Notes

Submitted to Indonesia: Earlier Cool Conflict Canadian Military services Policy and it is Influence on One particular Family's Knowledge.
AKs were detected in several invertebrates with specific antibodies and Der p 20 showed IgE cross-reactivity with AK from shrimp (Litopenaeus vannamei). Thus, Der p 20 is a cross-reactive HDM allergen and may serve as a diagnostic marker for HDM-induced lung symptoms such as asthma.
ImmunoCAP® (ImmunoCAP) and IMMULITE® 2000 3gAllergy™ (3gAllergy) systems are major quantitative allergen-specific immunoglobulin E (sIgE) assay methods. Due to the heterogeneous nature of allergenic extracts and differences in the assay format, quantitation of allergen-sIgEs is not expected to correlate well between different methods. However, we have recently reported good agreement between the methods in the diagnosis of egg allergy. This study aimed to determine and correlate the predictive values of sIgE by the two systems in the diagnosis of milk and wheat allergies.

Children who had undergone oral food challenge (OFC) for the diagnosis of milk and wheat allergies were enrolled. The OFCs were performed to diagnose either true allergy in the 1-year-old group (A) or tolerance in the 2- to 6-year-old group (B). Milk, casein and β-lactoglobulin, and wheat and ω-5 gliadin sIgE values were measured using the 2 systems. The predictive accuracy of each sIgE for the OFC outcome was assessed using receiver operating characteristic (ROC) curves. The probability of a positive OFC outcome was estimated by logistic regression analysis.

A total of 395 patients were recruited from 7 primary care clinics and 19 hospitals in Japan. Milk and wheat OFCs were performed for 87 and 102 group A patients, and 124 and 82 group B patients, respectively. ROC analysis yielded similar areas under the curve for the 2 assays (0.7-0.9). The log-transformed sIgE data showed a strong linear correlation with the estimated probabilities (R > 0.9).

The 2 systems may be interchangeable for diagnosis of milk and wheat allergies in young children.
The 2 systems may be interchangeable for diagnosis of milk and wheat allergies in young children.
Pet-derived allergens are the common indoor inhalant allergens. Among them, cat and dog allergens constitute more than 80% of animal allergic patients, which greatly affect the quality-of-life of patients and increase the burden of social health care. The aim of this study was to identify Cat-Niemann pick type C2 (NPC2) protein, a homologue of Can f 7, as a new allergen.

Cat-NPC2 complementary DNA (cDNA) was cloned and optimized for amplification and expression in
. Then, recombinant Cat-NPC2 (rCat-NPC2) was purified by Ni
affinity chromatography. The allergenicity was assessed by enzyme-linked immunosorbent assay (ELISA), western blot and basophil activation test (BAT). Based on the sequence similarity, the cross-reactivity between Cat-NPC2 and Can f 7 was investigated by inhibition ELISA. Circular dichroism spectroscopy and homology modeling were used to characterize the structure of Cat-NPC2.

The cDNA sequence of Cat-NPC2 was cloned with a 450-bp open reading frame coding for 149 amino acids (Gentified and characterized at both molecular and immunological levels. #link# The study will offer a deeper understanding of cat allergens and improve a component-resolved diagnosis in pet allergy.
The mechanisms of CC chemokine receptor 5 (CCR5) in the process of autophagy remain unknown. In CXCR inhibitor , we examined the role of HY peptide, which is an antagonistic peptide specifically binding the second extracellular loop of CCR5, in the expression of autophagy genes and β-arrestin 2 in lung tissues of asthmatic mice.

Experimental asthmatic mice were treated with HY peptide and dexamethasone sodium phosphate (Dex). Airway inflammation, autophagy-related genes, autophagic vacuoles (AVs) and β-arrestin 2 were examined in lung tissues, and the correlation between β-arrestin 2 and
expression was assessed.

HY peptide and Dex treatments alleviate airway inflammation. The expression of autophagy-related genes, such as
,
and
, was decreased in the lung tissues of the asthmatic mice. However, HY peptide and Dex treatments increased the expression of these genes as well as the formation of AVs. Additionally, the expression of the β-arrestin 2 protein was significantly increased in the HY peptide-treated group, and positive cells expressing β-arrestin 2 were mainly located in the membrane and cytoplasm of bronchial epithelial cells. The β-arrestin 2 expression was positively correlated with the expression of
in the model and HY peptide-treated groups.

HY peptide inhibits airway inflammation, autophagic dysfunction exists in asthmatic mice, and targeting HY peptide increases the expression of autophagy-related genes. Thus, β-arrestin 2 may participate in the mechanisms underlying these processes.
HY peptide inhibits airway inflammation, autophagic dysfunction exists in asthmatic mice, and targeting HY peptide increases the expression of autophagy-related genes. Thus, β-arrestin 2 may participate in the mechanisms underlying these processes.
Recent studies have demonstrated that macrophage migration inhibitory factor (MIF) is of importance in asthmatic inflammation. The role of MIF in modulating airway remodeling has not yet been thoroughly elucidated to date. In the present study, we hypothesized that MIF promoted airway remodeling by intensifying airway smooth muscle cell (ASMC) autophagy and explored the specific mechanisms.

MIF knockdown in the lung tissues of C57BL/6 mice was conducted by instilling intratracheally adeno-associated virus (AAV) vectors (MIF-mutant AAV9) into mouse lung tissues. Mice genetically deficient in the autophagy marker ATG5 (ATG5
) was used to detect the role of autophagy in ovalbumin (OVA)-asthmatic murine models. Moreover, to block the expression of MIF and CD74
models, inhibitors, antibodies and lentivirus transfection techniques were employed.

First, MIF knockdown in the lung tissues of mice showed markedly reduced airway remodeling in OVA murine mice models. Secondly, ASMC autophagy was increased in the OVA-challenged models. Mice genetically deficient in the autophagy marker ATG5 (ATG5
) that were primed and challenged with OVA showed lower airway remodeling than genetically wild-type asthmatic mice. Thirdly, MIF can induce ASMC autophagy
. Moreover, the cellular source of MIF which promoted ASMC autophagy was macrophages. Finally, MIF promoted ASMC autophagy in a CD74-dependent manner.

MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
MIF can increase asthmatic airway remodeling by enhancing ASMC autophagy. Macrophage-derived MIF can promote ASMC autophagy by targeting CD74.
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