No abstract available.
Diagnosis* ; Spondylarthropathies*

No abstract availalble.
Humans ; Lupus Erythematosus, Systemic* ; Pregnancy*

No abstract available.

No abstract available.
Hepatitis* ; Polymyositis*

Systemic lupus erythematosus is a prototype of systemic autoimmune disease which is characterized by polyclonal B cell activation and production of various autoantibodies, especially antibodies against nucleosome. The pathogenesis of lupus does not depend on a single gene defect but depend on multiple genetic and environmental factors. Lately defects of apoptosis have been focused as a potential etiologic factor of systemic autoimmune diasease. Apoptosis is an active programmed cell death which removes unwanted cells without any inflammatory sequelae. Cells of immune system are programmed to be deleted unless recruited into appropriate immune response. The fate of certain cell may be controlled by the balance between cell death signals and survival signals for each cells. The importance of these pathways in maintaining tolerance is highlighted by the development of lupus-like disease in three different mouse strains that have spontaneous mutations in the Fas or its ligand. We have a lot of reports on the relationship between apoptosis and systemic lupus erythematosus in terms of pathogenesis after then. We need to review all information on apoptosis and lupus and find appropriate direction toward research and clinical aspect, even though we don t have complete knowledge on signal transduction and regulators of apoptosis. Here relationships between systemic lupus erythematosus and apoptosis were reviewed on a few different viewpoints : 1) too little apoptosis of immune cell, 2) accelerated spontaneous apoptosis and nucleosome secretion, 3) defective phagocytosis of macrophage, 4) relationship between antiphospholipid antibody and apoptosis.
Animals ; Antibodies ; Antibodies, Antiphospholipid ; Apoptosis* ; Autoantibodies ; Autoimmune Diseases ; Cell Death ; Immune System ; Lupus Erythematosus, Systemic* ; Macrophages ; Mice ; Nucleosomes ; Phagocytosis ; Signal Transduction

Cigarette smoke is a complex mixture of 4,000 chemical compounds, including 43 known carcinogens. It is well known that smoke acts as the initiator and promoter in the process of carcinogenesis, and the risk of cancer is directly proportional to the amount and duration of smoking. Tobacco is the cause of 30% of all cancer deaths and one of the major risk factors for coronary heart disease, along with high blood pressure and hyperlipidemia. Cigarette smoking is estimated to be responsible for more than 20% of all coronary heart disease deaths in men over 86 years of age and for approximately 45% of such deaths in men aged less than 65 years. About 80% of mortality from chronic obstructive lung disease is attributable to cigarette smoking, and the age-adjusted death rate for COPD is 10-times higher in current smokers than in nonsmokers. Peptic ulcer disease, osteoporosis, skin wrinkling, and retarded fetal growth are all associated with cigarette smoking. Through passive smoking, 69% of individuals develop eye irritation, 29% have nasal symptoms, 32% have headaches, and 25% develop a cough. The infant admission rate increases with mother’s smoking amount, and the relative risk of lung cancer is 1.8 in smoker’s spouse. Tobacco is the single, chief, avoidable cause of death in our society, and the most important public issue of our time.
Carcinogenesis ; Carcinogens ; Cause of Death ; Coronary Disease ; Cough ; Fetal Development ; Headache ; Humans ; Hyperlipidemias ; Hypertension ; Infant ; Lung Neoplasms ; Male ; Mortality ; Osteoporosis ; Peptic Ulcer ; Pulmonary Disease, Chronic Obstructive ; Risk Factors ; Skin Aging ; Smoke ; Smoking* ; Spouses ; Tobacco ; Tobacco Products* ; Tobacco Smoke Pollution

No abstract available.
Arthritis, Rheumatoid*

No abstract available.

No abstract available.
Asthma* ; Theophylline*

No abstract available.