Therapists' experience of training and implementing an exoskeleton in a rehabilitation centre.

BACKGROUND: Lower limb exoskeletons are a recent intervention promoted to improve gait disorders. Available research has focused on clinical outcomes; however, little is known about therapists' experiences using the device in practice. PURPOSE: We explored the implementation of an exoskeleton at a tertiary rehabilitation center. METHOD: In this longitudinal qualitative study we conducted semi-structured interviews with 10 therapists. One group of therapists was formally trained using the device, whereas the other group only had clinical exposure to the device. The interviews were transcribed, coded, and analyzed for themes. RESULTS: Three main themes emerged: (1) A steep learning curve described challenges in learning to use the exoskeleton. (2) One step at a time illustrated the complex process of incorporating the exoskeleton in daily work. (3) Not a magic bullet revealed the tensions using this emergent technology in practice. CONCLUSION: The exoskeleton represents one of the most complicated and labor-intensive interventions provided by therapists. Implementation requires substantial resources, raising questions regarding its efficacy and cost-effectiveness relative to other approaches. Until more evidence becomes available around the use and effectiveness of this rapidly evolving technology, therapists must contend with a high degree of uncertainty.IMPLICATIONS FOR REHABILITATIONUsing a lower limb exoskeleton may reduce physical demands on therapists in high-intensity rehabilitation programs that involve repetitive, effortful movements.However, a number of potential barriers to implementing the exoskeleton into practice need to be taken into consideration, including calibration time, intensive training required to become qualified to administer the intervention, the cost of the device, and comfort and safety of the device affecting user acceptance and uptake.Therapists also need to manage patient expectations related to outcomes related to use of exoskeletons.

Assessing the impact of prehospital intubation on survival in out-of-hospital cardiac arrest.

UNLABELLED: There is a developing body of literature documenting adverse survival outcome of out-of-hospital endotracheal intubation for critical multiple trauma and head injury patients. OBJECTIVE: To compare the rates of survival to hospital admission and discharge of nontraumatic out-of-hospital cardiac arrest (OHCA) patients who received successful out-of-hospital endotracheal intubation and those who were not intubated. METHODS: We conducted a retrospective analysis from an ongoing database of OHCA patients brought to a large suburban tertiary care emergency department by paramedic services between 1995 and 2006. We dichotomized patients by whether they were successfully endotracheally intubated or not prior to hospital arrival. Utstein style cardiac arrest variables were abstracted for all cases. All survivors to hospital admission were reviewed to exclude those patients in whom intubation was not attempted or unnecessary, such as those who had successful first-shock recovery of spontaneous circulation. We used chi square and logistic regression techniques for analysis, using survival to discharge as the primary outcome and survival to admission as a secondary outcome. RESULTS: There were 1,515 total cases with 33 early survivors excluded. Overall, 1,220 (86.2%) were intubated; of those intubated, 270 (20.2%) survived to admission and 93 (7.0%) survived to discharge. Upon univariate analysis, there was no difference in survival between intubated and non intubated groups (6.5% vs 10.0%, OR = 0.63, 95% CI 0.37,1.08). For patients initially in ventricular fibrillation/ventricular tachycardia (VT/VF), in a multivariate Logit model, intubation significantly decreased survival to discharge, adjusted odds ratio (OR) = 0.52 (95% confidence interval 0.27, 0.998). Intubated non-VF patients were more likely to survive to admission, adjusted OR 2.96 (1.04, 8.43), but not to discharge (1.8% vs. 1.0%, p = 1.0). CONCLUSION: This observational study in an unselected population shows that patients in VF/VT arrest who underwent out-of-hospital intubation were less likely to survive to discharge than those not intubated. Out-of-hospital intubation of patients with non-VF arrest was associated with an increased rate of survival to admission, but not survival to discharge. Future prospective studies are needed to define the role of out-of-hospital endotracheal intubation in cardiac arrest patients.

Multiple forms of genetic instability within a 2-Mb chromosomal segment of 3q26.3-q27 are associated with development of esophageal adenocarcinoma.

Gene amplification is one of the mechanisms to activate oncogenes in many cancers, including esophageal adenocarcinoma (EA). In the present study, we used two-dimensional restriction landmark genome scanning to clone a NotI/DpnII fragment that showed increased genomic dosage in 1 of 44 EAs analyzed. This fragment maps to 3q26.3-q27, and subsequent experiments identified two intrachromosomal amplicons within a 10-Mb DNA segment in 7 of 75 (9%) EAs. The distal amplified-core region maps centromeric to the PIK3CA locus, and a microsatellite (D3S1754) within this region exhibited significant instability (MSI), in stark contrast to the genomewide microsatellite stability found in EA. D3S1754-MSI arises in premalignant Barrett's dysplastic cells and preceded amplification of the nascent MSI allele in the corresponding EA. Seven ESTs within the amplified-core were overexpressed in amplicon-containing EAs. One of these, EST AW513672, represents a chimeric transcript that initiated from an antisense promoter sequence in the 5'UTR of a full-length LINE-1 element (L1-5'ASP). Similar chimeric transcripts encoding portions of the MET oncogene and the BCAS3 gene also were overexpressed in EAs, suggesting that L1-5'ASP activation may occur at a broad level in primary EAs. Thus, the fine dissection of a 2-Mb amplified DNA segment in 3q26.3-q27 in EA revealed multiple genetic alterations that had occurred sequentially and/or concurrently during EA development.

The hepatocyte nuclear factor 3 alpha gene, HNF3alpha (FOXA1), on chromosome band 14q13 is amplified and overexpressed in esophageal and lung adenocarcinomas.

Genomic amplification is observed in many, if not all, types of human malignancy and is one of the mechanisms for the activation of dominant-acting oncogenes in tumorigenesis. In the present study, three amplified restriction fragments were identified in an esophageal adenocarcinoma (P16) using the restriction landmark genome scanning two-dimensional gel technique. These fragments were cloned, sequenced, and mapped to chromosome band 14q13. Using the sequence tagged site-amplification mapping approach, we defined the core-amplified domain by screening 75 normal-tumor paired esophageal samples. The frequency of 14q13 amplification is 6.7% in esophageal tumors, and the amplicon spans >6 Mb in 1 tumor but is contained in a region <0.3 Mb in all of the remaining amplified tumors. Quantitative reverse transcription-PCR (RT-PCR) of 8 genes and expressed sequence tags located within the core-amplified domain revealed that the HNF3alpha (FOXA1)(4) gene, a forkhead gene family member, was overexpressed in all of the amplified esophageal tumors. HNF3alpha amplification was confirmed by Southern blot and interphase fluorescence in situ hybridization analyses, and the results of real-time RT-PCR were consistent with that of the regular quantitative RT-PCR. Increased immunohistochemical nuclear staining of the HNF3alpha protein was detected in all of the tumors containing 14q13 amplification. Affymetrix oligonucleotide microarrays of 86 lung adenocarcinomas demonstrated that expression of the HNF3alpha mRNA was elevated (> or =2.5-fold of mean expression in normal lung) in 37% (32 of 86) of the tumors analyzed. Gene amplification of HNF3alpha was detected in 2 of the 5 overexpressed lung tumors examined. This is the first report of HNF3alpha amplification, and overexpression in esophageal and lung adenocarcinomas. Amplification of HNF3alpha in esophageal and lung tumors may suggest a potential oncogenic role for this gene in tumorigenesis.

Proteomic analysis of cytokeratin isoforms uncovers association with survival in lung adenocarcinoma.

Cytokeratins (CK) are intermediate filaments whose expression is often altered in epithelial cancer. Systematic identification of lung adenocarcinoma proteins using two-dimensional polyacrylamide gel electrophoresis and mass spectrometry has uncovered numerous CK isoforms. In this study, 93 lung adenocarcinomas (64 stage I and 29 stage III) and 10 uninvolved lung samples were quantitatively examined for protein expression. Fourteen of 21 isoforms of CK 7, 8, 18, and 19 occurred at significantly higher levels (P < .05) in tumors compared to uninvolved adjacent tissue. Specific isoforms of the four types of CK identified correlated with either clinical outcome or individual clinical-pathological parameters. All five of the CK7 isoforms associated with patient survival represented cleavage products. Two of five CK7 isoforms (nos. 2165 and 2091), one of eight CK8 isoforms (no. 439), and one of three CK19 isoforms (no. 1955) were associated with survival and significantly correlated to their mRNA levels, suggesting that transcription underlies overexpression of these CK isoforms. Our data indicate substantial heterogeneity among CK in lung adenocarcinomas resulting from posttranslational modifications, some of which correlated with patient survival and other clinical parameters. Therefore, specific isoforms of individual CK may have utility as diagnostic or predictive markers in lung adenocarcinomas.