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Canadian Neighbor Pharmacy: Chronic Airflow Limitation

pneumoconiosesWhile the classic diseases of dusty occupations, in particular the pneumoconioses, have not yet disappeared, they may be on the decline. In contrast, mortality rates due to the chronic nonmalignant pulmonary conditions including those characterized by airflow limitation are increasing in the industrialized countries of the world, and they are also responsible for high rates of morbidity and extended periods of disablement. Like other chronic lifestyle diseases, these are also almost certainly multifactorial in etiology, involving host factors as well as environmental factors. Among the latter, cigarette smoking is the most important. As chronic disease epidemiology has improved, it has become possible to investigate the role of environmental factors other than the cigarette, and there is now increasing evidence that exposures to other airborne pollutants also play a role, including those to which men and women are exposed at work. The purpose of this review is (1) to set in context some of the recently published information on the role of work in dusty occupations; (2) to assess its role visavis that of cigarettes; and (3) to reassess the evidence for causality. It addresses the question: can the exposures which men and women encounter in the course of their daily work lead to chronic airflow limitation sufficiently severe to disable them?

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Asthmatic airways

The first possible shortcoming of this study was that the methacholine challenge was performed in only 45 of 88 patients, which would have resulted in a selection bias. The most important reason for not performing the methacholine challenge concerned the patients’ respiratory state. It was difficult to perform the test when FEV1/FVC was reduced or when symptoms such as cough, dyspnea, and wheezing were present. Another reason was patient refusal. A much larger number of subjects would have to be studied in the future. Second, the male/ female ratio differed significantly between the control group and the asthmatic group. Therefore, we analyzed the association between sex and the polymorphisms (exon 1 +49 A/G, promoter —318 C/T) in all 174 subjects (54 male subjects and 120 female subjects) in the asthmatic and control groups.

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Discussion

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: DiscussionIn this study, the CTLA-4 promoter ( — 318 C/T) polymorphism was found to be associated with asthma severity, but not with asthma, atopy, or bronchial hyperresponsiveness. The CTLA-4 exon 1 (+ 49 A/G) polymorphism was shown to be associated with bronchial hyperresponsiveness, but not with asthma, atopy, or asthma severity. From these results, it appears that the CTLA-4 gene may not be a susceptibility gene, but rather a disease-modifying gene that can modify the asthma phenotype.

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Polymorphism

The distributions of genotypic frequencies were significantly different for the mild-to-moderate group and the severe group. In particular, the frequency of the T allele was 7.4% in the mild-to-moderate group and 20.4% in the severe group, and the association between severe asthma and the T allele was significant (p = 0.037; Table 3). The positive predictive value of a positive T allele for severe asthma was 55.0% and the negative predictive value was 72.4%. The relationship between bronchial hyperresponsiveness (PC20) and the CTLA-4 promoter (—318 C/T) polymorphism was also studied. PC20 was measured in 45 of the 88 asthma patients, divided into a CC genotype (wild type) group and a CT genotype +TT genotype (mutant-type) group. However, PC20 did not differ between the two groups (p = 0.758; Table 4).

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Statistical Analysis

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Statistical AnalysisSamples were denatured by 30 cycles of 30 s at 94°C, annealed for 30 s at 58°C, and extended for 30 s at 72°C, using the thermal cycler. A 152-bp fragment containing the +49 A/G polymorphism in exon 1 of CTLA-4 was amplified. The forward primer was designed with a single-base mismatch for the last nucleotide, which corresponded to the + 47 position, to introduce a base change in the sequence of the PCR product. This substitution created a BstEII restriction site in the A allele. Amplified products were incubated at 60°C for 2 h using 5 U BstEII per reaction. Digested products underwent electrophoresis on a 3.5% agarose gel. Buy allegra online so The digested A allele gave a fragment of 130 bp, and the G allele gave an intact 152-bp fragment (Fig 1).
Statistical analysis was performed using statistical software (SPSS, version 8.0; SPSS; Chicago, IL). The x2 test and t test were used when appropriate.

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Genotyping of CTLA-4 Gene

Classification of asthma severity was based on history, symptoms, clinical features, medication need, FEV1, and PEF according to the 1997 Expert Panel Report 2. Asthma severity was classified into mild intermittent, mild persistent, moderate persistent, and severe persistent. The investigator who assessed the severity of asthma was blinded to the genotyping of the CTLA-4 gene.
DNA was extracted from peripheral blood leukocytes following standard protocols and column purified (DNA midi kit; Qiagen; Hilden, Germany). The CTLA-4 promoter polymorphism at position —318 was defined using polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) with Tru9 I restriction enzymes (Bioneer; Seoul, Korea).

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Clinical Assessment

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Clinical AssessmentAll control subjects were nonsmokers and had normal findings on chest radiographs, normal airway reactivity, and normal pulmonary function test results. Moreover, they had experienced no current respiratory symptoms, were nonatopic, and had experienced no respiratory infections within the previous month. None were receiving any medications. The study protocol was approved by the ethics committee of the Korea University College of Medicine and written informed consent was obtained from all subjects. The methacholine challenge was performed using the following method. Acetyl methacholine chloride (Sigma; St. Louis, MO) was diluted with normal saline solution and divided into nine solutions ranging from 0.075 to 25 mg/mL. Each solution was inhaled five times through a nebulizer (DeVilbiss Pulmoaide Compressor/Nebulizer; SM Instruments; Doylestown, PA) and a dosimeter (Micro-Dosimeter; Sunrise Medical; Carlsbad, CA).

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism: Materials and Methods

Polymorphisms of the CTLA-4 gene, located on chromosome 2q33, could thus have effects on immune response. The following three CTLA-4 gene polymorphisms are known: a microsatellite (AT)n marker at position 642 of the 3′-untranslated region of exon 4; a single-nucleotide polymorphism in exon 1 (adenine or guanine at position +49); and another single-nucleotide polymorphism in the promoter region (cytosine or thymine at position —318). The A/G dimorphism at exon 1 position +49 results in an amino acid exchange (threonine to alanine) in the leader sequence.
To evaluate the possible role of CTLA-4 polymorphisms in bronchial asthma, we investigated the association between two polymorphisms (exon 1 +49 A/G, promoter —318 C/T) and atopy, asthma severity, and bronchial hyperresponsiveness, in bronchial asthma patients and a healthy control group.

Association of Asthma Severity and Bronchial Hyperresponsiveness With a Polymorphism

Association of Asthma Severity and Bronchial Hyperresponsiveness With a PolymorphismBronchial asthma is characterized by the infiltration of inflammatory cells into the airway submucosa. While the precise mechanisms by which inflammatory cells are recruited into the lungs are not fully understood, increasingly available evidence suggests that the activation of antigen-specific CD4+ T cells of the type 2 T-helper (Th2) subset in the lungs, which results in interleukin (IL)-5 secretion plays a major role in asthmatic airway inflam-mation comments canadianneighborpharmacy.com. CD4+ T-cell activation leading to cytokine production and effector function requires two signals from the antigen-presenting cell (APC). The first signal is triggered by the interaction between antigen-specific T-cell receptor and peptide-major histocompatibility complex II complexes on APCs.

Children With Asthma: Session 3

Children With Asthma: Session 3I. Review of asthma status and understanding of asthma
a. Discuss progress and problems
b. Play “Asthma Jeopardy” to review and reinforce the mastery of basic asthma facts by the parent(s) and child
II. Review progress in eliminating the child’s exposure to tobacco smoke
a. If participants were not at previous sessions, explain what cotinine is and what it means
b. Show “Secondhand Smoke Revised” video, and discuss the ideas with the family
c. Review the cotinine test results collected before the last session, and provide a copy of the result to parents to take home
d. Explain the relationship between the last cotinine results and the 4-day ETS exposure prior to the test, and compare it to previous cotinine results and exposures
e. Complete a new 4-day ETS exposure recall

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