BACKGROUND AND OBJECTIVE: Many chemical mediators such as histamine, prostaglandins, leukotrienes, bradykinin, angiotensisn II (A II), and even angiotensin converting enzyme (ACE) affect the pathophysiology of asthma. ACE exists in the epithelium, endothelium, neuroepithelium, plasma, and especially in high concentrations in human lung tissue. ACE converts A I to A II, which is highly vasoconstrictive, bronchoconstrictive, inflammatory substance, and can also inactivate bradykinin. ACE polymorphism determines the level of ACE such as DD, higher concentration of ACE, but II, lowest concentration of that, so in DD type, the level of A II increase, but that of bradykinin decrease. From that point we can speculate polymorphism of ACE gene anyhow affects asthma, so we carried out this study for evaluating relationships between the ACE genotype distribution and genesis and severity of asthma in Korean adult asthmatics. MATERIALS AND METHODS: The study population consisted of 150 asthmatics, 57 patients of non asthmatic lung diseases including lung cancer (n=10), pulmonary tuberculosis (n=27), empyema (n=3), pneumonia (n=11), bronchiectasis (n=5) and lung abscess (n=1) and 100 normal healthy subjects without hypertension, cardiovascular disease, diabetes mellitus and nephropathy which may bias the result. Bronchial asthmatics were classified into 3 groups according to the criteria of the NAPE. PCR (polymerase chain reaction) for ACE genotypes was performed. PCR products were electrophoresed in 1% agarose gels, and then DNA pattern was directly visualized under ethidium bromide staining. RESULTS: The frequency for II, ID, and DD genotypes were 46 (46%), 38 (38%), 16 (16%) in control group, 59 (39.6%), 74 (49.5%), 17 (10.9%) in asthma group and 28 (49.1%), 24 (42.1%), 5 (8.8%) in non-bronchial lung disease group, respectively. There was no signi- ficant difference in frequency of ACE genotype distribution among the 3 groups (p > 0.05). The frequency for II, ID, and DD genotypes in the 3 groups of asthmatics were 17 (34%), 27 (54%), 6 (12%) in mild subset, 13 (26%), 30 (60%), 7 (14%) in moderate subset, and 11 (22%), 33 (66%), 6 (12%) in severe subset. Even though there was also no significant difference among the 3 severity subsets in the asthma group, the frequency of non-DD subsets such as II and ID was higher in moderate and severe asthmatics. CONCLUSION: The results suggest that ACE gene polymorphism dose not affect the genesis but can progress asthma in Korean adult asthmatics. However, further mass studies on asthmatics will be needed to clarify the effect of ACE polymorphism on the severity of Korean adult asthmatics.
Adult* ; Angiotensin I* ; Angiotensins* ; Asthma* ; Bias (Epidemiology) ; Bradykinin ; Bronchiectasis ; Cardiovascular Diseases ; Diabetes Mellitus ; DNA ; Empyema ; Endothelium ; Epithelium ; Ethidium ; Gels ; Genotype ; Histamine ; Humans ; Hypertension ; Leukotrienes ; Lung ; Lung Abscess ; Lung Diseases ; Lung Neoplasms ; Peptidyl-Dipeptidase A* ; Plasma ; Pneumonia ; Polymerase Chain Reaction ; Prostaglandins ; Sepharose ; Tuberculosis, Pulmonary

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Cardiac disease is the second leading cause of mortality in Korea and the main cardiac disease is acute myocardial infarction (MI). Timely primary coronary intervention is the main treatment for acute MI and delay from symptom onset to intervention is the most important determinant of the prognosis and incidence of ischemic cardiomyopathy after acute MI. Treatment delay includes patient delay and system delay. The latter includes transfer and in-hospital delays. In-hospital delay improved greatly after introducing the critical pathway to Korea. However, there is still much room to improve patient and transfer delay.

Cardiac disease is the second leading cause of mortality in Korea and the main cardiac disease is acute myocardial infarction (MI). Timely primary coronary intervention is the main treatment for acute MI and delay from symptom onset to intervention is the most important determinant of the prognosis and incidence of ischemic cardiomyopathy after acute MI. Treatment delay includes patient delay and system delay. The latter includes transfer and in-hospital delays. In-hospital delay improved greatly after introducing the critical pathway to Korea. However, there is still much room to improve patient and transfer delay.

Sodium-glucose cotransporter 2 (SGLT2) inhibitors have transformed the treatment of both cardiovascular and renal diseases. Although originally developed for glycemic control in type 2 diabetes mellitus, these agents have demonstrated significant benefits by reducing cardiovascular events and slowing the progression of kidney disease, even in patients without diabetes. Landmark trials, including EMPA-REG OUTCOME, CANVAS, DECLARE-TIMI 58, and DAPA-HF, consistently demonstrated reductions in heart failure hospitalizations and renal deterioration among patients at high cardiovascular risk. However, many of these studies excluded patients with advanced chronic kidney disease (CKD), limiting the generalizability of their findings for this population. More recent investigations, such as CREDENCE, DAPA-CKD, and EMPA-KIDNEY, have focused on patients with CKD and confirmed that SGLT2 inhibitors offer significant renal and cardiovascular protection regardless of diabetic status. This review summarizes key clinical trials, outlining their design and outcomes with a particular emphasis on inclusion and exclusion criteria and the implications for CKD populations. Further, it discusses the practical application and safety considerations of SGLT2 inhibitors in nephrology, underscoring their emerging role as a fundamental therapeutic strategy in CKD management.

Cardiac disease is the second leading cause of mortality in Korea and the main cardiac disease is acute myocardial infarction (MI). Timely primary coronary intervention is the main treatment for acute MI and delay from symptom onset to intervention is the most important determinant of the prognosis and incidence of ischemic cardiomyopathy after acute MI. Treatment delay includes patient delay and system delay. The latter includes transfer and in-hospital delays. In-hospital delay improved greatly after introducing the critical pathway to Korea. However, there is still much room to improve patient and transfer delay.