RESUMEN
BACKGROUND: The prevalence of early childhood caries (ECC) varies with geographical region and population. The Uygur people, one of 55 officially recognized ethnic minorities in China, have a population of 10,069,346. We performed a preschool-based cross-sectional study of 670 Uygur children from the southern region of Xinjiang, China, to investigate the prevalence and severity of ECC and to identify factors related to the dental health condition of this population. METHODS: The study population of children ranging in age from 3 to 5 years was invited using a three-stage stratified sampling in Kashgar, the westernmost city in China. The "dmft" index was used to assess dental caries. The diagnosis of ECC or severe ECC was based on the oral health diagnostic criteria defined by the American Academy of Pediatric Dentistry. A questionnaire was completed by the children's caregivers. The survey included questions concerning the children's sociodemographic background; feeding and eating habits, particularly frequency of sweet beverage and food consumption; dental hygiene-related behaviors; the general oral health knowledge of caregivers; and the dental healthcare experience of caregivers and their children. RESULTS: A total of 670 Uygur children underwent complete dental caries examination. Most of the children (74.2%) had ECC, with a mean dmft ± SD of 3.95 ± 3.84. The prevalence of severe ECC was 40.1% (N =269), with a mean dmft of 7.72 ± 3.14. More than 99% of caries were untreated. Statistically significant correlations were found between higher ECC prevalence and increased age and lower socioeconomic background, while greater dental health knowledge of the caregiver and positive oral hygiene behaviors were found to be protective. Our findings confirm the multi-factorial etiology of ECC. CONCLUSIONS: The prevalence of ECC among preschool-aged Uygur children in Kashgar was high, particularly among those from lower socioeconomic backgrounds. Caries prevalence was associated with oral hygiene behaviors of children and the general oral health knowledge of caregivers. These factors could be modified through public health strategies, including effective publicity concerning general dental health and practical health advice.
Asunto(s)
Caries Dental/epidemiología , Etnicidad/estadística & datos numéricos , Grupos Minoritarios/estadística & datos numéricos , Factores de Edad , Cuidadores/educación , Preescolar , China/epidemiología , China/etnología , Estudios Transversales , Índice CPO , Atención Odontológica/estadística & datos numéricos , Caries Dental/etnología , Escolaridad , Composición Familiar , Conducta Alimentaria , Femenino , Conocimientos, Actitudes y Práctica en Salud , Humanos , Renta/estadística & datos numéricos , Masculino , Higiene Bucal/estadística & datos numéricos , Padres/educación , Prevalencia , Factores de Riesgo , Salud Rural/estadística & datos numéricos , Clase Social , Diente Primario/patología , Salud Urbana/estadística & datos numéricosRESUMEN
PURPOSE: To evaluate the effect of naringenin on improving PCOS and explore the mechanism. METHODS: Firstly, we carried out differential gene expression analysis from transcriptome sequencing data of human oocyte to screen the KEGG pathway, then the PCOS-like rat model was induced by letrozole. They were randomly divided into four groups: Normal group (N), PCOS group (P), Diane-35 group (D), and Naringenin group (Nar). The changes of estrus cycle, body weight, ovarian function, serum hormone levels, glucose metabolism, along with the expression of SIRT1, PGC-1É, claudin-1 and occludin of the ovary and colon were investigated. Furthermore, the composition of the gut microbiome of fecal was tested. RESULTS: By searching the KEGG pathway in target genes, we found that at least 15 KEGG pathways are significantly enriched in the ovarian function, such as AMPK signaling pathway, insulin secretion, and ovarian steroidogenesis. Interestingly, naringenin supplementation significantly reduced body weight, ameliorated hormone levels, improved insulin resistance, and mitigated pathological changes in ovarian tissue, up-regulated the expression of PGC-1É, SIRT1, occludin and claudin-1 in colon. In addition, we also found that the abundance of Prevotella and Gemella was down-regulated, while the abundance of Butyricimonas, Lachnospira, Parabacteroides, Butyricicoccus, Streptococcus, Coprococcus was up-regulated. CONCLUSION: Our data suggest that naringenin exerts a treatment PCOS effect, which may be related to the modulation of the gut microbiota and SIRT1/PGC-1É signaling pathway. Our research may provide a new perspective for the treatment of PCOS and related diseases.
Asunto(s)
Microbioma Gastrointestinal , Síndrome del Ovario Poliquístico , Animales , Peso Corporal , Claudina-1/genética , Claudina-1/farmacología , Femenino , Flavanonas , Hormonas , Humanos , Letrozol/efectos adversos , Ocludina , Síndrome del Ovario Poliquístico/inducido químicamente , Síndrome del Ovario Poliquístico/tratamiento farmacológico , Síndrome del Ovario Poliquístico/genética , Ratas , Ratas Sprague-Dawley , Transducción de Señal , Sirtuina 1/metabolismoRESUMEN
MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively modulate gene expression at the post-transcriptional level. A growing number of studies has shown that more and more miRNAs are aberrantly expressed and involved in the pathogenesis of several types of cancers. Here, we report that the down-regulated hsa-miR-34c was also involved in oncogenesis of laryngeal carcinoma. Our studies indicated that hsa-miR-34c functioned as a tumor suppressor which inhibited growth and invasion of human laryngeal carcinoma cells. Furthermore, in our study, an inverse relationship between the expression of hsa-miR-34c and c-Met was identified in 10 paired fresh samples from tumor tissues and adjacent normal tissues. Infection of hsa-miR-34c mediated by lentivirus suppressed the expression of c-Met directly. In addition, introduction of c-Met cDNA lacking 3'-UTR largely abrogated hsa-miR-34c-induced cell growth and invasion inhibition. These findings suggest aberrantly down-regulated hsa-miR-34c is a critical factor that contributes to malignancy in human laryngeal carcinoma by a mechanism involving targeting of c-Met.