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Food allergy plays an important role in atopic dermatitis (AD). Adequate predictors and guidelines for when dietary manipulation is indicated for AD are needed. The clinical significance of eosinophilia as a predictor for food allergy of late eczematous reactions in AD was investigated. Three hundred three patients with AD were studied, using elimination diets and food challenge tests. Food allergy prevalence was compared in groups of eczematoid AD patients with high or normal eosinophil levels. The effects on the blood eosinophil fraction of an elimination diet and milk allergy provocation of late eczematous reactions were evaluated. The prevalence of food allergy was 51.1% (135/264) in patients with eczematoid AD. The major type of food allergy in AD was late eczematous, rather than IgE mediated. Among eczematoid AD patients, 44.9% had high eosinophil levels. In patients with eczematoid AD, the food allergy prevalence was 70.8% (85/120) in the high eosinophil group and 34.7% (50/144) in the normal blood eosinophil group. An elimination diet improved clinical severity and decreased blood eosinophil levels. In milk allergy patients, a milk challenge significantly increased the blood eosinophil level. Skin-prick tests and food-specific IgE tests were useful for diagnosing IgE-mediated food allergy. Eosinophilia appeared to be a significant predictor of food allergy in AD and an indicating factor for diet manipulation, including an elimination diet. Food allergy may be responsible for eosinophilia in AD. Food allergy patterns for AD in Korea were different from those in western countries.

Food allergies are classified as IgE-mediated food allergies (IFAs) and non-IgE-mediated food allergies (NFAs). Recently, oral immunotherapy (OIT) has been found to be successful for treating both IFA and NFA, especially using interferon (IFN) gamma. This study was designed to clarify the clinical characteristics of IFA and NFA and compare the therapeutic characteristics of OIT using subcutaneously administered IFN-gamma for both types of food allergy. In this study, 148 patients were categorized into the IFA and NFA group following food challenge, skin-prick test and food-specific IgE tests. The patients were then treated using protocols specific for IFA and NFA using subcutaneous IFN-gamma injection as a randomized controlled trial. The principle of complete allergy resolution at prior dose in the case of IFA was also evaluated. Only the patients with IFA and NFA treated with OIT using IFN-gamma achieved tolerance successfully. Tolerance was achieved from low-dose range in IFA and in high-dose range for NFA. Complete tolerance was not obtained without achieving complete allergy resolution at each dose of the allergen before increasing the dosage in IFA. Both IFA and NFA can be successfully treated with OIT using IFN-gamma but show different clinical and therapeutic characteristics. IFN-gamma is necessary for the tolerance induction but not for tolerance maintenance. Additional study for the mechanisms of tolerance induction by IFN-gamma is needed.

A cDNA library was constructed from secondary xylem in the stem of a 2-year-old yellow poplar after being bent for 6 h with a 45° configuration to isolate genes related to cell wall modification during the early stages of tension wood formation. A total of 6,141 ESTs were sequenced to generate a database of 5,982 high-quality expressed sequence tags (ESTs). These sequences were clustered into 1,733 unigenes, including 822 contigs and 911 singletons. Homologs of the genes regulate many aspects of secondary xylem development, including those for primary and secondary metabolism, plant growth hormones, transcription factors, cell wall biosynthesis and modification, and stress responses. Although there were only 1,733 annotated ESTs (28.9%), the annotated ESTs obtained in this study provided sequences for a broad array of transcripts expressed in the stem upon mechanical bending, and the majority of them were the first representatives of their respective gene families in Liriodendron tulipifera. In the case of lignin, xylem-specific COMTs were identified and their expressions were significantly downregulated in the tension wood-forming tissues. Additionally, the majority of the auxin- and BR-related genes were downregulated significantly in response to mechanical bending treatment. Despite the small number of ESTs sequenced in this study, many genes that are relevant to cell wall biosynthesis and modification have been isolated. Expression analysis of selected genes allow us to identify the regulatory genes that may perform essential functions during the early stages of tension wood formation and associated cell wall modification.

Mechanical bending treatment was employed to cause tension wood formation in the stem of the fast-growing yellow poplar. The tension wood induced by mechanical bending had many characteristic features of tension wood, i.e., eccentric growth toward tension wood, increased frequency of fiber cell types, vessels with reduced size, and reduced lignin content in the developed xylem. The significant reduction of the guaiacyl (G) and p-hydroxyphenyl (H) units of lignin in the tension wood was clearly visualized in samples that had been subjected to bending for 7 and 14 days when analyzed by lignin histochemical analysis using phloroglucinol-HCl. The syringyl (S) unit in the tension wood lignin was also significantly decreased in the developed xylem of the 14-day bending treatment sample, as indicated by Maeule's staining. Expression analysis of several representative genes in the lignin biosynthetic pathway clearly demonstrated that the overall phenylpropanoid pathway toward biosynthesis for both the lignin monomers and the flavonoids was greatly downregulated on bending treatment. In addition, the genes encoding laccases, which have been reported to be involved in the polymerization of monolignols to produce lignin macromolecules, were significantly downregulated in the tension wood. Despite the very limited sequence information for the genes/enzymes in the phenylpropanoid pathway in yellow poplar, histochemical staining and expression analysis using quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) successfully demonstrated the anatomical and chemical characteristics associated with mechanical bending-induced tension wood formation in the yellow poplar.

ObjectiveCerebral amyloidosis and severe tauopathy in the brain are key pathological features of Alzheimer’s disease (AD). Despite a strong influence of the intestinal microbiota on AD, the causal relationship between the gut microbiota and AD pathophysiology is still elusive.DesignUsing a recently developed AD-like pathology with amyloid and neurofibrillary tangles (ADLPAPT) transgenic mouse model of AD, which shows amyloid plaques, neurofibrillary tangles and reactive gliosis in their brains along with memory deficits, we examined the impact of the gut microbiota on AD pathogenesis.ResultsComposition of the gut microbiota in ADLPAPT mice differed from that of healthy wild-type (WT) mice. Besides, ADLPAPT mice showed a loss of epithelial barrier integrity and chronic intestinal and systemic inflammation. Both frequent transfer and transplantation of the faecal microbiota from WT mice into ADLPAPT mice ameliorated the formation of amyloid β plaques and neurofibrillary tangles, glial reactivity and cognitive impairment. Additionally, the faecal microbiota transfer reversed abnormalities in the colonic expression of genes related to intestinal macrophage activity and the circulating blood inflammatory monocytes in the ADLPAPT recipient mice.ConclusionThese results indicate that microbiota-mediated intestinal and systemic immune aberrations contribute to the pathogenesis of AD in ADLPAPT mice, providing new insights into the relationship between the gut (colonic gene expression, gut permeability), blood (blood immune cell population) and brain (pathology) axis and AD (memory deficits). Thus, restoring gut microbial homeostasis may have beneficial effects on AD treatment.

Patients with atrial fibrillation are known to have a high risk of mortality. There is a paucity of population-based studies about the impact of atrial fibrillation on the mortality risk stratified by age, sex, and detailed causes of death. A total of 15,411 patients with atrial fibrillation from the Korean National Health Insurance Service-National Sample Cohort were enrolled, and causes of death were identified according to codes of the 10th revision of the International Classification of Diseases. From 2002 to 2013, a total of 4,479 (29%) deaths were confirmed, and the crude mortality rate for all-cause death was 63.3 per 1,000 patient-years. Patients with atrial fibrillation had a 3.7-fold increased risk of all-cause death compared with the general population. The standardized mortality ratio for all-cause death was the highest in young patients and decreased with increasing age (standardized mortality ratio 21.93, 95% confidence interval 7.60-26.26 in patients aged <20 years; standardized mortality ratio 2.77, 95% confidence interval 2.63-2.91 in patients aged ≥80 years). Women with atrial fibrillation exhibited a greater excess mortality risk than men (standardized mortality ratio 3.81, 95% confidence interval 3.65-3.98 in women; standardized mortality ratio 3.35, 95% confidence interval 3.21-3.48 in men). Cardiovascular disease was the leading cause of death (38.5%), and cerebral infarction was the most common specific disease. Patients with atrial fibrillation had an about 5 times increased risk of death due to cardiovascular disease compared with the general population. Patients with atrial fibrillation had a 4 times increased risk of mortality compared with the general population. However, the impact of atrial fibrillation on mortality decreased with age and in men. Cerebral infarction was the most common cause of death, and more attention should be paid to reducing the risk of stroke.

Tactile function is essential for human life as it enables us to recognize texture and respond to external stimuli, including potential threats with sharp objects that may result in punctures or lacerations. Severe skin damage caused by severe burns, skin cancer, chemical accidents, and industrial accidents damage the structure of the skin tissue as well as the nerve system, resulting in permanent tactile sensory dysfunction, which significantly impacts an individual’s daily life. Here, we introduce a fully-implantable wireless powered tactile sensory system embedded artificial skin (WTSA), with stable operation, to restore permanently damaged tactile function and promote wound healing for regenerating severely damaged skin. The fabricated WTSA facilitates (i) replacement of severely damaged tactile sensory with broad biocompatibility, (ii) promoting of skin wound healing and regeneration through collagen and fibrin-based artificial skin (CFAS), and (iii) minimization of foreign body reaction via hydrogel coating on neural interface electrodes. Furthermore, the WTSA shows a stable operation as a sensory system as evidenced by the quantitative analysis of leg movement angle and electromyogram (EMG) signals in response to varying intensities of applied pressures. Although artificial skins can facilitate the healing of damaged skin, the restoration of tactile functions remain a challenge. Here, Kang et al. report an artificial skin with an implantable tactile sensor that can simultaneously replace the tactile function by nerve stimulation and promote skin regeneration.

Hygroscopic and acidic nature of organic hole transport layers (HTLs) insisted to replace it with metal oxide semiconductors due to their favorable charge carrier transport with long chemical stability. Apart from large direct bandgap and high optical transmittance, ionization energy in the range of −5.0 to −5.4 eV leads to use NiO as HTL due to good energetic matching with lead halide perovskites. Analyzing X‐ray photoelectron spectroscopic (XPS) data of NiO, it is speculated that p‐type conductivity is related to the NiOOH or Ni2O3 states in the structure and the electrical conductivity can be modified by altering the concentration of nickel or oxygen vacancies. However, it is difficult to separate the contribution from nonlocal screening, surface effect and the presence of vacancy induced Ni3+ ion due to very strong satellite structure in the Ni 2p XPS spectrum of NiO. Thus, an effective approach to analyze the NiO XPS spectrum is presented and the way to correlate the presence of Ni3+ with the conductivity results which will help to avoid overestimation in finding the oxygen‐rich/deficient conditions in NiO. The shoulder peak of Ni2p XPS spectrum is important to understand p‐type semiconducting behavior. Both the Ni 2p and O 1s XPS spectra shall be carefully recorded with fixed take‐off angle (and/or depending on take‐off angle) and compare results with transport measurements.

BACKGROUNDMolecular characterization in pediatric papillary thyroid cancer (PTC), distinct from adult PTC, is important for developing molecularly targeted therapies for progressive radioiodine-refractory (131I-refractory) PTC.METHODSPTC samples from 106 pediatric patients (age range: 4.3-19.8 years; n = 84 girls, n = 22 boys) who were admitted to SNUH (January 1983-March 2020) were available for genomic profiling. Previous transcriptomic data from 125 adult PTC samples were used for comparison.RESULTSWe identified genetic drivers in 80 tumors: 31 with fusion oncogenes (RET in 21 patients, ALK in 6 patients, and NTRK1/3 in 4 patients); 47 with point mutations (BRAFV600E in 41 patients, TERTC228T in 2 patients [1 of whom had a coexisting BRAFV600E], and DICER1 variants in 5 patients); and 2 with amplifications. Fusion oncogene PTCs, which are predominantly detected in younger patients, were at a more advanced stage and showed more recurrent or persistent disease compared with BRAFV600E PTCs, which are detected mostly in adolescents. Pediatric fusion PTCs (in patients <10 years of age) had lower expression of thyroid differentiation genes, including SLC5A5, than did adult fusion PTCs. Two girls with progressive 131I-refractory lung metastases harboring a TPR-NTRK1 or CCDC6-RET fusion oncogene received fusion-targeted therapy; larotrectinib and selpercatinib decreased the size of the tumor and restored 125I radioiodine uptake. The girl with the CCDC6-RET fusion oncogene received 131I therapy combined with selpercatinib, resulting in a tumor response. In vitro 125I uptake and 131I clonogenic assays showed that larotrectinib inhibited tumor growth and restored radioiodine avidity.CONCLUSIONSIn pediatric patients with fusion oncogene PTC who have 131I-refractory advanced disease, selective fusion-directed therapy may restore radioiodine avidity and lead to a dramatic tumor response, underscoring the importance of molecular testing in pediatric patients with PTC.FUNDINGThe Ministry of Science, ICT and Future Planning (NRF-2016R1A2B4012417 and 2019R1A2C2084332); the Korean Ministry of Health and Welfare (H14C1277); the Ministry of Education (2020R1A6A1A03047972); and the SNUH Research Fund (04-2015-0830).TRIAL REGISTRATIONTwo patients received fusion-targeted therapy with larotrectinib (NCT02576431; NAVIGATE) or selpercatinib (LOXO-RET-18018).