RESUMEN
Simulation-based medical training provides learners a method to develop technical skills without exposing patients to harm. Although fluoroscopic phantoms are already adopted in some areas of radiology, this has historically not been for lumbar puncture. Commercially available phantoms are expensive. We report a cost-effective, accessible solution by creation of an inexpensive phantom for resident training to perform fluoroscopically guided lumbar puncture, as well as instructions on how to make a phantom for residency education. An anthropomorphic ballistics-gel phantom that contains a plastic lumbar vertebral column and simulated CSF space was created. Radiology residents with minimum or no experience with fluoroscopically guided lumbar punctures were given a brief education and practiced fluoroscopically guided lumbar punctures on the phantom. A survey from the residents was then done. The phantom was qualitatively quite durable and deemed adequate for educational purposes. All the residents surveyed expressed the desire to have this phantom available and it increased comfort, knowledge, and perceived likelihood of success. Few articles have been published that focused on low-cost phantom creation for fluoroscopic-procedure training. This study supports the benefits of using phantoms for fluoroscopic training as well as step-by-step instructions for creation of this phantom. The residents responded positively and felt more confident in their fluoroscopically guided techniques. The ability to make a long-term training device for resident education would be inexpensive and relatively easy to implement in academic programs.
Asunto(s)
Modelos Anatómicos , Fantasmas de Imagen , Radiología/educación , Punción Espinal , Competencia Clínica , Educación de Postgrado en Medicina/métodos , Fluoroscopía , Humanos , Internado y Residencia , Vértebras Lumbares , Punción Espinal/métodosRESUMEN
We have PCR-amplified and sequenced the immediate (841 bp) 5'-flanking region of murine p16INK4a (MTS1, CDKN2) tumor suppressor gene. Comparing to recently published 5'-flanking region of the human alpha form of p16INK4a, homologies were found in several regions of murine p16INK4a-alpha putative promoter sequence.
Asunto(s)
Proteínas Portadoras/genética , Animales , Secuencia de Bases , Inhibidor p16 de la Quinasa Dependiente de Ciclina , ADN , Genes Supresores de Tumor , Humanos , Ratones , Datos de Secuencia Molecular , Regiones Promotoras Genéticas , Homología de Secuencia de AminoácidoRESUMEN
The genes of murine cyclin D-dependent kinase inhibitors, p15INK4b and p16INK4a, are located in a region of chromosome 4 where overlapping deletions were found in lung adenocarcinomas. The p16INK4a gene uniquely consists of alternative first exons (E1alpha and E1beta), which are spliced to exon 2 in alternative reading frames to either encode p16INK4a (alpha form) or another potential tumor suppressor, p19ARF (beta form). We examined 99 lung adenocarcinomas of C3H/HeJ x A/J F1(C3AF1) and A/J x C3H/HeJ F1(AC3F1) mouse hybrids and 18 (13 metastatic, 5 nonmetastatic) tumorigenic mouse lung epithelial cell lines for p15INK4b and p16INK4a gene inactivation. Homozygous codeletion occurred in eight of the 13 (62%) metastatic, four of the five (80%) nonmetastatic cell lines, but in only six of 99 (6%) adenocarcinomas. Neither p15INK4b nor p16INK4a gene was individually deleted in any of the tumors or cell lines, and all deletions of the p16INK4a gene extended into exon 2, which would be expected to disrupt the functions of both p16INK4a and p19ARF. We also detected no intragenic mutations of either gene in 44 tumors that displayed loss of heterozygosity at the p16INK4a locus or in any of the cell lines. Transcript levels of p16INK4a-alpha, p16INK4a-beta and p15INK4b also were examined in each of the cell lines that retained copies of these genes. Whereas an immortal mouse lung epithelial cell line (E10) and two metastatic tumor cell lines (LM1 and E9) expressed p16INK4a-beta and p15INK4b mRNA, the alpha transcript of p16INK4a was detected in only the LM1 cell line. These results suggest that both p15INK4b and p16INK4a (alpha and beta) are targets of inactivation in mouse lung tumorigenesis.