STAT6 and IL-10 are required for the anti-arthritic effects of Schistosoma mansoni via different mechanisms.

To investigate possible roles of T helper type 2 (Th2) cytokines in the anti-arthritic effects of a blood fluke, Schistosoma mansoni (Sm), for mouse collagen-induced arthritis (CIA), wild-type (WT), signal transducer and activator of transcription 6 (STAT6) knock-out (KO) and interleukin (IL)-10 KO mice were infected with Sm. Three weeks after infection, the mice were immunized with bovine type II collagen (IIC). Arthritis severity was monitored by scoring, measurement of paw thickness and the presence of ankylosis. Serum anti-IIC IgG levels, splenic cytokine production and cytokine gene expression in the popliteal lymph nodes (PLNs) were measured and compared among WT and gene-KO mice. Consistent with our previous findings, Sm infection reduced the arthritis severity in WT mice. Splenic production of IL-17A and tumor necrosis factor (TNF)-α was reduced by the infection. In contrast, Sm infection markedly exacerbated CIA in STAT6 KO mice. In the KO mice, IL-17A production was increased by the infection. Conversely, Sm infection did not affect the exacerbated arthritis in IL-10 KO mice, although IL-17A production was reduced by the helminth. Our results suggest that signaling via STAT6 (presumably IL-4 and/or IL-13) and IL-10 is required for the suppression of CIA by Sm infection, but through different mechanisms. STAT6 was essential for helminth-induced reduction of IL-17A, whereas regulation of the basal arthritis severity by IL-10 was needed in order for it to be sufficiently suppressed by the helminth.

Interleukin-33 enhances programmed oncosis of ST2L-positive low-metastatic cells in the tumour microenvironment of lung cancer.

The proinflammatory interleukin-33 (IL-33) binds to its receptor ST2L on the surface of immune cells and stimulates the production of Th2 cytokines; however, the effects of IL-33 on tumour cells are poorly understood. Here we show that ST2 was significantly downregulated in human lung cancer tissues and cells compared with normal lung tissues and cells. IL-33 expression was also inversely correlated with the stages of human lung cancers. In accordance with this finding, low-metastatic cells but not high-metastatic cells derived from Lewis lung carcinoma expressed functional ST2L. IL-33 was abundantly present in the tumours established by the low-metastatic cells compared with those formed by the high-metastatic cells. Although the low-metastatic cells scarcely expressed IL-33 in vitro, these cells did expry 6ess this molecule in vivo, likely due to stimulation by intratumoural IL-1ß and IL-33. Importantly, IL-33 enhanced the cell death of ST2L-positive low-metastatic cells, but not of ST2L-negative high-metastatic cells, under glucose-depleted, glutamine-depleted and hypoxic conditions through p38 MAPK and mTOR activation, and in a mitochondria-dependent manner. The cell death was characterised by cytoplasmic blisters and karyolysis, which are unique morphological features of oncosis. Inevitably, the low-metastatic cells, but not of the high-metastatic cells, grew faster in IL-33(-/-) mice than in wild-type mice. Furthermore, IL-33 selected for the ST2L-positive, oncosis-resistant high-metastatic cells under conditions mimicking the tumour microenvironment. These data suggest that IL-33 enhances lung cancer progression by selecting for more malignant cells in the tumour microenvironment.

Lack of IL-21 signal attenuates graft-versus-leukemia effect in the absence of CD8 T-cells.

Previously, we have shown that IL-21R(-/-) splenocytes ameliorate GVHD as compared with wild-type splenocytes. Here, we investigated whether or not IL-21R(-/-) splenocytes diminish the graft-versus-leukemia (GVL) effect. Surprisingly, IL-21R(-/-) splenocytes efficiently eliminate leukemic cells as well as wild-type splenocytes, suggesting the retention of GVL effects in the absence of IL-21 signaling. To compare the GVL effect between IL-21R(-/-) and wild-type cells, we titrated the number of splenocytes required for the elimination of leukemic cells and found that the threshold of GVL effect was obtained between 5 × 10(5) and 5 × 10(6) with both types of splenocytes. Cotransplantation with CD8-depleted splenocytes but not with purified CD8 T-cells resulted in a significant reduction in anti-leukemic effect of IL-21R(-/-) cells compared with wild-type cells, suggesting that the lack of IL-21 signaling primarily impairs CD4 T-cell rather than CD8 T-cell function and the comparable GVL effect with IL-21R(-/-) bulk splenocytes results from cooperative compensation by CD8 T-cells.

Therapeutic silencing of an endogenous gene by siRNA cream in an arthritis model mouse.

Recent advances of biotechnology have laid the groundwork for potent and specific molecular-targeting therapies including RNA interference. The largest remaining hurdle for widespread use of this technology in skin is an effective delivery system. Here, we demonstrate an effective topical delivery system using a cream formulation containing a small-interfering RNA (siRNA) that specifically targets osteopontin (OPN). OPN is a validated target in numerous inflammatory diseases, including rheumatoid arthritis (RA). The siRNA targeting OPN was incorporated into a cream formulation GeneCream that penetrates the stratum corneum, depositing siRNA in the epidermis, dermis, and to a lesser extent, subcutaneous tissue. In addition, when the OPN siRNA cream was topically applied to the skin of a collagen antibody-induced RA mouse model, the siRNA cream prevented the occurrence of severe, irreversible damage to bone and cartilage. Thus, the siRNA cream provides effective delivery of active OPN siRNA, suggesting this formulation may represent a platform technology for delivery of siRNAs for treating various disorders including RA.

The role of TNFalpha and IL-17 in the development of excess IL-1 signaling-induced inflammatory diseases in IL-1 receptor antagonist-deficient mice.

IL-1 receptor antagonist (IL-1Ra)-deficient mice spontaneously develop several inflammatory diseases, resembling rheumatoid arthritis, aortitis, and psoriasis in humans. As adoptive T cell transplantation could induce arthritis and aortitis in recipient mice, it was suggested that an autoimmune process is involved in the development of diseases. In contrast, as dermatitis developed in scid/scid-IL-IRa-deficient mice and could not be induced by T cell transfer, a T cell-independent mechanism was suggested. The expression of proinflammatory cytokines was augmented at the inflammatory sites. The development of arthritis and aortitis was significantly suppressed by the deficiency of TNFalpha or IL-17. The development of dermatitis was also inhibited by the deficiency of TNFalpha. These observations suggest that TNFalpha and IL-17 play a crucial role in the development of autoimmunity downstream of IL-1 signaling, and excess IL-1 signaling-induced TNFalpha also induces skin inflammation in a T cell-independent manner.

Biosynthesis of poly(3-hydroxybutyrate-co-3-hydroxyalkanoates) copolymer from sugars by recombinant Ralstonia eutropha harboring the phaC1Ps and the phaGPs genes of Pseudomonas sp. 61-3.

Heterologous expression of the phaGPs and the phaClPs genes encoding 3-hydroxyacyl acyl carrier protein-coenzyme A transacylase and polyhydroxyalkanoate (PHA) synthase from Pseudomonas sp. 61-3, respectively, was performed in the phbCRe negative mutant, Ralstonia eutropha PHB-4. The recombinant strain of the R. eutropha PHB-4 produced PHA copolymers consisting of 3-hydroxybutyrate (3HB) and medium-chain-length 3-hydroxyalkanoate (mcl-3HA) units of 6-12 carbon atoms from sugars. The 3HB fraction in copolymers was very high (95-97 mol%). The PHA content in the recombinant strain could further be increased by the additional introduction of the phbABRe genes from R. eutropha encoding beta-ketothiolase and NADPH-depedent acetoacetyl-coenzyme A reductase. Differential scanning calorimetry analysis of the PHA copolymers produced by the recombinant R. eutropha PHB-4 have indicated that the PHA is a random copolymer of 3HB and mcl-3HA units.

IL-1 alpha, but not IL-1 beta, is required for contact-allergen-specific T cell activation during the sensitization phase in contact hypersensitivity.

Contact hypersensitivity (CHS) is a T cell-mediated cellular immune response caused by epicutaneous exposure to contact allergens. In this reaction, after the first epicutaneous allergen sensitization, Langerhans cells (LC) catch allergens and migrate from the skin to draining lymph nodes (LN) and activate naive T cells. Although IL-1 is suggested to be involved in these processes, the mechanisms have not been elucidated completely. In this report, to elucidate roles of IL-1alpha and IL-1beta in CHS, we analyzed ear swelling in 2,4,6-trinitrochlorobenzene (TNCB)-induced CHS using gene-targeted mice. We found that ear swelling was suppressed in IL-1alpha-deficient (IL-1alpha(-/-)) mice but not in IL-1beta(-/-) mice. LC migration from the skin into LN was delayed in both IL-1alpha(-/-) and IL-1beta(-/-) mice, suggesting that this defect was not the direct cause for the reduced CHS in these mice. However, we found that the proliferative response of trinitrophenyl (TNP)-specific T cells after sensitization with TNCB was specifically reduced in IL-1alpha(-/-) mice. Furthermore, adoptive transfer of TNP-conjugated IL-1-deficient epidermal cells (EC) into wild-type mice indicated that only IL-1alpha, but not IL-1beta, produced by antigen-presenting cells in EC could prime allergen-specific T cells. These observations indicate that IL-1alpha, but not IL-1beta, plays a crucial role in TNCB-induced CHS by sensitizing TNP-specific T cells.

Modulation of serotonin2A receptor function in rats after repeated treatment with dexamethasone and L-type calcium channel antagonist nimodipine.

1. It has been conceivable that the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity plays an important role in the pathophysiology of depression. In the present study, we have investigated the effect of repeated treatment with dexamethasone on serotonin (5-HT) 1A, 5-HT2A and alpha1-adrenergic receptors in the rat frontal cortex. Moreover, several studies have suggested the effectiveness of L-type calcium channel antagonist nimodipine for the treatment of depression. We also investigated the effect of repeated treatment with nimodipine on 5-HT2A receptor in rats with repeated dexamethasone treatment. 2. Repeated treatment with dexamethasone (1 mg/kg/day for 14 days) increased the density of 5-HT2A receptor, but not 5-HT1A and alpha1-adrenergic receptors in the rat frontal cortex. 3. The density of 5-HT2A receptor in the rat frontal cortex was significantly increased 1 day after repeated treatment with dexamethasone, but was not increased 7 or 14 days after repeated treatment. Wet dog shakes (WDS) induced by (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI), a 5-HT2A receptor agonist, in rats were significantly enhanced 1, 7 and 14 days after repeated treatment with dexamethasone, although the frequency of WDS gradually decreased after repeated treatment. 4. Repeated treatment with nimodipine (5 mg/kg/day for 14 days) attenuated DOI-induced WDS enhanced by repeated treatment with dexamethasone (1 mg/kg/day for 14 days), however, it did not change the density of 5-HT2A receptor. Repeated treatment with dexamethasone decreased locomotor activity and body weight, but repeated treatment with nimodipine did not recover these parameters. 5. The results of the present study suggest that repeated treatment with dexamethasone may selectively increase the 5-HT2A receptor in the rat frontal cortex and affect 5-HT2A receptor-mediated signal transduction. In addition, the intracellular calcium homeostasis by blocking calcium influx through L-type calcium channel may play an important role in the regulation of the 5-HT2A receptor function by dexamethasone.

IL-1 enhances T cell-dependent antibody production through induction of CD40 ligand and OX40 on T cells.

IL-1 is a proinflammatory cytokine that plays pleiotropic roles in host defense mechanisms. We investigated the role of IL-1 in the humoral immune response using gene-targeted mice. Ab production against SRBC was significantly reduced in IL-1alpha/beta-deficient (IL-1(-/-)) mice and enhanced in IL-1R antagonist(-/-) mice. The intrinsic functions of T, B, and APCs were normal in IL-1(-/-) mice. However, we showed that IL-1(-/-) APCs did not fully activate DO11.10 T cells, while IL-1R antagonist (-/-) APCs enhanced the reaction, indicating that IL-1 promotes T cell priming through T-APC interaction. The function of IL-1 was CD28-CD80/CD86 independent. We found that CD40 ligand and OX40 expression on T cells was affected by the mutation, and the reduced Ag-specific B cell response in IL-1(-/-) mice was recovered by the treatment with agonistic anti-CD40 mAb both in vitro and in vivo. These observations indicate that IL-1 enhances T cell-dependent Ab production by augmenting CD40 ligand and OX40 expression on T cells.

Effect of acute lipopolysaccharide administration on (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2 aminopropane-induced wet dog shake behavior in rats: comparison with body weight change and locomotor activity.

1. Several reports have shown that serotonin (5-HT)2A receptor density and its function are altered after physiological or pharmacological stress. To examine whether an acute administration of lipopolysaccharide (LPS), a bacterial endotoxin, affected 5-HT2A receptor function, wet dog shakes of male Wistar rats were observed after a subcutaneous injection of DOI, a 5-HT2A receptor agonist following LPS treatment. Body weight change and locomotor activity were also observed. 2. DOI (1 mg/kg)-induced WDS significantly decreased after 400 or 1000 microg/kg LPS treatment compared with that of control rats 1 and 3 hr after injection, and WDS completely recovered 8 hr after LPS treatment. Treatment with 10 mg/kg indomethacin (IND) or 1 mg/kg naltrexone (NLTX) canceled the effect of 400 microg/kg LPS on DOI-induced WDS. 3. Body weight decrease was significantly greater in LPS-treated rats compared with control rats 3, 5 and 8 hr after treatment. Treatment with IND (10 mg/kg) significantly recovered the reduction in body weight induced by 400 microg/kg LPS. Treatment with NLTX (1 mg/kg) also prevented the LPS effect on body weight decrease. 4. Eight hr after treatment with LPS (400 microg/kg), the rats showed significant attenuation of locomotor activity. IND (10 mg/kg) treatment abolished the inhibitory effect of LPS on locomotor activity, and NLTX (1 mg/kg) also improved the decrease in locomotion 8 hr after LPS treatment. 5. Plasma tumor necrosis factor (TNF)-alpha concentration dramatically increased 1 hr after the injection of 400 microg/kg LPS, and returned almost to the basal level 3 hr later. Next, rats were injected with 50 microg/kg TNF-alpha intraperitoneally, and body weight change and DOI-induced WDS was determined 3 hr after TNF-alpha injection. Body weight loss was significantly greater in rats treated with TNF-alpha. On the other hand, DOI-induced WDS was not altered when rats were treated with TNF-alpha. 6. These results suggest that acute treatment with LPS inhibited 5-HT2A receptor-mediated behavior via cyclooxygenase and opioid receptor activation, but that the inhibition of the WDS by LPS appears to be independent of TNF-alpha production.

Interleukin-1 beta, but not interleukin-1 alpha, is required for T-cell-dependent antibody production.

Interleukin-1 (IL-1) consists of two molecules, IL-1 alpha and IL-1 beta, and IL-1 receptor antagonist (IL-1Ra) is a natural inhibitor of these molecules. Although the adjuvant effects of exogenously administered IL-1 in the humoral immune response are well known, the roles of endogenous IL-1 and the functional discrimination between IL-1 alpha and IL-1 beta have not been elucidated completely. In this report, we investigated the role of IL-1 in the humoral immune response using gene-targeted mice. Both primary and secondary antibody production against T-dependent antigen, sheep red blood cells (SRBC), was significantly reduced in IL-1 alpha/beta-/- mice, and was enhanced in IL-1Ra-/- mice. The intrinsic functions of B cells, such as antibody production against type 1 T-independent antigen, trinitrophenyl-lipopolysaccharide and proliferative responses against mitogenic stimuli, were normal in IL-1 alpha/beta-/- mice. The proliferative response of T cells and cytokine production upon stimulation with anti-CD3 monoclonal antibody were also normal, as was the phagocytotic ability of antigen-presenting cells (APCs). However, SRBC-specific proliferative response and cytokine production of T cells through the interaction with APCs were markedly impaired in IL-1 alpha/beta-/- mice, and enhanced in IL-1Ra-/- mice. Moreover, we show that SRBC-specific antibody production was reduced in IL-1 beta-/- mice, but not in IL-1 alpha-/- mice. These results show that endogenous IL-1 beta, but not IL-1 alpha, is involved in T-cell-dependent antibody production, and IL-1 promotes the antigen-specific T-cell helper function through the T-cell-APC interaction.

Development of chronic inflammatory arthropathy resembling rheumatoid arthritis in interleukin 1 receptor antagonist-deficient mice.

Interleukin (IL)-1 is a proinflammatory cytokine that plays important roles in inflammation, host defense, and the neuro-immuno-endocrine network. IL-1 receptor antagonist (ra) is an endogenous inhibitor of IL-1 and is supposed to regulate IL-1 activity. However, its pathophysiological roles in a body remain largely unknown. To elucidate the roles of IL-1ra, IL-1ra-deficient mice were produced by gene targeting, and pathology was analyzed on different genetic backgrounds. We found that all of the mice on a BALB/cA background, but not those on a C57BL/6J background, spontaneously developed chronic inflammatory polyarthropathy. Histopathology showed marked synovial and periarticular inflammation, with articular erosion caused by invasion of granulation tissues closely resembling that of rheumatoid arthritis in humans. Moreover, elevated levels of antibodies against immunoglobulins, type II collagen, and double-stranded DNA were detected in these mice, suggesting development of autoimmunity. Proinflammatory cytokines such as IL-1beta, IL-6, and tumor necrosis factor alpha were overexpressed in the joints, indicating regulatory roles of IL-1ra in the cytokine network. We thus show that IL-1ra gene deficiency causes autoimmunity and joint-specific inflammation and suggest that IL-1ra is important in maintaining homeostasis of the immune system. Possible involvement of IL-1ra gene deficiency in RA will be discussed.

Peculiar respiratory response observed during sleep-onset REM sleep of an infant with Ondine's curse.

We treated an infant with congenital central hypoventilation syndrome ("Ondine's curse"). She was cyanotic and given ventilatory support at the first hour after birth. An investigation of sleep state and respiration performed at the age of 3 months led to this diagnosis. Hypoventilation persisted in all sleep stages, with the most severely reduced tidal volumes occurring during delta-wave sleep (stages 3 and 4). In addition, severe secondary reduction in tidal volumes occurred in sleep-onset REM sleep. This phenomenon was absent in non sleep-onset REM sleep. At 4 months of age, her respiratory treatment was successfully converted to positive-pressure ventilation via a nasal mask, thus avoiding tracheotomy. This transition to noninvasive ventilatory support dramatically improved her quality of life during wakefulness. This report may be a clue to discuss the function of sleep-onset REM sleep seen in the early stage of life and suggests that nasal mask ventilation is a viable option in selected cases with congenital central hypoventilation syndrome (CCHS).

Expression of nm23-H1 in colorectal cancer: no association with metastases, histological stage, or survival.

The correlations of nm23-H1 expression in primary cancer lesions with the already confirmed 14 prognostic variables and survival were examined in 52 advanced colorectal cancer patients, because the clinical roles of nm23-H1 expression in the cancer lesions remain controversial. An immunohistochemical expression of nm23-H1 was found in 23 lesions (positive group) but not found in 29 lesions (negative group). No significant difference between the positive and negative groups was found according to 12 clinicopathological variables including vascular invasion, lymph node and liver metastases, and histological stage. The carcinoembryonic antigen levels (21.5+/-33.4 ng/ml) of the draining venous blood and argyrophilic nucleolar organizer regions score (3.35+/-1.36 per nucleus) of the cancer cells in the positive group were not significantly diffeent from those (34.1+/-102.9 ng/ml and 3.32+/-1.00 per nucleus, respectively) in the negative group. In addition, no significant difference was found in the survival curves or the 5-year survival rates of the positive and negative groups. From these results, it may be concluded that the nm23-H1 expression was not associated with the aforementioned prognostic variables and the prognosis of advanced colorectal cancer patients.

Prospective echocardiographic analysis of progressive obstruction of the proximal pulmonary artery in congenital heart disease and obstructed pulmonary flow.

BACKGROUND: It is uncertain whether proximal pulmonary artery (PA) obstruction exists soon after birth and whether its progress relates directly to postnatal ductal constriction in congenital heart disease and obstructed pulmonary flow. METHODS: Serial morphometric analyses of the PA branches by echocardiogram were performed in 28 patients (mean age at initial study 2.5 days) until severe constriction of the ductus occurred (mean age 47 days). These patients were divided into 2 groups by subsequent angiographic or postmortem confirmation; 10 with proximal PA obstruction (group 1) and 18 without obstruction (group 2). RESULTS: At the time of initial examination, the mean indexed diameter of the proximal PA on the side of the ductus arteriosus in group 1 was significantly smaller than that on the contralateral side (5.2+/-0.7 versus 9.0+/-0.7 mm/BSA0.5, P < .001) or that in group 2 (8.0+/-0.4 mm/BSA0.5, P < .001). In group 1, 8 patients had a proximal PA index on the ductal side < or = 5.5 mm/BSA0.5, which was less than those of any group 2 patients. After severe constriction of the ductus, the proximal PA index on the ductal side further decreased only in group 1 (P < .01). CONCLUSIONS: These data indicate that unilateral obstructive lesion of branch PA is present shortly after birth and its progression relates directly to ductal constriction. Neonates with branch PA obstruction can be identified on their initial echocardiogram as having a proximal PA index on the ductal side < or = 5.5 mm/BSA0.5.

Evaluation of argyrophilic nucleolar organizer region and proliferating cell nuclear antigen in colorectal cancer.

BACKGROUND AND OBJECTIVES: Information on cellular proliferation is gaining importance for predicting prognosis in several cancers. To clarify the clinicopathological significance of argyrophilic nucleolar organizer region (AgNOR), proliferating cell nuclear antigen (PCNA), and DNA ploidy pattern, we studied their correlations with clinicopathological factors in colorectal cancer. METHODS: Fifty-two patients with colorectal cancer were examined by AgNOR staining, immunohistochemical study of PCNA expression, and DNA flow cytometry. RESULTS: The AgNOR score and the PCNA labeling rate (PCNA LR) were significantly higher in patients with deep invasion (P = 0.0072, P = 0.0355), liver metastasis (P = 0.0022, P = 0.0001), and Dukes D classification (P = 0.0002, P = 0.0001) than in patients without these factors. In patients with high AgNOR score (>3.83) or with high PCNA LR (>48.8), prognosis was significantly worse (P = 0.0002, P = 0.0123) than in those with low AgNOR score (<3.83) or in those with low PCNA LR (<48.8), respectively. No significant association was observed between AgNOR score and PCNA LR. Combined analysis revealed that the survival curve for patients with high AgNOR score and high PCNA LR was significantly lower (P = 0.0156) than that for patients with high AgNOR score and low PCNA LR. There was no significant correlation between DNA ploidy pattern and clinicopathological findings. CONCLUSIONS: PCNA LR and AgNOR score were correlated not only with local progression but also with metastasis. Their determination provided useful prognostic information, and these parameters are probably independent. Their simultaneous determination was useful for accurate evaluation of prognosis. The value of DNA ploidy pattern was uncertain.

Effect of suture closure of coronary artery fistula on aneurysmal coronary artery and myocardial ischemia.

This study indicates the importance of coronary angiography and myocardial scintigraphy on long-term follow-up of patients after surgery for coronary arterial fistula in view of the progression to coronary artery obstruction and myocardial ischemia.

A case of intraductal papilloma of breast in advanced age.

Breast tumors have their various biological characteristics as to advanced age of patients. Intraductal papilloma is a benign tumor of the breast which is known to occur in the premenopausal young females. Tumors of the breast in the senile females are found mainly to be breast cancers. No any cases of intraductal papilloma over 80-years were reported in Japan to date. We have recognized mammary tumors in old aged patients to be cancers, but it is necessary to put it into mind there are a few intraductal papillomas even if advanced in age. In this report, we present the most senile case with intraductal papilloma in our institute.

Correction of truncus arteriosus with autologous arterial flap in neonates and small infants.

BACKGROUND: This study describes the results of techniques using the autologous truncal wall and part of the pulmonary artery for correction in anticipation of the growth of the pulmonary tract in patients with truncus arteriosus. METHODS: Seven consecutive patients with truncus arteriosus were reviewed. The posterior wall of the pulmonary tract was obtained by anastomosing the lower edge of the truncal arteriotomy to the upper corner of the ventriculotomy from the truncus in types I and II. Anterior translocation of the pulmonary artery was performed in a type III. A pericardial patch with or without a monocusp was placed to complete the right ventricular outflow tract. RESULTS: There were two hospital deaths, one of which was unrelated to a cardiac problem. Postoperative right-to-left ventricular peak pressure ratio was less than 0.55. There was one left pulmonary stenosis due to monocusp adherence in the late postoperative period. The sizes of the pulmonary tract at anastomosis were between 107% and 166% of the normal value between 7 months and 3.8 years of follow-up. CONCLUSIONS: The use of autologous arterial wall instead of a conduit is recommended for the repair of truncus arteriosus to expect growth of the pulmonary tract.