Role of small nucleolar RNAs in alternative splicing of the doublesex gene in the silkworm, Bombyx mori.

More and more evidence shows that small noncoding RNAs (ncRNAs) play diverse roles in development, stress response and other cellular processes, but functional study of intermediate-size ncRNAs is still rare. Here, the expression profile of 16 intermediate-size ncRNAs in ovary and testis of silkworm Bombyx mori were analyzed. Twelve ncRNAs, including 5 small nucleolar RNAs (snoRNAs) and 7 unclassified ncRNAs, accumulated more in the testis than in the ovary of silkworm, especially Bm-163, Bm-51 and Bm-68. Four ncRNAs (including three orphan snoRNAs and one unclassified ncRNA) had higher expression level in the ovary than in the testis, especially Bm-86. Overexpression of the testis-enriched snoRNA Bm-68 in the female led to the accumulation of male-specific isoform of doublesex (BmdsxM) and increased the expression ratio of BmdsxM: BmdsxF. While overexpression of ovary-enriched snoRNA Bm-86 in the male decreased the expression ratio of BmdsxM: BmdsxF, indicating the roles of the two snoRNAs played in the alternative splicing of Bmdsx of silkworm, which will provide new clues for the functional study of snoRNAs in insects.

How does chronic disease influence subjective life expectancy among middle-aged and older adults? Evidence from the China Health and Retirement Longitudinal Study (CHARLS) 2018 cross-sectional data.

Chronic diseases have become one of the most important factors threatening human health. Subjective life expectancy (SLE) describes an individual's expectation or subjective perception of lifespan. This article aims to explore the relationship between chronic diseases and SLE, as well as the differences among different age groups and different types of chronic diseases in this relationship. China Health and Retirement Longitudinal Study (CHARLS) is a nationwide longitudinal study that evaluates the social, economic, and health conditions of middle-aged and older adult families and individuals aged 45 and above in China. In this study, CHARLS used probability proportional to size sampling (PPS sampling) to ensure the breadth and representativeness of the sample. This study selected cross-sectional data from CHARLS 2018, removed missing values, and obtained a valid sample of 10,658 middle-aged and older individuals, of whom 8564 had chronic diseases. After controlling demographic, health behavior, socioeconomic, psychological, and social security factors, an ordered logistic regression was performed to explore the relationship between chronic disease and SLE in middle-aged and older adults. The results show that chronic diseases negatively correlate with SLE in middle-aged and older adults. Middle-aged and older adults with chronic diseases are 36.2% less likely to have high life expectancy than those without chronic diseases. Many different types of chronic diseases are negatively correlated with SLE. Cancer is most negatively correlated with SLE, far exceeding other chronic diseases. Chronic disease and SLE of middle-aged and older adults have age-heterogeneous differences. For middle-aged people aged 45-59 and young older adults aged 60-79, there is a significant correlation between chronic diseases and SLE. However, there is no correlation between chronic diseases and subjective life expectancy in the older population aged 80 and above. The government and society should pay close attention to the prevention and treatment of chronic diseases among middle-aged and older adults and adjust policies and measures according to the population's age structure. In addition, the government and society should pay attention to the spiritual needs of middle-aged and older adults. The government and society should pay more attention to cancer patients. Finally, the scientific research team should also strengthen research on chronic diseases, research and development of specific drugs and vaccines, improve the cure rate of chronic diseases, promote people's health, and make people no longer afraid of diseases.

5-ARI induces autophagy of prostate epithelial cells through suppressing IGF-1 expression in prostate fibroblasts.

OBJECTIVES: 5α-reductase inhibitor (5-ARI) is a commonly used medicine in the treatment of lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH). Our study mainly focuses on the mechanism of BPH development after 5ARI treatment. MATERIALS AND METHODS: Prostate specimens from patients were collected. Insulin-like growth factor 1 (IGF-1), Beclin-1, LC3 levels, was analysed by immunohistochemistry. The role IGF-1 on autophagic flux in prostate epithelial cells was studied. Additionally, effect of autophagy on recombinant grafts consisting of prostate stromal and epithelial cells in nude mice was investigated. RESULTS: We demonstrated that IGF-1 expression is down-regulated in prostate fibroblasts after long-term 5-ARI application. A decrease in IGF-1 levels was found to activate autophagic flux through the mTOR pathway in prostate epithelial cells, while the inhibition of IGF-1 receptor function induced autophagy in prostate epithelial cells. In addition, we revealed that blocking autophagic flux initiation can reduce the volume of recombinant grafts in vivo. Finally, our findings suggest that long-term 5-ARI application reduces IGF-1 secretion by prostatic stromal cells, thereby inducing autophagy of prostatic epithelial cells, which is one of the mechanisms underlying BPH pathogenesis and progression. CONCLUSIONS: Focusing on the autophagy induced by low levels of IGF-1 in prostatic epithelial cells, after elucidating AR signalling impairment of prostate stromal cells, might provide a novel strategy for the treatment and prevention of BPH development.

Involvement of MAPK ERK activation in upregulation of water channel protein aquaporin 1 in a mouse model of Bell's palsy.

The aim of this study is to immunolocalize the aquaporin 1 water channel protein (AQP1) in Schwann cells of idiopathic facial nerve and explore its possible role during the development of facial palsy induced by herpes simplex virus type 1 (HSV-1). HSV-1 was inoculated into the surface of posterior auricle of mouse to establish a paralyzed animal model. In HSV-1-induced facial palsy mice, protein levels of AQP1 significantly increased on the 9th to 16th day after inoculation of HSV-1. The upregulation of AQP1 was closely related to the intratemporal facial nerve edema in facial nerve canal, which was also consistent with the symptom of facial palsy in mice. In a hypoxia model of Schwann cells in vitro, we found that U0126, an ERK antagonist, inhibited not only morphological changes of cultures Schwann cells but also upregulation of both AQP1 and phosphorylated ERK. Combined with increased phosphorylated ERK in HSV-1-induced facial palsy mice, we inferred that ERK MAPK pathway might also be involved in increased AQP1 in mouse model of Bell's palsy. Although the precise mechanism needs to be further explored, our findings suggest that AQP1 in Schwann cells of intratemporal facial nerve is involved in the evolution of facial palsy induced by HSV-1 and may play an important role in the pathogenesis of this disease. AQP1 might be a potential target, and the ERK antagonist U0126 could be a new drug for the treatment of HSV-1-induced Bell's palsy in an early stage.