A luteinising hormone (LH) surge is fundamental to the induction of ovulation in mammalian females. The administration of a preovulatory level of oestrogen evokes an LH surge in ovariectomised females, whereas the response to oestrogen in castrated males differs among species; namely, the LH surge-generating system is sexually differentiated in some species (e.g. rodents and sheep) but not in others (e.g. primates). In the present study, we aimed to determine whether there is a functional LH surge-generating system in male goats, and whether hypothalamic kisspeptin neurones in male goats are involved in the regulation of surge-like LH secretion. By i.v. infusion of oestradiol (E2; 6 μg/h) for 16 h, a surge-like LH increase occurred in both castrated male and ovariectomised female goats, although the mean peak LH concentration was lower and the mean peak of the LH surge was later in males compared to females. Dual staining with KISS1 in situ hybridisation and c-Fos immunohistochemistry revealed that E2 treatment significantly increased c-Fos expression in the medial preoptic area (mPOA) KISS1 cells in castrated males, as well as ovariectomised females. By contrast, dual-labelled cells were scarcely detected in the arcuate nucleus (ARC) after E2 treatment in both sexes. These data suggest that kisspeptin neurones in the mPOA, but not those in the ARC, are involved in the induction of surge-like LH secretion in both male and female goats. In summary, our data show that the mechanism that initiates the LH surge in response to oestrogen, the mPOA kisspeptin neurones, is functional in male goats. Thus, sexual differentiation of the LH surge-generating system would not be applicable to goats.

Colorectal cancer is a common cancer and a leading cause of cancer‐related death worldwide. The liver is a dominant metastatic site for patients with colorectal cancer. Molecular mechanisms that allow colorectal cancer cells to form liver metastases are largely unknown. Activation of epithelial–mesenchymal transition is the key step for metastasis of cancer cells. We recently reported that dual‐specificity tyrosine‐regulated kinase 2 (DYRK2) controls epithelial–mesenchymal transition in breast cancer and ovarian serous adenocarcinoma. The aim of this study is to clarify whether DYRK2 regulates liver metastases of colorectal cancer. We show that the ability of cell invasion and migration was abrogated in DYRK2‐overexpressing cells. In an in vivo xenograft model, liver metastatic lesions were markedly diminished by ectopic expression of DYRK2. Furthermore, we found that patients whose liver metastases expressed low DYRK2 levels had significantly worse overall and disease‐free survival. Given the findings that DYRK2 regulates cancer cell metastasis, we concluded that the expression status of DYRK2 could be a predictive marker for liver metastases of colorectal cancer.

Our findings suggest that serum creatinine begins to decrease before the onset of clinical symptoms and is a biomarker for disease progression and the efficacy of therapeutics in preclinical SBMA.

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Reactions of excess H 2 SiEt 2 and H 2 SiHex 2 with [Pt(PCy 3 ) 2 ] at room temperature form mononuclear cis-hydrido(silyl)platinum complexes, cis-[Pt(H)(SiHR 2 )(PCy 3 ) 2 ] (1: R ) Et, 2: R ) Hex), which are converted into diplatinum complexes with bridging dialkylsilyl ligands, [{Pt(PCy 3 )} 2 (µ-η 2 -HSiR 2 ) 2 ] (3: R ) Et, 4: R ) Hex), upon heating at 80 °C. Complex 3 reacts with excess H 2 SiPhMe and H 2 SiPh 2 to afford dinuclear complexes [{Pt(PCy 3 )} 2 (µ-η 2 -HSiPhR) 2 ] (5: R ) Me, 6: R ) Ph) via exchange of the bridging silyl ligands. An equimolar reaction of H 2 SiPh 2 with 3 yields a mixture of diplatinum complexes [{Pt(PCy 3 )} 2 (µ-η 2 -HSiEt 2 )(µ-η 2 -HSiPh 2 )] (7) and [{Pt(PCy 3 )} 2 (µ-η 2 :η 2 -H 2 SiEt 2 )(µ-SiPh 2 )] (8). Use of D 2 SiPh 2 in the reaction results in distribution of deuterium in the diethylsilyl and diphenylsilyl ligands of 7, the diethylsilane ligand of 8, and the diphenylsilyl ligand of 6. Complex 6 undergoes exchange of the phosphine ligands with dmpe (1,2-bis(dimethylphosphino)ethane) and with dppe (1,2-bis(diphenylphosphino)ethane) to afford diplatinum complexes with bridging silylene ligands and the chelating diphosphine ligands, [{Pt(dmpe)} 2 (µ-SiPh 2 ) 2 ] (9) and [{Pt(dppe)} 2 (µ-SiPh 2 ) 2 ] (10). Short contact between the two Si atoms (2.718(2) and 2.646(2) Å) suggests a weak Si • • • Si interaction.

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A diplatinum complex with bridging diethylsilyl ligands, [{Pt(PCy3)}2(μ-η2-HSiEt2)2] (1), reacted with an excess of H2SiPh2 to yield [{Pt(PCy3)}2(μ-η2-HSiPh2)2] (2) via exchange of the bridging SiHEt2 ligands with SiHPh2 groups. An equimolar reaction of H2SiPh2 with 1 afforded a mixture of the dinuclear complexes [{Pt(PCy3)}2(μ-η2-HSiEt2)(μ-η2-HSiPh2)] (3) and [{Pt(PCy3)}2(μ-η2:η2-H2SiEt2)(μ-SiPh2)] (4). X-ray crystallographic structure determination of 4 showed bridging coordination of the H2SiEt2 ligand to two Pt centers via two Pt−H−Si three-center two-electron bonds (Pt−Si = 2.375(8) and 2.39(1) Å).

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