Different procedures are recommended for different sympathetic disorders according to the classification. The higher the level of sympathetic ganglion blockade, the higher is the regret rate. Therefore, for T2 and T3 ganglion, endoscopic thoracic sympathetic block by the clipping method is strongly recommended because of its reversibility.

Type 2 pleural tags on conventional CT images can increase the accuracy of early diagnosis of visceral pleural invasion by NSCLC that does not abut the pleura.

The risks of betel quid chewing with or without tobacco, alcohol drinking and cigarette smoking have been well explored in the oral cavity but not in the pharynx and larynx. We conducted a case-control study to investigate the association of these three risk factors to cancers of the pharynx and larynx in Taiwan. A total cases of 148 pharyngeal cancer, 128 laryngeal cancer and 255 hospital controls, all men, were recruited. Betel quid chewing was a significant independent risk factor (adjusted odds ratio [aOR] 5 7.7; 95% confidence interval [CI] 5 4.1-15.0) similar to that of alcohol drinking (aOR 5 6.6; 95% CI 5 3.5-13.0) for pharyngeal cancer, but not for laryngeal cancer (aOR 5 1.3; 95% CI 5 0.7-2.5) on which cigarette smoking (aOR 5 7.1) exerts a stronger significant independent risk than alcohol drinking (aOR 5 3.8). For pharyngeal cancers, chewers who consumed >20 quid/day, chewed with inflorescence in the quid or swallowed the betel quid juice were at higher risks; significant dose-response effects were found in daily quantity of drinking and chewing, and cumulative quantity of drinking. Synergistic effects from the 3 risk factors existed both on the pharynx (aOR 5 96.9) and the larynx (aOR 5 40.3), and attributed for 93.1% and 92.9% respectively. Our study is the first evidence to show that betel quid chewing without tobacco has different impact on the pharynx (digestive tract) and the larynx (airway), and supports the concept that exposure quantity and direct mucosal contact with the betel quid juice may contribute to carcinogenesis. Our results show an important insight into the impact of betel quid chewing on other sites of the digestive tract other than the oral cavity. ' 2005 Wiley-Liss, Inc.Key words: risk factors; areca; laryngeal neoplasms; pharyngeal neoplasms; betel; alcohol; cigarette Cigarette smoking and alcohol drinking are risk factors for cancers of the oral cavity, pharynx and larynx.1-6 Betel quid chewing with or without tobacco, a widespread habit in south and east Asian countries, is an important risk factor having both independent and synergistic effects with cigarette smoking and alcohol drinking for oral cancer.7-13 The risk of betel quid chewing without tobacco on the pharynx and larynx in humans has not been explored and is unknown.Betel nut (areca nut) is consumed by an estimated 400-600 million people worldwide, mainly IndoAsian, Chinese and Taiwanese. It has a long history of use and is deeply ingrained in many sociocultural and religious activities. 7,14 Betel nut is the seed of the fruit of the oriental palm, Areca catechu. It is seldom chewed alone but is usually consumed in the form of betel quid, which is most often prepared by adding different ingredients to the areca nut, for example, the betel fruit (unripe fruit, inflorescence of Piper betle), betel leaf (leaf of Piper betle), slaked lime, catechu and tobacco, mainly according to the local tradition and for the purpose of flavor enhancing. 11,14 In general, although chewers from different countries prepare betel quid ...

The consumption of alcohol, tobacco and betel quid has been found to be an important contributor to esophageal squamous cell carcinoma (ESCC) in Taiwan. The genotoxic effect of the ADH1B and ALDH2 genes modulating an individual's alcohol-metabolizing capacity on ESCC may be linked to drinking behavior, intake pattern and other exogenous factors. To investigate the interplay of these genetic and environmental factors in determining the risk of ESCC, a multicenter case-control study was conducted. Here, 406 patients with pathology-proven ESCC, as well as 656 gender, age and study hospital matched controls were recruited. Genetic polymorphisms of ADH1B and ALDH2 appeared to correlate with the abstinence of alcohol, though not with tobacco and betel quid. Within the same levels of alcohol consumption, carcinoma risks increased along with an increase in the numbers of ADH1B*1 and ALDH2*2 alleles. The inactive ALDH2*1/*2 genotype was found to multiplicatively interact with a low-to-moderate (0.1-30 g/day) and a heavy (>30 g/day) ethanol intake to increase the ESCC risk (the joint aOR 5 14.5 and 102.6, respectively). Among low-tomoderate drinkers, a smoking-dependent carcinogenetic effect for the ADH1B*1/*1 and ALDH2*1/*21*2/*2 genotypes was recognized, with significant risks found in smokers, but not in nonsmokers. Further, a supra-multiplicative combined risk of ESCC for alcohol and tobacco use was identified among carriers of the ADH1B*1/*1 genotype (p for interaction 5 0.042). In conclusion, the interplay of the ADH1B and ALDH2 genotypes, in conjunction with a behaved drinking habit and a practiced drinking pattern, along with continued tobacco consumption, plays an important pathogenic role in modulating ESCC risk. ' 2007 Wiley-Liss, Inc.Key words: alcohol drinking; esophageal neoplasms; genetic polymorphism; tobacco; areca Alcohol consumption has been causally linked to the cancerization of the esophagus in humans. 1 Epidemiological surveys offered ample evidence that esophageal cancer risk due to this agent is not homogeneous across gender and populations, or even socioeconomic classes. 1 Although discrepancies in the characteristics of alcohol intake have clarified parts of this issue, 2 interindividual dissimilarities in regard to the capabilities of alcohol metabolism may be crucial in accounting for the diverse effect of alcohol in populations, since acetaldehyde, the primary intermediate metabolite of ethanol, has been well recognized as a carcinogen in animal models. 3 Though the variant allele of the alcohol dehydrogenase-1B gene (ADH1B*2) that confers the ''fast'' metabolism of ethanol to acetaldehyde, and the mutant allele of the aldehyde dehydrogenase-2 gene (ALDH2*2) that results in a catalytically inactive subunit to oxidize acetaldehyde to acetate, are prevalent in Orientals, they are uncommon in Caucasians. 4 Alcohol flushing syndrome, characterized by a facial flushing accompanied by palpitation, drowsiness, breathlessness or nausea is a condition related to a toxic accumulation of acetaldehyde i...

Summary Intubation with a double‐lumen tube is important for achieving one‐lung ventilation and facilitating thoracic surgery. The GlideScope® videolaryngoscope (Verathon Inc., Bothell, WA, USA) is designed to assist tracheal intubation for patients with a difficult airway. We wished to compare the GlideScope and direct laryngoscopy for double‐lumen tube intubation. Sixty adult patients requiring a double‐lumen tube for thoracic surgery and predicted uncomplicated laryngoscopy were randomly assigned to a direct Macintosh laryngoscopy group (n = 30) or a GlideScope group (n = 30). The mean (SD) duration of intubation was longer in the Macintosh group (62.5 (29.7) s) than in the GlideScope group (45.6 (10.7) s; p = 0.007). There was no difference in the success of the first attempt at intubation (26/30 (87%) and 30/30 (100%) for Macintosh and GlideScope groups, respectively; p = 0.112). The incidence of sore throat and hoarseness was higher in the Macintosh group (18 (60%) and 14 (47%), respectively) than in the GlideScope group (6 (20%) and 4 (13%), respectively; p = 0.003 and 0.004). We conclude that double‐lumen tube intubation in patients with predicted normal laryngoscopy is easier using the GlideScope videolaryngoscope than the Macintosh laryngoscope.

Research on molecular mechanisms underlying the carcinogenesis of non-small cell lung cancer (NSCLC) may provide gene targets in critical pathways valuable for improving the efficacy of therapy and survival of patients with NSCLC. However, the molecular markers highly sensitive for the prognosis and treatment evaluation of NSCLC are not yet available. To explore candidates, we conducted an oligonucleotide microarray study with three pairs of NSCLC and normal lung tissue, and determined 8 differentially expressed genes including the Human MutT homologue (hMTH1), Surfactant protein D (SPD), Human hyaluronan binding protein 2 (HABP2), Crystalline-mu (CRYM), Ceruloplasmin (CP), Integrin alpha-11 subunit (ITGA11), Collagen type XI alpha I (COL11A1), and Lungspecific X protein (Lun X). Four lung cancer-related markers MUC-1, hTERT, hnRNP B1, and CK-19 were also incorporated for further analysis. The expression profiles of the twelve genes in seventy pairs of NSCLC tumor and normal lung tissue were then detected quantitatively by using membrane array and quantitative real-time PCR (qRT-PCR). The data of the membrane array and qRT-PCR were compared for consistency and the potential of these mRNA markers in clinical application. The results showed that membrane array and qRT-PCR obtained consistent data for the tested genes in both sensitivity and specificity (correlation coefficient 0.921, p<0.0001). For patients' clinicopathological characteristics, the overexpression of hMTH1, SPD, HABP 2, ITGA11, COL11A1, and CK-19 was significantly correlated with the pathological stage (p<0.05). In addition, the overexpression of hMTH1, SPD, ITGA11, and COL11A1 was correlated with lymph node metastasis and poor prognosis. This is the first report relating SPD to a prognosis marker for NSCLC. Moreover, the combined detection of these four mRNA markers by membrane array had a sensitivity of 89% and a specificity of 84% for NSCLC, significantly higher than these markers had achieved separately. In conclusion, we identified mRNA markers for NSCLC prognosis and therapy evaluation from differentially expressed genes determined by using microarray. Further studies are needed to collect the data of the mRNA markers used in clinical practice.

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