Evaluation of Risk Factors for Asthma in Taipei City

BackgroundAsthma has rarely been studied by evaluating all of its trigger factors in 1 study population. Thus, correlations between the concentration of allergen immunoglobulin (Ig) E antibodies and airway limitation or asthma severity remain unclear.MethodsFive hundred and seventy-nine asthmatic patients were enrolled, and serum specific IgE antibodies to allergens were analyzed. All suspected trigger factors were assessed by questionnaire, case histories over a 4-year period, and diary card recordings; possible trigger factors were then re-evaluated.ResultsAntibodies to the following allergens were found: Dermatophagoides pteronyssinus (59.8% of patients), D. microceras (58.8%), D. farinae (56.8%), cockroach (38.3%), dog dander (26.3%), Candida albicans (13.3%), cat dander (10%), and Cladosporium herbarum (6.6%). A greater prevalence of allergy to dog and cat dander was found than previously. Younger patients were more often positive for mite allergens, and had higher titers of antibodies against such allergens, than older patients. Further, females had a lower concentration of mite allergen antibodies than males. No correlation between the concentration of allergen antibodies and forced expiratory volume in 1 second (FEV1), or the ratio of FEV1:forced vital capacity (FEV1:FVC), was found. In addition, there was no significant change in antibody titers with varying asthma severity. Non-allergenic trigger factors were irritant air inhalants (94.6% of patients), respiratory infection (92.2%), exercise (75.2%), emotional factors (58.8%), drugs and chemical substances (16%).ConclusionThere are multiple trigger factors in asthma. Allergenic trigger factors are more common in younger than older patients, whereas non-allergenic trigger factors are more common in older patients. There was no linear correlation between the concentration of specific IgE antibodies and asthma severity or airway limitation; therefore, to prevent asthma attacks in individual asthmatic patients, greater attention should be paid to avoiding all potential trigger factors, and not just house dust mite allergens

Synergistic effect of phosphodiesterase 4 inhibitor and serum on migration of endotoxin-stimulated macrophages.

Macrophage migration is an essential step in host defense against infection and wound healing. Elevation of cAMP by inhibiting phosphodiesterase 4 (PDE4), enzymes that specifically degrade cAMP, is known to suppress various inflammatory responses in activated macrophages, but the role of PDE4 in macrophage migration is poorly understood. Here we show that the migration of Raw 264.7 macrophages stimulated with LPS was markedly and dose-dependently induced by the PDE4 inhibitor rolipram as assessed by scratch wound healing assay. Additionally, this response required the involvement of serum in the culture medium as serum starvation abrogated the effect. Further analysis revealed that rolipram and serum exhibited synergistic effect on the migration, and the influence of serum was independent of PDE4 mRNA expression in LPS-stimulated macrophages. Moreover, the enhanced migration by rolipram was mediated by activating cAMP/exchange proteins directly activated by cAMP (Epac) signaling, presumably via interaction with LPS/TLR4 signaling with the participation of unknown serum components. These results suggest that PDE4 inhibitors, together with serum components, may serve as positive regulators of macrophage recruitment for more efficient pathogen clearance and wound repair

Inhibition of NKCC1 Modulates Alveolar Fluid Clearance and Inflammation in Ischemia-Reperfusion Lung Injury via TRAF6-Mediated Pathways

Background: The expression of Na-K-2Cl cotransporter 1 (NKCC1) in the alveolar epithelium is responsible for fluid homeostasis in acute lung injury (ALI). Increasing evidence suggests that NKCC1 is associated with inflammation in ALI. We hypothesized that inhibiting NKCC1 would attenuate ALI after ischemia-reperfusion (IR) by modulating pathways that are mediated by tumor necrosis-associated factor 6 (TRAF6).Methods: IR-ALI was induced by producing 30 min of ischemia followed by 90 min of reperfusion in situ in an isolated and perfused rat lung model. The rats were randomly allotted into four groups comprising two control groups and two IR groups with and without bumetanide. Alveolar fluid clearance (AFC) was measured for each group. Mouse alveolar MLE-12 cells were cultured in control and hypoxia-reoxygenation (HR) conditions with or without bumetanide. Flow cytometry and transwell monolayer permeability assay were carried out for each group.Results: Bumetanide attenuated the activation of p-NKCC1 and lung edema after IR. In the HR model, bumetanide decreased the cellular volume and increased the transwell permeability. In contrast, bumetanide increased the expression of epithelial sodium channel (ENaC) via p38 mitogen-activated protein kinase (p38 MAPK), which attenuated the reduction of AFC after IR. Bumetanide also modulated lung inflammation via nuclear factor-κB (NF-κB). TRAF6, which is upstream of p38 MAPK and NF-κB, was attenuated by bumetanide after IR and HR.Conclusions: Inhibition of NKCC1 by bumetanide reciprocally modulated epithelial p38 MAPK and NF-κB via TRAF6 in IR-ALI. This interaction attenuated the reduction of AFC via upregulating ENaC expression and reduced lung inflammation

Risk Factors for Recurrent Hypoglycemia in Hospitalized Diabetic Patients Admitted for Severe Hypoglycemia

Purpose: Severe hypoglycemia can result in neural damage, impaired cognitive function, coma, seizures, or death. The decision to admit diabetic patients after initial treatment in the emergency department remains unclear. Our purpose is to identify risk factors for developing recurrent hypoglycemia in diabetic patients admitted for severe hypoglycemia. Materials and Methods: We reviewed the records of 233 subjects (92 males, 141 females; mean age, 74.1 ± 9.8 years) with type 2 diabetes treated at a tertiary care teaching hospital and hospitalized for severe hypoglycemia. Results: Seventy-four (31.8%) patients were categorized with recurrent hypoglycemia and 159 (68.2%) with non-recurrent. Multivariate logistic regression analysis revealed that patients with loss of a recent meal, coronary artery disease, infection, and poor renal function (lower estimated glomerular filtration rate) were at risk for recurrent hypoglycemia. The use of calcium-channel blockers appeared to be a protective factor for the development of recurrent hypoglycemia. Conclusion: There may be a subset of patients with severe hypoglycemia and certain risk factors for recurrent hypoglycemia that should be admitted

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Influenza-Related Postinfectious Encephalomyelitis Complicated by a Perforated Peptic Ulcer

Influenza virus infection is extremely common and raises global concern due to the increasing prevalence of pandemic H1N1 infection. Influenza may occasionally be associated with neurologic complications and, also, rarely with gastrointestinal complications. Here, we report a rare case complicated with appendicitis, duodenum perforation, and transient delirious behavior after influenza A viral infection in a pediatric patient aged 14 years. The transient delirious behavior could be attributed to postinfectious encephalopathy. The perforated peptic ulcer could have resulted from influenza infection, could have been an adverse event related to oseltamivir administration, or could have been a complication of preceding gastroenteritis. Our case highlights the importance of pediatric healthcare workers to be aware of possible complications arising from both influenza infection and oseltamivir therapy, even though some of these complications may be relatively rare