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The title compound, C12H20N42+·2BF4−, was prepared by the anion exchange of a dibromide ionic liquid with sodium tetrafluoroborate. The asymmetric unit contains one half of the imidazolium cation, which lies about an inversion centre at the mid-point of the central C—C bond of the linking butyl chain. The two planar imidazole rings (r.m.s. deviation = 0.0013 Å) are strictly parallel and separated by 2.625 (7) Å [vertical distance between the centroids of two imidazole rings], giving the molecule a stepped appearance. In the crystal structure, intermolecular C—H...F hydrogen bonds link the cations and anions, generating a three-dimensional network.

The title compound, C9H11N3S, was prepared by reacting 4-methylbenzaldehyde with thiosemicarbazide. An intramolecular N—H...N hydrogen bond helps to establish the observed molecular conformation. The crystal packing is realized by intermolecular N—H...S hydrogen bonds.

Background The association between the TDRD6 variants and human infertility remains unclear, as only one homozygous missense variant of TDRD6 was found to be associated with oligoasthenoteratozoospermia (OAT). Methods Whole-exome sequencing and Sanger sequencing were employed to identify potential pathogenic variants of TDRD6 in infertile men. Histology, immunofluorescence, immunoblotting and ultrastructural analyses were conducted to clarify the structural and functional abnormalities of sperm in mutated patients. Tdrd6-knockout mice were generated using the CRISPR-Cas9 system. Total RNA-seq and single-cell RNA-seq (scRNA-seq) analyses were used to elucidate the underlying molecular mechanisms, followed by validation through quantitative RT-PCR and immunostaining. Intracytoplasmic sperm injection (ICSI) was also used to assess the efficacy of clinical treatment. Results Bi-allelic TDRD6 variants were identified in five unrelated Chinese individuals with OAT, including homozygous loss-of-function variants in two consanguineous families. Notably, besides reduced concentrations and impaired motility, a significant occurrence of acrosomal hypoplasia was detected in multiple spermatozoa among five patients. Using the Tdrd6-deficient mice, we further elucidate the pivotal role of TDRD6 in spermiogenesis and acrosome identified. In addition, the mislocalisation of crucial chromatoid body components DDX4 (MVH) and UPF1 was also observed in round spermatids from patients harbouring TDRD6 variants. ScRNA-seq analysis of germ cells from a patient with TDRD6 variants revealed that TDRD6 regulates mRNA metabolism processes involved in spermatid differentiation and cytoplasmic translation. Conclusion Our findings strongly suggest that TDRD6 plays a conserved role in spermiogenesis and confirms the causal relationship between TDRD6 variants and human OAT. Additionally, this study highlights the unfavourable ICSI outcomes in individuals with bi-allelic TDRD6 variants, providing insights for potential clinical treatment strategies. [ABSTRACT FROM AUTHOR]