RESUMO
Flooding is the main natural factor in snail diffusion, and it has a negative impact on schistosomiasis transmission. There are few studies on the spread and migration of snails following a flood; therefore, we aimed to investigate the influence of flooding on snail diffusion and explore the characteristics and laws of snail diffusion in Jiangxi Province. By using a retrospective survey and cross-sectional survey, the data on snail spreading in Jiangxi Province from 2017 to 2021 were collected. The distribution, nature, and area of snail spread were systematically analyzed in combination with the hydrological situation, types of region, and types of flood. From 2017 to 2021, a total of 120 snail-spread environments were found, including in 92 hilly areas and in 28 lake areas. The areas caused by flood and by other means numbered 6 and 114, respectively. The proportions of recurrence, expansion, and first-time occurrences were 43.42%, 38.16%, and 18.42%, respectively, and the 14 new snail environments were only distributed in the hilly areas. With the exception of 2018, the ratio of snail-spread areas in the hilly region was higher than that in lake region in other years. The average density of live snails was 0.0184-1.6617 no./0.1 m2 and 0.0028-0.2182 no./0.1 m2 in the hilly region. Among the 114 environments affected by floods, 86 consisted of hilly environments, including 66 spreading environments affected by rainstorm floods, and 20 rainstorm debris flow environments. There were 28 lake areas, of which 10 were in the Jiangxi section of Yangtze River and were affected by rainstorm floods. Snail spread following flooding has a certain 'lag effect,' and = simple annual changes in hydrological characteristics have little effect on the diffusion of snails or on their density = in the affected environment, but it is more closely related to local floods. The hilly environments are more susceptible to floods than the lake region, and the risk of snail spread is much higher in the hilly than in the lake region.
RESUMO
OBJECTIVE: Supracondylar humerus fractures are the most frequent fractures of the paediatric elbow. The present study introduced a modified surgical procedure for treatment of supracondylar humerus fractures in children. METHODS: From February 2015 to August 2019, 73 patients with Gartland's type II and III supracondylar fractures were treated with this modified method. Totally, 68 of all patients were followed up for 3-12 months (mean 8.25 months). The evaluation results included fracture nonunion, ulnar nerve injury, pin track infection, carrying angle and elbow joint Flynn score. RESULTS: The results showed that bone union was observed in all children, one case had an iatrogenic ulnar nerve injury, and the symptoms were completely relieved in 4 months after removing of the medial-side pin. All children had no cubitus varus deformity and no pin track infection, and the rate of satisfactory results according to Flynn's criteria score was 100%. CONCLUSION: The modified closed reduction and Kirschner wires internal fixation could effectively reduce the rate of open reduction, the risk of iatrogenic ulnar nerve injury, and the incidence of cubitus varus deformity in treatment of supracondylar humerus fractures in children.
Assuntos
Fixação Interna de Fraturas/métodos , Fraturas do Úmero/cirurgia , Úmero/cirurgia , Procedimentos de Cirurgia Plástica , Fios Ortopédicos , Criança , Pré-Escolar , Feminino , Humanos , Fraturas do Úmero/fisiopatologia , Úmero/fisiopatologia , Masculino , PediatriaRESUMO
Osteosarcoma is a bone cancer that develops commonly in children and adolescents. However, osteosarcoma treatments often fail by the development of chemoresistance to apoptosis, and the molecular mechanisms remain unclear. In this study, we propose that autophagy is responsible for osteosarcomatous resistance to apoptosis. We implicate PERK-mediated autophagy as a significant contributor to apoptosis resistance due to ER stress in osteosarcoma cells. By immunostainings and western blots, we identified that PERK activated osteosarcomatous autophagy via inhibiting mTORC1 pathway, thereby preventing cell apoptosis. While using RNAi, we knocked down PERK and found that autophagy was suppressed, result in osteosarcomatous apoptosis. Our results identify a novel role of PERK-mediated autophagy as a significant mechanism for osteosarcoma cell survival. These results will help to understand the mechanism of chemoresistance in osteosarcoma cells, and indicate a novel target for improving osteosarcoma therapy.
Assuntos
Apoptose/fisiologia , Autofagia/fisiologia , Estresse do Retículo Endoplasmático/fisiologia , Osteossarcoma/metabolismo , eIF-2 Quinase/metabolismo , Análise de Variância , Western Blotting , Linhagem Celular Tumoral , Primers do DNA/genética , Humanos , Alvo Mecanístico do Complexo 1 de Rapamicina , Complexos Multiproteicos/metabolismo , Osteossarcoma/fisiopatologia , Interferência de RNA , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo , eIF-2 Quinase/farmacologiaRESUMO
The onset of lipid peroxidation within cellular membranes is associated with changes in their physiochemical properties and enzymatic dysfunction of the membrane environment. There are increasing bodies of evidence indicating that aldehydic molecules generated endogenously during the process of lipid peroxidation are causally involved in most of the pathophysiological effects associated with oxidative stress in cells and tissues. 4-Hydroxy-2-nonenal (4-HNE), among them, is believed to be largely responsible for cytopathological effects observed during oxidative stress in vivo and has achieved the status of one of the best recognized and most studied of the cytotoxic products of lipid peroxidation. Here, we reported that 4-HNE treatment may induce cell death in MG63 human osteosarcoma cells. The 4-HNE treatment could activate caspase-3 and alter the Bax/Bcl-2 apoptotic signaling. All these changes are due to the inhibition of AKT activity by 4-HNE treatment, and we also found that the p70S6K activity, downstream factors of AKT, was also blocked by 4-HNE. Our results revealed the molecular mechanism of how 4-HNE induces cell death in MG63 human osteosarcoma cells, which contributes to the clinical treatment of cancer therapy.