This report describes a case of portal hypertension caused by periportal tuberculous lymphadenitis. There were a few reports of portal hypertension associated with tuberculosis. A 27-year-old man was admitted to the hospital because of recurrent hematemesis for 7 days. There was a history of mediastinal tuberculous lymphadenitis 3 years earlier that was treated with isoniazide, rifampin, ethambutol, and pyrazinamide for 2 years. Clinical evaluation revealed esophageal variceal bleeding and main portal vein obstruction by enlarged periportal lymph nodes. The patient underwent distal splenorenal shunt. Pathologic examination of the excised periportal lymph node revealed chronic granulomatous inflammation with central caseous necrosis. Thereafter the patient took antituberculous medication for 12 months. The patient has not re-bled 3 years since the shunt operation.
Adult ; Case Report ; Human ; Hypertension, Portal/*etiology/therapy ; Male ; Tuberculosis, Lymph Node/*complications

BACKGROUND AND OBJECTIVES: Electrical dyssynchronicity (Dsyn) appears to be prognostic of survival in congestive heart failure (CHF). Recent study has shown some discrepancy between the electrical Dsyn and the Doppler tissue image (DTI) assessed mechanical Dsyn. The aim of our study was to evaluate the relationship between the QRS duration and DTI assessed Dsyn. SUBJCETS AND METHODS: One hundred and forty patients, with CHF and left ventricular ejection fractions < or =40%, were enrolled. DTI was performed on 5-basal and 5-mid segments to assess the time from the R-wave to the peak systolic velocity (RS time). A QRS duration >130 msec, standard deviation (SD) of the RS time >40 msec, or a difference in the maximal and minimal RS times (RS time-diff) >100 msec were indicators of'Dsyn'. RESULTS: The prevalence of myocardial Dsyn, by QRS duration, SD of the RS time and the RS time-diff were 19, 43 and 47%, respectively. The SD of the RS time (49.8+/-23.6 vs. 36.6+/-20.7, p<0.01) and the RS time-diff (139.2+/-63.2 vs. 98.0+/-54.3, p<0.01) were prolonged in the wide (>130 msec) compared with the narrow QRS group. There was also a weak positive correlation between the QRS duration and the SD of the RS time (R=0.34, p<0.001) and the RS time-diff (R=0.38, p<0.001). However, from a cross-tabulation analysis, more than one third of patients had a discrepancy between QRS duration and DTI assessed mechanical Dsyn. From a multivariate analysis, a major determinant of the SD of the RS time was the QRS duration. CONCLUSION: Although a major determinant of the DTI assessed Dsyn was the QRS duration, more than one-third of patients had a discrepancy between electrical and mechanical Dsyn. Therefore, not only the QRS duration, but the DTI assessed Dsyn, should be measured when considering cardiac resynchronization therapy.
Cardiac Resynchronization Therapy ; Diagnosis* ; Electrocardiography* ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Humans ; Multivariate Analysis ; Prevalence ; Stroke Volume

BACKGROUND AND OBJECTIVES: Electrical dyssynchronicity (Dsyn) appears to be prognostic of survival in congestive heart failure (CHF). Recent study has shown some discrepancy between the electrical Dsyn and the Doppler tissue image (DTI) assessed mechanical Dsyn. The aim of our study was to evaluate the relationship between the QRS duration and DTI assessed Dsyn. SUBJCETS AND METHODS: One hundred and forty patients, with CHF and left ventricular ejection fractions < or =40%, were enrolled. DTI was performed on 5-basal and 5-mid segments to assess the time from the R-wave to the peak systolic velocity (RS time). A QRS duration >130 msec, standard deviation (SD) of the RS time >40 msec, or a difference in the maximal and minimal RS times (RS time-diff) >100 msec were indicators of'Dsyn'. RESULTS: The prevalence of myocardial Dsyn, by QRS duration, SD of the RS time and the RS time-diff were 19, 43 and 47%, respectively. The SD of the RS time (49.8+/-23.6 vs. 36.6+/-20.7, p<0.01) and the RS time-diff (139.2+/-63.2 vs. 98.0+/-54.3, p<0.01) were prolonged in the wide (>130 msec) compared with the narrow QRS group. There was also a weak positive correlation between the QRS duration and the SD of the RS time (R=0.34, p<0.001) and the RS time-diff (R=0.38, p<0.001). However, from a cross-tabulation analysis, more than one third of patients had a discrepancy between QRS duration and DTI assessed mechanical Dsyn. From a multivariate analysis, a major determinant of the SD of the RS time was the QRS duration. CONCLUSION: Although a major determinant of the DTI assessed Dsyn was the QRS duration, more than one-third of patients had a discrepancy between electrical and mechanical Dsyn. Therefore, not only the QRS duration, but the DTI assessed Dsyn, should be measured when considering cardiac resynchronization therapy.
Cardiac Resynchronization Therapy ; Diagnosis* ; Electrocardiography* ; Estrogens, Conjugated (USP)* ; Heart Failure* ; Humans ; Multivariate Analysis ; Prevalence ; Stroke Volume

BACKGROUND AND OBJECTIVES: Several echocardiographic methods, such as ejection fraction, fractional shortening, and Doppler tissue imaging (DTI), have been developed to quantify systolic function but all had several important limitations. The purpose of this study was to quantify the regional wall motion abnormality, using strain, in an acute myocardial infarction, compared with a visual estimation. SUBJECTS AND MEHTODS: Forty-five patients, with acute anterior (n=28) and inferior myocardial (n=17) infarctions, who underwent color DTI, were examined using longitudinal strain and standard echocardiography, and the results were compared with 54 normal controls. A total of 594 segments [3 segments (apical, mid and basal portion) of septum and inferior wallx99 patients] were evaluated. RESULTS: In the normal control group, the strain was uniformly distributed in all segments (-20%~-23%). In the infarction groups, the strain was negatively related with the wall motion score. The strain of the apical segments and mid-septum was decreased in the anterior wall infarctions, and the strain of basal septum and mid to basal inferior wall was decreased in the inferior wall infarctions. The dyskinetic segments showed positive strain. CONCLUSION: This study validates strain as a superior method for the quantification of the regional wall motion abnormality in an acute myocardial infarction than visual estimation.
Echocardiography ; Humans ; Infarction ; Myocardial Infarction*

BACKGROUND AND OBJECTIVES: The recovery of the left ventricular ejection fraction (LVEF) appeared to be prognostic of survival in congestive heart failure (CHF). The aim of our study was to evaluate the parameters that appear to predict the LVEF recovery in CHF. SUBJECTS AND METHODS: Forty-nine patients, with CHF and a LVEF< 35%, were enrolled. Doppler myocardial imaging was performed on 5-basal and 5-mid segments in order to assess the systolic duration, the time from the R-wave to the peak systolic velocity (RS time) and the time from the R-wave to the peak early diastolic velocity (RE time). The standard deviation (SD) of the RS time was an indicator of the 'systolic synchronicity'. After at least 3 months of full medical therapy, a follow-up echocardiography was performed. According to the changes in the LVEF, the patients were divided into groups I (< 5%, n=29) and II (> or =5%, n=20). RESULTS: The baseline clinical and echocardiographic parameters were similar in both groups. In group II, the LV end-systolic and end-diastolic volumes were decreased, but the LVEF was increased by up to 44% at the follow-up. The right ventricular annulus velocity (group I: 6.7+/-2.1 vs. group II: 8.0+/-2.0 cm/sec, p< 0.05), the use of beta-blocker (69 vs. 100%, p< 0.05) and the SD of the RS time (46+/-21 vs. 21+/-12, p< 0.01) were significantly different between the two groups. However, the systolic duration and the SD of the RE time were similar in the two groups. From a multivariate analysis, only the SD of the RS time was an independent predictor of the LVEF recovery. CONCLUSION: Myocardial systolic synchronicity is an important predictor of the LVEF recovery.
Echocardiography ; Estrogens, Conjugated (USP)* ; Follow-Up Studies ; Heart Failure* ; Heart Ventricles* ; Humans ; Multivariate Analysis ; Recovery of Function* ; Stroke Volume

BACKGROUND AND OBJECTIVES: Recent studies have implicated inflammation in the pathogenesis of coronary artery disease. The aim of this study was to determine whether C-reactive protein (CRP) levels are predictive of major adverse cardiac events (MACE) following stenting. SUBJECTS AND METHODS: The study comprised 193 patients (90 men, 152 unstable angina, mean age 63 years) between October 1999 and March 2001. The patients were classified into 2 groups according to their MACE, [group A; MACE (+), n=46 and group B; MACE (-), n=147]. RESULTS: During clinical follow-up at a mean duration of 15 months, there was 1death, 7 myocardial infarctions, 25 cases of revascularization therapy, and 13 recurrent anginas. At 24 hours after stenting, the CRP levels were significantly higher in group A compared to group B (5.4, 0.6-15.2 vs. 3.1, 0.1-9.8 mg/L, respectively, p<0.01), with the elevation of the CRP level ( >8.0 mg/L) occurring more commonly in group A than group B (24% vs. 9%, p<0.05). The differences in the CRP levels between the baseline and 24 hours following stenting (CRP 24h-base ) were also significantly higher in group A than in group B. After adjustment for age, sex, and cardiovascular risk factor, multi-variate analysis using logistic regression revealed the CRP levels 24 hours after stenting were predictive of MACE, with an odd ratio of 1.6 (95% CI 1.1-2.2, p=0.01). CONCLUSION: CRP levels, 24 hours following intervention, are powerful predictor of cardiac events in patients with stable or unstable angina undergoing coronary stenting. These results suggest that the inflammatory responsiveness to coronary intervention can plays an important role in predicting cardiac events.
Angina, Unstable ; Angioplasty, Balloon, Coronary ; C-Reactive Protein* ; Coronary Artery Disease ; Follow-Up Studies ; Humans ; Inflammation ; Logistic Models ; Male ; Myocardial Infarction ; Risk Factors ; Stents*

Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

Anticancer activities of Licochalcone D (LCD) in human colorectal cancer (CRC) cells HCT116 and oxaliplatin-resistant HCT116 (HCT116-OxR) were determined. Cell viability assay and soft agar assay were used to analyze antiproliferative activity of LCD.Flow cytometry was performed to determine effects of LCD on apoptosis, cell cycle distribution, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) dysfunction, and multi-caspase activity in CRC cells. Western blot analysis was used to monitor levels of proteins involved in cell cycle and apoptosis signaling pathways. LCD suppressed the growth and anchorageindependent colony formation of both HCT116 and HCT116-OxR cells. Cell cycle analysis by flow cytometry indicated that LCD induced cell cycle arrest and increased cells in sub-G1 phase. In parallel with the antiproliferative effect of LCD, LCD up-regulated levels of p21 and p27 while downregulating cyclin B1 and cdc2. In addition, phosphorylation levels of JNK and p38 mitogen-activated protein kinase (MAPK) were increased by LCD. Inhibition of these kinases somehow prevented the antiproliferative effect of LCD. Moreover, LCD increased ROS and deregulated mitochondrial membrane potential, leading to the activation of multiple caspases. An ROS scavenger N-acetyl-cysteine (NAC) or pan-caspase inhibitor Z-VAD-FMK prevented the antiproliferative effect of LCD, supporting that ROS generation and caspase activation mediated LCD-induced apoptosis in CRC cells. In conclusion, LCD exerted antitumor activity in CRC cells by inducing ROS generation and phosphorylation of JNK and p38 MAPK. These results support that LCD could be further developed as a chemotherapeutic agent for treating CRC.

BACKGROUND: Inflammation plays a key role in the pathogenesis of an in-stent restenosis because it promotes neointimal proliferation. This study was performed to determine responses of the C-reactive protein (CRP) in unstable angina patients with an in-stent restenosis undergoing repeated percutaneous transluminal coronary angioplasty (re-PTCA). METHODS: The study subjects (unstable angina) were classified into 2 groups:Group A (n=30, 15 men, mean age 62 years) had a re-PTCA for an in-stent restenosis lesion and Group B (n=60, 33 men, mean age 63 years) underwent a stent implantation for a de novo lesion. RESULTS: The baseline CRP levels in group A were significantly lower than in group B, as well as 6 and 24 hours after intervention. Twenty four hours after intervention, the CRP levels increased (>4 mg/L) in 3 out of 30 patients (10%) of group A but increased in 32 out of 60 patients (53%) in group B (p<0.001). The differences in the CRP levels between the baseline and 24 hours after intervention were significantly lower in group A than in group B (0.8 and 2.15 mg/L, respectively, p<0.001). In group B, the serum CRP levels 24 hours after intervention were significantly higher than the baseline levels (p<0.05), but not in group A. CONCLUSION: The CRP expression level is significantly lower in unstable angina patients undergoing a re-PTCA for an in-stent restenosis than those undergoing a stent implantation for a de novo lesion.
Angina, Unstable* ; Angioplasty* ; Angioplasty, Balloon, Coronary ; C-Reactive Protein ; Coronary Restenosis ; Humans ; Inflammation ; Male ; Stents