The incidence of gastric cancer is high in old age group and low in young age group, extremely rare in child age. So the diagnosis of gastric cancer in young age is often delayed, and this, with other factors such as poorly differentiated histopathologic tendency and rapid growing nature, makes the prognosis poorer than in other age guoup. Therefore it should always be remembered that the young who has gastric symptom may have malignancy in his stomach in spite of the age. We report a case of early gastric cancer in a 16-years old male with the review of the literature.
Adolescent ; Child ; Diagnosis ; Humans ; Incidence ; Male ; Prognosis ; Stomach ; Stomach Neoplasms*

BACKGROUND: Pericardiocentesis is not routinely recommended in most patients with pericardial effusion (PE), except for patients with cardiac tamponade. However, the long-term follow-up results in patients with clinically not significant PE are few. METHODS: Sixty-five consecutive patients (mean age:57 yrs, 26 males) out of 87 patients with PE, who were clinically not serious, were studied prospectively once in every two month for mean 6 months (2-12 months) without any specific treatment. The amount of PE was measured at the enddiastole period of parasternal long axis view and apical four chamber view. RESULTS: The incidence of insignificant PE in our echocardiographic laboratory is 3.4% (n=87 from 2461). The maximal accumulation site of PE was posterior (n=51, 79%). The next is anterior (n=11, 17%) and right ventricular side (3, 5%). The amount of PE is less (0.37+/-0.17cm vs 0.64+/-0.54cm, p=0.018) in localized PE (n=24, 37%) than that of diffuse form (n=41, 63%), which spreads to more than 2 chambers. The presumptive etiologies of PE were unknown (n=41), heart failure (n=5), myocardial infarction (n=6), viral (n=3), and others (n=10). The amount of PE was decreased from 0.54+/-0.46 cm to 0.30+/-0.26 cm, 0.23+/-0.24 cm, and 0.21+/-0.23 cm 2, 4, and 6 months after intial evaluation, respectively, without any complication. CONCLUSION: The patients with PE, not combining >KERN= Axis, Cervical Vertebra ; Cardiac Tamponade ; Echocardiography ; Follow-Up Studies* ; Heart Failure ; Humans ; Incidence ; Myocardial Infarction ; Pericardial Effusion* ; Pericardiocentesis ; Prospective Studies

6-Hydroxydopamine (6-OHDA) is a neurotoxin and is commonly used to generate experimental models of Parkinson's disease (PD). In this study, we investigated the signaling molecules involved in the 6-OHDA-induced cell death using a neuronal catecholaminergic cell line (SK-N-SH cells), and the protective effect of fustin, a flavonoid from Rhus verniciflua Stokes, on 6-OHDA-induced neuronal death. 6-OHDA significantly increased levels of reactive oxygen species (ROS), intracellular Ca2+ ([Ca2+](i)), and p38 phosphorylation. In addition, this ROS increase by 6-OHDA was reduced by pretreatment with N-acetylcysteine (NAC), a free radical scavenger, but not by bis-(o-aminophenoxy)-ethane-N,N,N,N-tetraacetic acid (BAPTA), a Ca2+ chelator. However, the [Ca2+](i) increase induced by 6-OHDA was suppressed by NAC. Moreover, pretreatment with NAC or BAPTA significantly prevented the 6-OHDA-induced increases in p38 phosphorylation, Bax/Bcl-2 ratio, and caspase-3 activity. Although 6-OHDA-increased phosphorylation of p38 was prevented by NAC or BAPTA, inhibition of p38 by SB203580 did not suppress ROS, Bax/Bcl-2 ratio, or caspase-3 activity increases, and only partially prevented 6-OHDA-induced cell death, thus demonstrating that p38 activation is a component of a signaling pathway leading to the initiation of 6-OHDA-induced cell death, which acts in parallel with an ROS-Ca2+ -Bcl-2-caspase-3 pathway. Moreover, fustin not only suppressed 6-OHDA-induced cell death in a concentration-dependent manner but also blocked 6-OHDA-induced increases in ROS, [Ca2+](i), Bax/Bcl-2 ratio, caspase-3 activity, and p38 phosphorylation. These results suggest that fustin exerts neuroprotection against 6-OHDA-induced cell death.
Acetylcysteine/pharmacology ; Apoptosis ; Calcium/metabolism ; Caspase 3/metabolism ; Cell Death/drug effects ; Cell Line, Tumor ; Cytoprotection ; Egtazic Acid/analogs & derivatives/pharmacology ; Enzyme Activation ; Flavonoids/*pharmacology ; Humans ; Imidazoles/pharmacology ; Neurons/cytology/*drug effects ; Oxidopamine/*toxicity ; Phosphorylation ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Pyridines/pharmacology ; Reactive Oxygen Species/metabolism ; Rhus/*chemistry ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism

The powers of the low-frequency(LF) and high-frequency(HF) components characterizing heart rate variability (HRV) appear to reflect, in their reciprocal relationship, changes in the state of the sympatho-vagal balance occurring during orthostatic stress with head-up tilt. We studied 24 healthy volunteers (median age, 23.1 years) who were subjected after a rest period to a series of passive head-up tilt steps chosen from the following angles: 0 degree. 15 degrees, 30degrees, 45degrees, 70degrees, and 90degrees under the condition of frequency controlled respiration(0.25Hz) in order to get data of the Korean young adults. During head-up tilt, heart rate and normalized low frequency power(LF(N : 0.05-0.15 Hz) of HRV showed significant increase(p=0.000), but normalized high frequency power(HFN : 0.2-0.3 Hz) and total power showed progressive decrease(p=0.000, p<0.01 respectively). Male showed significantly higher LF(N and lower HFN than female at tilt table angle 0degree(p<0.01). Power spectral analysis of HRV appears to be capable of providing a noninvasive quantitatibve evaluation of graded changes in the state of the sympatho-vagal balance.
Female ; Healthy Volunteers ; Heart Rate* ; Heart* ; Humans ; Male ; Young Adult*

Human SIRT1 controls various physiological responses including cell fate, stress, and aging, through deacetylation of its specific substrate protein. In processing DNA damage signaling, SIRT1 attenuates a cellular apoptotic response by deacetylation of p53 tumor suppressor. The present study shows that, upon exposure to radiation, SIRT1 could enhance DNA repair capacity and deacetylation of repair protein Ku70. Ectopically over-expressed SIRT1 resulted in the increase of repair of DNA strand breakages produced by radiation. On the other hand, repression of endogenous SIRT1 expression by SIRT1 siRNA led to the decrease of this repair activity, indicating that SIRT1 can regulate DNA repair capacity of cells with DNA strand breaks. In addition, we found that SIRT1 physically complexed with repair protein Ku70, leading to subsequent deacetylation. The dominant-negative SIRT1, a catalytically inactive form, did not induce deacetylation of Ku70 protein as well as increase of DNA repair capacity. These observations suggest that SIRT1 modulates DNA repair activity, which could be regulated by the acetylation status of repair protein Ku70 following DNA damage.
Sirtuins/genetics/*metabolism ; RNA, Small Interfering/genetics ; Humans ; DNA-Binding Proteins/*metabolism ; DNA Repair/*genetics ; DNA/*genetics ; Cell Line ; Antigens, Nuclear/*metabolism ; Acetylation