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해외 시각 - "기후 변화는 에너지 문제, 원자력에 대해 솔직하게 이야기해야"

Grimes, David Robert 한국원자력산업회의 2017 원자력산업 Vol.37 No.7
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원자력 에너지에 대한 사람들의 두려움이 매우 깊지만 그와 같은 문제점이 있음에도 불구하고 원자력 발전은 현재 우리가 활용할 수 있는 것 가운데 가장 효율적이고 청정한 에너지원이라고 할 수 있다.
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Should Lutetium-prostate specific membrane antigen radioligand therapy for metastatic prostate cancer be used earlier in men with lymph node only metastatic prostate cancer?

William John Yaxley,Rhiannon McBean,David Wong,David Grimes,Paul Vasey,Mark Frydenberg,John William Yaxley 대한비뇨의학회 2021 Investigative and Clinical Urology Vol.62 No.6
Purpose: Lutetium labelled prostate-specific membrane antigen radioligand therapy (Lu-PSMA RLT) has shown pleasing early results in management of high-volume metastatic castration resistant prostate cancer (mCRPC), but its role in the early treatment of men with only lymph node metastasis (LNM) is unknown. The aim was to assess the outcome of Lu-PSMA RLT earlier in the treatment of men with only LNM. Materials and Methods: Single institution retrospective review of men with only LNM on staging Ga-PSMA PET PSMA who proceeded with Lu-PSMA RLT. Results: There were 17 men with only LNM, including 13 with mCRPC and 3 who were both hormone and chemotherapy naïve. The median PSA was 3.7 (0.46–120 ng/mL). A PSA decline of ≥50% occurred in 10/17 (58.8%), decreasing to <0.2 ng/mL in 35.3% (6/17). The PSA continues to decline or remain stable in 10/17 (58.8%) with a median follow-up of 13 months, and 8/17 (47.1%) have not reached their pre-treatment levels. There were no significant side effects. There was a better PSA response in men without prior chemotherapy (p=0.05). The prostate cancer specific and overall survival is 82.4% (14/17). Conclusions: Our results identify improved PSA response to Lu-PSMA RLT in men with only LNM, especially in the chemotherapy naïve cohort, compared to previous series with more advanced mCRPC. These findings provide important proof of principle to aid with planning of future prospective randomized trials evaluating the role of Lu-PSMA RLT earlier in the management of node metastatic prostate cancer, including men naïve of ADT and chemotherapy.
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Defective erythropoiesis caused by mutations of the thyroid hormone receptor α gene

Park, Sunmi,Han, Cho Rong,Park, Jeong Won,Zhao, Li,Zhu, Xuguang,Willingham, Mark,Bodine, David M.,Cheng, Sheue-yann,Grimes, H. Leighton Public Library of Science 2017 PLoS genetics Vol.13 No.9
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<▼1>Patients with mutations of the THRA gene exhibit classical features of hypothyroidism, including erythroid disorders. We previously created a mutant mouse expressing a mutated TRα1 (denoted as PV; Thra1PV/+ mouse) that faithfully reproduces the classical hypothyroidism seen in patients. Using Thra1PV/+ mice, we explored how the TRα1PV mutant acted to cause abnormalities in erythropoiesis. Thra1PV/+ mice exhibited abnormal red blood cell indices similarly as reported for patients. The total bone marrow cells and erythrocytic progenitors were markedly reduced in the bone marrow of Thra1PV/+ mice. In vitro terminal differentiation assays showed a significant reduction of mature erythrocytes in Thra1PV/+ mice. In wild-type mice, the clonogenic potential of progenitors in the erythrocytic lineage was stimulated by thyroid hormone (T3), suggesting that T3 could directly accelerate the differentiation of progenitors to mature erythrocytes. Analysis of gene expression profiles showed that the key regulator of erythropoiesis, the Gata-1 gene, and its regulated genes, such as the Klf1, β-globin, dematin genes, CAII, band3 and eALAS genes, involved in the maturation of erythrocytes, was decreased in the bone marrow cells of Thra1PV/+ mice. We further elucidated that the Gata-1 gene was a T3-directly regulated gene and that TRα1PV could impair erythropoiesis via repression of the Gata-1 gene and its regulated genes. These results provide new insights into how TRα1 mutants acted to cause erythroid abnormalities in patients with mutations of the THRA gene. Importantly, the Thra1PV/+ mouse could serve as a preclinical mouse model to identify novel molecular targets for treatment of erythroid disorders.</▼1><▼2>Author summaryPatients with mutations of the THRA gene exhibit erythroid disorders. The molecular pathogenesis underlying erythroid abnormalities is poorly understood. In Thra1PV/+ mice expressing a dominant negative mutant TRα1PV, we found abnormal red blood cell indices similar to patients. Total bone marrow cells, the clonogenic potential of erythrocytic progenitors, and terminal differentiation of erythrocytes were markedly decreased in Thra1PV/+ mice. We elucidated that Gata-1, a key erythroid gene, was directly positively regulated by TRα1. The erythroid defects in Thra1PV/+ mice were due, at least partly, to the TRα1PV-mediated suppression of the Gata-1 gene and its down-stream target genes. Over-expression of Gata-1 rescued impaired terminal differentiation. Our studies elucidated molecular mechanisms by which TRα1 mutants caused erythroid disorders in patients. The present study suggests that therapies aimed at GATA1 could be tested as a potential target in treating erythroid abnormalities in patients.</▼2>

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