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Background & objectives: Interleukin 4 (IL4) and IL13 genes are believed to be responsible for inflammation of the airways in asthmatics. These share a common receptor component called IL4Rα which is another potentially important candidate gene linked to asthma phenotypes. Another gene Toll-like receptor 4 (TLR4) might affect the incidence or progression of asthma through the expression of proinflammatory genes. Several single nucleotide polymorphisms (SNPs) in IL4, IL13, IL4Rα and TLR4 have been reported to be linked to asthma or related phenotypes in several ethnic populations using linkage studies and association studies. However, the results have not been consistent. We investigated five SNPs (C-589T and C-33T of IL4, G+2044A of IL13, A+1902G of IL4Rα, and A+896G of TLR4) in patients with adult onset asthma to evaluate their role in manifestation and severity of asthma. Methods: Adult (>18 yr of age) patients with asthma (n=100) and healthy controls (n=50) were included in the study. Genotyping was performed using sequenom MassARRAY technology. Results: The mutant alleles of the C-589T and C-33T SNPs in the promoter region of IL4 were present in 4 per cent patients with asthma but absent from the control group suggesting that the variations in IL4 may contribute to asthma occurrence. The SNPs of other genes were seen in both controls and patients. Interpretation & conclusions: The results suggest the possible association between the genetic distribution of C-589T and C-33T SNPs of IL4 with asthma in Indian adults.

Three Neogobius species are common in the southern Caspian Sea. Identification of these species, especially from remains, is not fully understood. The present study compares the morphological characteristics of sagittal otoliths of N. caspius, N. pallasi and N. melanostomus. Furthermore, it also provides a dichotomous identification key based on otoliths morphology.

Serum protein analysis for noninvasive quantification of airway inflammation in asthma is a promising research tool in the field of lung diseases. Cytokines are believed to have major role in inflammatory process of the airways of the lung. There is an imbalance between T-helper (Th)-2 cells, which secrete interleukin (IL)-4 and interleukin (IL)-13, and Th1 cells, which secrete interferon (IFN)-gamma in asthma. To test the hypothesis that serum IL-13 and IL-4 levels may be elevated whereas IFN-gamma would be decreased in this cohort of patients, a property that could make them possible candidate biomarkers in determining asthma occurrence and severity, we measured concentrations of IL-4, IL-13 and IFN-gamma in serum samples of 88 subjects (44 normal, 12 with mild asthma, 16 with moderate asthma, and 16 with severe asthma). Serum Levels of IL-4, IL-13, and IFN-gamma were determined by an enzyme-linked immune-sorbent assay (ELISA). Median serum level of IFN-gamma in asthmatic patients was 8.0 pg/ml, while it was 11.4 pg/ml in healthy controls. However, the difference was not significant. Among the different age groups in whom IFN-gamma was assessed, the highest median value in both cases and controls was observed in the age group of 31-40 years. The median serum level of IL-13 was 40.0 pg/ml in asthmatic patients and 58.25 pg/ml in healthy controls. The difference was not significant. On subgroup analysis, no significant difference of IFN-gamma and IL-13 between asthma of different severities was observed. The study also revealed nonsignificant difference of serum cytokines with the duration of asthma, number of allergens, and severity of sensitization. Normal serum levels of IFN-gamma and IL-13 in asthmatic patients suggest their neutral role in the inflammatory process; however, more studies are required to establish the effect of these cytokines in adulthood asthma in different ethnic populations.

To study the pure catalytic activity of metallic nanoparticles, the formation of methane on gasborne Ni nanoparticles, so called aerosol catalysis experiments, were performed. Beside effects typical for the methanation such as poisoning of the particle surface at temperatures above 385°C, the maximum of the catalytic activity was observed for Ni particles of about 14 nm, i.e. in a size range, which is quite uncommon for typical nanoeffects of metallic particles. To clarify, which catalytic phenomena are related to the aerosol state, the same reaction was performed on supported Ni nanoparticles, which were also generated and conditioned in the gas phase and deposited on a SiO2 surface by thermophoresis. For these supported particles, the same reaction conditions were established as before for the gasborne Ni nanoparticles. However, differences in the mass transport characteristics of educt and product molecules to the particles were encountered and led to lower overall reaction rates. While qualitatively poisoning kinetics and activation energies agreed for both cases, significant differences were observed for the size dependence of the catalytic activity and for the sintering kinetics. The observed shift of the optimum size for the methanation from 14 nm (aerosol) to 25 nm (on support) can be explained by different adsorption enthalpies of the educt gases on aerosol and supported Ni nanoparticles, respectively.

Sir, Asthma is one of the most common chronic disorders worldwide. Epidemiological twin and family studies mainly on childhood asthma have offered evidence for familial aggregation of asthma and atopy. Asthma heritability of as high as > 90 per cent has been reported in separate studies1,2. Segregation analyses on asthma have revealed different modes of inheritance such as polygenic inheritance with major gene involved3,4, co-dominant inheritance5, and polygenic/multifactorial influence with a recessive component inheritance6. Risk factors for developing asthma in adults, particularly in those who did not have asthma in childhood, are less defined. With an aim to demonstrate the parental effect of asthma and to determine the relative contribution of family history as a potential risk factor in adult onset asthma and its mode of inheritance, and to investigate the effect of consanguinity in adult onset asthma, the present study was undertaken on consecutive patients attending a tertiary care asthma centre (Allergy, Asthma, and Chest Center) in Mysore, Karnataka, India, during 2009-2010. The laboratory work was performed in the Genomics Laboratory of University of Mysore. The study protocol was approved by the Institutional Human Ethical Committee (IHEC) of the University of Mysore and informed written consent was obtained from cases and controls who participated in the study. Assuming history of maternal and paternal asthma of 20 per cent in cases and 10 per cent in controls with a 1:2 case control ratio, a sample of 195 cases and 390 controls was required to detect the level of significance at 0.05 with a power of 90 %. The sample size of 200 index cases and their family members were selected. Asthma in the index adult was diagnosed according to Global Initiative for Asthma (GINA) guidelines7 and American Thoracic Society Guidelines8. The patients with asthma were included only if they had theirfirst respiratory symptoms after the age of 18 yr. A total of 400 families were randomly selected in four administrative wards and these wards were randomly selected from the 30 units that were part of a large epidemiology study on asthma in urban Mysore. Only one adult subject from each family was considered as index control. A genetic register was designed to collect data on demographics, respiratory symptoms, triggers, age of onset of asthma and medications. Also detailed family history that included data in the pedigrees was collected. Adult patients with asthma were asked about the diagnosis of asthma in the first family members including parents, grandparents, siblings, uncle/aunt and their children. Odds ratio and 95 % confidence interval were estimated to quantify the relation between determinants of interest and the risk of asthma. Logistic regression analysis was performed to assess independent association of variables found to be significant in univariate analysis. The mean age of patients was 40±13 yr and that of controls was 39±13 yr. the male: female ratios were 1:1.35 in cases and 1:1.4 in controls. Family history of asthma was observed in 128 (64%) cases and 52 (13%) controls (P=0.001), revealing a significant association of asthma with family history of the disease in univariate analysis (OR = 13.29, 95% CI = 8.77 - 20.14) (Table). Parental consanguinity did not show any effect on adult onset asthma in this study. The independent association of maternal and paternal asthma with adult onset asthma was confirmed with paternal asthma associated with a higher risk of asthma in the offspring (OR = 11.82; P=0.003) than the maternal asthma (OR = 10.23; P=0.03) (Table). Sibling and aunt/uncle history of asthma was also found to be independently associated with adult onset asthma in our study population. Of the 128 families with asthma patient, the most common mode of asthma inheritance observed was dominant (61%). Of these families, only 6 per cent had consanguineous marriages, indicating null effect of consanguinity in the manifestation of asthma. Table Logistic regression analysis of patients with asthma (n=200) and healthy controls (n=400) In this study, paternal asthma was observed to be more significantly associated with asthma than the maternal asthma. This is in line with another study from India9 where the paternal history of asthma was found to confer a greater risk than the maternal asthma. To investigate the role of maternal asthma in the offspring and to determine if a parent-of-origin effect exists, a meta-analysis of multiple studies was performed. It was concluded that maternal asthma predisposed offspring to the disease more than paternal asthma10. Limitations of this study include patients being selected from a tertiary care center which may not be reflective of the general population. The control population though identified from the general population was limited to four administrative wards and may not be representative of Mysore city. There are also possibilities of information bias if the index cases and controls did not have a precise knowledge of their family members having asthma. In conclusion, it was observed that family history of asthma conferred a great risk in developing new onset asthma in adults. Paternal asthma was observed to be more significantly associated with asthma than the maternal asthma. Further studies on a larger population of adults with new onset of the disease are needed to confirm these findings.