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Hexokinase (HK) catalyzes the first irreversible rate-limiting step in glycolysis that converts glucose to glucose-6-phosphate. HK1 is ubiquitously expressed in the brain, erythrocytes, and other tissues where glycolysis serves as the major source of ATP production. Spermatogenic cell-specific type 1 hexokinase (HK1S) is expressed in sperm but its physiological role in male mice is still unknown. In this study, we generate Hk1s knockout mice using the CRISPR/Cas9 system to study the gene function in vivo. Hk1s mRNA is exclusively expressed in testes starting from postnatal day 18 and continuing to adulthood. HK1S protein is specifically localized in the outer surface of the sperm fibrous sheath (FS). Depletion of Hk1s leads to infertility in male mice and reduces sperm glycolytic pathway activity, yet they have normal motile parameters and ATP levels. In addition, by using in vitro fertilization (IVF), Hk1s deficient sperms are unable to fertilize cumulus-intact or cumulus-free oocytes, but can normally fertilize zona pellucida-free oocytes. Moreover, Hk1s deficiency impairs sperm migration into the oviduct, reduces acrosome reaction, and prevents capacitation-associated increases in tyrosine phosphorylation, which are probable causes of infertility. Taken together, our results reveal that HK1S plays a critical role in sperm function and male fertility in mice. Author summary: About 8%-12% of couples worldwide are infertile, and male infertility is associated with about half of these cases. Common defects of male infertility include low sperm count, reduced sperm motility, abnormal sperm morphology, and unexplained male infertility with normal sperm parameters but infertility. The cause of over 50% of male infertility cases remains unidentified. Research on male reproduction has helped to unravel male infertility. In this study, we used a knockout mouse model to study the function of HK1S in the male mouse reproductive system. We showed that depletion of Hk1s leads to infertility in male mice but with normal sperm morphology and motility. These phenotypes are similar to patients with unexplained male infertility. Furthermore, HK1S is essential for sperm glycolysis. Hk1s deficiency in mice results in decreased glycolysis activity and leads to impaired sperm migration into the oviduct, reduced acrosome reaction, and defective capacitation-associated increase in tyrosine phosphorylation. These results suggested that HK1S is necessary for male fertility in mice. Our study suggests a new avenue for the development of new therapeutic strategies for male infertility. [ABSTRACT FROM AUTHOR]

Structure optimization of stretchable AMOLED for high stretchability and high reliability was studied. High stretchability (>10%) was achieved. To improve the key reliability performance of stretchable OLED, pixel‐size hybrid encapsulation was developed, with which the panel can pass 60o C/90% 360h reliability test. A dynamic stretchable AMOLED module was fabricated. [ABSTRACT FROM AUTHOR]

The RIIβ subunit of cAMP‐dependent protein kinase A (PKA) is expressed in the brain and adipose tissue. RIIβ‐knockout mice show leanness and increased UCP1 in brown adipose tissue. The authors have previously reported that RIIβ reexpression in hypothalamic GABAergic neurons rescues the leanness. However, whether white adipose tissue (WAT) browning contributes to the leanness and whether RIIβ‐PKA in these neurons governs WAT browning are unknown. Here, this work reports that RIIβ‐KO mice exhibit a robust WAT browning. RIIβ reexpression in dorsal median hypothalamic GABAergic neurons (DMH GABAergic neurons) abrogates WAT browning. Single‐cell sequencing, transcriptome sequencing, and electrophysiological studies show increased GABAergic activity in DMH GABAergic neurons of RIIβ‐KO mice. Activation of DMH GABAergic neurons or inhibition of PKA in these neurons elicits WAT browning and thus lowers body weight. These findings reveal that RIIβ‐PKA in DMH GABAergic neurons regulates WAT browning. Targeting RIIβ‐PKA in DMH GABAergic neurons may offer a clinically useful way to promote WAT browning for treating obesity and other metabolic disorders. [ABSTRACT FROM AUTHOR]

Polyacrylamide (PAM), SrAl2O4 (SAO), and PAM/SAO composites were synthesized by hydrothermal method, polymer network method and low temperature sintering method, respectively. The phase structure and functional group information confirm that the as-prepared PAM/SAO composites contain only PAM and SAO and does not contain any other impurities. The microstructure and nitrogen adsorption experiments confirmed that the PAM/SAO composites possess porous structure, and the diameter of the pores increased with the increase of the mass percentage of SAO. The coupling of PAM and SAO broadened the light response range of PAM/SAO composites to visible light. The PAM/SAO composites showed two emission peaks at 370 and 470 nm are assigned to the 260 nm absorption of PAM and interface defects between PAM and SAO, respectively. The photocatalytic experiments confirmed that PAM/SAO composites had high photocatalytic activity for the degradation of methyl red dye. With the increase of the mass percentage of SAO, the intensity of emission peak decreased, while the photocatalytic activity increased. The high photocatalytic activity for the PAM/90 wt % SAO composites can be assigned to the high charge transfer and separation efficiency. Based on the experimental structure, the intrinsic relationship between luminescence and photocatalysis is discussed in detail. [ABSTRACT FROM AUTHOR]