental diets to apparent satiation (5-6 times a day, from 08:00 to 18:00 h at 2-h intervals) for 10 weeks. At the end of the feeding trial, the weight gain and specific growth rate of fish fed P46L14 (46% protein and 14% lipid), P50L10 (50% protein and 10% lipid) and P50L14 (50% protein and 14% lipid) were significantly (P<0.05) higher than those of fish fed P42L18 (42% protein and 18% lipid). The feed conversion ratios (FCR) of the fish were affected by dietary lipid levels (P<0.039), but not dietary protein levels. The FCR tended to increase with increasing dietary lipid levels from 10% to 18% with the 46% and 50% protein levels. The weight gain, protein efficiency ratio, specific growth rate, feed intake and survival of fish were not affected by either dietary protein or lipid levels. Myeloperoxidase activity in the group fed P50L14 (50% protein and 14% lipid) was significantly higher than that in the group fed P42L10 (42% protein and 10% lipid) or P50L18 (50% protein and 18% lipid). However, the myeloperoxidase activity of fish was not affected by either dietary protein or lipid level. The fish fed P46L14 (46% protein and 14% lipid) and P46L18 (46% protein and 18% lipid) showed significantly higher superoxide dismutase activity than did the fish fed P46L10 (46% protein and 10% lipid), P50L10 (50% protein and 10% lipid) of P50L18 (50% protein and 18% lipid). In conclusion, the optimum protein and lipid levels for the growth and feed utilization of juvenile red seabream were 46% and 14%, respectively, and the optimum dietary protein to energy ratio was 27.4 g/MJ.

  • https://doi.org/10.5657/KFAS.2015.0308 인용 PDF KSCI KPUBS HTML

NK cell-activating receptor NKp46 does not participate in the development of obesity-induced inflammation and insulin resistance

  • Gracia Nathalie;Beatriz Dal Santo Francisco Bonamichi;Jieun Kim;Jiwon Jeong;Haneul Kang;Emirrio Reinaldie Hartland;Eveline Eveline;Jongsoon Lee
    • Molecules and Cells
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    • v.47 no.3
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    • pp.100007.1-100007.11
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    • 2024

  • Recent evidence establishes a pivotal role for obesity-induced inflammation in precipitating insulin resistance and type-2 diabetes. Central to this process is the proinflammatory M1 adipose-tissue macrophages (ATMs) in epididymal white adipose tissue (eWAT). Notably, natural killer (NK) cells are a crucial regulator of ATMs since their cytokines induce ATM recruitment and M1 polarization. The importance of NK cells is shown by the strong increase in NK-cell numbers in eWAT, and by studies showing that removing and expanding NK cells respectively improve and worsen obesity-induced insulin resistance. It has been suggested that NK cells are activated by unknown ligands on obesity-stressed adipocytes that bind to NKp46 (encoded by Ncr1), which is an activating NK-cell receptor. This was supported by a study showing that NKp46-knockout mice have improved obesity-induced inflammation/insulin resistance. We therefore planned to use the NKp46-knockout mice to further elucidate the molecular mechanism by which NKp46 mediates eWAT NK-cell activation in obesity. We confirmed that obesity increased eWAT NKp46+ NK-cell numbers and NKp46 expression in wild-type mice and that NKp46-knockout ablated these responses. Unexpectedly, however, NKp46-knockout mice demonstrated insulin resistance similar to wild-type mice, as shown by fasting blood glucose/insulin levels and glucose/insulin tolerance tests. Obesityinduced increases in eWAT ATM numbers and proinflammatory gene expression were also similar. Thus, contrary to previously published results, NKp46 does not regulate obesity-induced insulin resistance. It is therefore unclear whether NKp46 participates in the development of obesity-induced inflammation and insulin resistance. This should be considered when elucidating the obesity-mediated molecular mechanisms that activate NK cells.

  • https://doi.org/10.1016/j.mocell.2023.100007 인용 PDF