A New Ultrasonographic “Fluttering Sign” for Hepatic Hemangioma

The aim of the study described here was to clarify the diagnostic value of the fluttering sign, a new sign that characterizes hepatic hemangiomas in gray-scale ultrasonography (US). It refers to a phenomenon in which the speckled echogenicity inside the hemangioma changes continuously and seems to be moving. A total of 172 hemangiomas diagnosed with contrast-enhanced US were evaluated. The fluttering sign was found in 123 of 172 hemangiomas (71.5%). Its prevalence was significantly higher than that of the marginal strong echo (89/172, 51.7%, p < 0.001), posterior acoustic enhancement (103/172, 59.9%, p = 0.031) and chameleon sign (100/172, 58.1%, p = 0.013). In addition, the fluttering sign was observed significantly more frequently in mixed or hypo-echoic tumors than in hyper-echoic tumors (p < 0.001), relatively large tumors (p < 0.001) and tumors that were less than 5 cm from the body surface (p = 0.015). The fluttering sign in gray-scale US has great potential to be a new complementary sign for the diagnosis of hemangioma.     

Specificity of co-promoting effects of caffeine on thyroid carcinogenesis in rats pretreated with N-bis(2-hydroxypropyl)nitrosamine

The specificity of copromotion effects of caffeine with known goitrogenic factors on thyroid carcinogenesis was examined in rats pretreated with N-bis(2-hydroxypropyl)nitrosamine (DHPN). Male F344 rats were divided into 8 groups, each consisting of 10 animals, and received a single sc injection of 2,800 mg/kg DHPN. From one week after the DHPN initiation, they were given basal diet, iodine deficiency (ID) diet, 500 ppm phenobarbital (PB) solution or 1,000 ppm sulfadimethoxine (SDM) solution with or without 1,500 ppm caffeine feeding for 12 weeks. The caffeine, PB, SDM, and ID treatments significantly (p < 0.05 or 0.01) increased the relative thyroid weights, and the increases with PB or ID were further (p < 0.05 or 0.01) enhanced in combination with caffeine. SDM drastically promoted thyroid carcinogenesis in association with increased serum TSH levels regardless of the caffeine treatment. Thyroid follicular carcinomas and adenomas were more frequently observed in the additional caffeine groups than in the ID alone groups. The incidence and multiplicity of focal thyroid follicular hyperplasias in the ID-treated groups were significantly (p < 0.05 and 0.01) elevated in the case of combination with caffeine. Increases in serum TSH levels with PB or ID were also further enhanced in combination with caffeine. Serum thyroid hormone levels were significantly (p < 0.01) decreased by SDM but significantly (p < 0.05 or 0.01) increased by caffeine, PB or ID. Our results clearly indicate that dietary caffeine at a high dose of 1,500 ppm interacts with ID, but neither SDM nor PB, to promote rat thyroid carcinogenesis although the combined caffeine + PB treatment somewhat affected thyroid weights as well as thyroid hormone levels.     

Re-evaluation of exercise intensity for overweight Japanese men by ventilatory threshold

AIM: To re-evaluate exercise intensity for overweight Japanese men by ventilatory threshold (VT). METHODS: Cross sectional clinical intervention study. Subjects and materials: One hundred and ten overweight Japanese men aged 32-59 years were recruited. The average body mass index was 28.5+/-2.5 kg/m(2). Aerobic exercise level was evaluated by measuring VT. Fifty per cent heart rate (HR) reserve by Karvonen's formula was calculated and compared with HR at VT. Fat distribution was evaluated by visceral fat and subcutaneous fat areas measured with computed tomography scanning at umbilical levels. Anthropometric parameters such as height, body weight and body fat percentage were also measured. RESULTS: There was significant correlation between HR at VT and 50% HR reserve by Karvonen's formula (r=0.642, p<0.01). However, HR at VT was significantly lower than 50% HR reserve by Karvonen's formula (HR at VT 103.6+/-10.6 beat/min vs. 50% HR reserve 125.0+/-7.1 beat/min, p<0.01) and HR at VT was corresponded to 28.5+/-8.3% HR reserve by Karovonen's formula. CONCLUSION: The present study indicated that exercise intensity of 30% HR reserve should be recommended for overweight Japanese men.     

Adenosine monophosphate-activated protein kinase suppresses vascular smooth muscle cell proliferation through the inhibition of cell cycle progression

Vascular smooth muscle cell (VSMC) proliferation is a critical event in the development and progression of vascular diseases, including atherosclerosis. We investigated whether the activation of adenosine monophosphate-activated protein kinase (AMPK) could suppress VSMC proliferation and inhibit cell cycle progression. Treatment of human aortic smooth muscle cells (HASMCs) or isolated rabbit aortas with the AMPK activator 5-Aminoimidazole-4-carboxamide ribonucleoside (AICAR) induced phosphorylation of AMPK and acetyl Co-A carboxylase. AICAR significantly inhibited HASMC proliferation induced by both platelet-derived growth factor-BB (PDGF-BB) and fetal calf serum (FCS). Treatment with AICAR inhibited the phosphorylation of retinoblastoma gene product (Rb) induced by PDGF-BB or FCS, and increased the expression of cyclin-dependent kinase inhibitor p21(CIP) but not that of p27(KIP). Pharmacological inhibition of AMPK or overexpression of dominant negative-AMPK inhibited both the suppressive effect of AICAR on cell proliferation and the phosphorylation of Rb, suggesting that the effect of AICAR is mediated through the activation of AMPK. Cell cycle analysis in HASMCs showed that AICAR significantly increased cell population in G0/G1-phase and reduced that in S- and G2/M-phase, suggesting AICAR induced cell cycle arrest. AICAR increased both p53 protein and Ser-15 phosphorylated p53 in HASMCs, which were blocked by inhibition of AMPK. In isolated rabbit aortas, AICAR also increased Ser-15 phosphorylation and protein expression of p53 and inhibited Rb phosphorylation induced by FCS. These data suggest for the first time that AMPK suppresses VSMC proliferation via cell cycle regulation by p53 upregulation. Therefore, AMPK activation in VSMCs may be a therapoietic target for the prevention of vascular diseases.     

Mediastinoscopy-assisted esophagectomy for thoracic esophageal cancer after right thoracotomy for lung cancer: report of two cases

We herein report two cases of thoracic esophageal cancer operated on by mediastinoscopy-assisted esophagectomy (MAE) via the neck and the esophageal hiatus after right thoracotomy for primary lung cancer. Case 1 was a 78-year-old man who had undergone a lower lobectomy of the right lung 5 years earlier and had also undergone a pleuroparietopexy for postoperative chylothorax via right thoracotomy again. A squamous cell carcinoma of the middle thoracic esophagus was detected by endoscopy. Although radiotherapy was performed on the patient, the esophageal tumor was locally recurrent. Thus, MAE was performed because it would have been difficult to approach the esophageal tumor by right thoracotomy again, and the patient was successfully treated. Case 2 was a 71-year-old-man who had undergone an upper lobectomy of the right lung 5 years earlier. For a squamous cell carcinoma located between the middle and lower esophagus, MAE was performed. Metastatic lymph nodes surrounding the middle and lower thoracic esophagus were sufficiently dissected. Although esophageal cancer patients with metachronous lung cancer are rare, therapeutic issues for these patients remain. MAE via the neck and the esophageal hiatus for esophageal cancer patients who had previously undergone a lobectomy of the right lung may be considered a tool for surgical approach. Furthermore, MAE may be considered to be a salvage operation such as in case 1.     

ACE inhibitor and angiotensin II type 1 receptor blocker differently regulate ventricular fibrosis in hypertensive diastolic heart failure

BACKGROUND: Promoted myocardial stiffening has a crucial role in the transition to overt diastolic heart failure (DHF) in hypertensive hearts and is attributed to progressive ventricular fibrosis. Previous studies revealed the effects of an angiotensin II type 1 receptor blocker (ARB) and an angiotensin-converting enzyme inhibitor (ACEI) on the synthesis and degradation of collagens in the other phenotype of heart failure, systolic heart failure, which has a different pathophysiology; however, little is known about their effects in DHF. OBJECTIVE: To investigate effects of an ACEI and an ARB on the regulatory system of ventricular fibrosis in hypertensive DHF. DESIGN AND METHODS: Dahl salt-sensitive rats fed a diet containing 8% NaCl from age 7 weeks (DHF model) were divided into three groups: six untreated rats, six rats treated with a subdepressor dose of an ARB, candesartan cilexetil (1 mg/kg per day), from age 8 weeks, and six rats treated with a subdepress or dose of an ACEI, temocapril hydrochloride (0.2 mg/kg per day), from age 8 weeks. Six Dahl salt-sensitive rats fed on normal chow served as controls. Data were collected when animals were aged 20 weeks. RESULTS: The administration of an ARB or an ACEI inhibited ventricular fibrosis to the same degree. The ACEI decreased the level of type I collagen mRNA, but the decrease was less than that induced by the ARB. The difference in collagen synthesis was probably cancelled out by that in degradation: both in-vitro and in-situ zymography showed that gelatinase activity was greater in the rats treated with the ACEI than in those treated with the ARB. CONCLUSIONS: An ARB and an ACEI inhibited ventricular fibrosis through different mechanisms in hypertensive DHF.     

Assessment of coronary artery disease in hemodialysis patients with delayed systolic blood pressure response after exercise testing

BACKGROUND: We evaluated usefulness of the postexercise systolic blood pressure (SBP) response for detecting coronary artery disease (CAD) in hemodialysis patients. METHODS: A treadmill exercise testing was done, and the SBP response was measured in 44 hemodialysis patients (30 men, 14 women; age 41 to 81 years). The postexercise SBP response was defined as the ratio of SBP after 3 minutes of recovery to SBP at peak exercise. RESULTS: The SBP ratio of the 25 subjects with coronary artery stenosis (1.01+/- 0.13) was significantly greater (p<0.01) than 19 subjects without coronary artery stenosis (0.83+/- 0.10). An SBP ratio greater than 0.92 identified CAD with higher sensitivity, specificity, and accuracy than did the conventional ST-segment depression criterion (76 vs. 56%, 90 vs. 53%, and 82 vs. 55%, respectively). CONCLUSION: Determination of the SBP ratio is a clinically useful, noninvasive method for accurately detecting CAD in hemodialysis patients.