RESUMEN
PURPOSE: This study aims to evaluate the efficacy and satisfaction of using a multi-angle laser device (MLD) for C-arm fluoroscopy to assist novice learners during lumbar spine surgery. METHODS: Forty novice learners were randomly assigned to Group A using an MLD-equipped C-arm or Group B using a traditional C-arm. Both groups performed X-ray fluoroscopy on a lumbar spine model in supine and rotated positions. Time, number of shots, and deviation from the target were compared. A questionnaire was used to assess the learning experience. RESULTS: Group A required less time (13.66 vs. 25.63 min), and fewer shots (15.05 vs. 32.50), and had a smaller deviation (22.9% vs. 61.5%) than Group B (all p<0.05). The questionnaire revealed higher scores in Group A for comfort, efficiency, and knowledge mastery (all p<0.05). CONCLUSION: The MLD significantly improves novice learning of C-arm fluoroscopy during lumbar spine surgery.
Asunto(s)
Vértebras Lumbares , Cirugía Asistida por Computador , Fluoroscopía , Vértebras Lumbares/diagnóstico por imagen , Vértebras Lumbares/cirugía , Encuestas y Cuestionarios , HumanosRESUMEN
Convection-enhanced delivery (CED) is a promising technique for the delivery of drugs directly into the central nervous system (CNS) and, more specifically, the brain. CED can increase drug concentration within a brain tumour, thereby improving the therapeutic efficacy and limiting the systemic toxicity of tumoricidal agents. In this study, we evaluated a drug-liposome construct in vitro and in vivo using U87 tumour-bearing nude mice. Dipalmitoylphosphatidylcholine (DPPC)-based liposomes were designed to deliver a lipophilic temozolomide (TMZ) formulation (LipoTMZ). The LipoTMZ displayed good release of TMZ in vitro over a suitable range of time and temperatures. Encapsulating the TMZ into liposomes enhanced its tumoricidal activity against U87MG human glioma cells. The LipoTMZ also displayed good release and distribution of TMZ when delivered intracerebrally to U87MG tumour-bearing mice by CED infusion. Histological examination revealed that CED did not damage normal brain tissue. Our data indicate that CED was an effective method to deliver LipoTMZ to U87MG tumour-bearing mice, significantly inhibiting tumour growth without evidence of systemic toxicity.
Asunto(s)
Neoplasias Encefálicas/tratamiento farmacológico , Sistemas de Liberación de Medicamentos , Glioma/tratamiento farmacológico , Temozolomida/administración & dosificación , 1,2-Dipalmitoilfosfatidilcolina/química , Animales , Antineoplásicos Alquilantes/administración & dosificación , Antineoplásicos Alquilantes/farmacocinética , Antineoplásicos Alquilantes/farmacología , Encéfalo/efectos de los fármacos , Encéfalo/patología , Línea Celular Tumoral , Convección , Preparaciones de Acción Retardada , Liberación de Fármacos , Humanos , Liposomas , Masculino , Ratones , Ratones Desnudos , Temozolomida/farmacocinética , Temozolomida/farmacología , Distribución Tisular , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
PM2.5 (aerodynamic diameter ≤2.5 µm) has been a dominating and ubiquitous air pollutant and has become a global concern. Emerging evidences suggest a positive correlation between PM2.5 and leukemia, but the underlying molecular mechanisms remain unclear and need to be elucidated. Here, we assessed the impacts of PM2.5 on the progression and inflammation of human myeloid leukemia at lower environmental doses and explored the possible pathway. We showed that PM2.5 exposure significantly induced the leukemia cell growth and enhanced the release of inflammatory mediators in both in vitro and in vivo models. Additionally, NF-κB p65 and p-STAT3 were activated in PM2.5-treated leukemia cells, with a concomitant increase in both ROS formation and NADPH oxidase expressions. Strikingly, the supplement of inhibitors, including NAC (ROS), PDTC (NF-κB), or WP1066 (STAT3), contributed to a decline in leukemia cell growth. Furthermore, enhanced expressions of inflammatory cytokines were attenuated by the addition of NAC or PDTC, but not affected by WP1066. This study demonstrates that PM2.5 promotes leukemia progression, identifies a potential intervention target, and provides further understanding of the detrimental effect of PM2.5 exposure on human health.
Asunto(s)
Contaminantes Atmosféricos/toxicidad , Proliferación Celular/efectos de los fármacos , Citocinas/metabolismo , Leucemia Experimental/inmunología , Leucemia Mieloide/inmunología , Material Particulado/toxicidad , Animales , Supervivencia Celular/efectos de los fármacos , Supervivencia Celular/inmunología , Progresión de la Enfermedad , Relación Dosis-Respuesta a Droga , Células HL-60 , Humanos , Células K562 , Leucemia Experimental/patología , Leucemia Mieloide/patología , Ratones Desnudos , Trasplante de Neoplasias , Especies Reactivas de Oxígeno/metabolismo , Factor de Transcripción STAT3/metabolismo , Factor de Transcripción ReIA/metabolismoRESUMEN
Exposure to 2-amino-1-methyl-6-phenylimidazo [4, 5-b] pyridine (PhIP), a typical example of heterocyclic amine compounds, increases colon cancer risk. Seabuckthorn (SBT) seed oil is a biologically active substance extracted from seeds of wild Hippophae rhamnoides L. Here, we sought to investigate the toxicological mechanisms underlying oxidative stress and cancer-related gene expression in the rat colons as well as the protective effect of SBT seed oil against colonic oxidative damage. Our results showed that PhIP significantly decreased the anti-oxidative enzyme activities whereas increased the malondialdehyde (MDA) contents, protein carbonyl (PCO) levels and DNA-protein cross-links (DPC) coefficients in the rat colons compared with the solvent-control group. Moreover, PhIP activated expression of c-fos and c-jun and inhibited p16 and Rb expression. Additionally, SBT seed oil plus PhIP significantly improved antioxidant markers and reduced the levels of MDA, PCO and DPC compared to those in rats exposed to PhIP alone. These data indicated that PhIP could induce oxidative stress and abnormal alterations of cancer-related gene expression in the rat colons while SBT seed oil may be beneficial because of its ability to alleviate the PhIP-induced oxidative damage to the rats.