RESUMEN
BACKGROUND: Aedes albopictus is among the 100 most invasive species worldwide and poses a major risk to public health. Photoperiodic diapause provides a crucial ecological basis for the adaptation of this species to adverse environments. Ae. albopictus is the vital vector transmitting dengue virus in Guangzhou, but its diapause activities herein remain obscure. METHODS: In the laboratory, yeast powder and food slurry were compared for a proper diapause determination method, and the critical photoperiod (CPP) was tested at illumination times of 11, 11.5, 12, 12.5, 13, and 13.5 h. A 4-parameter logistic (4PL) regression model was selected to estimate the CPP. In the field, the seasonal dynamics of the Ae. albopictus population, egg diapause, and hatching of overwintering eggs were investigated monthly, weekly, and daily, respectively. A distributed lag non-linear model (DLNM) was used to assess the associations of diapause with meteorological factors. RESULTS: In the laboratory, both the wild population and the Foshan strain of Ae. albopictus were induced to diapause at an incidence greater than 80%, and no significant difference (P > 0.1) was observed between the two methods for identifying diapause. The CPP of this population was estimated to be 12.312 h of light. In the field, all of the indexes of the wild population were at the lowest levels from December to February, and the Route Index was the first to increase in March. Diapause incidence displayed pronounced seasonal dynamics. It was estimated that the day lengths of 12.111 h at week2016, 43 and 12.373 h at week2017, 41 contributed to diapause in 50% of the eggs. Day length was estimated to be the main meteorological factor related to diapause. CONCLUSIONS: Photoperiodic diapause of Ae. albopictus in Guangzhou of China was confirmed and comprehensively elucidated in both the laboratory and the field. Diapause eggs are the main form for overwintering and begin to hatch in large quantities in March in Guangzhou. Furthermore, this study also established an optimized investigation system and statistical models for the study of Ae. albopictus diapause. These findings will contribute to the prevention and control of Ae. albopictus and mosquito-borne diseases.
Asunto(s)
Aedes/fisiología , Dengue/prevención & control , Modelos Estadísticos , Mosquitos Vectores/fisiología , Adaptación Fisiológica , Aedes/virología , Animales , China/epidemiología , Dengue/epidemiología , Dengue/transmisión , Virus del Dengue/patogenicidad , Diapausa/fisiología , Femenino , Masculino , Mosquitos Vectores/virología , Fotoperiodo , Dinámica Poblacional , Estaciones del Año , Cigoto/fisiologíaRESUMEN
The autonomic nervous system contributes to prostate cancer proliferation and metastasis. However, the exact molecular mechanism remains unclear. In this study, muscarinic acetylcholine receptor M1 (CHRM1) expression was measured via immunohistochemical analysis in human prostate cancer tissue array slides. PC-3, LNCaP, and A549 cells were treated with pirenzepine or carbachol, and the cell migration and invasion abilities were evaluated. Western blotting and quantitative real-time PCR were performed to measure GLI family zinc finger 1 (GLI1), patched 1 (PTCH1), and sonic hedgehog (SHH) expression levels. High expression of CHRM1 was found in early-stage human prostate cancer tissues. In addition, the selective CHRM1 antagonist pirenzepine inhibited PC-3, LNCaP, and A549 cell migration and invasion, but the agonist carbachol promoted the migration and invasion of these three cell lines. Muscarinic signaling can be relayed by hedgehog signaling. These data show that CHRM1 is involved in the regulation of prostate cancer migration and invasion through the hedgehog signaling pathway.
Asunto(s)
Proteínas Hedgehog/genética , Neoplasias de la Próstata/patología , Receptor Muscarínico M1/genética , Carbacol/farmacología , Movimiento Celular/genética , Proliferación Celular , Humanos , Masculino , Agonistas Muscarínicos/farmacología , Antagonistas Muscarínicos/farmacología , Receptor Patched-1/genética , Pirenzepina/farmacología , Neoplasias de la Próstata/genética , Receptor Muscarínico M1/antagonistas & inhibidores , Proteína con Dedos de Zinc GLI1/genéticaRESUMEN
Insulin resistance (IR) links Alzheimer's disease (AD) with oxidative damage, cholinergic deficit, and cognitive impairment. Peroxisome proliferator-activated receptor γ (PPARγ) agonist pioglitazone previously used to treat type 2 diabetes mellitus (T2DM) has also been demonstrated to be effective in anti-inflammatory reaction and anti-oxidative stress in the animal models of AD and other neuroinflammatory diseases. Here, we investigated the effect of pioglitazone on learning and memory impairment and the molecular events that may cause it in fructose-drinking insulin resistance rats. We found that long-term fructose-drinking causes insulin resistance, oxidative stress, down-regulated activity of cholinergic system, and cognitive deficit, which could be ameliorated by pioglitazone administration. The results from the present study provide experimental evidence for using pioglitazone in the treatment of brain damage caused by insulin resistance.
Asunto(s)
Encefalopatías/tratamiento farmacológico , Hiperinsulinismo/complicaciones , Resistencia a la Insulina/fisiología , Aprendizaje por Laberinto/efectos de los fármacos , Memoria/efectos de los fármacos , PPAR gamma/antagonistas & inhibidores , Tiazolidinedionas/farmacología , Análisis de Varianza , Animales , Encefalopatías/etiología , Fructosa/toxicidad , Insulina/sangre , Masculino , Pioglitazona , Ratas , Ratas Wistar , Especies Reactivas de Oxígeno/metabolismo , Tiazolidinedionas/uso terapéutico , Sustancias Reactivas al Ácido TiobarbitúricoRESUMEN
Advanced glycation endproducts (AGEs) are elevated in aging and neurodegenerative diseases such as Alzheimer's disease (AD), and they can stimulate the generation of reactive oxygen species (ROSs) via NADPH oxidase, induce oxidative stress that lead to cell death. In the current study, we investigated the molecular events underlying the process that AGEs induce cell death in SH-SY5Y cells and rat cortical neurons. We found: (1) AGEs increase intracellular ROSs; (2) AGEs cause cell death after ROSs increase; (3) oxidative stress-induced cell death is inhibited via the blockage of AGEs receptor (RAGE), the down-regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and the increase of scavenging by anti-oxidant alpha-lipoic acid (ALA); (4) endoplasmic reticulum (ER) stress was triggered by AGE-induced oxidative stress, resulting in the activation of C/EBP homologous protein (CHOP) and caspase-12 that consequently initiates cell death, taurine-conjugated ursodeoxycholic acid (TUDCA) inhibited AGE-induced ER stress and cell death. Blocking RAGE-NADPH oxidase, and RAGE-NADPH oxidase-ROSs and ER stress scavenging pathways could efficiently prevent the oxidative and ER stresses, and consequently inhibited cell death. Our results suggest a new prevention and or therapeutic approach in AGE-induced cell death.