No abstract available.
Diagnosis* ; Low Back Pain*

No abstract available.

Catheter-based techniques to treat coronary artery diseases have been developed rapidly during the past half a century. After the first performance in 1977, the percutaneous transluminal coronary angioplasty has attained clinical relevance and become a viable option for medical and surgical treatment in patients with a coronary artery disease. However, the high incidence of acute closure and restenosis following balloon angioplasty limits its widespread use. Among the various medical and technical efforts to prevent the untoward effects of balloon angioplasty, coronary artery stenting was most successful and has been the turning point in the management of coronary occlusive diseases in 1990's. Intravascular ultrasound and doppler pressure wire have facilitated the optimal procedure of coronary stenting. However, the stent restenosis and in-stent restenotic lesion present a new and an even more challenging dilemma due to the widespread use of coronary stent. With better understanding of pathophysiology of stent restenosis, new approaches and therapies are encouraged and provide unique insight in the treatment of restenosis. Intracoronary brachytherapy with beta- and gamma-radiation was successful in decreasing the occurrence of in-stent restenotic lesions. Drug-eluting stents using various antiproliferative drugs are the most exciting modality in preventing restenosis and are currently under clinical trials. Newer percutaneous coronary interventional techniques including gene therapy and targeted drug delivery are also under investigation. This article presents the review of the current practice of percutaneous coronary intervention in the treatment of coronary occlusive diseases.
Angioplasty, Balloon ; Angioplasty, Balloon, Coronary ; Arteries ; Brachytherapy ; Coronary Artery Disease ; Drug-Eluting Stents ; Genetic Therapy ; Humans ; Incidence ; Myocardial Ischemia* ; Percutaneous Coronary Intervention* ; Stents ; Ultrasonography

No abstract available.
Intercellular Signaling Peptides and Proteins*

As degenerative changes of lumbar spine and surrounding structures progress with aging, the strength of not only the bony tissues but also the supporting structures become weak and dysfunctional with pain. This phenomenon is increasingly evident as elderly population increases rather progressively in contemporary era. Therefore, the chronic back pain in this subpopulation group is relatively common and comprise of various pain syndromes originating from vertebral bodies, joints, muscles, and other soft tissues. The causes of chronic low back pain in elders also differ patient to patient. but common presentations seen in clinical setting are disorders related to intervertebral disc, spinal stenosis, spondylolisthesis, compression fracture related to osteoporosis, and pain originating from zygapophysial joints and other surrounding structures. Less common but other important causes include metastatic lesions, infection, and myofacical pain syndromes. Here, evidence-based literature review on common disorders affecting elderly patients causing chronic low hack pain is presented with special attention focused on diagnostic and therapeutic approaches based on etiologic processes and clinical presentations Every effort should be made to contemplate all possible factors that might have played roles in generating the chronic pain in these patients. Also, whatever management chosen it should have been decided based upon the clinical presentation that closely correlated with definitive findings from studies best available whenever possible.
Aged ; Aging ; Back Pain ; Chronic Pain ; Diagnosis ; Fractures, Compression ; Humans ; Intervertebral Disc ; Joints ; Low Back Pain* ; Muscles ; Osteoporosis ; Spinal Stenosis ; Spine ; Spondylolisthesis

No abstract available.
Acute Coronary Syndrome*

No abstract availalbe.
Diabetes Mellitus* ; Humans ; Stents*

PURPOSE: Among children who visited hospital because of short stature, malnutrition-related short stature(MRSS) is often observed. Most of these children showed significantly decreased appetite without medical cause. Leptin is a very important weight regulating protein through a feedback signal between adipose tissue and the satiety center. IGF-I and insulin are also very important weight regulating hormones with adipogenic and somatotropic effects. Therefore, we have undertaken this study to examine the levels of leptin, IGF-I and insulin in MRSS and to analyze the relationship among these growth factors. METHODS: Twenty children more than 5 years old, who visited Sanggye Paik Hospital due to poor growth were enrolled. Their weight and height are less than 10 percentile of the Korean weight standard curve. All subjects had no organic disorders and their growth hormone levels were normal. Twenty healthy children whose height and weight were between the 25-75 percentiles were enrolled as a control group. The serum levels of leptin, IGF-I and insulin were measured by RIA method. RESULTS: 1)Leptin concentration was significantly lower in the MRSS than in the control group(2.35+/-1.05 vs 3.20+/-2.31 ng/mL, P<0.05, Fig. 1). 2)IGF-I concentration was significantly lower in the MRSS than in the control group(176.4+/-93.1 vs 258.2+/-221.3 ng/mL, P<0.05, Fig. 2). 3)Insulin concentration was lower in the MRSS than in the control group but showed no significant differences(17.9+/-13.9 vs 21.8+/-14.0 microIU/mL, Fig. 3). 4)Leptin was positively correlated with body weight(r=0.49, P<0.05) and BMI (r=0.55, P=0.01) in the control group, but was not correlated in the MRSS group. 5)IGF-I was positively correlated with body weight(r=0.61, P<0.05) and height (r=0.56, P<0.05) and BMI(r=0.50, P=0.05) in the control group, but was not correlated in the MRSS group. 6)There were no correlations among leptin, IGF-I and insulin both in the control and MRSS group. CONCLUSION: We speculate that low leptin and IGF-I concentrations in MRSS group might be related to the result of a poor nutritional state and might be an adaptive mechanism to reduce energy expenditure to increase appetite. To elucidate the underlying mechanism of poor appetite and adaptational changes of leptin, IGF-I and insulin, further studies with more cases are needed.
Adipose Tissue ; Appetite* ; Child* ; Child, Preschool ; Energy Metabolism ; Growth Hormone ; Humans ; Insulin* ; Insulin-Like Growth Factor I* ; Intercellular Signaling Peptides and Proteins ; Leptin*

No abstract available.
Growth Hormone*

No abstract available.
Erythropoietin* ; Humans ; Kidney Failure, Chronic*