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Abstract Background The emergence of Spodoptera frugiperda (fall armyworm; FAW) in the world has raised concerns regarding its impact on crop production, particularly on corn and sorghum. While chemical control and Bt crops have been effective in managing FAW damage, the development of pesticide-resistant and Bt-resistant strains necessitates alternative control methods. The push-pull farming system has gained attention, but direct utilization of African plant species in Taiwan faces challenges due to invasive potential and climatic disparities. Therefore, identifying and evaluating suitable local plant species, such as Napier grass (Pennisetum purpureum), Desmodium species, and signal grass (Brachiaria brizantha), is crucial for implementing effective FAW management strategies in Taiwan. Results In screening fifty Napier grass germplasms, all demonstrated an antibiotic effect, reducing leaf consumption compared to corn. Notably, thirty-five germplasms exhibited robust antibiotic traits, decreasing FAW consumption and increasing mortality rates. Three Napier grass germplasms also attracted more female moths for oviposition. Further evaluation of selected Napier grass germplasms and signal grass demonstrated efficacy in reducing FAW larval weight and survival duration. Additionally, Desmodium species, particularly D. uncinatum, showed promising toxicity against FAW larvae. Conclusion Our findings support the effectiveness of selected Napier grass germplasms and signal grass as pull plants, and highlight the potential of D. uncinatum as a push plant in FAW management strategies in Taiwan.

Abstract Background Nitrogen is an essential macronutrient for plant growth and development. Crops with a high nitrogen input usually have high yields. However, outbreaks of brown planthoppers (Nilaparvata lugens; BPH) frequently occur on rice farms with excessive nitrogen inputs. Rice plants carrying BPH resistance genes are used for integrated pest management. Thus, the impact of nitrogen on the resistance of rice near-isogenic lines (NILs) with BPH resistance genes was investigated. Results We tested these NILs using a standard seedbox screening test and a modified bulk seedling test under different nitrogen treatments. The amount of nitrogen applied had an impact on the resistance of some lines with BPH resistance genes. In addition, three NILs (NIL-BPH9, NIL-BPH17, and NIL-BPH32) were further examined for antibiosis and antixenosis under varying nitrogen regimes. The N. lugens nymph population growth rate, honeydew excretion, female fecundity, and nymph survival rate on the three NILs were not affected by different nitrogen treatments except the nymph survival rate on NIL-BPH9 and the nymph population growth rate on NIL-BPH17. Furthermore, in the settlement preference test, the preference of N. lugens nymphs for IR24 over NIL-BPH9 or NIL-BPH17 increased under the high-nitrogen regime, whereas the preference of N. lugens nymphs for IR24 over NIL-BPH32 was not affected by the nitrogen treatments. Conclusions Our results indicated that the resistance of three tested NILs did not respond to different nitrogen regimes and that NIL-BPH17 exerted the most substantial inhibitory effect on N. lugens growth and development.

Rationale: Little is known about effects of paternal tobacco smoke (PTS) on the offspring’s asthma and its prenatal epigenetic programming.Objective: To investigate whether PTS exposure was associated with the offspring’s asthma and correlated to epigenetic CG methylation of potential tobacco-related immune genes: LMO2, GSTM1 or/and IL-10 genes.Measurements and Main Results: In a birth cohort of 1,629 newborns, we measured exposure rates of PTS (23%) and maternal tobacco smoke (MTS, 0.2%), cord blood DNA methylation, infant respiratory tract infection, childhood DNA methylation, and childhood allergic diseases. Infants with prenatal PTS exposure had a significantly higher risk of asthma by the age of 6 than those without (p = 0.026). The PTS exposure doses at 0,

A form of systemic vasculitis, Kawasaki disease (KD) occurs most frequently in children under the age of five years old. Previous studies have found that Prostaglandin E2 (PGE2) correlates with KD, although the related mechanisms are still unknown. CD40L may also be a marker of vasculitis in KD, so this study focuses on PGE2 and CD40L expression in KD.This study consisted of a total of 144 KD patients, whose intravenous immunoglobulin (IVIG)/coronary arterial lesion (CAL) formation resistance was evaluated. PGE2 levels were evaluated in vitro to study the effect of CD40L on CD4+ T lymphocytes.PGE2 levels significantly increased after IVIG treatment (p

BackgroundKawasaki disease (KD) of unknown immunopathogenesis is an acute febrile systemic vasculitis and the leading cause of acquired heart diseases in childhood. To search for a better strategy for the prevention and treatment of KD, this study compared and validated human KD immunopathogenesis in a mouse model of Lactobacillus casei cell wall extract (LCWE)-induced coronary arteritis.MethodsRecruited subjects fulfilled the criteria of KD and were admitted for intravenous gamma globulin (IVIG) treatment at the Kaohsiung Chang Gung Memorial Hospital from 2001 to 2009. Blood samples from KD patients were collected before and after IVIG treatment, and cardiovascular abnormalities were examined by transthoracic echocardiography. Wild-type male BALB/c mice (4-week-old) were intraperitoneally injected with LCWE (1 mg/mL) to induce coronary arteritis. The induced immune response in mice was examined on days 1, 3, 7, and 14 post injections, and histopathology studies were performed on days 7 and 14.ResultsBoth human KD patients and LCWE-treated mice developed coronary arteritis, myocarditis, valvulitis, and pericarditis, as well as elevated plasma levels of interleukin (IL)-2, IL-6, IL-10, monocyte chemoattractant protein (MCP)-1, and tumor necrosis factor (TNF)-α in acute phase. Most of these proinflammatory cytokines declined to normal levels in mice, whereas normal levels were achieved in patients only after IVIG treatment, with a few exceptions. Toll-like receptor (TLR)-2, but not TLR4 surface enhancement on circulating CD14+ monocytes, was augmented in KD patients before IVIG treatment and in LCWE-treated mice, which declined in patients after IVIG treatment.ConclusionThis result suggests that that not only TLR2 augmentation on CD14+ monocytes might be an inflammatory marker for both human KD patients and LCWE-induced CAL mouse model but also this model is feasible for studying therapeutic strategies of coronary arteritis in human KD by modulating TLR2-mediated immune activation on CD14+ monocytes.

Background. Kawasaki disease (KD) is characterized by systemic vasculitis of unknown etiology. Our previous studies showed expression of CD40 ligand on CD4+ T cells correlated to the coronary artery lesion (CAL) and disease progress in KD. Other studies from Japan suggested the role of CD40L in the pathogenesis of CAL, and this might help explain the excessive number of males affected with KD but cannot be reproduced by Taiwanese population. This study was conducted to investigate the CD40 polymorphism in KD and CAL formation. Methods. A total of 950 subjects (381 KD patients and 569 controls) were investigated to identify 2 tagging single-nucleotide polymorphisms (tSNPs) of CD40 (rs4810485 and rs1535045) by using the TaqMan allelic discrimination assay. Results. A significant association was noted with regards to CD40 tSNPs (rs1535045) between controls and KD patients (P=0.0405, dominant model). In KD patients, polymorphisms of CD40 (rs4810485) showed significant association with CAL formation (P=0.0436, recessive model). Haplotype analysis did not yield more significant results between polymorphisms of CD40 and susceptibility/disease activity of KD. Conclusions. This study showed for the first time that polymorphisms of CD40 are associated with susceptibility to KD and CAL formation, in the Taiwanese population.

It remains unclear whether the GSTM1 genotype interacts with tobacco smoke exposure (TSE) in asthma development. This study aimed to investigate the interactions among GSTM1 genotype, gender, and prenatal TSE with regard to childhood asthma development. In a longitudinal birth cohort in Taiwan, 756 newborns completed a 6-year follow-up, and 591 children with DNA samples available for GSTM1 genotyping were included in the study, and the interactive influences of gender-GSTM1 genotyping prenatal TSE on childhood asthma development were analyzed. Among these 591 children, 138 (23.4%) had physician-diagnosed asthma at 6 years of age, and 347 (58.7%) were null-GSTM1. Prenatal TSE significantly increased the prevalence of childhood asthma in null-GSTM1 children relative to those with positive GSTM1. Further analysis showed that prenatal TSE significantly increased the risk of childhood asthma in girls with null-GSTM1. Furthermore, among the children without prenatal TSE, girls with null-GSTM1 had a significantly lower risk of developing childhood asthma and a lower total IgE level at 6 years of age than those with positive GSTM1. This study demonstrates that the GSTM1 null genotype presents a protective effect against asthma development in girls, but the risk of asthma development increases significantly under prenatal TSE. [ABSTRACT FROM AUTHOR]

Background: Exposure to cow's milk protein in early infancy could lead to increased rates of allergic diseases later in life. We investigated whether feeding a protein-hydrolyzed formula (HF) in the first 6 months of life decreased allergic diseases up to 36 months later. Methods: Newborns who had at least 1 first-degree family member with a history of atopy and could not breast-feed were enrolled. They were fed with HF or cow's milk infant formula (CM) for at least 6 months via an open-label protocol and were monitored prospectively at 6, 18 and 36 months of age to assess allergy sensitization and allergic diseases. Results: A total of 1,002 infants were enrolled and 679 infants were consistently fed the same formula for the first 6 months of life (345 HF and 334 CM). The percentage of food sensitization (especially to milk protein) was significantly lower in the HF group than in the CM group at 36 months (12.7 vs. 23.4%, p = 0.048). There was no significant difference in the prevalence of aeroallergen sensitization between the groups. Occurrence of allergic diseases during the first 3 years of life was significantly correlated with aeroallergen sensitization, but not to food allergen sensitization, parental atopy or feeding types. Conclusions: Infants fed with HF during the first 6 months of life had a significantly lower percentage of sensitization to milk protein allergens, but not allergic diseases during the first 3 years of life. Avoidance of cow's milk protein alone in infancy is not enough to decrease rates of allergic diseases. Copyright © 2010 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is the leading cause of acquired heart disease during childhood in the developed countries. Coronary artery lesions (CAL) are the major complications of KD. A unique proteomic profiling with increased or decreased fibrinogen, alpha-1-antitrypsin, clusterin, and immunoglobulin free light chains were noted in KD in our previous study. The purpose of this study was to evaluate relations between these biomarkers and CAL in KD and to establish within the markers the appropriate cut-off value with which to predict the occurrence of CAL. A total of 47 KD patients were enrolled, including 14 with CAL and 33 without CAL. Plasma samples from patients with KD before intravenous immunoglobulin administration were indicated for measurement of these biomarkers. A potential relation among CAL, clinical characteristics, and these biomarkers was investigated, and a receiver operating characteristic curve was used to identify a cut-off value of the significant marker that best predicated the occurrence of CAL. Among these biomarkers, only plasma clusterin level was associated with the occurrence of CAL. Using a cut-off value of clusterin <12.0 mg/l, the relative risk for CAL was 4.53-fold (95% confidence interval [CI] 1.060-19.347%, P = 0.014). Results from this study suggest that plasma clusterin level <12.0 mg/l in KD is significantly associated with the occurrence of CAL. Results from this study provide a potential biomarker of KD that may help predict the occurrence of CAL. [ABSTRACT FROM AUTHOR]

Objectives: Kawasaki disease (KD) is a systemic vasculitis primarily affecting children who are <5 years old. Intravenous immunoglobulin (IVIG) is the standard therapy for KD. However, many patients with KD still show poor response to initial IVIG treatment. This study was conducted to investigate the risk factors for initial IVIG treatment failure in KD. Methods: Children who met KD diagnosis criteria and were admitted for IVIG treatment were retrospectively enrolled for analysis. Patients were divided into IVIG-responsive and IVIG-resistant groups. Initial laboratory data before IVIG treatment were collected for analysis. Results: A total of 131 patients were enrolled during the study period. At 48 h after completion of initial IVIG treatment, 20 patients (15.3%) had an elevated body temperature. Univariate analysis showed that patients who had initial findings of high neutrophil count, abnormal liver function, low serum albumin level (≤2.9 g/dL) and pericardial effusion were at risk for IVIG treatment failure. Multivariate analysis with a logistic regression procedure showed that serum albumin level was considered the independent predicting factor of IVIG resistance in patients with KD (p = 0.006, OR = 40, 95% CI: 52.8–562). There was no significant correlation between age, gender, fever duration before IVIG treatment, haemoglobin level, total leucocyte and platelet counts, C-reactive protein level, or sterile pyuria and initial IVIG treatment failure. The specificity and sensitivity for prediction of IVIG treatment failure in this study were 96% and 34%, respectively. Conclusion: Pre-IVIG treatment serum albumin levels are a useful predictor of IVIG resistance in patients with KD. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is the leading cause of acquired heart disease during childhood in the developed countries. The mechanism and biomarkers of KD remain to be determined. In this study, we sought to elucidate potential plasma proteomic markers in KD patients in comparison to that in febrile controls. Plasma samples from KD patients and febrile controls were subjected to two-dimensional polyacrylamide gel electrophoresis analysis. Differential protein displays between KD patients and febrile controls were determined. Fibrinogen beta and gamma chains, alpha-1-antitrypsin (A1AT), CD5 antigen-like precursor (CD5L), and clusterin were increased in KD patients, whereas immunoglobulin free light chains were decreased, as compared with controls. The differential protein displays were validated with enzyme-linked immunosorbent assay tests. We found higher fibrinogen-related proteins (fibrinogen, A1AT, clusterin, and CD5L), along with a lower level of the immunoglobulin free light chains that involve fibrin degradation in KD. Results from this study showing a unique proteomic profiling with abnormal fibrinogen cascade may afford a good biomarker of KD and a better strategy to prevent cardiovascular complications of KD by correcting abnormal fibrin deposition or degradation. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) is a systemic febrile vasculitis particular coronary artery involvement. Eosinophilia has been found in our and other studies in KD. This study further investigates whether eosinophil-related T helper 2 (Th2) cytokines or the activation marker (eosinophil cationic protein – ECP) is involved in KD with coronary artery lesions (CAL). A total of 95 KD patients were enrolled for this study. Plasma samples were subjected to the measurement of interleukin (IL)-4, IL-5, and eotaxin by Luminex-Bedalyte multiplex beadmates system and to the measurement of ECP by fluoroimmunoassay. Patients with KD had higher eosinophils than controls. Eosinophil-related mediators: IL-4, IL-5, eotaxin, and ECP levels were also higher in KD patients than controls before intravenous immunoglobulin (IVIG) treatment. After IVIG treatment, ECP decreased but IL-4, IL-5, and eotaxin increased significantly. The higher the IL-5 and eosinophil levels after IVIG treatment, the lower rate of CAL was found. Changes of eosinophils after IVIG treatment were positively correlated to changes of IL-5 levels but not ECP levels. An increase of eosinophils and IL-5, but not ECP levels after IVIG treatment, was inversely correlated with CAL formation in KD. [ABSTRACT FROM AUTHOR]

Although maternal amniotic and vaginocervical cytokines are known to play a role in triggering preterm delivery, the effects of activating fetal phagocytes and platelets are not clear. In an attempt to clarify this issue, we measured levels of myeloperoxidase (MPO), a phagocyte activation marker, and soluble p-selectin (sCD62p), a platelet activation marker, in umbilical cord blood samples from 2200 consecutive cord blood collections, 106 of which were from preterm infants. MPO and sCD62p levels were correlated to gestational age and preterm delivery. It was found that MPO levels were significantly higher in preterm infants and were not significantly correlated to gestational age. In contrast, sCD62p levels were lower in preterm infants and were negatively correlated to gestational age. In summary, we showed that fetal phagocyte activation as demonstrated by higher cord blood MPO levels is associated with preterm delivery, but platelet activation as shown by lower sCD62p levels is not. This suggests that fetal phagocyte activation may be implicated in preterm delivery, and subsequently in prematurity- related inflammatory insults. [ABSTRACT FROM AUTHOR]

Describes a case of a newborn with scrub typhus. Results of the medical examinations; Treatment administered to the patient; Information on scrub typhus. INSET: METHYLPHENIDATE AND THIORIDAZINE IN THE TREATMENT OF....