| 1. |
- Proletov, Ian, et al.
(författare)
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Primary and secondary glomerulonephritides 1.
- 2014
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Ingår i: Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association. - : Oxford University Press (OUP). - 1460-2385. ; 29 Suppl 3:May, s. 186-200
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Tidskriftsartikel (refereegranskat)
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| 2. |
- Okita, Yukari, et al.
(författare)
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The transcription factor MAFK induces EMT and malignant progression of triple-negative breast cancer cells through its target GPNMB
- 2017
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Ingår i: Science Signaling. - : AMER ASSOC ADVANCEMENT SCIENCE. - 1945-0877 .- 1937-9145. ; 10:474
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Tidskriftsartikel (refereegranskat)abstract
- Triple-negative breast cancer (TNBC) is particularly aggressive and difficult to treat. For example, the transforming growth factor-beta (TGF-beta) pathway is implicated in TNBC progression and metastasis, but its opposing role in tumor suppression in healthy tissues and early-stage lesions makes it a challenging target. Therefore, additional molecular characterization of TNBC may lead to improved patient prognosis by informing the development and optimum use of targeted therapies. We found that musculoaponeurotic fibrosarcoma (MAF) oncogene family protein K (MAFK), a member of the small MAF family of transcription factors that are induced by the TGF-beta pathway, was abundant in human TNBC and aggressive mouse mammary tumor cell lines. MAFK promoted tumorigenic growth and metastasis by 4T1 cells when implanted subcutaneously in mice. Overexpression of MAFK in mouse breast epithelial NMuMG cells induced epithelial-mesenchymal transition (EMT) phenotypes and promoted tumor formation and invasion in mice. MAFK induced the expression of the gene encoding the transmembrane glycoprotein nmb(GPNMB). Similar to MAFK, GPNMB overexpression in NMuMG cells induced EMT, tumor formation, and invasion, in mice, whereas knockdown of MAFK in tumor cells before implantation suppressed tumor growth and progression. MAFK and GPNMB expression correlated with poor prognosis in TNBC patients. These findings suggest that MAFK and its target gene GPNMB play important roles in the malignant progression of TNBC cells, offering potentially new therapeutic targets for TNBC patients.
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| 3. |
- Suzuki, Kohei, 1976, et al.
(författare)
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Impact of municipal mergers on local population growth: an assessment of the merger of Japanese municipalities
- 2016
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Ingår i: Asia Pacific Journal of Public Administration. - : Informa UK Limited. - 2327-6665 .- 2327-6673. ; 38:4, s. 223-238
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Tidskriftsartikel (refereegranskat)abstract
- Municipal mergers have been widely used as a tool for administrative reform at the municipal level in various countries. While there are many studies of such reform initiatives, most have overlooked the issue of the unequal distribution of merger benefits among merged municipalities. This article responds to this research gap by assessing the impact of municipal mergers on local population growth in Japan – and, in doing so, appreciates that mergers differ within each of the merger partners, and also that the extent to which pre-merger municipalities can benefit from municipal mergers is contingent on their size relative to that of their merging partners. A unique dataset of Japanese local governments both pre-merger and post-merger facilitates an analysis of the impact of municipal mergers on local population growth. By employing propensity score-matching, it is found that, in Japan, municipal mergers negatively affect population growth for municipalities if they are not the largest municipalities among their merging partners. This finding suggests that not all pre-merger areas benefit from municipal mergers; rather, smaller municipalities are likely to incur considerable costs from municipal mergers.
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| 4. |
- Zhang, Rong, et al.
(författare)
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ISL1 is a major susceptibility gene for classic bladder exstrophy and a regulator of urinary tract development
- 2017
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Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7
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Tidskriftsartikel (refereegranskat)abstract
- Previously genome-wide association methods in patients with classic bladder exstrophy (CBE) found association with ISL1, a master control gene expressed in pericloacal mesenchyme. This study sought to further explore the genetics in a larger set of patients following-up on the most promising genomic regions previously reported. Genotypes of 12 markers obtained from 268 CBE patients of Australian, British, German Italian, Spanish and Swedish origin and 1,354 ethnically matched controls and from 92 CBE case-parent trios from North America were analysed. Only marker rs6874700 at the ISL1 locus showed association (p = 2.22 x 10(-08)). A meta-analysis of rs6874700 of our previous and present study showed a p value of 9.2 x 10(-19). Developmental biology models were used to clarify the location of ISL1 activity in the forming urinary tract. Genetic lineage analysis of Isl1-expressing cells by the lineage tracer mouse model showed Isl1-expressing cells in the urinary tract of mouse embryos at E10.5 and distributed in the bladder at E15.5. Expression of isl1 in zebrafish larvae staged 48 hpf was detected in a small region of the developing pronephros. Our study supports ISL1 as a major susceptibility gene for CBE and as a regulator of urinary tract development.
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