Radiofrequency tumor ablation for lung tumors: is there a role for neoadjuvant and/or adjuvant chemotherapy?
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Catheter Ablation↗
Biomedical subjects
L Joos
Publications and source records attributed to L Joos.
Polymorphisms in the beta2 adrenergic receptor and bronchodilator response, bronchial hyperresponsiveness, and rate of decline in lung function in smokers.
BACKGROUND: Non-specific bronchial hyperresponsiveness (NSBH) is a known predictor of accelerated rate of decline in lung function in smokers. Polymorphisms of the beta(2) adrenergic receptor (ADRB2) have previously been associated with NSBH and bronchodilator response (BDR) in asthmatics. Based on these associations, we hypothesised that ADRB2 polymorphisms would be associated with NSBH and BDR as well as an accelerated rate of decline in lung function among smokers. METHODS: The prevalence of two ADRB2 polymorphisms, Arg16-->Gly and Gln27-->Glu, was examined in 587 smokers chosen from the NHLBI Lung Health Study for having the fastest (n=282) and slowest (n=305) 5 year rate of decline in forced expiratory volume in 1 second (FEV(1); mean DeltaFEV(1) -4.14 and +1.08% predicted/year, respectively). RESULTS: Contrary to our hypothesis, no ADRB2 allele or haplotype was associated with NSBH, BDR, or rate of decline in lung function. However, there was a significant negative association between heterozygosity at position 27 and a fast decline in lung function (adjusted odds ratio 0.56, 95% CI 0.40 to 0.78, p=0.0007). CONCLUSIONS: Heterozygosity at position 27 may be protective against an accelerated rate of decline in lung function. The polymorphism at position 16 does not contribute to the rate of decline in lung function, measures of NSBH, or BDR in smokers.
Administration, Inhalation↗
Pulmonary rehabilitation in outpatients with asthma or chronic obstructive lung disease. A pilot study of a "modular" rehabilitation programme.
STUDY/PRINCIPLES: Pulmonary rehabilitation programmes are often costly and dependent on the infrastructure of specialised centres. We developed a modular, outpatient-based rehabilitation programme, which is inexpensive and can be implemented in a variety of settings. The aim of this study was to determine the effects and feasibility of this programme. METHODS: Thirteen patients with COPD and 7 patients with asthma were enrolled by their primary care physician because of dyspnoea. Initial assessment included cardiopulmonary exercise testing, six-minute walking distance, lung function testing and multiple questionnaires addressing dyspnoea, depression and quality of life issues. The training consisted of 36 sessions of high intensity training of 2 hours duration to improve exercise tolerance, including 30 minutes of stationary cycling at the anaerobic threshold. Another complete assessment was done on completion of the study at 3 months. RESULTS: The six-minute walking distance improved significantly from 401 to 551 m (p < 0.0001). The maximal exercise capacity increased significantly from 85 W to 99 W (p < 0.001). The anaerobic threshold remained unchanged despite the high intensity training. There was a reduction of dyspnoea and an improvement of quality of life. CONCLUSION: This study shows that our outpatient rehabilitation programme leads to a benefit in exercise tolerance and health related quality of life comparable to other programmes published in the literature. The rehabilitation programme was very well accepted among patients, primary care physicians and health insurers.
Adult↗
beta(2)-Adrenergic receptor polymorphisms and asthma.
The idea that an abnormality in the beta(2)-adrenergic receptor contributes to asthma has been a long-standing hypothesis. Since the discovery of functionally relevant polymorphisms in the beta(2)-adrenergic receptor gene, there has been intensive research on their impact on asthma and related phenotypes, particularly the responsiveness to bronchodilators. It is the aim of this chapter to summarize the latest developments in this interesting field of research.
Adrenergic beta-Agonists↗
Association of IL-1beta and IL-1 receptor antagonist haplotypes with rate of decline in lung function in smokers.
BACKGROUND: There is increasing evidence that the cytokine network is central to the immunopathology of inflammatory airway diseases. The interleukin 1 (IL-1) receptor antagonist (IL-1RN) is a naturally occurring anti-inflammatory agent that binds to the IL-1 receptor but does not possess agonist activity. Each of the genes of the IL-1 locus on chromosome 2q14 is polymorphic. The IL1RN gene contains an 86 bp tandem repeat and allele 2 of this polymorphism has been associated with various inflammatory diseases. The IL-1beta (IL1B) gene contains a promoter polymorphism (C-511T) that has been associated with inflammatory diseases and is in linkage disequilibrium with the IL1RN polymorphism. METHODS: We investigated whether polymorphisms in the IL1B and IL1RN genes were associated with rate of decline of lung function. Genotypes were determined in 284 smokers with a rapid decline in lung function and 306 smokers with no decline in lung function. RESULTS: None of the genotypes was associated with the rate of decline of lung function. However, the distribution of IL1B/IL1RN haplotypes was different between smokers with a rapid decline in lung function and those with no decline in lung function (p=0.0005). CONCLUSION: These results suggest that IL1B/IL1RN haplotypes play a role in the rate of decline in lung function in smokers.
Algorithms↗
Recent developments in the genetics of asthma.
Asthma is a complex genetic disease with multiple genes involved in the pathogenesis. Some of these genes have been investigated to determine whether they influence an individual's response to asthma medication. We summarise the recent developments in the genetics of asthma as they pertain to the three main treatments available - inhaled glucocorticoids (GCs), (2)-agonists and leukotriene modulators. It has been shown that polymorphisms in the (2)-adrenergic receptor ((2)AR) gene influence responsiveness to (2)-agonists. Polymorphisms in the 5-lipoxygenase (5-LO) gene and the leukotriene C(4) (LTC4) synthase gene have been associated with response to medications that target the LT pathway. However, no polymorphisms have been identified that influence response to anticholinergics or are involved in steroid resistance. In the future, knowledge of an individual's genotype may help us tailor treatment to make it the most appropriate form for that asthmatic individual.
Adrenergic beta-Agonists↗
Cutaneous pseudolymphoma associated with bromocriptine therapy.
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Adult↗
[Amoebic liver abscess in chronic colitis: revision of "Crohn disease" diagnosis].
We present two cases initially diagnosed as Crohn's disease which were treated with immunosuppressive drugs. In both patients the development of an amoebic liver abscess led to the correct diagnosis of amoebic dysentery. The pitfalls of the diagnosis of amoebic colitis and the possible influence of immunosuppression in the development of extraintestinal amoebiasis are discussed.
Adult↗
[Unexpected development during rehabilitation for suspected rheumatic disorder].
The 57 year old woman presented with diffuse muscle spasms and delirium. Prior to presentation, she complained of progressive muscle pain, weakness and a weight loss of 10 kg over several months. Laboratory investigation showed hypopituitarism and a syndrome of inappropriate antidiuretic hormone secretion. Magnetic resonance imaging revealed an empty sella. The primary and secondary syndromes of empty sella are discussed.
Empty Sella Syndrome↗
Bronchoprotection by salmeterol: cell stabilization or functional antagonism? Comparative effects on histamine- and AMP-induced bronchoconstriction.
Salmeterol provides bronchoprotection against a number of constrictor stimuli for more than 12 h after a single dose. This effect could be due either to functional antagonism at the level of airway smooth muscle or to cell-stabilizing effects of the compound. In this study, we attempted to clarify this mechanism by comparing the effects of salmeterol (50 micrograms), salbutamol (200 micrograms) and placebo on the airway responsiveness to histamine (to assess functional antagonism), and to adenosine 5'-monophosphate (AMP) (to assess additional cell-stabilizing effects), 14 h after drug treatment. Thirteen patients with mild allergic asthma were studied in a double-blind, randomized protocol on 6 days, at least 48 h apart. Forced expiratory volume in one second (FEV1) was measured before and 15 min after inhalation of the study medication. Then, 14 h later (8 a.m. the following morning), a bronchoprovocation test with histamine or AMP was performed. We found that 14 h after inhalation, salmeterol still had a significant effect on FEV1 in comparison to placebo and salbutamol. The provocative dose producing a 20% fall in FEV1 (PD20histamine) was significantly increased after salmeterol, whilst the increase in PD20AMP did not reach significance. The shift in PD20 (in doubling dose steps) induced by salmeterol pretreatment was not different between histamine and AMP. We conclude that the prolonged protective effect of salmeterol occurs via an extended bronchodilating and functional antagonistic action and not via a cell-stabilizing effect.
Adenosine Monophosphate↗
Effect of phalloidin and viroisin on Acanthamoeba castellanii after permeabilization of the cell.
We have developed a new technique for the permeabilization of the membrane of Acanthamoeba castellanii. This technique involves the use of digitonin which alters neither the morphology nor the motility of the cell, but favours the penetration of phalloidin and viroisin. Treatment of permeabilized cells with phalloidin or viroisin induces, in the cortex of the cell, an intensive proliferation of filaments which have been identified as actin. This cortical filamentous layer detaches from the membrane and slowly contracts, acting as a fine mesh sieve which concentrates the organelles in the middle of the cell, causing therefore the formation of a central granuloplasm and a cortical hyaloplasm. During this process, cell motility is irreversibly lost. The results indicate that extensive proliferation and reorganization of actin filaments cannot support cell motility and they are discussed in terms of a general understanding of amoeboid movement.
Actin Cytoskeleton↗