Adenovirus Infections, Human ; pathology ; virology ; Glomerulonephritis, Membranous ; pathology ; virology ; HIV Infections ; pathology ; virology ; Hepatitis B ; pathology ; virology ; Hepatitis C ; pathology ; virology ; Herpes Zoster ; pathology ; virology ; Herpesvirus 3, Human ; isolation & purification ; Humans ; Kidney ; pathology ; virology ; Kidney Diseases ; pathology ; virology ; Nephritis, Interstitial ; pathology ; virology ; Parvoviridae Infections ; pathology ; virology ; Parvovirus B19, Human ; isolation & purification

ObjectiveTo investigate the role of caspase 3 in HMME-induced apoptosis in hypertrophic scar fibroblasts (HSFs).MethodsFibroblasts were obtained from 10 patients with untreated hypertrophic scar,and subjected to a primary culture.After 4 to 6 passages of culture,the HSFs were divided into 3 groups to remain untreated(control group),be treated with HMME followed by photodynamic therapy (HMME-PDT group),or the combination of HMME and Z-DEVD-FMK followed by photodynamic therapy (caspase 3 inhibitor group).At 12 hours after the therapy,HSFs were collected and immunofluorescence microscopy was used to observe the fluorescence intensity of caspase 3 after staining with fluorescein isocyanate (FITC) and popodium iodide (PI),flow cytometry was performed to determine the percentage of caspase 3-positive HSFs and apoptosis rate in HSFs after single staining with FITC and PI respectively.Results The fluorescence intensity of caspase 3 was weak in the control group and caspase 3 inhibitor group,but was strong in the HMME-PDT group.An increased percentage of caspase 3-positive HSFs was noted in the HMMEPDT group compared with the control group and caspase 3 inhibitor group(30.86％ ± 1.21％ vs.3.12％ ±0.28％ and 2.46％ ± 0.18％,t =19.92,21.76,both P ＜ 0.05).The apoptosis rate in HSFs was significantly higher in the HMME-PDT group and caspase 3 inhibitor group than in the control group(30.54％ ± 3.78％ and 10.46％ ± 2.15％ vs.2.45％ ± 0.22％,t =35.90,27.97,both P＜ 0.05),and higher in the HMME-PDT group than in the caspase 3 inhibitor group.ConclusionsThe apoptosis in HSFs induced by HMME-PDT is closely related to the activation of caspase 3,while caspase 3 seems to be dispensable for the apoptosis.

This paper analyse the problem of medical probation,suggests solutions with the application of new medical education methods to improve teaching quality and cultivate the high quality talents that can meet the fundmental requirement of global medical education.

No abstract available.
Temporomandibular Joint*

No abstract available.
Temporomandibular Joint*

BACKGROUND: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.
Angina, Stable ; Angina, Unstable ; Angioplasty* ; Atherosclerosis ; C-Reactive Protein* ; Coronary Artery Disease ; Humans ; Inflammation ; Troponin T

We experinced a case of 4p+ syndrome in male infant. He had multiple anomalies such as flat occiput, hypertelorism, low set malformed ear, lower anterior hair line, depressed nose, broad nasal bridge, bilateral complete cleft lip and palate, short neck, unusual position of fingers, ventricular septal defect and umblical hernia. He menifested growth and developmental retardation. Karyotype with banding revealed an extra short arm of chromosome 4. The mother's karyotype was normal. His father and father's sister had a translocation between the short arm of chromosome 4 and the short arm of chromosome 9; their karyotypes were 46, XY, t(4;9) and 46, XX, t(4;9), respectively. In this case, trisomy 4p was the result of parental balanced translocatiom. As this is the first case in Korea, it is worthwhile to report with reviewing literature.
Arm ; Chromosomes, Human, Pair 4 ; Chromosomes, Human, Pair 9 ; Cleft Lip ; Ear ; Fathers ; Fingers ; Growth and Development ; Hair ; Heart Septal Defects, Ventricular ; Hernia ; Humans ; Hypertelorism ; Infant ; Karyotype ; Korea ; Male ; Neck ; Nose ; Palate ; Parents ; Siblings ; Trisomy

Fetal echocardiography is used by means of decleration of fetal cardiac anaztomy, to estabilish the diagnosis of congenital heart disease in utero. We attemped fetal echocardiography to ninty three pregnant women after intra uterine period 24 weeks, and estimated cardiac circumference, cardiac axis, pulmonary atery root diameter, arortic root diameter, diameter of inferior vena cava, diameter of superior ve studied how these estimates associate with following gestational na cava, and fractional shortening of ventricles. We ages. Cardiac axis was on the average 37.28 degree and cardiac apex was located in anterior left side of chest area. Aortic root diameter was 0.227 GA-0.043mm (GA=gestational age) at systolic phase, 0.203 GA+0.421mm at diastolic phase. Pulmonaly root diameter was 0.271 GA-0.029mm at systolic phase, 0.251 GA-0.067mm at diastolic phase. Thoracic aorta diameter was 0.195 GA+0.109mm at systolic phase, 0.198 GA+0.794mm at diastolic phase. Fractional shortening was 0.24 (1 Standard Deviation=0.11) in right ventricle, 0.23(1 SD=0.154) at left ventricle, and so ratio of right and left ventricle was 1.04(1 SD=0.51). Once normal fetal cardiac anatomy is understood, structural defects and/or alternation of function can be evaluated antenatally.
Aorta, Thoracic ; Axis, Cervical Vertebra ; Diagnosis ; Echocardiography* ; Female ; Heart Defects, Congenital ; Heart Ventricles ; Humans ; Pregnant Women ; Thorax ; Vena Cava, Inferior

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Two phases of the effect of preconditioning has been explored, early protection and second window of protection at 24 hours. The late protection was seen in some animal model, but the precise mechanism is controversal. This study was designed to evaluate the late cardioprotective effect and role of HSP70 in ischemic preconditioning of cat heart. METHODS: Two groups of cats were studied. Control animals were subjected to an episode of 40-min coronary artery occlusion followed by 30-min reperfusion. Experimental animals were subjected to ischemic preconditioning before the 40-min ishcemia/reperfusion. The preconditioning protocol was comprised of three 5-min episodes of ischemia interspersed by 10-min episodes of reperfusion. After sustained ischemia and reperfusion, left ventricular risk area and infart area were measured by injection of Evans blue bye and triphenyltetrazolium staining, and myocardial HSP70 mRNA was examined in risk(left ventricular anterior wall) and nonrisk(left ventricular posterior wall) area using northern blot hybridization. HSP70 mRNA expression was quantified as a percent of GAPDH. The late cardioprotective effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Infarct size was markedly limited by ischemic preconditioning when compared with the control group (18.5+/-6.9% vs 38.5+/-11.1%; p<0.001). HSP70 mRNA expression in risk area was much higher in preconditioning group than control group(78+/-12% vs 41+/-11%; p<0.01). But, there was no significant difference of HSP70 mRNA expression in the posterior wall between control and ischemic preconditioning group. CONCLUSIONS: These data suggest that ischemic preconditioning have delayed myocardial protective effect from ischemia. The increase in myocardial HSP70 mRNA may be one of the contributing factors to the delayed cardioprotective effects of ischemic preconditioning in cats.
Animals ; Arrhythmias, Cardiac ; Blotting, Northern ; Cats* ; Coronary Vessels ; Evans Blue ; Heart* ; Heat-Shock Proteins* ; Hot Temperature* ; HSP70 Heat-Shock Proteins ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Models, Animal ; Reperfusion ; RNA, Messenger

Adult ; Colon, Transverse ; pathology ; Hernia, Diaphragmatic ; pathology ; Humans ; Male ; Respiratory Insufficiency ; pathology ; Spleen ; pathology ; Stomach ; pathology