No abstract available.
Democratic People's Republic of Korea* ; Health Services*

No abstract available.
Rickets*

No abstract available.
Dentigerous Cyst*

The pharmacological therapy of cardiac arrhythmias is still challenging. As is well known, antiarrhythmic drugs have a narrow therapeutic-toxic window and can induce lethal proarrhythmia (antiarrhythmic drug-induced arrhythmia). The harmful effect of antiarrhythmic drug was proven by CAST and so many clinical trials. Thus we need strict indications for prescription and objective parameters for monitoring of the drug action and side effects. The cardiac arrhythmias are classified as ectopic beats, bradyarrhythmia, and tachyarrhythmia. The main target of antiarrhythmic drugs is tachyarrhythmia. The clinical role of antiarrhythmic drugs is the acute conversion of arrhythmia to sinus rhythm and the chronic suppression/prevention of tachycardia. The cardiac arrhythmia (arrhythmogenesis) occurs in harmony of 3 components, namely, substrate, precipitating (modulating) factors, and trigger. The acute modification of arrhythmogenic environment by drug may be efficient, but the chronic suppression of arrhythmia only by the drug may not be complete. Recently, the clinical role of chronic drug therapy is replaced by RFCA (in patients with SVT except atrial fibrillation) and ICD (VT/SCD). The antiarrhythmic drugs are usually classified into Class I (sodium channel blocker), Class II (beta-blocker), Class III (potassium channel blocker), Class IV (calcium channel blocker), and others (digoxin and adenosine), according to Vaughn-Williams suggestion. Nowadays, the clinical electrophysiologist reclassified the agents into calcium channel-dependent drug (Class II, IV, digoxin, and adenosine) and sodium/potassium channel-dependent drug (Class I and III). The drug is effective only when the concentration in blood or tissue is sufficient to modify the arrhythmogenic substrate. We need to know the pharmacokinetic and pharmacodynamic properties of antiarrhythmic drugs exactly. We can expect the blood concentration of a drug if we know the elimination half-life and the dosing schedule of the drug because most drugs (including antiarrhythmic agents) have the first-order (elimination) kinetic. For a new steady-state of drug concentration, we should wait for 3 to 4 times of the half-life after changing the dosage (prescription). Finally, the consideration and management of the underlying heart disease and precipitating/modulating factors are needed for the effective antiarrhythmic drug therapy.
Anti-Arrhythmia Agents ; Appointments and Schedules ; Arrhythmias, Cardiac ; Bradycardia ; Calcium ; Digoxin ; Drug Therapy ; Half-Life ; Heart Diseases ; Humans ; Prescriptions ; Tachycardia

No abstract available.
Adrenal Hyperplasia, Congenital* ; Genetic Association Studies*

No abstract available.
Ghrelin* ; Prader-Willi Syndrome*

No abstract available.
Ghrelin* ; Prader-Willi Syndrome*

Objective To analyse the therapeutic effect of Carvedilol in patients with severe heart failure.Methods The clinical data of 89 Carvedilol patients treated with dilated cardiomyopathy were retrospective analysis.Results The overall therapeutic effective rate was 98.88％,because of one death related to discontinued use of medication.Before and after treatment,systolic left ventricular cavity diameter (LVDD) were (68.25 ± 2.15) mm,(56.89 ±4.21) mm,respectively,and left ventricular ejection fraction(LVEF) were (28.63 ±0.33)％,(40.56 ±3.98) ％,respectively,there were significantly differences (t =7.215,16.877,all P ＜ 0.05).Conclusion Carvedilol is the cornerstone in the drug treatments of patients with dilated cardiomyopathy.

Objective To explore the expression of cathepsin L in hepatocellular carcinoma and to analyze its relationship with clinical and pathological features. Methods Fifty-eight specimens of hepatocellular carcinoma were studied, including 18 well-differentiated, 18 moderately differentiated and 22 poorly differentiated. Classified by TNM clinical stage, 26 were in Ⅰ/Ⅱ stage and 32 in Ⅲ/Ⅳ stage. The expressions of cathepsin L were detected with immunohistochemistry and RT-PCR. Their relationship with the clinical and pathological features of hepatocellular carcinoma was analyzed. Results The positive rate of cathepsin L protein was 72.4% (42/58), and the expressions of cathepsin L protein were significantly different among the specimens of pathological grades of tumor, of TNM clinical stages and with/without metastasis. The positive rate of cathepsin L mRNA was 65.5% (38/58). The expression of cathepsin L mRNA in hepatocellular carcinoma was correlated with pathological grades of tumor, TNM clinical stages and lymph node metastasis. Conclusion Cathepsin L plays an important role in the occurrence of hepatocellular carcinoma for its correlation with infiltration and metastasis of hepatocellular carcinoma. Cathepsin L can be used as a useful marker for the prognosis of hepatocellular carcinoma patients.

Objective To investigate the effect of natriuretic peptide on vascular endothelial function and inflammatory factors of patients with heart failure complicating myocardial infarction.Methods Two hundred and twenty-six patients with heart failure complicating myocardial infarction admitted into Hanzhong Central Hospital from March 2012 to March 2016 were randomly divided into experimental group (n =138) and control group (n =128).Patients in control group were treated with conventional drug,and patients in experimental group were treated with natriuretic peptide based on conventional drug treatment.The vascular endothelial function,contents of NO and eddthelin 1,and inflammatory factors including CRP,IL-6,and TNF-α were detected.Results After 2 weeks of treatment,the flow-mediated vasodilation (FMD) and NO in experimental group were remarkably higher than those in control group,and eddthelin 1 was significantly lower than those of control group (P ＜ 0.05).Additionally,CRP,IL-6,and TNF-α in experimental group were significantly lower than those in control group after treatment for 5 d (P ＜ 0.05).Conclusion Natriuretic peptide could improve the vascular endothelial function of patients with heart failure complicating myocardial infarction via increasing the content of NO and decreasing content of eddthelin 1,and was benefit to cardiac function by inhibiting release of inflammatory factors.