54 research outputs found

    Endoscopic Nd:YAG Laser Treatment in the Perioperative Management of Tracheobronchoplasty

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    The objective of this study was to determine the role of endoscopic Nd:YAG laser treatment in the preoperative or postoperative management of tracheobronchoplasty. Eighteen patients with severe stenotic lesions of the trachea or bronchus underwent Nd:YAG laser treatment. Nd:YAG laser treatment was performed in the preoperative period in 14 patients and in the postoperative period in 4 patients. The indications for Nd:YAG laser treatment included emergency airway dilatation, confirmation of the distal margin of tumor, and safe tracheal intubation in patients with severe tracheal stenosis. The indications for Nd:YAG laser treatment in patients with severe stenosis of the mainstem bronchus were confirmation of the distal margin of tumor and recovery of lung ventilation during the preoperative period and reopening of the bronchial lumen to prevent obstructive pneumonia in the postoperative period. Among patients treated with Nd:YAG laser preoperatively, the indications were completely achieved in all 14 patients, except for 1 patient with adenoid cystic carcinoma who underwent treatment of the right mainstem bronchus. Among patients treated with Nd:YAG laser postoperatively the indications also were achieved in all 4 patients with severe granulomatous stenosis of the bronchial end-to-end anastomosis following sleeve lobectomy. In conclusion, endoscopic Nd:YAG laser treatment played an important role in the perioperative management of patients undergoing tracheobronchoplasty

    Two distinct prions in fatal familial insomnia and its sporadic form

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    Abstract Fatal familial insomnia is a genetic prion disease, which is associated with the aspartic acid to asparagine substitution at codon 178 of the prion protein gene. Although the hallmark pathological feature is thalamic and olivary degeneration, there is a patient with an atypical fatal familial insomnia without the hallmark feature. The cause of the pathological variability is unclear. We analysed a Japanese fatal familial insomnia kindred and compared one atypical clinicopathological fatal familial insomnia phenotype case and typical fatal familial insomnia phenotype cases with transmission studies using multiple lines of knock-in mice and with protein misfolding cyclic amplification. We also analysed the transmissibility and the amplification properties of sporadic fatal insomnia. Transmission studies revealed that the typical fatal familial insomnia with thalamic and olivary degeneration showed successful transmission only using knock-in mice expressing human–mouse chimeric prion protein gene. The atypical fatal familial insomnia with spongiform changes showed successful transmission only using knock-in mice expressing bank vole prion protein gene. Two sporadic fatal insomnia cases with thalamic and olivary degeneration showed the same transmissibility as the typical fatal familial insomnia phenotype. Interestingly, one sporadic fatal insomnia case with thalamic/olivary degeneration and spongiform changes showed transmissibility of both the typical and atypical fatal familial insomnia phenotypes. Protein misfolding cyclic amplification could amplify both typical fatal familial insomnia cases and sporadic fatal insomnia cases but not the atypical fatal familial insomnia phenotype or other sporadic Creutzfeldt–Jakob disease subtypes. In addition to clinical findings and neuropathological features, the transmission properties and the amplification properties were different between the typical and atypical fatal familial insomnia phenotypes. It is suggested that two distinct prions were associated with the diversity in the fatal familial insomnia phenotype, and these two prions could also be detected in sporadic fatal insomnia

    Aberrant methylation of N-methyl-D-aspartate receptor type 2B (NMDAR2B) in non-small cell carcinoma

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    <p>Abstract</p> <p>Background</p> <p>N-methyl-D-aspartate receptors (NMDAR) act as tumor suppressors of digestive malignancies. The expression and genetic methylation patterns of <it>NMDAR2B </it>in non-small cell lung cancer (NSCLC) are unknown.</p> <p>Methods</p> <p>The relationship between gene methylation and expression of <it>NMDAR2B </it>was analyzed in NSCLC cell lines (N = 9) and clinical tissues (N = 216). The cell lines were studied using RT-PCR and 5-aza-2'-deoxycytidine treatment, while the clinical tissues were examined by methylation specific real-time quantitative PCR and immunohistochemistry. Retrospective investigation of patient records was used to determine the clinical significance of <it>NMDAR2B </it>methylation.</p> <p>Results</p> <p><it>NMDAR2B </it>was silenced in five of the nine cell lines; 5-aza-2'-deoxycytidine treatment restored expression, and was inversely correlated with methylation. Aberrant methylation of <it>NMDAR2B</it>, detected in 61% (131/216) of clinical NSCLC tissues, was inversely correlated with the status of protein expression in 20 randomly examined tumors. Aberrant methylation was not associated with clinical factors such as gender, age, histological type, or TNM stage. However, aberrant methylation was an independent prognostic factor in squamous cell carcinoma cases.</p> <p>Conclusions</p> <p>Aberrant methylation of the <it>NMDAR2B </it>gene is a common event in NSCLC. The prognosis was significantly better for cases of squamous cell carcinoma in which <it>NMDAR2B </it>was methylated. It may have different roles in different histological types.</p

    Cancer risk in patients with chronic obstructive pulmonary disease

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    Purpose: The goal of this study was to compare the risk of developing cancer between patients with or without chronic obstructive pulmonary disease (COPD), and to assess the role of gender as well as the use of respiratory medication on the risk of developing lung cancer in COPD patients.Patients and methods: We used the UK-based General Practice Research Database to conduct a follow-up study with a nested case-control analysis. We identified all patients with a first-time COPD diagnosis aged 40–79 years between 1995 and 2005 and a matched COPD-free comparison group. We then identified all patients who received an incident cancer diagnosis during follow-up. Results: Among 35,772 COPD patients and 35,772 COPD-free patients, we identified 4506 patients with an incident cancer diagnosis, of whom 2585 (57.4%) had a previous COPD diagnosis, yielding a crude incidence rate ratio of 1.64 (95% CI 1.55–1.74). The increased risk was mainly driven by a high lung cancer risk among COPD patients, while other cancers not associated with smoking were not statistically significantly associated with an altered COPD risk. In the nested case-control analysis, the odds ratio (OR) for lung cancer associated with COPD was higher for women (OR 5.26, 95% CI 3.64–7.61) than for men (OR 2.10, 95% CI 1.70–2.60). In the nested case-control analysis, none of the respiratory drugs were associated with a substantially altered risk of developing lung cancer among COPD patients.Conclusion: Our findings provide further evidence that COPD is associated with an elevated lung cancer risk, and that women with COPD may be more susceptible to developing lung cancer than men. Overall, respiratory medication did not have an influence on cancer risk

    Association of decreased variation of coefficient R-R interval with ischemic colitis and small bowel obstruction.

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    BACKGROUND:The parasympathetic nervous system exerts and controls intestinal tone. Several studies have suggested that the coefficient of the R-R intervals (CVRR) is useful for evaluating the parasympathetic nervous system. OBJECTIVES:This study aimed to evaluate the relationship between gastrointestinal emergencies, specifically ischemic colitis (IC) and small bowel obstruction (SBO), and the autonomic nervous system. METHODS:In this retrospective study, a total of 13 patients with IC or SBO aged ≧65 years were analyzed. CVRR was measured in patients with IC and SBO and controls. RESULTS:CVRR averaged to 8.8% ± 2.5% in controls, 1.4% ± 0.4% in patients with IC, and 2.4% ± 1.0% in SBO groups (p < 0.001). CVRR was significantly lower in patients with IC and SBO than that in controls. CONCLUSION:The results of this study demonstrate the possibility that CVRR may serve as a clinical index for assessing the functioning of the parasympathetic nervous system in patients with IC or SBO
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