Impacts of Heavy Rain and Typhoon on Allergic Disease

AbstractObjectivesAllergic disease may be increased by climate change. Recent reports have shown that typhoon and heavy rain increase allergic disease locally by concentration of airborne allergens of pollen, ozone, and fungus, which are causes of allergic disease. The objective of this study was to determine whether typhoon and heavy rain increase allergic disease in Korea.MethodsThis study included allergic disease patients of the area declared as a special disaster zone due to storms and heavy rains from 2003 to 2009. The study used information from the Korea Meteorological Administration, and from the National Health Insurance Service for allergic diseases (asthma, allergic rhinitis, and atopic dermatitis).ResultsDuring a storm period, the numbers of allergy rhinitis and atopic dermatitis outpatients increased [rate ratio (RR) = 1.191; range, 1.150–1.232] on the sixth lag day. However, the number of asthma outpatients decreased (RR = 0.900; range, 0.862–0.937) on the sixth lag day after a disaster period. During a storm period, the numbers of allergic rhinitis outpatients (RR = 1.075; range, 1.018–1.132) and atopy outpatients increased (RR = 1.134; range, 1.113–1.155) on the seventh lag day. However, the number of asthma outpatients decreased to RR value of 0.968 (range, 0.902–1.035) on the fifth lag day.ConclusionThis study suggests that typhoon and heavy rain increase allergic disease apart from asthma. More study is needed to explain the decrease in asthma

Role of interleukin-10 in endochondral bone formation in mice: Anabolic effect via the bone morphogenetic protein/Smad pathway

Objective: Interleukin-10 (IL-10) is a pleiotropic immunoregulatory cytokine with a chondroprotective effect that is elevated in cartilage and synovium in patients with osteoarthritis. However, the role of IL-10 during endochondral bone formation and its mechanism of action have not been elucidated. Methods: IL-10-/- mice and IL-10-treated tibial organ cultures were used to study loss and gain of IL-10 functions, respectively, during endochondral bone formation. Primary chondrocytes from the long bones of mouse embryos were cultured with and without IL-10. To assess the role of IL-10 in chondrogenic differentiation, we conducted mesenchymal cell micromass cultures. Results: The lengths of whole skeletons from IL-10-/- mice were similar to those of their wild-type littermates, although their skull diameters were smaller. The tibial growth plates of IL-10-/- mice showed shortening of the proliferating zone. Treatment with IL-10 significantly increased tibial lengths in organ culture. IL-10 also induced chondrocyte proliferation and hypertrophic differentiation in primary chondrocytes in vitro. Mechanistically, IL-10 activated STAT-3 and the Smad1/5/8 and ERK-1/2 MAP kinase pathways and induced the expression of bone morphogenetic protein 2 (BMP-2) and BMP-6 in primary chondrocytes. Furthermore, the blocking of BMP signaling attenuated the IL-10-mediated induction of cyclin D1 and RUNX-2 in primary chondrocytes and suppressed Alcian blue and alkaline phosphatase staining in mesenchymal cell micromass cultures. Conclusion: These results indicate that IL-10 acts as a stimulator of chondrocyte proliferation and chondrogenic or hypertrophic differentiation via activation of the BMP signaling pathway. © 2013, American College of Rheumatology

C-1 Root Schwannoma with Aggressive Lateral Mass Invasion

Schwannomas are relatively common, benign tumors that are thought to arise from the nerve sheath cell. Schwannomas of the C1 root are extremely rare and seldom invade lateral masses because they gradually increase in size and can extend through the wide space behind the lateral mass instead of the intervertebral foramen. We present here an unusual case of a benign schwannoma that aggressively invaded the lateral mass of C-1

Korean Guideline Development for the Evaluation of Permanent Impairment of the Spine: Proposal by the Korean Academy of Medical Sciences Committee

The criteria for the evaluation of spinal impairment are diverse, complex, and have no standardized form. This makes it difficult and somewhat troublesome to accurately evaluate spinal impairment patients. A standardized guideline was studied for the evaluation of spinal impairment, based on the American Medical Association (AMA) Guides and the McBride method. This guideline proposal was developed by specialty medical societies under the Korean Academy of Medical Sciences. In this study, the grades of impairment were assessed by dividing patients into three different categories: spinal cord impairment, spinal injury impairment and spinal disorder impairment. The affected regions of the spine are divided into three: the cervical region, the thoracic region, and the lumbosacral region. The grade of impairment was differentially evaluated according to the affected region. The restricted range of motion was excluded in the evaluation spinal impairment because of low objectivity. Even though the new Korean guideline for the evaluation of spinal impairment has been proposed, it should be continuously supplemented and revised

Clinical Characteristics of a Nationwide Hospital-based Registry of Mild-to-Moderate Alzheimer's Disease Patients in Korea: A CREDOS (Clinical Research Center for Dementia of South Korea) Study

With rapid population aging, the socioeconomic burden caused by dementia care is snowballing. Although a few community-based studies of Alzheimer's disease (AD) have been performed in Korea, there has never been a nationwide hospital-based study thereof. We aimed to identify the demographics and clinical characteristics of mild-to-moderate AD patients from the Clinical Research Center for Dementia of Korea (CREDOS) registry. A total of 1,786 patients were consecutively included from September 2005 to June 2010. Each patient underwent comprehensive neurological examination, interview for caregivers, laboratory investigations, neuropsychological tests, and brain MRI. The mean age was 74.0 yr and the female percentage 67.0%. The mean period of education was 7.1 yr and the frequency of early-onset AD (< 65 yr old) was 18.8%. Among the vascular risk factors, hypertension (48.9%) and diabetes mellitus (22.3%) were the most frequent. The mean score of the Korean version of Mini-Mental State Examination (K-MMSE) was 19.2 and the mean sum of box scores of Clinical Dementia Rating (CDR-SB) 5.1. Based on the well-structured, nationwide, and hospital-based registry, this study provides the unique clinical characteristics of AD and emphasizes the importance of vascular factors in AD in Korea

Ischemic and Bleeding Events Associated with Thrombocytopenia and Thrombocytosis after Percutaneous Coronary Intervention in Patients with Acute Myocardial Infarction

The early and late ischemic and bleeding clinical outcomes according to baseline platelet count after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) remain unclear. Overall, 10,667 patients from the Cardiovascular Risk and identification of potential high-risk population in AMI (COREA-AMI) I and II registries were classified according to the following universal criteria on baseline platelet counts: (1) moderate to severe thrombocytopenia (platelet \u3c 100 K/µL, n = 101), (2) mild thrombocytopenia (platelet = 100~149 K/µL, n = 631), (3) normal reference (platelet = 150~450 K/µL, n = 9832), and (4) thrombocytosis (platelet \u3e 450 K/µL, n = 103). The primary endpoint was the occurrence of major adverse cardiovascular events (MACE). The secondary outcome was Bleeding Academic Research Consortium (BARC) 2, 3, and 5 bleeding. After adjusting for confounders, the moderate to severe thrombocytopenia (HR, 2.03; 95% CI, 1.49–2.78); p \u3c 0.001), mild thrombocytopenia (HR, 1.15; 95% CI, 1.01–1.34; p = 0.045), and thrombocytosis groups (HR, 1.47; 95% CI, 1.07–2.03; p = 0.019) showed higher 5-year MACE rates than the normal reference. In BARC 2, 3, and 5 bleeding outcomes, the bleedings rates were higher than the normal range in the moderate to severe thrombocytopenia (HR, 2.18; 95% CI, 1.36–3.49; p = 0.001) and mild thrombocytopenia (HR, 1.41; 95% CI, 1.12–1.78; p = 0.004) groups. Patients with AMI had higher 5-year MACE rates after PCI if they had lower- or higher-than-normal platelet counts. Thrombocytopenia revealed higher early and late bleeding rates whereas thrombocytosis showed long-term bleeding trends, although these trends were not statistically significant

Ionizing radiation modulates human macrophages towards a pro-inflammatory phenotype preserving their pro-invasive and pro-angiogenic capacities

In order to improve the efficacy of conventional radiotherapy, attention has been paid to immune cells, which not only modulate cancer cell response to therapy but are also highly recruited to tumours after irradiation. Particularly, the effect of ionizing radiation on macrophages, using therapeutically relevant doses, is not well understood. To evaluate how radiotherapy affects macrophage behaviour and macrophage-mediated cancer cell activity, human monocyte derived-macrophages were subjected, for a week, to cumulative ionizing radiation doses, as used during cancer treatment (2Gy/fraction/day). Irradiated macrophages remained viable and metabolically active, despite DNA damage. NF-kappaB transcription activation and increased Bcl-xL expression evidenced the promotion of pro-survival activity. A significant increase of pro-inflammatory macrophage markers CD80, CD86 and HLA-DR, but not CCR7, TNF and IL1B was observed after 10Gy cumulative doses, while anti-inflammatory markers CD163, MRC1, VCAN and IL-10 expression decreased, suggesting the modulation towards a more proinflammatory phenotype. Moreover, ionizing radiation induced macrophage morphological alterations and increased their phagocytic rate, without affecting matrix metalloproteases (MMP)2 and MMP9 activity. Importantly, irradiated macrophages promoted cancer cell-invasion and cancer cell-induced angiogenesis. Our work highlights macrophage ability to sustain cancer cell activities as a major concern that needs to be addressed to improve radiotherapy efficacy

A Novel Core Genome-Encoded Superantigen Contributes to Lethality of Community-Associated MRSA Necrotizing Pneumonia

Bacterial superantigens (SAg) stimulate T-cell hyper-activation resulting in immune modulation and severe systemic illnesses such as Staphylococcus aureus toxic shock syndrome. However, all known S. aureus SAgs are encoded by mobile genetic elements and are made by only a proportion of strains. Here, we report the discovery of a novel SAg staphylococcal enterotoxin-like toxin X (SElX) encoded in the core genome of 95% of phylogenetically diverse S. aureus strains from human and animal infections, including the epidemic community-associated methicillin-resistant S. aureus (CA-MRSA) USA300 clone. SElX has a unique predicted structure characterized by a truncated SAg B-domain, but exhibits the characteristic biological activities of a SAg including Vβ-specific T-cell mitogenicity, pyrogenicity and endotoxin enhancement. In addition, SElX is expressed by clinical isolates in vitro, and during human, bovine, and ovine infections, consistent with a broad role in S. aureus infections of multiple host species. Phylogenetic analysis suggests that the selx gene was acquired horizontally by a progenitor of the S. aureus species, followed by allelic diversification by point mutation and assortative recombination resulting in at least 17 different alleles among the major pathogenic clones. Of note, SElX variants made by human- or ruminant-specific S. aureus clones demonstrated overlapping but distinct Vβ activation profiles for human and bovine lymphocytes, indicating functional diversification of SElX in different host species. Importantly, SElX made by CA-MRSA USA300 contributed to lethality in a rabbit model of necrotizing pneumonia revealing a novel virulence determinant of CA-MRSA disease pathogenesis. Taken together, we report the discovery and characterization of a unique core genome-encoded superantigen, providing new insights into the evolution of pathogenic S. aureus and the molecular basis for severe infections caused by the CA-MRSA USA300 epidemic clone