Increased level of MSU crystal-bound protein apolipoprotein A-I in acute gouty arthritis.

BACKGROUND: Gout is a common form of inflammatory arthritis that is triggered by the crystallization of monosodium urate (MSU). We investigated the potential proteins that relate to the pathogenesis or the spontaneous resolution of acute gouty arthritis. METHOD: We screened for differentially expressed proteins in the plasma of patients with acute gouty arthritis using two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) identification. We confirmed these findings in a population study of 209 subjects, and further determined the protein profile of the synovial fluid (SF) from 24 gouty patients during acute attack by liquid chromatography coupled with tandem MS (LC/MS/MS). RESULTS: The highly expressed apolipoprotein A-I (apoA-I) was identified in the plasma of acute gouty patients compared with healthy controls. Moreover, we detected high levels of SF apoA-I in 83.3% of acute gouty patients during attack. From the population study, apoA-I was increasingly associated with normouricaemia, hyperuricaemia, and acute gouty arthritis (ptrend < 0.001), and plasma uric acid (UA) and apoA-I were positively correlated (p = 0.0156). We used a human liver cell model and found that UA enhanced the hepatic apoA-I mRNA expression level (ptrend < 0.01) and apoA-I secretion level (ptrend = 0.002) in a dose-dependent manner. An elevated MSU concentration caused the endogenous apoA-I to deplete gradually. CONCLUSIONS: Based on the role of apoA-I in anti-inflammation, our observational data in acute gout support the hypothesis that apoA-I expression can be induced under the condition of a high concentration of UA and its elevated level may be implicated in the spontaneous resolution of acute gouty arthritis.

Psoriasis as initiator or amplifier of the systemic inflammatory march: impact on development of severe vascular events and implications for treatment strategy.

BACKGROUND: Psoriasis is a systemic disease associated with metabolic disorders and vascular complications. Both psoriasis and metabolic disorders are associated with systemic inflammation. We hypothesized that the sequence of events between the onset of psoriasis and metabolic disorder may affect the risk for subsequent development of vascular complications. METHODS: Nested case-control study was performed using the Taiwan National Health Insurance database. Accordingly, a total of 8180 psoriatic patients and 163,600 controls were included. Psoriasis was considered as the initiator of inflammatory march if metabolic disorder, including hypertension, diabetes mellitus and dyslipidemia, developed after onset of psoriasis. In patients with pre-existing metabolic disorder, psoriasis was considered as the amplifier of inflammatory march. RESULTS: In patients whose psoriasis served as the disease initiator, a lower risk for developing vascular disease (HR = 1.49; 95% CI = 1.11-2.00 and HR = 1.64; 95% CI = 1.31-2.05 for cerebrovascular and cardiovascular events, respectively) was found compared with patients whose psoriasis served as the disease amplifier (HR = 2.26; 95% CI = 1.72-2.97 and HR = 2.78; 95% CI = 2.26-3.42 for cerebrovascular and cardiovascular events, respectively) after adjusting for age and gender. In terms of treatment implications, methotrexate was associated with reduced risk for developing cerebrovascular event (HR = 0.22; 95% CI = 0.05-0.88) only in patients with psoriasis serving as the disease amplifier. CONCLUSIONS: Our results suggested that two scenarios of systemic inflammatory marches are present among psoriatic patients with metabolic disorder and judicious use of methotrexate may reduce the risk of cerebrovascular event, especially when psoriasis served as the disease amplifier of the systemic inflammatory march.

Mechanistic correlations between two itch biomarkers, cytokine interleukin-31 and neuropeptide ß-endorphin, via STAT3/calcium axis in atopic dermatitis.

BACKGROUND: Itch is the cardinal symptom of atopic dermatitis (AD). ß-Endorphin, a neuropeptide, is increased in both AD skin and sera. Interleukin (IL)-31, an itch-relevant cytokine, activates IL-31 receptors in keratinocytes. However, how IL-31 and ß-endorphin interact in AD skin remains elusive. OBJECTIVES: To investigate the mechanistic interaction of IL-31 and ß-endorphin in AD. METHODS: This was a prospective cross-sectional study. We recruited adult patients with AD and controls according to Hanifin's AD criteria. Serum levels of IL-31 and ß-endorphin were measured by enzyme-linked immunosorbent assay. Expressions of IL-31 receptor A (IL-31RA) and ß-endorphin in the skin were assessed by immunohistochemistry. Their expression in the skin and blood was compared and correlated in patients with AD and in controls. We also treated primary keratinocytes with IL-31 and measured calcium influx, ß-endorphin production and signalling pathways to define their mechanistic interactions. RESULTS: ß-Endorphin was increased in the supernatant from IL-31-treated keratinocytes. IL-31 receptor activation resulted in calcium influx and STAT3 activation; pretreatment with STAT3 inhibitor stopped the increase of ß-endorphin. Notably, either replacement of extracellular calcium or treatment with 2-aminoethoxydiphenyl borate, an inhibitor for the store-operated channel, blocked STAT3 activation. We found higher levels of blood ß-endorphin and IL-31, which were significantly correlated, in patients with AD. Moreover, IL-31RA and ß-endorphin were increased and colocalized both in AD human skin and TPA-painted mouse skin. CONCLUSIONS: IL-31 receptor activation in keratinocytes induces calcium influx and STAT3-dependent production of ß-endorphin. These results might contribute to an understanding of the regulatory mechanisms underlying peripheral itch.

Signalling pathway of isophorone diisocyanate-responsive interleukin-8 in airway smooth muscle cells.

This study is the first to analyse the soluble factors secreted by the bronchial epithelium after exposure to isophorone diisocyanate (IPDI) that are responsible for increasing migration and proliferation of primary normal human bronchial smooth muscle cells (BSMCs). We treated immortalised, nontumorigenic human bronchial epithelial cells (cell line BEAS-2B) and primary normal human bronchial epithelial cells (HBEC) with IPDI, and then collected the conditioned culture media (IPDI-BEAS-2B-CM and IPDI-HBEC-CM, respectively), which was added to BSMCs. Exposure of BEAS-2B cells and HBECs to IPDI increased interleukin (IL)-8 production. Culture of BSMCs with IPDI-BEAS-2B-CM and IPDI-HBEC-CM increased BSMC proliferation and migration, which are major features in asthma-related airway remodelling. Induction of BSMC proliferation and migration by IPDI-BEAS-2B-CM and IPDI-HBEC-CM was associated with increased focal adhesion kinase (FAK), Src, extracellular signal-regulated kinase (ERK)1/2 and AKT activation. Blocking FAK with a specific inhibitor significantly decreased BSMC migration and proliferation by inhibiting ERK1/2 activation. FAK and ERK1/2 inhibitor also decreased IPDI-BEAS-2B-CM-, IPDI-HBEC-CM- and recombinant human IL-8-mediated BSMC proliferation and migration, whereas blocking Rnd3 using small interfering RNA failed to affect BSMC proliferation, suggesting that Rnd3 was only involved in the regulation of BSMC migration. Our study suggests that inhibition of IL-8 or IL-8-mediated FAK/ERK/Rnd3 signalling is an attractive therapeutic target for IPDI-mediated asthma.

Role of gender disparity of circulating high-sensitivity C-reactive protein concentrations and obesity on asthma in Taiwan.

BACKGROUND: Several studies have suggested that the association between obesity and asthma may be stronger in females than in males, but the reason is still unclear. OBJECTIVE: The aim of this study was to investigate whether differences in high-sensitivity C-reactive protein (hs-CRP) levels explain why obesity is associated with asthma in females but not in males. METHODS: This study prospectively enrolled 754 subjects ≥ 18 years old from hospital-based asthma patients and population-based controls. We measured adiposity factors [body mass index (BMI), waist circumference and waist-hip ratio], hs-CRP and total IgE levels. RESULTS: After adjusting for potential confounding factors, we found a significant association between BMI and asthma in females with a significant interaction of gender and BMI on asthma (χ(2) =10.2, P=0.004). If hs-CRP was added to the logistic model, the interaction was attenuated but still significant (χ(2) =7.02, P=0.03). After adjusting for BMI, we did not find that circulating hs-CRP concentrations were significantly associated with asthma in males and females. CONCLUSION: We found that BMI was associated with asthma in females, but our results do not support the suggestion that hs-CRP levels contribute significantly to the link between obesity and asthma with respect to gender disparity.

The polymorphisms of C-reactive protein gene modify the association between central obesity and lung function in taiwan asthmatics.

High-sensitivity C-reactive protein (hs-CRP) concentrations and obesity are proposed to have a significant relationship with impairment of lung function, but little has been reported to date on the association between CRP gene and lung function. We studied the association of three tagSNPs (tag single nucleotide polymorphisms) of CRP gene and their interactions with central obesity on lung function. A total of 384 asthmatic adults and 384 controls who were 1:1 matched by sex and age were recruited for this study. Three tagSNPs polymorphisms for CRP rs1417938, rs1800947 and rs1205 were selected from HapMap data and genotyping by using TaqMan allelic discrimination assay. A questionnaire interview, body composition and pulmonary function tests were performed. CRP single nucleotide polymorphisms (SNPs) did not increase the risk of asthma, but CRP rs1205 CC genotype significantly decreased the predictive value of forced vital capacity (FVC) in the asthma group (adjusted mean change = -7.54%, 95% CI = -13.82 to -1.25%). Waist-to-hip ratio, not body mass index, also decreased the predictive value of FVC in asthmatics. The subjects with central obesity who carried CRP SNPs have a significant reduction effect in lung function. The current results suggest that central obesity may play a major role in lung function, and these effects were modified significantly by the polymorphisms for CRP gene.

Lifetime exposure to cigarette smoking and the development of adult-onset atopic dermatitis.

BACKGROUND: Adult-onset atopic dermatitis (AD) has recently been recognized as a distinct disease entity, but its risk factors have not yet been clearly defined. Although gestational and perinatal exposure to tobacco smoking may be associated with the development of classic AD, the association between active/passive smoking and adult-onset AD remains controversial. OBJECTIVES: To determine if exposure to smoking, including environmental tobacco smoke (ETS), is associated with the risk of adult-onset AD. METHODS: Tobacco smoking and exposure to ETS were measured in a case-control association analysis in 83 patients with physician-diagnosed adult-onset AD and 142 age- and sex-matched controls. RESULTS: Multiple logistic regression analyses showed that, among the potential environmental risk factors, both current and ever smoking were significant risk factors for adult-onset AD [odds ratio (OR) 4·994 and 3·619, respectively], compared with never smoking. Also, packs per year was significantly associated with adult-onset AD (OR 1·058, 95% confidence interval 1·028-1·089), suggesting a lifelong cumulative risk in current smokers. Moreover, nonsmokers with adult-onset AD reported significantly more exposure to ETS. CONCLUSIONS: Early and/or current exposure to cigarette smoking may contribute cumulatively to the development of adult-onset AD. Exposure to ETS in childhood is associated with the development of adult-onset AD. Adults should be discouraged from smoking to prevent adult-onset AD in themselves and their family members.

The cyclic GMP-dependent protein kinase II gene associates with gout disease: identified by genome-wide analysis and case-control study.

OBJECTIVE: To identify the position of a gout susceptibility gene. METHODS: A genome-wide scan was performed using 382 random polymorphic microsatellite markers spread across 22 autosomes in a Taiwanese family with gout to screen for the gout susceptibility genetic marker. Its association with gout by 33 single nucleotide polymorphisms (SNP) in 148 matched case-control subjects was confirmed. The family with gout comprised eight patients with gout and 10 gout-free subjects; case-control subjects were 74 male patients with gout and 74 healthy controls matched by age. RESULTS: Analysis of the genome-wide scan results by a non-parametric linkage method found that chromosome 4q21 contains a locus significantly linked with gout (D4S3243 at 81 289 553 bp; p = 0.004; LOD score = 5.13). In SNP genotyping analysis at the neighbourhood regions of marker D4S3243 for the case-control subjects, the polymorphisms rs7688672 and rs6837293, located on the cGMP-dependent protein kinase II (cGK II) gene, were found to relate significantly to gout disease in a recessive model after adjustment of hyperuricaemia (OR = 2.89, 95% CI 1.19 to 7.02 and OR = 2.72, 95% CI 1.13 to 6.54, respectively). CONCLUSIONS: This study suggests that the cGK II gene on chromosome 4q21 is most likely to harbour gout disease independently of hyperuricaemia and is inherited recessively.

Association study between keratinocyte-derived growth factor gene polymorphisms and susceptibility to vitiligo vulgaris in a Taiwanese population: potential involvement of stem cell factor.

BACKGROUND: Vitiligo vulgaris is a depigmentary disorder resulting from the disappearance of functional melanocytes. Currently, the pathogenesis of this disorder remains obscure. OBJECTIVES: Genetic analysis of patients with vitilgo may provide important clues for elucidating the complex pathomechanisms involved in the disease process. Because dysfunctional keratinocytes have recently been implicated in the pathogenesis of vitiligo vulgaris, we conducted a case-control association study to investigate this phenomenon. PATIENTS AND METHODS: Fifty-one patients with vitiligo vulgaris and 118 healthy controls from Taiwan were recruited to investigate the association between relevant keratinocyte-related genes and the occurrence of vitiligo vulgaris. This study genotyped 11 single-nucleotide polymorphisms (SNPs) in five genes including stem cell factor (SCF, also known as KITLG), basic fibroblast growth factor (bFGF, also known as NuDT6), endothelin-1 (EDN1), hepatocyte growth factor (HGF) and stem cell growth factor (SCGF, also known as CLEC11A). RESULTS: Our results revealed that the A allele for SNP rs11104947 in the SCF gene and the T allele for SNP rs13866 in the SCGF gene were, respectively, associated with a 1.95- and a 2.14-fold risk of developing vitiligo vulgaris. A higher risk was also detected among subjects who carried the SCF rs995029/rs11104947 C/A haplotype (odds ratio = 2.45). Furthermore, the at-risk alleles for SCF rs11104947 (A allele) and for SCGF SNP rs13866 (T allele) were found to display a 7.92-fold increased gene-gene combined risk. No significant relationship between polymorphic frequency for genes bFGF, EDN1 as well as HGF and occurrence of vitiligo vulgaris was observed. CONCLUSIONS: These novel genetic findings provide new insights in relation to the mechanisms that might be involved in the development of vitiligo vulgaris.

Peri-ictal normalization of visual cortex excitability in migraine: an MEG study.

To delineate if the change in cortical excitability persists across migraine attacks, visual evoked magnetic fields (VEF) were measured in patients with migraine without aura during the interictal (n = 26) or peri-ictal (n = 21) periods, and were compared with 30 healthy controls. The visual stimuli were checkerboard reversals with four different check sizes (15', 30', 60' and 120'). For each check size, five sequential blocks of 50 VEF responses were recorded to calculate the percentage change of the P100m amplitude in the second to the fifth blocks in comparison with the first block. At check size 120', interictal patients showed a larger amplitude increment than controls [28.1 +/- 38.3% (s.d.) vs. 8.7 +/- 21.3%] in the second block and a larger increment than peri-ictal patients in the second (28.1 +/- 38.3% vs. -3.2 +/- 19.2%), fourth (22.7 +/- 31.2% vs. -5.7 +/- 22.3%) and fifth (20.5 +/- 30.4% vs. -10.8 +/- 30.1%) blocks (P < 0.05). There was no significant difference at other check sizes or between peri-ictal patients and controls. In conclusion, there may be peri-ictal normalization of visual cortical excitability changes in migraine that is dependent on the spatial frequency of the stimuli and reflects a dynamic modulation of cortical activities.

Associations between gout tophus and polymorphisms 869T/C and -509C/T in transforming growth factor beta1 gene.

OBJECTIVES: To investigate the associations between gout tophus and polymorphisms 869T/C and -509C/T in TGF-beta1 gene. METHODS: The polymorphisms 869T/C and -509C/T were determined in 73 gout patients and 114 healthy controls among male Taiwanese using the PCR-restriction fragment length polymorphism method. Each patient was matched with 1-2 controls by age within 1-2 yrs. The tophus number was measured from all the patients' arms and legs. RESULTS: Neither 869T/C nor -509C/T showed a significant association between patients and controls in the proportions of genotypes, allele frequency or dominant and recessive models. The mean number of tophi for all patients was 1.53 +/- 3.44, showing a significant difference in distribution among the genotypes at polymorphism 869T/C (P = 0.006), but not those in polymorphism -509C/T (P > 0.05). Those carrying genotype CC at polymorphism 869T/C have a mean number of tophi 0.35 (+/- 1.11), which is significantly lower than those carrying genotype TT (3.73 +/- 4.67; P < 0.05). Those with genotype TT at polymorphism 869T/C also had 11.06 times the likelihood of having at least one tophus compared with the genotype CC after adjustment of hyperuricaemia (95% CI = 1.84, 66.36; P = 0.009). However, except for the tophus number, these two polymorphisms did not show any significant association with the clinical characteristics or biochemical markers. CONCLUSIONS: The polymorphism 869T/C in TGF-beta1 gene has a significant association with the occurrence of tophus in gout patients.

Anterior spinal artery as a collateral channel in cases of bilateral vertebral arterial steno-occlusive diseases.

BACKGROUND AND PURPOSE: We report 6 cases of retrograde flow through the anterior spinal artery (ASA) from cervical vertebral artery (VA) to intracranial distal VA because the perfusion from bilateral vertebral arteries was tenuous. Its hemodynamic and clinical implications are discussed. METHODS: In association with bilateral steno-occlusive disease of vertebral arteries, 6 cases of retrograde flow through ASA were reviewed in terms of clinical and angiographic characteristics. All 6 patients presented with stroke in the posterior fossa and underwent conventional angiography as part of diagnostic evaluation and/or therapeutic intervention. RESULTS: On the angiography, 2 patients showed bilateral VA occlusion, and the other 4 patients showed VA occlusion on 1 side and severe stenosis in the other VA. Distal perfusion by ASA was prominent in 2, and not prominent in 4. Reversal or disappearance of the retrograde flow through ASA was observed after successful recanalization of the occluded VA in 4 patients. In 1 patient, increased perfusion through ASA was observed because the stenosed VA was completely occluded. CONCLUSION: When the vertebral arteries were occluded bilaterally or when a single VA was occluded and the other carried a severe stenosis and, as a result, the basilar arterial blood supply was tenuous, retrograde flow through ASA could be observed. This is a potentially important source of collateral supply to the posterior fossa neural contents. The degree and extent of perfusion via this collateral channel varied depending on presence of other collateral routes and patency of the vertebrobasilar junction.

Impact of socioeconomic status on vision-related quality of life in primary open-angle glaucoma.

PurposeTo investigate the impact of socioeconomic status (SES) on vision-related quality of life (VRQOL) in patients with primary open-angle glaucoma (POAG).Patients and methodsThis prospective cross-sectional study included consecutive patients with POAG at a tertiary hospital between March 2012 and January 2013. All patients had visual acuity no worse than 20/60 in the better eye and reliable visual field tests. VRQOL was assessed by the validated Taiwan version 25-item National Eye Institute Visual Functioning Questionnaire (NEI VFQ-25). Sociodemographic characteristics, medical history, and ocular parameters were recorded. SES was evaluated based on educational attainment and monthly income, both stratified into three levels. Analysis of variance and linear regression analysis were used to evaluate the relationship between SES, VRQOL, and clinical parameters.ResultsAmong the 186 patients recruited, intergroup differences were not observed among educational or monthly income levels for binocular vision or integrated visual field defects. Patients of lower educational and monthly income levels had lower self-reported general health ratings. After adjustment for visual function, treatment complexity, and general health in the multiple linear regression model, patients with a college degree or higher reported better NEI VFQ-25 scores for the composite score (P=0.041), mental health (P=0.035), and peripheral vision (P=0.05) than did those with education below junior high school. Monthly income levels did not affect the NEI VFQ-25 scores.ConclusionEducational attainment significantly affects VRQOL in patients with POAG. Additional counseling may be provided to patients with lower educational background to help them cope with the disease.

Seven-year incidence of uncorrected refractive error among an elderly Chinese population in Shihpai, Taiwan: The Shihpai Eye Study.

PURPOSE: To report the 7-year incidence of uncorrected refractive error in a metropolitan Chinese elderly population. METHODS: The Shihpai Eye Study 2006 included 460/824 (55.8%) subjects (age range 72-94 years old) of 1361 participants in the 1999 baseline survey for a follow-up eye examination. Visual acuity was assessed using a Snellen chart, uncorrected refractive error was defined as presenting visual acuity (naked eye if without spectacles and with distance spectacles if worn) in the better eye of <6/12 that improved to no impairment (≥6/12) after refractive correction. RESULTS: The 7-year incidence of uncorrected refractive error was 10.5% (95% confidence interval (CI): 7.6-13.4%). 92.7% of participants with uncorrection and 77.8% with undercorrection were able to improve at least two lines of visual acuity by refractive correction. In multivariate analysis controlling for covariates, uncorrected refractive error was significantly related to myopia (relative risk (RR): 3.15; 95% CI: 1.31-7.58) and living alone (RR: 2.94; 95% CI 1.14-7.53), whereas distance spectacles worn during examination was protective (RR: 0.35; 95% CI: 0.14-0.88). CONCLUSION: Our study indicated that the incidence of uncorrected refractive error was high (10.5%) in this elderly Chinese population. Living alone and myopia are predisposing factors, whereas wearing distance spectacles at examination is protective.

Survival and distribution pattern of childhood liver cancer in Taiwan.

Studies of survival and distribution of liver cancer in children are scarce. In this study, using data from the cancer registry of Taiwan, from 1979 to 1992, we identified 377 young patients (0-15 years of age) suffering from liver cancer, coded 155 according to the International Classification of Diseases. Among these patients, 122 were histopathologically proven hepatocellular carcinoma (HCC) and 43 hepatoblastoma (HB). For survival analysis, we also searched for cases of liver cancer in 0-16 year old children in the Taiwan cancer registry for the period between 1988 and 1992. We found 109 cases with identification numbers and birth dates which allowed our cases to be linked with the death registry of the National Health Department of Taiwan enabling the calculation of 5-year survival rates using actuarial life tables. Between 1979 and 1992, for 122 HCC cases, there was a peak incidence at the age of 1 year, then a decline to a trough at the age of 4 years, after which the number of cases increased to the age of 15 years. After the age of 4 years boys outnumbered the girls by 2:1. 36 (84%) of 43 HB cases were under the age of 5 years and boys tended to outnumber girls by 2.9:1. Between 1988 and 1992, of the 109 patients, 49 were diagnosed histopathologically and 60 patients clinically. Their overall 5-year survival rate was 19%. The 5-year survival rate of the 28 HCC patients was 17%, whereas that of the 17 HB patients was 47%. In conclusion, our epidemiological findings indicate that the HCC distribution among children is different according to age and to some extent sex. The overall 5-year survival rate of children suffering from liver cancer was still unfavourable.

Cancer aggregation and complex segregation analysis of families with female non-smoking lung cancer probands in Taiwan.

Previous studies have found that having a first-degree blood relative with lung cancer was a possible predictor of lung cancer risk, but some studies have indicated that the association is non-significant or only significant for a subset of the studied population. To determine the familial aggregation and whether there is any evidence for a gene controlling the susceptibility to developing lung cancer in female non-smokers, multiple logistic regression methods for estimating covariate effects and maximum likelihood segregation analyses were performed using data from 216 female non-smoking lung cancer probands (2328 individuals) in a population-based case-control study. Having a family history of lung cancer was found to be a significant predictor of lung cancer for non-smoking females (Adjusted Odds Ratio (OR)=5.7, 95% Confidence Interval (CI)=1.9-16.9). Having a female relative with lung cancer (adjusted OR=14.4, 95% CI=2.7-75.5) was more strongly associated with the lung cancer risk than was having a male relative with lung cancer. This association was stronger for probands aged less than 60 years at onset (adjusted OR=11.2, 95% CI=2.2-56.9). All of the Mendelian models fitted the data significantly better than the sporadic (no major type) model or the environmental model (P<0.00l). The Mendelian codominant models provided the best fit of the data for the early onset probands and showed a stronger effect for a major susceptibility locus for non-smoking lung cancer probands. The results of this study provide evidence that a rare autosomal codominant gene may influence the risk lung cancer in non-smoker and is responsible for the familial aggregation observed in non-smoking lung cancer patients.

Isotypic and allotypic analysis with monoclonal antibodies and jacalin of 309 serum monoclonal IgA from French and Japanese myeloma patients.

The subclass and allotype distribution of serum monoclonal IgA from myeloma patients was determined by ELISA with monoclonal antibodies in two French and one Japanese laboratory. In addition, the French sera were tested for their reactivity with the lectin jacalin. No significant difference in the isotypic distribution between French and Japanese series could be demonstrated: kappa/lambda ratios were 0.99 and 1.17, and the IgA1 subclass accounted for 93.9% and 91% of cases in the French and Japanese studies, respectively. Five out of 7 myeloma IgA2 from Japan and only one of the 12 IgA2 from France belonged to the A2m(2) allotype (P less than 0.01). All 219 IgA1 tested reacted with jacalin by immunoelectrophoresis (IEP), although with variable intensities. Among IgA2 proteins, only one (of the A2m(1) allotype) yielded a precipitating line with jacalin by IEP. Molecular analysis demonstrated that this protein was an IgA1-IgA2 hybrid bearing most of the A2m(1) epitopes.

Climate, traffic-related air pollutants, and asthma prevalence in middle-school children in taiwan.

This study compared the prevalence of asthma with climate and air pollutant data to determine the relationship between asthma prevalence and these factors. We conducted a nationwide survey of respiratory illness and symptoms in middle-school students in Taiwan. Lifetime prevalences of physician-diagnosed asthma and of typical symptoms of asthma were compared to air monitoring station data for temperature, relative humidity, sulfur dioxide, nitrogen oxides, ozone, carbon monoxide, and particulate matter with aerodynamic diameter [less than/equal to] 10 microm (PM(10)). A total of 331,686 nonsmoking children attended schools located within 2 km of 55 stations. Asthma prevalence rates adjusted for age, history of atopic eczema, and parental education were associated with nonsummer (June-August) temperature, winter (January-March) humidity, and traffic-related air pollution, especially carbon monoxide and nitrogen oxides, for both girls and boys. Nonsummer temperature, winter humidity, and traffic-related air pollution, especially carbon monoxide and nitrogen oxides, were positively associated with the prevalence of asthma in middle-school students in Taiwan.

Segregation analysis of asthma: recessive major gene component for asthma in relation to history of atopic diseases.

Although asthma has a significant heritable component, the mode of inheritance remains controversial because of the complexity of the disease and the influence of environmental factors. Segregation analysis for asthma are performed with and without a history of atopic diseases (dermatitis and rhinitis) after adjusting for environmental factors. To investigate whether asthma may be inherited through a major gene with two alleles, the REGD program of the Statistical Analysis for Genetic Epidemiology (SAGE) package was conducted in 1,990 individuals from 227 families with at least one asthmatic child in a cross-sectional study of respiratory diseases in Southern Taiwan. Other covariates adjusted for included age, sex, current smoking, and environmental tobacco smoking. The hypothesis of Mendelian model and no parent-offspring transmission was rejected. However, when the variables of atopic disease and environmental factors were included in the model as covariates, the models for a two-allele gene with a recessive or codominant inheritance could not be rejected, and Akaike's Information Criterion was smaller (1,377. 13) for the recessive model than all of the other models tested, assuming a major gene with a population frequency of 0.56 +/- 0.04. However, Mendelian model without family effect was rejected. In conclusion, a history of asthma in parents is a strong risk factor for asthma in offspring. Under the assumptions of the applied segregation, at least one major gene exists that could be a gene involved also in allergy. However, the data suggest that a single locus gene explains a portion of asthma that is related to the history of atopic diseases. In addition, a polygenic/multifactorial (genetic and environmental factors) influence with a recessive component inheritance may be involved in the pathogenesis of asthma.

Risk factors for primary lung cancer among non-smoking women in Taiwan.

BACKGROUND: Although cigarette smoking is considered to be the most important cause of lung cancer, smoking behaviour cannot fully explain the epidemiological characteristics of lung cancer in Taiwanese women, who rarely smoke but contract lung cancer relatively often. There are other causes of lung cancer that have produced variability in lung cancer incidence. METHODS: A case-control study involving interviews with 117 female patients (including 106 non-smoking) suffering from lung cancer and the same number of individually matched hospital controls was conducted in Kaohsiung, Taiwan between 1992 and 1993. The questionnaire administered to cases and controls collected information on cigarette smoking and suspected risk factors for lung cancer. Multivariate logistic regression analysis was applied to assess smoking for all women and suspected risk factors for non-smoking women. RESULTS: The relationship between cigarette smoking and lung cancer was statistically significant although only a small proportion (9.4%) of female patients had smoked. However, the risk of contracting cancer for non-smoking women appears to be associated with certain cooking practices, especially preparing meals in kitchens not equipped with a fume extractor at cooking age of 20-40 years (odds ratio [OR] = 8.3; 95% confidence interval [CI]: 3.1-22.7. These factors and a history of pulmonary tuberculosis plus low consumption of fresh vegetables explained 78% of the summary attributable risks for non-smoking women in a multivariate logistic regression model. CONCLUSIONS: Exposure to fumes from cooking oils, when not reduced by an extractor, may be an important factor in causing lung cancer in non-smoking Taiwanese women.