[Long term outcome of arterial switch surgery for transposition of the great arteries: evaluation of the reconstruction of the pulmonary artery].

We assessed the effect of reconstructing the pulmonary artery during arterial switch surgery for transposition of the great arteries on late pulmonary stenosis. Sixty-five patients who underwent Lecompte procedure between September 1991 and December 2006 were divided, by the procedure used chronologically to reconstruct the pulmonary artery, into group XP (single pantaloon patch with equine pericardium, n = 11), group P (direct reconstruction, n = 47), and group AP (single pantaloon patch with fresh autopericardium, n = 7). Outcome and pulmonary stenosis on the most recent ultrasound cardiography (UCG) were compared in the 3 groups. The median follow-up was 13, 7.5, and 1.3 years, respectively. Both early and late mortalities were 1.5% (1/65). Although percutaneous trans-pulmonary angioplasty was necessary in 1, 13, and 3 patients, there was 1, 1, and 0 reoperation for pulmonary stenosis in the 3 groups, respectively. Pulmonary stenosis (pulmonary arterial maximum flow velocity > 3 m/sec on UCG) was present in 4 (40%). 14 (30%). and 3 patients (43%). Although there was no significant difference among the 3 procedures in preventing pulmonary stenosis 10 years after arterial switch surgery, direct reconstruction of the pulmonary artery may show a superior outcome, in particular, over 10 years after arterial switch surgery.

Brain natriuretic peptide as a hormonal marker of ventricular diastolic dysfunction in children with Kawasaki disease.

Although an increased level of serum brain natriuretic peptide (BNP) has been reported in children in the acute phase of Kawasaki disease (KD), no precise relation was documented between the serum BNP level and left ventricular (LV) systolic function. We hypothesized that the increased BNP levels may be explained by diastolic abnormalities in those with KD. We prospectively studied 25 patients in the acute phase of KD. Patients with abnormal systolic function were excluded. Pediatric cardiologists making the assessment of LV diastolic function were blinded to the BNP levels. Doppler interrogation was applied to measure LV inflow velocities, which were transformed to z scores using control measurements obtained from 83 healthy subjects. In the patients, the BNP levels ranged from 2.0 to 450.0 pg/ml, with a mean of 54.0 +/- 102.8 pg/ml. Six patients with abnormal velocities (> 2 SD in z score) showed significantly higher levels of BNP (152 +/- 173 pg/ml) than those in the remaining patients (p < 0.01). The BNP levels correlated positively with diastolic atrial velocity in z score (r = 0.51, p < 0.05), and negatively with diastolic early velocity to atrial velocity ratio in z score (r = -0.75, p < 0.01). This study suggests that LV diastolic dysfunction may occur in some children in the acute phase of KD, causing an increased level of BNP.

CDK-inhibitors-associated kinase activity: a possible determinant of malignant potential in smooth muscle tumors of the external soft tissue.

There has been accumulating histological observation of leiomyoma and leiomyosarcoma of the external soft tissue regarding their differential diagnosis. The definitive diagnostic tools have not been established, however, nor have the pathological mechanisms of cell proliferation in these tumors been clarified. Herein, expression of the cyclin-dependent kinase inhibitors (CKIs), p21, p27 and p57 and their associated kinase activities were examined in 61 cases of soft tissue smooth muscle tumors. Immunohistochemical staining showed that all 3 inhibitor proteins were expressed in all cases of leiomyoma and leiomyosarcoma, but that the mean values of their labeling indices (LIs) were higher in the cases of leiomyosarcoma. In addition, the LIs of p21 and p27 were inversely correlated in total cases. Immunoblotting revealed that these proteins are expressed at higher levels in tumors, in particular, in leiomyosarcoma. When CKIs were immunoprecipitated from tissue extracts, cyclin/cdk protein complexes associated with, at least, 1 CKI were detectable only in tumor tissues. Furthermore, cdk2 or cdk4 kinase activity manifested by these cyclin/cdk/CKI complexes (CKI-associated kinase activity) was detectable exclusively from leiomyosarcoma, but not from leiomyoma. Among the cases of leiomyosarcoma, cdk2 activity was generally found associated either with p21 or p27, but not both. Statistical analysis indicated that p21- and p27 LIs are predictive of positive or negative clinical outcome, respectively. In conclusion, the participation of CKIs in active cyclin/cdk complexes in a reciprocal and redundant manner and subsequent CKI- associated kinase activity are the characteristic profiles of malignant phenotype in these tumors. Moreover, immunohistochemical detection of CKIs may provide a useful tool for evaluating patients' prognosis.

Hyalinizing spindle cell tumor with giant rosettes: report of a case showing remarkable myofibroblastic differentiation.

We examined the proliferative activity and the differentiation line of tumor cells in a case of "hyalinizing spindle cell tumor with giant rosettes" (HSCGR). A 6 cm tumor within the right deltoid muscle of a 58-year-old female was found by physical and radiographical examinations. A biopsy revealed the histological features of a spindle cell tumor with rosette-like structures. Wide excision was done under the diagnosis of HSCGR. The tumor presented as a gray-whitish, solid mass with focal pseudocystic degeneration. Immunohistochemically, the tumor cells were diffusely positive for vimentin and were also focally positive for S-100, but negative for desmin and alpha-smooth muscle actin. The cells stained positively for Ki-67 with even distribution, there being a correlation with the cellularity of the areas, with a labeling index ranging from 0.3 to 0.5%. In addition, flow cytometry revealed an almost normal diploid DNA pattern and 5.8% S-phase fraction, indicating low proliferative activity. Ultrastructurally, many tumor cells displayed discontinuous basal lamina, pinocytotic vesicles, dilated rough endoplasmic reticulum, and microfilaments with focal dense bodies. The main component of the rosette was collagenous fibrils with normal diameter and normal periodic banding. We interpreted this case of HSCGR as a low grade fibrosarcoma with remarkable differentiation of myofibroblastic lineage, and with focally accumulated, morphologically normal collagenous fibrils.

Creep motion in a granular pile exhibiting steady surface flow.

We investigate experimentally granular piles exhibiting steady surface flow. Below the surface flow, it has been believed that a "frozen" bulk region exists, but our results show no such frozen bulk. We report here that even the particles in layers deep in the bulk exhibit very slow flow and that such motion can be detected at an arbitrary depth. The mean velocity of the creep motion decays exponentially with depth, and the characteristic decay length is approximately equal to the particle size and is independent of the flow rate. It is expected that the creep motion we have seen is observable in all sheared granular systems.

Mechanisms for slow strengthening in granular materials

Several mechanisms cause a granular material to strengthen over time at low applied stress. The strength is determined from the maximum frictional force F(max) experienced by a shearing plate in contact with wet or dry granular material after the layer has been at rest for a waiting time tau. The layer strength increases roughly logarithmically with tau only if a shear stress is applied during the waiting time. The mechanisms of strengthening are investigated by sensitive displacement measurements, and by imaging of particle motion in the shear zone. Granular matter can strengthen due to a slow shift in the particle arrangement under shear stress. Humidity also leads to strengthening, but is found not to be its sole cause. In addition to these time dependent effects, the static friction coefficient can also be increased by compaction of the granular material under some circumstances, and by a cycling of the applied shear stress.

Neuron-specific enolase-producing epithelioid leiomyosarcoma with gross vascular invasion and intracardiac involvement.

We present an unusual case of epithelioid leiomyosarcoma in the right shoulder. A 10-cm tumor eroding the right scapula occurred in a 59-year-old man and grew into the subclavian vein with extension to the right atrium. An elevated serum level of neuron-specific enolase was also detected. Clinical presentation suggested small cell carcinoma of the lung (Pancoast tumor) with intravenous extension. Eventually, the patient died of respiratory insufficiency. Autopsy revealed a primary tumor in the right shoulder, numerous tumor emboli in the pulmonary arteries, and associated hemorrhagic infarction. Histopathologic features revealed an epithelioid leiomyosarcoma. Furthermore, immunohistochemical and immunoblotting analyses of the tumor demonstrated positive reactions for neuron-specific enolase. We interpreted this peculiar case to be a neuron-specific enolase-producing epithelioid leiomyosarcoma of the soft tissue associated with gross vascular invasion.

Investigation of soy sauce treated with nitrite in the chromosomal aberration test in vitro and the micronucleus test in vivo.

Soy sauce pretreated with 2300 ppm nitrite caused no more aberrations than did untreated soy sauce in the chromosomal aberration test in vitro using a Chinese hamster fibroblast cell line with or without S9 mixture. The aberration induction by soy sauce is likely to be caused by the 17% sodium chloride it contains. Soy sauce with or without pretreatment with 2300 ppm nitrite was orally given to ICR mice at a dose of 14 ml/kg body weight once or 6 ml/kg body weight/day for 5 consecutive days. This oral administration did not induce any significant increase in micronuclei in the micronucleus test in vivo.

Relation of nitrite concentration to mutagen formation in soy sauce.

When soy sauce was mixed with nitrite solutions at pH 1.0 and 3.0, only mixtures containing nitrite concentrations above 250 ppm were mutagenic in the Salmonella/mammalian microsome test. In buffered aqueous solution (pH 3) the mutagen precursor, (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid [(1S,3S)-MTCA] and its stereoisomer ( - )-(1R,3S)-MTCA reacted with 10 ppm or more of sodium nitrite; but at least 250 ppm nitrite was required for them to react in soy sauce (pH 3). Similarly, another mutagen precursor, tyramine, did not react even with 2300 ppm nitrite in soy sauce (pH 1), although pure tyramine in aqueous solution (pH 1) reacted with as little as 50 ppm nitrite. Nitrite concentration in human saliva and gastric juice does not generally exceed 50 ppm. Therefore, the most probable source of mutagens--nitrosation of MTCAs and tyramine--is likely to be very restricted in vivo and soy sauce is unlikely to be significantly mutagenic.

Polygalacturonic acid trans-eliminase of Xanthomonas campestris.

Polygalacturonic acid trans-eliminase from the culture fluid of Xanthomonas campestris was purified 66-fold by acetone precipitation, citrate extraction and chromatography on diethylaminoethyl- and carboxymethyl-cellulose. The optimum pH is 9.5 in glycine-sodium hydroxide buffer. Up to 1mm-calcium chloride brings about a remarkable stimulation of the enzyme activity and, at this concentration, no other cations promote or inhibit enzyme action except Ba(2+) ions, which cause complete inhibition. The enzyme degrades polygalacturonic acid in a random manner; it does not act upon polygalacturonate methyl glycoside, although it can cleave partially (68%) esterified pectin. The end products from polygalacturonic acid at 46% breakdown are unsaturated di- and tri-galacturonic acids, in addition to saturated mono-, di- and tri-galacturonic acids. Pentagalacturonic acid is split preferentially into saturated dimer plus unsaturated trimer, or into saturated trimer plus unsaturated dimer; at a lower rate, it is also split into monomer and unsaturated tetramer. Unsaturated pentamer is split into unsaturated dimer plus unsaturated trimer. Tetragalacturonic acid is split some-what preferentially at the central bond to form dimer and unsaturated dimer, but it is also split into monomer and unsaturated trimer. Unsaturated tetramer is split only at the central bond to yield only unsaturated dimer. Trigalacturonic acid is split into monomer and unsaturated dimer. Unsaturated trimer is cleaved into saturated dimer and probably 4-deoxy-l-5-threo-hexoseulose uronic acid, which has not yet been directly identified. Neither saturated nor unsaturated digalacturonic acid is attacked. The unsaturated digalacturonic acid was isolated and proved to be O-(4-deoxy-beta-l-5-threo-hexopyranos-4-enyluronic acid)-(1-->4)-d-galacturonic acid.