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Background Lower urinary tract symptoms (LUTS) comprise a highly prevalent chronic condition among the aging male population. Existing literature on the experiences of men with LUTS is scarce given that only a few studies explored medical care-seeking behaviors and coping strategies. The current understanding of the experiences of elderly males with LUTS is considerably limited. Therefore, the present study aimed to identify the experiences of living with moderate-to-severe LUTS among community-dwelling Chinese ageing males and their coping strategies to facilitate the management of LUTS by healthcare providers. Methods and findings A qualitative exploratory design using thematic analysis was used. Semi-structured interviews with 24 Chinese ageing males with moderate-to-severe LUTS were conducted. According to the participants, LUTS adversely affect the physical aspects of their daily lives. Most of them were unwilling to seek social support and were even embarrassed to share this topic with their peers. A range of psychological responses could be observed from the participants that range from regarding the condition as a natural life course to loss of one’s self-esteem. Most of the interviewees lacked knowledge and held misconceptions toward LUTS, which prevented them from pursuing medical advice. Most of the participants also sought alternative treatments and developed self-help methods to cope with their symptoms. Conclusion LUTS affects the physical and social aspects of sufferers. The findings of this qualitative study can raise awareness about the life experiences, perceptions, misconceptions, and help-seeking behaviors of Chinese elderly with LUTS. Proper health education and advice can be provided for this population.

BackgroundAdar2 deaminates selective adenosines to inosines (A-to-I RNA editing) in the double-stranded region of nuclear transcripts. Although the functions of mouse Adar2 and its biologically most important substrate gria2, encoding the GluA2 subunit of AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor, have been extensively studied, the substrates and functions of zebrafish Adar2 remain elusive.Methods/principal findingsExpression of Adar2 was perturbed in the adar2 morphant (adar2MO), generated by antisense morpholio oligonucleotides. The Q/R editing of gria2α was reduced in the adar2MO and was enhanced by overexpression of Adar2, demonstrating an evolutionarily conserved activity between zebrafish and mammalian Adar2 in editing the Q/R site of gria2. To delineate the role of Q/R editing of gria2α in the developmental defects observed in the adar2MO, the Q/R editing of gria2α was specifically perturbed in the gria2αQRMO, generated by a morpholio oligonucleotide complementary to the exon complementary sequence (ECS) required for the Q/R editing. Analogous to the adar2-deficient and Q/R-editing deficient mice displaying identical neurological defects, the gria2αQRMO and adar2MO displayed identical developmental defects in the nervous system and cranial cartilages. Knockdown p53 abolished apoptosis and partially suppressed the loss of spinal cord motor neurons in these morphants. However, reducing p53 activity neither replenished the brain neuronal populations nor rescued the developmental defects. The expressions of crestin and sox9b in the neural crest cells were reduced in the adar2MO and gria2αQRMO. Overexpressing the edited GluA2αR in the adar2MO restored normal expressions of cresting and sox9b. Moreover, overexpressing the unedited GluA2αQ in the wild type embryos resulted in reduction of crestin and sox9b expressions. These results argue that an elevated GluA2αQ level is sufficient for generating the cranial neural crest defects observed in the adar2MO. Our results present a link between dysfunction of AMPA receptors and defective development of the nervous system and cranial neural crest in the zebrafish.