• Publications of The Korean Astronomical Society
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• v.32 no.1
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• pp.117-121
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• 2017

We show Akari data, Herschel data and data from the SCUBA2 camera on JCMT, of molecular clouds. We focus on pre-stellar cores within the clouds. We present Akari data of the L1147-1157 ring in Cepheus and show how the data indicate that the cores are being externally heated. We present SCUBA2 and Herschel data of the Ophiuchus region and show how the environment is also affecting core evolution in this region. We discuss the effects of the magnetic field in the Lupus I region, and how this lends support to a model for the formation and evolution of cores in filamentary molecular clouds.

• Childhood Kidney Diseases
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• v.19 no.1
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• pp.43-47
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• 2015

Hemolytic anemia and thrombocytopenia are rare clinical manifestations of acute glomerulonephritis. Initially, in all such cases, a diagnosis of hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, systemic lupus erythematosus, and amyloidosis should be ruled out. The presence of hemolytic anemia and thrombocytopenia is rare, but possible, in a case of acute poststreptococcal glomerulonephritis, and may result in delayed diagnosis or misdiagnosis. Correct and timely diagnosis would ensure adequate treatment in such patients. We report of a 22-month-old boy with acute glomerulonephritis coexistent with hemolytic anemia and idiopathic thrombocytopenia.

• Bulletin of the Korean Space Science Society
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• 2005.04a
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• pp.30-30
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• 2005

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.1-15
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• 2018

Inflammasomes are intracellular multiprotein complexes that coordinate anti-pathogenic host defense during inflammatory responses in myeloid cells, especially macrophages. Inflammasome activation leads to activation of caspase-1, resulting in the induction of pyroptosis and the secretion of pro-inflammatory cytokines including interleukin $(IL)-1{\beta}$ and IL-18. Although the inflammatory response is an innate host defense mechanism, chronic inflammation is the main cause of rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and $Sj{\ddot{o}}gren^{\prime}s$ syndrome (SS). Since rheumatic diseases are inflammatory/autoimmune disorders, it is reasonable to hypothesize that inflammasomes activated during the inflammatory response play a pivotal role in development and progression of these diseases. Indeed, previous studies have provided important observations that inflammasomes are actively involved in the pathogenesis of inflammatory/autoimmune rheumatic diseases. In this review, we summarize the current knowledge on several types of inflammasomes during macrophage-mediated inflammatory responses and discuss recent research regarding the role of inflammasomes in the pathogenesis of inflammatory/autoimmune rheumatic diseases. This avenue of research could provide new insights for the development of promising therapeutics to treat inflammatory/autoimmune rheumatic diseases.

• Journal of Veterinary Clinics
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• v.34 no.6
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• pp.434-436
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• 2017

Nine dogs with history of lameness and anorexia were presented. On physical examination, all dogs had gait abnormality and six dogs had high body temperature. Their clinical signs were mostly episodic, and only non-specific symptoms were occasionally observed. Arthrocentesis was performed in all dogs, and immune-mediated polyarthritis (IMPA) was diagnosed. Definitive rheumatoid arthritis (RA) and systemic lupus erythematous (SLE) were diagnosed in one dogs, one each. Prednisolone (PDS) was chosen as the first-line therapy for all dogs, except for the one with RA. Most cases responded to PDS but some cases including those of SLE and RA were refractory to PDS. IMPA can be challenging to diagnose due to its vague symptom and is commonly implicated in 'fever of unknown origin'. Therefore, clinicians should consider IMPA as a differential diagnosis when the patient has fever with systemic, non-specific signs, such as anorexia and depression, but does not respond to antibiotics.

• Journal of Trauma and Injury
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• v.33 no.2
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• pp.112-118
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• 2020

In trauma patients, coagulopathy and abnormal increases or decreases in cell counts are frequently observed, and are associated with high mortality and morbidity in the acute phase of trauma. Because major trauma is often life-threatening, and hematologic abnormalities are multi-factorial and transient, major blood loss is usually suspected to be the primary cause of these abnormalities, and much time and cost may be spent attempting to identify a focus of hemorrhage that might or might not actually exist. Persistent abnormalities in the complete blood count, however, require clinical suspicion of other hematologic diseases to minimize improper transfusions and to improve outcomes, including mortality. Physicians at trauma centers should be familiar with the clinical characteristics of hematologic diseases and should consider these diseases in trauma patients. In this report, we present cases of two hematologic disorders found in trauma patients: autoimmune hemolytic anemia induced by systemic lupus erythematosus and myelodysplastic syndrome.

• Tuberculosis and Respiratory Diseases
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• v.74 no.4
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• pp.151-162
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• 2013

Diffuse alveolar hemorrhage (DAH) is a life-threatening and medical emergency that can be caused by numerous disorders and presents with hemoptysis, anemia, and diffuse alveolar infiltrates. Early bronchoscopy with bronchoalveolar lavage is usually required to confirm the diagnosis and rule out infection. Most cases of DAH are caused by capillaritis associated with systemic autoimmune diseases such as anti-neutrophil cytoplasmic antibody-associated vasculitis, anti-glomerular basement membrane disease, and systemic lupus erythematosus, but DAH may also result from coagulation disorders, drugs, inhaled toxins, or transplantation. The diagnosis of DAH relies on clinical suspicion combined with laboratory, radiologic, and pathologic findings. Early recognition is crucial, because prompt diagnosis and treatment is necessary for survival. Corticosteroids and immunosuppressive agents remain the gold standard. In patients with DAH, biopsy of involved sites can help to identify the cause and to direct therapy. This article aims to provide a general review of the causes and clinical presentation of DAH and to recommend a diagnostic approach and a management plan for the most common causes.

• Clinical and Experimental Pediatrics
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• v.53 no.2
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• pp.136-145
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• 2010

Natural killer T (NKT) cell is a special type of T lymphocytes that has both receptor of natural killer (NK) cell (NK1.1, CD161c) and T cell (TCR) and express a conserved or invariant T cell receptor called $V{\alpha}14J{\alpha}18$ in mice or Va24 in humans. Invariant NKT (iNKT) cell recognizes lipid antigen presented by CD1d molecules. Marine-sponge-derived glycolipid, ${\alpha}-galactosylceremide$ (${\alpha}-GalCer$), binds CD1d at the cell surface of antigen-presenting cells and is presented to iNKT cells. Within hours, iNKT cells become activated and start to secrete Interleukin-4 and $interferon-{\gamma}$. NKT cell prevents autoimmune diseases, such as type 1 diabetes, experimental allergic encephalomyelitis, systemic lupus erythematous, inflammatory colitis, and Graves' thyroiditis, by activation with ${\alpha}-GalCer$. In addition, NKT cell is associated with infectious diseases by mycobacteria, leshmania, and virus. Moreover NKT cell is associated with asthma, especially CD4+ iNKT cells. In this review, I will discuss the characteristics of NKT cell and the association with inflammatory diseases, especially asthma.

• Clinical and Experimental Pediatrics
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• v.58 no.7
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• pp.239-244
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• 2015

The complement system is part of the innate immune response and as such defends against invading pathogens, removes immune complexes and damaged self-cells, aids organ regeneration, confers neuroprotection, and engages with the adaptive immune response via T and B cells. Complement activation can either benefit or harm the host organism; thus, the complement system must maintain a balance between activation on foreign or modified self surfaces and inhibition on intact host cells. Complement regulators are essential for maintaining this balance and are classified as soluble regulators, such as factor H, and membrane-bound regulators. Defective complement regulators can damage the host cell and result in the accumulation of immunological debris. Moreover, defective regulators are associated with several autoimmune diseases such as atypical hemolytic uremic syndrome, dense deposit disease, age-related macular degeneration, and systemic lupus erythematosus. Therefore, understanding the molecular mechanisms by which the complement system is regulated is important for the development of novel therapies for complement-associated diseases.

• The Bulletin of The Korean Astronomical Society
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• v.30 no.1
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• pp.31.2-31.2
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• 2005