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A growing body of research suggests an association between attention deficit hyperactivity disorder (ADHD) and allergic disorders, but little work has been done to explore the role of external factors such as parental smoking at home in the development of comorbid ADHD and allergic disorders. This study aimed to examine the association between allergic diseases and ADHD adjusted for exposure to parental smoking at home in early adolescents. We recruited 250 male (41.7%) and 350 female (58.3%) adolescents (mean [SD] age, 13.29 [0.52] years) via chain-referral sampling. Their ADHD symptoms were assessed by the parent proxy-report version of the Chinese Strengths and Weaknesses of Attention-Deficit/Hyperactivity-symptoms and Normal-behaviours (SWAN) rating scale. Data on the participants' history of clinician-diagnosed allergic diseases, family socio-demographics, and parental smoking habit were collected using a parent-completed questionnaire. Regression analyses were performed to examine the associations of interest. The levels of ADHD symptoms were comparable between allergic and non-allergic participants after controlling for child and family demographics and parental smoking at home. Notably, the risk of probable ADHD was particularly high in participants with food allergies (odd ratio = 4.51, p = 0.011) but not in those with allergic rhinitis after adjusting for parental smoking at home. Our findings suggest that second-hand smoke exposure at home is a potential risk factor underlying the link between ADHD and allergic diseases. Current management guidelines should emphasize the importance of early identification and cessation of tobacco smoke exposure for prevention of comorbidity of ADHD and allergic disorders. Clinical Trial Registration (if any): NA., Author(s): Rosa S. Wong [sup.1] [sup.2] [sup.3] , Keith T. S. Tung [sup.1] , Hugo E. Leung [sup.1] , Reena Chow [sup.1] , Gilbert T. Chua [sup.1] , Macro H. [...]

Byline: Bharat. Gurnani, Kirandeep. Kaur Subtenon's block is commonly used to achieve akinesia, analgesia, and anesthesia for ophthalmic surgeries. This case study detailed a rare hypersensitivity report in a 65-year-old [...]

Background/Objectives: The potential immune functions related to the damages induced by oxygen-free radicals suggest that antioxidants may have a role in the development of allergies. The objective was to investigate the association between maternal intake of antioxidants during pregnancy and the risk of asthma, rhinitis and eczema in 5-year-old children. Subjects/Methods: This study was on the basis of the Finnish Type 1 Diabetes Prediction and Prevention Nutrition Study, a population-based birth cohort study with 5-year follow-up. Complete information on maternal food frequency questionnaire data and ISAAC (International Study of Asthma and Allergies in Childhood)-based allergic outcomes were available for 2441 children. Cox proportional regression and logistic regression were used for the analyses. Results: Maternal intake of any of the antioxidants was not significantly associated with the risk of asthma, rhinitis or eczema in the offspring, except for dietary intake of magnesium, which was independently associated with protection against eczema (OR 0.78;95% CI 0.62-0.97). Conclusion: Maternal intake of dietary magnesium during pregnancy may protect against the risk of eczema in the offspring. We did not confirm previous observations concerning other antioxidants. This may be due to the variable amount of antioxidant intake across studies and also indicative of the hypothesis that there may be a critical time window in pregnancy during which antioxidants might modify the risk of allergies in the offspring. European journal of Clinical Nutrition (2011) 65, 937-943; doi: 10.1038/ejcn.2011.67; published online 11 May 2011 Keywords: allergies; antioxidants; asthma; children; maternal diet; pregnancy, Introduction Allergic disorders are a consequence of immune processes that promote a shift in the balance between the Th1 and Th2 cytokines, favoring Th2 dominance (Kay, 2001). This process is [...]

Diminished exposure to harmless micro-organisms, such as lactobacilli, has been suggested to play a role in the increased prevalence of allergic disorders in Westernized communities. The development of allergies depends on both environmental factors and genetic variations, including polymorphisms in genes encoding pattern recognition receptors. The present study examines the effects of both colonization with specific Lactobacillus species and genetic variations in DC-SIGN, a pattern recognition receptor on dendritic cells that recognizes lactobacilli, on the development of atopic dermatitis (AD) and sensitization in infancy. Within the KOALA Birth Cohort Study, faecal samples of 681 one-month-old infants were collected and quantitatively screened for five Lactobacillus species: L. casei, L. paracasei, L. rhamnosus, L. acidophilus and L. reuteri. Eleven haplotype-tagging polymorphisms in the DC-SIGN gene were genotyped in these children. Allergic outcomes were a clinical diagnosis of AD and sensitization (specific IgE) at age 2 years. L. rhamnosus (31.5 %), L. paracasei (31.3 %) and L. acidophilus (14.4 %) were frequently detected in the faecal samples of one-month-old infants, whereas L. casei (2.5 %) and L. reuteri (< 1%) were rare. Colonization with L. paracasei decreased the risk of AD significantly (odds ratio 0.57, 95 % confidence interval 0.320.99), whereas effects of L. acidophilus were of borderline statistical significance (0.46, 0.20-1.04). Two DC-SIGN polymorphisms, rs11465413 and rs8112555, were statistically significantly associated with atopic sensitization. The present study supports the 'old friends' hypothesis suggesting that certain health-beneficial micro-organisms protect us from developing allergies and that these protective effects are species-dependent. Firm conclusions on the potential interaction between lactobacillus colonization and genetic variations in DC-SIGN in association with the development of allergic disorders cannot be drawn, given the limited power of our study. Therefore, incorporation of consecutive faecal sampling in newly started (birth) cohort studies would be a first requisite to further increase our understanding of host-microbial interactions in health and disease. DOI 10.1099/mic.0.042069-0

ABSTRACT There are currently more than 20 FDA-approved fillers in the United States (U.S.), noteworthy considering that it was only six years ago that the first hyaluronic acid filler was [...]

BACKGROUND: It has been demonstrated that ambient particulate matter (PM) can act as an adjuvant for allergic sensitization. Redox-active organic chemicals on the particle surface play an important role in [...]

BACKGROUND: The relationship of domestic endotoxin exposure to allergy and asthma has been widely investigated. However, few studies have evaluated predictors of household endotoxin, and none have done so for [...]

Barrier epithelial cells and airway dendritic cells (DCs) make up the first line of defense against inhaled substances such as house dust mite (HDM) allergen and endotoxin (lipopolysaccharide, LPS). We hypothesized that these cells need to communicate with each other to cause allergic disease. We show in irradiated chimeric mice that Toll-like receptor 4 (TLR4) expression on radioresistant lung structural cells, but not on DCs, is necessary and sufficient for DC activation in the lung and for priming of effector T helper responses to HDM. TLR4 triggering on structural cells caused production of the innate proallergic cytokines thymic stromal lymphopoietin, granulocyte-macrophage colony-stimulating factor, interleukin-25 and interleukin-33. The absence of TLR4 on structural cells, but not on hematopoietic cells, abolished HDM-driven allergic airway inflammation. Finally, inhalation of a TLR4 antagonist to target exposed epithelial cells suppressed the salient features of asthma, including bronchial hyperreactivity. Our data identify an innate immune function of airway epithelial cells that drives allergic inflammation via activation of mucosal DCs., Aberrant innate and adaptive immune responses to allergens and environmental pollutants lead to respiratory disease, including asthma and chronic obstructive pulmonary disease (1). Airway DCs continuously sample inhaled air for [...]

We identified English-language publications on hypersensitivity reactions to xenobiotics through the PubMed database, using the search terms drug and/or xenobiotic, hypersensitivity reaction, mechanism, and immune mediated. We analyzed articles pertaining [...]

Background; Childhood respiratory allergies, which contribute to missed school days and other activity limitations, have increased in recent years, possibly due to environmental factors. OBJECTIVE: In this study we examined [...]

We have tested the entire Keio collection of close to 4,000 single-gene knockouts in Escherichia coli for increased susceptibility to one of seven different antibiotics (ciprofloxacin, rifampin, vancomycin, ampicillin, sulfamethoxazole, gentamicin, or metronidazole). We used high-throughput screening of several subinhibitory concentrations of each antibiotic and reduced more than 65,000 data points to a set of 140 strains that display significantly increased sensitivities to at least one of the antibiotics, determining the MIC in each case. These data provide targets for the design of 'codrugs' that can potentiate existing antibiotics. We have made a number of double mutants with greatly increased sensitivity to ciprofloxacin, and these overcome the resistance generated by certain gyrA mutations. Many of the gene knockouts in E. coli are hypersensitive to more than one antibiotic. Together, all of these data allow us to outline the cell's 'intrinsic resistome,' which provides innate resistance to antibiotics.

We have identified colorectal distension (CRD)-responsive neurons in the anterior cingulate cortex (ACC) and demonstrated that persistence of a heightened visceral afferent nociceptive input to the ACC induces ACC sensitization. In the present study, we confirmed that rostral ACC neurons of sensitized rats [induced by chicken egg albumin (EA)] exhibit enhanced spike responses to CRD. Simultaneous in vivo recording and reverse microdialysis of single ACC neurons showed that a low dose of glutamate (50 [micro]M) did not change basal ACC neuronal firing in normal rats but increased ACC neuronal firing in EA rats from 18 [+ or -] 2 to 32 [+ or -] 3.8 impulses/10 s. A high dose of glutamate (500 [micro]M) produced 1.95-fold and a 4.27-fold increases of ACC neuronal firing in shamtreated rats and in EA rats, respectively, suggesting enhanced glutamatergic transmission in the ACC neurons of EA rats. Reverse microdialysis of the 3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainite receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 [micro]M) reduced basal and abolished CRD-induced ACC neuronal firing in normal rats. In contrast, microdialysis of N-methyt-D-aspartate (NMDA) receptor antagonist AP5 had no effect on ACC neuronal firing in normal rats. However, AP5 produced 86% inhibition of ACC neuronal firing evoked by 50 mmHg CRD in the EA rats. In conclusion, ACC nociceptive transmissions are mediated by glutamate AMPA receptors in the control rats. ACC responses to CRD are enhanced in viscerally hypersensitive rats. The enhancement of excitatory glutamatergic transmission in the ACC appears to mediate this response. Furthermore, NMDA receptors mediate ACC synaptic responses after the induction of visceral hypersensitivity. anterior cingulate cortex; visceral hypersensitivity; NMDA and nonNMDA receptors

A study to investigate the high prevalence of hypersensitivity reactions to monoclonal antibody cetuximab, used in the treatment of colorectal cancer and carcinoma of the head and neck is conducted. Findings reveal that all the reactions were associated with IgE antibodies against galactose-[alpha]-1, 3-galactose that was present before the treatment with cetuximab.

A study to check the effectiveness of HLA-B*5701 screening to prevent hypersensitivity to abacavir is conducted. Results confirm the hypothesis that HLA-B*5701 screening reduced hypersensitivity to abacavir.

BACKGROUND: Recent studies have identified associations between the concentration of phthalates in indoor dust and allergic symptoms in the airways, nose, and skin. OBJECTIVES: Our goal was to investigate the [...]

Atherosclerosis is an inflammatory disease that is associated with monocyte recruitment and subsequent differentiation into lipid-laden macrophages at sites of arterial lesions, leading to the development of atherosclerotic plaques. PLC is a key member of signaling pathways initiated by G protein--coupled ligands in macrophages. However, the role of this enzyme in the regulation of macrophage function is not known. Here, we studied macrophages from mice lacking PLC [beta]2, PLC [beta]3, or both PLC isoforms and found that PLC [beta]3 is the major functional PLC [beta] isoform in murine macrophages. Although PLC [beta]3 deficiency did not affect macrophage migration, adhesion, or phagocytosis, it resulted in macrophage hypersensitivity to multiple inducers of apoptosis. PLC [beta]3 appeared to regulate this sensitivity via PKC-dependent upregulation of Bcl-XL. The significance of PLC [beta] signaling in vivo was examined using the apoE-deficient mouse model of atherosclerosis. Mice lacking both PLC [beta]3 and apoE exhibited fewer total macrophages and increased macrophage apoptosis in atherosclerotic lesions, as well as reduced atherosclerotic lesion size when compared with mice lacking only apoE. These results demonstrate what we believe to be a novel role for PLC activity in promoting macrophage survival in atherosclerotic plaques and identify PLC [beta]3 as a potential target for treatment of atherosclerosis., Introduction PLC hydrolyzes phosphatidylinositol 4,5-bisphosphate to generate 2 second messengers, inositol 1,3,4-triphosphate and diacylgl-ycerol. While inositol 1,3,4-triphosphate regulates [Ca.sup.2+] efflux, it and diacylglycerol activate PKC (1). The [beta] family of [...]

BACKGROUND: In utero environmental tobacco smoke (ETS) exposure exacerbates initial lung responses of adult mice to ovalbumin (OVA), a common allergen in rodent models of allergicasthma. OBJECTIVE: We tested the hypothesis that in utero ETS exposure alters expression of genes (including asthma-related and inflammatory genes) in the lungs of adult mice and that this differential expression is reflected in differential respiratory and immune responses to nontobacco allergens. METHODS: Using Affymetrix Mouse Genome 430 2.0 arrays, we examined gene expression changes in lungs of BALB/c mice exposed to ETS in utero, OVA, or saline aerosol at weeks 7-8, and OVA sensitization and challenge at weeks 11-15. Data sets were filtered by transcript p-value ([less than or equal to] 0.05), false discovery rate ([less than or equal to] 0.05), and fold change ([greater than or equal to] 1.5). Differential expression of selected genes was confirmed by polymerase chain reaction (PCR). RESULTS: Genes differentially expressed as a result of in utero ETS exposure are involved in regulation of biological processes (immune response, cell proliferation, apoptosis, cell metabolism) through altered cytoskeleton, adhesion, transcription, and enzyme molecules. A number of genes prominent in lung inflammation were differentially expressed on PCR but did not pass selection criteria for microarray, including arginase (Arg1), chitinases (Chia, Chi3l3, Chi3l4), eotaxins (Ccl11, Ccl24), small proline-rich protein 2a (Sprr2a), and cytokines (Il4, Il6, Il10, Il13, Tnfa) . CONCLUSION: The differential lung gene expression reported here is consistent with previously reported functional changes in lungs of mice exposed in utero to ETS and as adults to the non-tobacco allergen OVA. KEY WORDS: allergy, asthma, environmental tobacco smoke (ETS), gene regulation, in utero, inflammation, lung, ovalbumin. Environ Health Perspect 115:1757-1766 (2007). doi:10.1289/ehp.10358 available via http://dx.doi.org/ [Online 19 September 2007], The incidence of asthma and allergy has increased dramatically during the past 30 years, primarily in industrialized countries (Eder et al. 2006). Although improved availability and quality of medical care [...]

[A.sub.2A] adenosine receptor ([A.sub.2A]AR) has potent anti-inflammatory properties, which may be important in the regulation of airway reactivity and inflammation. Inflammatory cells that possess [A.sub.2A]AR also produce nitrosative stress, which is associated with pathophysiology of asthma, so we hypothesized that [A.sub.2A]AR deficiency may lead to increased airway reactivity and inflammation through nitrosative stress. Thus the present study was carried out to investigate the role of [A.sub.2A]AR on airway reactivity, inflammation, NF-[kappa]B signaling, and nitrosative stress in [A.sub.2A]AR knockout (KO) and wild-type (WT) mice using our murine model of asthma. Animals were sensitized intraperitoneally on days 1 and 6 with 200 [micro]g of ragweed, followed by aerosolized challenges with 0.5% ragweed on days 11, 12, and 13, twice a day. On day 14, airway reactivity to methacholine was assessed as enhanced pause (Penh) using whole body plethysmography followed by bronchoalveolar lavage (BAL) and lung collection for various analyses. Allergen challenge caused a significant decrease in expression of [A.sub.2A]AR in [A.sub.2A] WT sensitized mice, with AzAAR expression being undetected in [A.sub.2A] KO sensitized group leading to decreased lung cAMP levels in both groups. [A.sub.2A]AR deletion/downregulation led to an increase in Penh to methacholine and influx of total cells, eosinophils, lymphocytes, and neutrophils in BAL with highest values in [A.sub.2A] KO sensitized group. [A.sub.2A] KO sensitized group further had increased NF-[kappa]B expression and nitrosative stress compared with WT sensitized group. These data suggest that [A.sub.2A]AR deficiency leads to airway inflammation and airway hyperresponsiveness, possibly via involvement of nitrosative stress in this model of asthma. NF-[kappa]B signaling doi:10.1152/ajplung.00416.2006.