Optimization of acoustic coupling for bottom actuated scattering based subsurface scanning probe microscopy.

The characterization of buried nanoscale structures nondestructively is an important challenge in a number of applications, such as defect detection and metrology in the semiconductor industry. A promising technique is Subsurface Scanning Probe Microscopy (SSPM), which combines ultrasound with Atomic Force Microscopy (AFM). Initially, SSPM was used to measure the viscoelastic contrast between a subsurface feature and its surrounding medium. However, by increasing the ultrasonic frequency to >1 GHz, it has been shown that SSPM can also measure acoustic impedance based contrasts. At these frequencies, it becomes difficult to reliably couple the sound into the sample such that the AFM is able to pick up the scattered sound field. The cause is the existence of strong acoustic resonances in the sample, the transducer, and the coupling layer-the liquid layer used to couple the sound energy from the transducer into the sample-in combination with the nonlinearity of the tip-sample interaction. Thus, it is essential to control and measure the thickness of the coupling layer with nanometer accuracy. Here, we present the design of a mechanical clamp to ensure a stable acoustic coupling. Moreover, an acoustic method is presented to measure the coupling layer thickness in real-time. Stable coupling layers with thicknesses of 700 ± 2 nm were achieved over periods of 2-4 h. Measurements of the downmixed AFM signals showed stable signal intensities for >1 h. The clamp and monitoring method introduced here makes scattering based SSPM practical, robust, and reliable and enables measurement periods of hours.

Synthesis of monolayer platinum nanosheets.

Platinum (Pt) nanosheets were developed by exfoliating layered platinum oxide. Moreover, we succeeded in synthesizing monolayer Pt nanosheets for the first time by adjusting the conditions for reduction. Monolayer Pt nanosheets were highly active in oxygen reduction reaction.

Osteoprotegerin is secreted into the coronary circulation: a possible association with the renin-angiotensin system and cardiac hypertrophy.

The circulating osteoprotegerin (OPG) level reflects a series of cardiovascular diseases; however, the source(s) of circulating OPG remain(s) to be determined. This study explored whether OPG is released in the coronary circulation and whether it is associated with cardiac structure and function. Fifty-six patients (67±10 years old, male 57%, hypertension 73%, coronary artery disease 50%) were enrolled, and blood samples were collected simultaneously from the orifice of the left coronary artery (CA) and the coronary sinus (CS) after angiography. The concentration of OPG was higher in the CS than in the CA (7.7±4.1 vs. 6.7±3.6 pmol/l, p<0.001). The trans-cardiac OPG concentration was significantly (p=0.019) decreased in patients who have been prescribed either an angiotensin converting enzyme inhibitor or an angiotensin II type 1 receptor blocker (ACEI/ARB). In patients subgroup who did not take an ACEI/ARB (n=27), the trans-cardiac OPG level was positively correlated with age (r=0.396, p=0.041) and relative wall thickness of left ventricle (r=0.534, p=0.004). In multivariate linear regression analysis, relative wall thickness remained to be the independent variable for the trans-cardiac OPG level (p=0.004). Moreover, trans-cardiac OPG was significantly (p=0.021) increased in patients with relative wall thickness greater than 0.45 but it did not differ if the left ventricular mass index was increased (≥116 for males, or ≥ 104 for females, g/m(2)) or not (p=0.627). This study suggests that OPG is secreted into the coronary circulation and is associated with concentric remodeling/hypertrophy of LV, possibly in interactions with the renin-angiotensin system.

Associations of intrauterine growth restriction with placental pathological factors, maternal factors and fetal factors; clinicopathological findings of 257 Japanese cases.

Intrauterine growth restriction (IUGR) is the leading cause of fetal mortality and morbidity. As an etiology, each of placental findings, maternal factors and fetal factors has been reported to be associated with IUGR, although a comprehensive approach to examine all of these parameters as a cause of IUGR has not been reported. In the present study, therefore, we comprehensively examined the placental findings and maternal and fetal factors in the cases of IUGR (n=257, mean maternal age, 30 years; gestational weeks, 34 weeks) and normal growth pregnancies (n=258, mean maternal age, 30 years; gestational weeks, 33 weeks), and determined risk factors for IUGR. The prevalence of pregnancy hypertension (PHT) (19% vs. 8%, P<0.01), smoking habit (3% vs. 0.7%, P<0.05) and fetal anomaly (3.5% vs. 0.8%, P<0.05) were higher in IUGR cases than normal growth pregnancies. Pathologically, the prevalence of infarction (33% vs. 14%, P<0.05), fetal vessel thrombosis (22% vs. 6%, P<0.001) and chronic villitis (11% vs. 3%, P<0.001) were higher in IUGR cases than those in normal growth pregnancies. A multivariable regression analysis revealed that maternal factors (PHT), fetal factors (anomaly), and placental findings (infarction, fetal vessel thrombosis, and chronic villitis) are independently associated with increased risk of IUGR (all P<0.01).

Total pancreatectomy combined with partial pancreas autotransplantation for recurrent pancreatic cancer: a case report.

We describe a patient presenting with a resectable carcinoma of the remnant pancreas at 3 years after undergoing a pylorus-preserving pancreaticoduodenectomy for invasive ductal carcinoma of the pancreatic head. We also performed a distal pancreas autotransplantation using a part of the resected pancreas to preserve endocrine function. Final histologic findings showed the second tumor to be an invasive ductal carcinoma consisting of a well-differentiated tubular adenocarcinoma with similar histopathologic findings as the first tumor. There were no microscopic lymph node metastases and no evidence of microvascular invasion (pStage IA [pT1, pN0, M0] and R0 according to the International Union Against Cancer TNM classification). The patient was discharged at 20 days after surgery without any trouble and followed by adjuvant chemotherapy with S-1. The carbohydrate antigen 19-9 value was again normalized after the second surgery. Twenty months after the second operation, the patient is alive without cancer recurrence. The pancreas graft is functioning with a blood glucose of 108 mg/dL, HbA1C of 6.2%, and serum C-peptide of 1.4 ng/mL.

Magnetic compression anastomosis for bile duct stenosis after donor left hepatectomy: a case report.

Magnetic compression anastomosis (MCA) provides a minimally invasive treatment creating a nonsurgical, sutureless enteric anastomosis in conjunction with an interventional radiologic technique by using 2 high-power magnets. Recently, the MCA technique has been applied to bile duct strictures after living donor liver transplantation or major hepatectomy. Herein we described use of MCA for bile duct stenosis 5 months after donor left hepatectomy in a 24-year-old man who presented with a stricture at the porta hepatis and intrahepatic bile duct dilatation. Unsuccessful transpapillary biliary drainage and balloon dilatation through a percutaneous transhepatic biliary drainage (PTBD) route led to the MCA. A 4-mm-diameter cylindrical samarium-cobalt (Sm-Co) daughter magnet with a long nylon wire was placed at the superior site of the obstruction through the PTBD route. A 5-mm-diameter Sm-Co parent magnet with an attached nylon handle was endoscopically inserted into the common bile duct and placed at the inferior site of obstruction. The 2 magnets were attracted, sandwiching the stricture and establishing a reanastomosis. In conclusion, the MCA technique was a unique procedure for choledochocholedochostomy in a patient with bile duct stenosis after donor hepatectomy.

Successful laparoscopic-assisted hemostasis of intrathoracic massive vericeal rupture during living related liver transplantation: a case report.

End-stage liver disease that requires transplantation is usually accompained by esophagogastric or another collateral vessel varices. Sometimes, the esophagogastric varices rupture intraoperatively during liver transplantation. However we have reported rare case of rupture of an intercostal varicose vein, which was controlled successfully by flexible laparoscopy. The patient was a 62-year-old man, who suffered decompensated liver cirrhosis with hepatocellular carcinoma. The Child-Pugh score was 11 and the Model for End-stage Liver Diseases score was 14. Preoperative gastrointestinal fiberscopy and colon fiberscopy examinations revealed esophagogastric and rectal varices. He underwent living related liver transplantation from his son on February 10, 2010. Just after the liver transplantation, the patient's blood pressure tended to decrease. Chest radiography demonstrated a massive right pleural effusion. We drained 3000 mL of blood by thoracic puncture. Therefore we reoperated him for the question an intrathoracic variceal hemorrhage. We confirmed variceal bleeding after removal of the massive hematoma by opening the diaphragm. However, we could neigher show directly the bleeding point in the anterior thorax nor stop it because of the constriction of the diaphragm. Therefore we used a flexible laparoscope to both confirm the bleeding point and to achieve hemostasis. We believe that theoperative compression of the intercostal varicose vein by a retractor induced the vascular rupture.

Regulatory T-cell activation among patients who displayed operational tolerance following intra-portal administration of donor-specific antigens in living donor liver transplantation.

Immunologic tolerance is the goal for all transplant surgeons. We have reported that repeated donor-specific antigen transfusion (DST) via the portal vein allowed rapid reduction of immunosuppressants with decreased acute cellular rejection episodes among living donor liver transplantations (LDLT). Moreover, we demonstrated that intraportal DST induced macrochimerism of donor type CD56+ T cells in the liver graft. We examined the impact of FoxP3+CD4+CD25+ T cells in recipients who acquired almost tolerance after LDLT with intraportal DST. We defined the amount of immunosuppressants administered less than one time per week as "almost tolerance" after LDLT, which occurred among 14% of DST patients after adult-to-adult LDLT. Two patients (4%) have gotten been we used from immunosuppressants more than 2 years after LDLT 4 years prior. We examined the impact of FoxP3+CD4+CD25+ T cells both in recipients with almost daily immunosuppressants and those who acquired almost tolerance. The proportion of FoxP3+/CD4+CD25+ T cells in the almost tolerance group was significantly higher than that in the almost daily immunosuppressant group (P<.05). The increased proportion of FoxP3+/CD4+CD25+ T cells significantly correlated with time after LRLT (y=0.0964x+42.02, R2=0.8854). Repeated intraportal DST may be a goot tool to induce immunologic tolerance after LDLT. Both donor type CD56+ T cells and FoxP3+/CD4+CD25+ T cells may act as important regulatory cells for tolerance. The period after LDLT is important for acquiring immunologic tolerance.

De novo ulcerative colitis and autoimmune hepatitis after living related liver transplantation from cytomegalovirus-positive donor to cytomegalovirus-negative recipient: a case report.

BACKGROUND: De novo autoimmune hepatitis (AIH) after liver transplantation (OLT) has been reported; however, de novo ulcerative colitis (UC) combined with AIH after OLT is rare. MATERIALS AND METHODS: We report a patient who suffered de novo UC with AIH after living related OLT (LRLT) due to fulminant hepatitis using a cytomegalovirus (CMV)-positive donor to a CMV-negative recipient. RESULTS: A 32-year-old man underwent LRLT due to fuluminant hepatis 4 years prior. He was admitted for colitis with diarrhea, abdominal pain, and high fever in March 2010. The abdominal computed tomography revealed severe jejunal edema. Anti-infectious therapies for bacterial, fungal, and CMV cases were ineffective. Small bowel endoscopy demonstrated erosion, redness, ulceration, and edema from the stomach to the jejunum. However, the origin of the colitis was not clear. Thereafter he displayed melena with a high fever and abdominal pain. The colon revealed diffuse inflammation with pseudopolyposis. De novo UC or CMV infection was suspected. His symptoms improved upon administration of salazopyrin and denosine. Moreover, he suffered de novo AIH, which was diagnosed by liver biopsy 3 months after the de novo UC. Steroid therapy improved the AIH. CONCLUSIONS: It has been reported that CMV is involved with UC and rejection. Our case suggested that CMV might induce de novo UC or AIH in CMV-negative recipients.

Liver transplantation surgical techniques for extensive retroperitoneal tumor with major blood vessel involvement: a case report.

A case of a 71-year-old man with a huge retroperitoneal tumor situated behind the liver, which strongly compressed the liver inferior vena cava (IVC), and gastrointestinal tract is described. With the techniques of whole liver extraction and autologous orthotopic liver transplantation, we successfully removed the tumor. We have the surgical techniques, essential elements, and indications for this procedure.

Isolated dissection of the superior mesenteric artery after living donor liver transplantation: a case report.

Isolated dissection of the superior mesenteric artery (SMA) not associated with aortic dissection is rare, particularly after living donor liver transplantation (LDLT). We experienced a case of isolated dissection of the SMA after LDLT performed in a 56-year-old man diagnosed with hepatitis B virus-related cirrhosis and hepatocellular carcinoma within the Milan criteria. He had no past history of hypertension or diabetes mellitus. At 6 days after LDLT, the patient underwent an emergency portal vein thrombectomy with ligation of a huge left gastric vein shunt. Thereafter anticoagulant and antiplatelet therapy were initiated. At 12 days after LDLT, a contrast-enhanced computer assisted tomography (CT) scan revealed the presence of a thrombus in a false lumen and a thin flap enlarged in the SMA. Because he presented neither abdominal pain nor biochemical data suggesting mesenteric ischemia, he was treated with antihypertensive agents in addition to anticoagulant and antiplatelet therapy. The thrombus in the false lumen was reduced and the intimal flap in the SMA disappeared according to the results of a CT scan 4 months after LDLT. He has remained free of symptoms for 4 years. The strategy to treat isolated SMA dissection is not well established. Urgent surgery is indicated for acute symptomatic forms with a suspicion of mesenteric ischemia; conservative treatment is indicated for patients with minimal, resolving, or no pain, but requires close follow-up.

The inferior mesenteric vein to the left gonadal vein shunt for gastroesophageal varices and extrahepatic portal vein thrombosis after living donor liver transplantation: a case report.

This 59-year-old woman underwent living donor liver transplantation using a left lobe graft as an aid for autoimmune hepatitis in 2003. Splenectomy was also performed because of blood type incompatibility. Follow-up endoscopic and computed tomography examinations showed gastroesophageal varices with extra hepatic portal vein thrombosis in 2007 that increased (esophageal varices [EV]: locus superior [Ls], moderately enlarged, beady varices [F2], Blue varices [Cb], presence of small in number and localized red color sign [RC1] and telangiectasia [TE+], gastric varices [GV]: extension from the cardiac orifice to the fornix [Lg-cf], moderately enlarged, beady varices [F2], white varices [Cw], absence of red color sign [RC-]). Portal venous flow to the gastroesophageal varices was also confirmed from a large right gastric vein. The splenic vein was thrombosed. Blood flow to the liver graft was totally supplied from the hepatic artery. The graft was functioning well. Because these gastroesophageal varices had a high risk of variceal bleeding, we decided to proceed with a portal reconstruction of a surgical portosystemic shunt in 2008. Severe adhesions were observed around the portal vein. It was impossible to perform portal reconstruction. There were relatively fewes adhesious in the left lower side of the abdominal cavity. We decided to create an inferior mesenteric vein to left gonadal vein shunt. The portal vein pressure decreased from 31.0 to 21.5 cm H2O thereafter. The postoperative course was smooth without any complication. This patient was discharged on the postoperative day 15. Follow-up endoscopic study showed the improvement in the gastroesophageal varices (EV: Ls, F2, Cb, RC(-), GV: Lg-c, F2, Cw, RC-) at 3 months after the operation. We also comfirmed the patency of the shunt by serial computed tomography examinations.

Clinical significance of CADM1/TSLC1/IgSF4 expression in adult T-cell leukemia/lymphoma.

Cell adhesion molecule 1 (CADM1/TSLC1) was recently identified as a novel cell surface marker for adult T-cell leukemia/lymphoma (ATLL). In this study, we developed various antibodies as diagnostic tools to identify CADM1-positive ATLL leukemia cells. In flow cytometric analysis, the percentages of CD4(+)CADM1(+) double-positive cells correlated well with both the percentages of CD4(+)CD25(+) cells and with abnormal lymphocytes in the peripheral blood of patients with various types of ATLL. Moreover, the degree of CD4(+)CADM1(+) cells over 1% significantly correlated with the copy number of the human T-lymphotropic virus type 1 (HTLV-1) provirus in the peripheral blood of HTLV-1 carriers and ATLL patients. We also identified a soluble form of CADM1 in the peripheral blood of ATLL patients, and the expression levels of this form were correlated with the levels of soluble interleukin 2 receptor alpha. Moreover, lymphomas derived from ATLL were strongly and specifically stained with a CADM1 antibody. Thus, detection of CD4(+)CADM1(+) cells in the peripheral blood, measurement of serum levels of soluble CADM1 and immunohistochemical detection of CADM1 in lymphomas would be a useful set of markers for disease progression in ATLL and may aid in both the early diagnosis and measurement of treatment efficacy for ATLL.

Eµ/miR-125b transgenic mice develop lethal B-cell malignancies.

MicroRNA-125b-1 (miR-125b-1) is a target of a chromosomal translocation t(11;14)(q24;q32) recurrently found in human B-cell precursor acute lymphoblastic leukemia (BCP-ALL). This translocation results in overexpression of miR-125b controlled by immunoglobulin heavy chain gene (IGH) regulatory elements. In addition, we found that six out of twenty-one BCP-ALL patients without t(11;14)(q24;q32) showed overexpression of miR-125b. Interestingly, four out of nine patients with BCR/ABL-positive BCP-ALL and one patient with B-cell lymphoid crisis that had progressed from chronic myelogenous leukemia overexpressed miR-125b. To examine the role of the deregulated expression of miR-125b in the development of B-cell tumor in vivo, we generated transgenic mice mimicking the t(11;14)(q24;q32) (Eµ/miR-125b-TG mice). Eµ/miR-125b-TG mice overexpressed miR-125b driven by IGH enhancer and promoter and developed IgM-negative or IgM-positive lethal B-cell malignancies with clonal proliferation. B cells obtained from the Eµ/miR-125b-TG mice were resistant to apoptosis induced by serum starvation. We identified Trp53inp1, a pro-apoptotic gene induced by cell stress, as a novel target gene of miR-125b in hematopoietic cells in vitro and in vivo. Our results provide direct evidence that miR-125b has important roles in the tumorigenesis of precursor B cells.

Human C-reactive protein enhances thrombus formation after neointimal balloon injury in transgenic rabbits.

BACKGROUND: High plasma levels of C-reactive protein (CRP) constitute a powerful predictive marker of cardiovascular events. Several lines of evidence suggest that CRP has prothrombogenic effects. However, whether CRP directly participates in the pathogenesis of thrombosis in vivo has not been fully clarified. OBJECTIVE: To test whether human CRP (hCRP) affects arterial thrombus formation after balloon injury of smooth muscle cell (SMC)-rich or macrophage-rich neointima. METHODS: We compared the susceptibility of transgenic (Tg) rabbits expressing hCRP (46.21 ± 13.85 mg L(-1), n = 22) and non-Tg rabbits to arterial thrombus formation after balloon injury of SMC-rich or macrophage-rich neointima. RESULTS: Thrombus size on SMC-rich or macrophage-rich neointima was significantly increased, and was accompanied by an increase in fibrin content in hCRP-Tg rabbits, as compared with non-Tg rabbits. Thrombus size did not significantly differ between SMC-rich and macrophage-rich neointima in hCRP-Tg rabbits. Tissue factor (TF) mRNA expression and activity in these neointimal lesions were significantly increased in hCRP-Tg rabbits as compared with non-Tg rabbits. The degree of CRP deposition correlated with the elevated TF expression and thrombus size on injured neointima. In addition, hCRP isolated from hCRP-Tg rabbit plasma induced TF mRNA expression and activity in rabbit cultured vascular SMCs. CONCLUSIONS: These results suggest that elevated plasma hCRP levels promote thrombus formation on injured SMC-rich neointima by enhancing TF expression, but have no additive effects in macrophage-rich neointima.

Dysspondyloenchondromatosis: Another COL2A1-Related Skeletal Dysplasia?

Dysspondyloenchondromatosis (DSC) is a rare skeletal dysplasia that has currently been classified into the group of spondylometaphyseal dysplasias. To date, only 12 affected individuals have been reported. All cases are sporadic, and the etiology remains unknown. Distinctive features of DSC are anisospondyly and enchondroma-like lesions in the metaphyseal and diaphyseal portions of the long tubular bones. Affected individuals usually develop kyphoscoliosis and asymmetric limb shortening at an early age. Interestingly, some of the skeletal changes overlap with spondyloepimetaphyseal dysplasia (SEMD) Strudwick type, a rare type II collagen disorder. Based on this resemblance we postulated that DSC may be allelic to SEMD Strudwick type and therefore performed a COL2A1 analysis in an affected boy who was diagnosed as having DSC at the age of 3 years. The identification of a novel heterozygous COL2A1 missense mutation (p.Gly753Asp) in the proband confirms our hypothesis and suggests that DSC may be another type II collagen disorder.

Auxiliary partial orthotopic living donor liver transplantation for fulminant hepatic failure with flat electroencephalogram: a case report.

A 54-year-old woman with hepatic encephalopathy grade IV (coma) and flat electroencephalogram (EEG) due to fulminant liver failure (FHF) due to hepatitis B virus infection was admitted to our hospital on May 24, 2002. We performed a living donor auxiliary partial orthotopic liver transplantation (APOLT) emergently on the day of admission. The donor was the patient's son, whose ABO blood group was identical. The immunosuppressant regimen consisted of tacrolimus and low-dose steroids. The left lobe (260 g) of the recipient, which was removed using a Pringle maneuver, was reconstructed with a left lobe (417 g) graft from the donor, which was orthotopically positioned as an auxiliary support. The patient remained in a coma for the first 5 days but on day 6 her eyes opened and followed objects. Finally, she recovered an almost normal appearance. Abdominal compartment syndrome, bile leak, and a mild rejection episode occurred during the postoperative course; all were treated successfully. The patient was discharged on the postoperative day 142. Computed tomography (CT) scan and biopsy were used to follow the changes in the graft and the native liver. On postoperative day 520, a CT scan showed a remarkable improvement in native liver size (493 cm3). Immunosuppression was tapered off and stopped on the postoperative day 635 to surrender the grafted liver. The graft liver biopsy specimen showed severe chronic rejection. The present status of the patient, who is now more than 7 years after transplantation, is an absence of neurological findings with normal liver function.

The new method of time-lag ligation for portosystemic shunt using coronary artery bypass graft occluder for adult living donor liver transplantation.

We performed a living donor liver transplantation (LDLT) for a 57-year-old man who had end-stage liver failure with portal hypertension and an inferior mesenteric vein-left testicular vein (IMV-LTV) shunt. At operation, we did not clamp the shunt but encircled it with a coronary artery bypass graft (CABG) occluder (Sumitomo Bakelite K.K., Japan), which was passed outside the body through the abdominal wall to time-lag ligation (TLL). On postoperative day (POD) 5, we observed decreased portal flow. We performed TLL of the shunt using the CABG occluder without re-laparotomy. The portal flow increased, while the portal vein pressure increased slightly. In LDLT, portosystemic shunt has been reported to be a cause of portal thrombus formation or graft liver atrophy due to decreased PV flow in the mid postoperative period. However, perioperative ligation of a portosystemic shunt may prevent regeneration of the grafted liver because of excessive portal hypertension. Therefore the technique of time-lag ligation of a portosystemic shunt using a CABG occluder may be a minimally invasive, useful method to achieve physiological liver graft regeneration.

Schwannoma of the esophagus: a case exhibiting high 18F-fluorodeoxyglucose uptake in positron emission tomography imaging.

Esophageal schwannoma is rare and it is difficult preoperatively to confirm a definitive diagnosis, even using current imaging techniques. We present a case of a benign esophageal schwannoma that was surgically excised and confirmed by immunohistochemical staining. Conventional radiological studies, including barium meal, computed tomography and endoscopic examination had shown a solid submucosal tumor of the upper thoracic esophagus but had been unable to confirm the diagnosis. Positron emission tomography was carried out to evaluate the malignant potential and showed a high uptake of 18F-fluorodeoxyglucose (FDG) into the tumor in both the early and delayed phase, suggesting that the tumor was a potentially malignant tumor such as a gastrointestinal stromal tumor. This is the first reported case of esophageal schwannoma that indicated a high FDG uptake. Although consensus has not been reached regarding the precise mechanism of FDG accumulation in schwannomas, we discuss our clinicopathological findings and review other studies of the subject.

Impact of intraportal donor-specific leukocyte transfusion for adult ABO-incompatible liver transplantation.

INTRODUCTION: We have reported that repeated donor-specific leukocyte transfusions (DSLT) via the portal vein allow rapid reduction of immunosuppressants and decrease the occurrence of acute cellular rejection. Herein, we examined the immunological benefits of DSLT in adult ABO-incompatible living donor liver transplantation (LDLT). MATERIALS AND METHODS: Ten adult patients (MELD score, 19.4 +/- 7.3; range, 12-29) underwent LDLT from ABO-incompatible donors from August 2003 to November 2007. The antirejection therapy included multiple perioperative plasmaphereses, splenectomy, and quadruple immunosuppression. In addition to these conventional approaches, we performed 4 intraportal administrations of DSLT after transplantation. RESULTS: There was no humoral rejection in any patient. Two patients experienced mild cellular rejection requiring steroid pulse therapy. Both donor-specific immunoglobulin (Ig)M and IgG A/B antibodies in all patients decreased following transplantation by 16 fold. By flow cytometry, donor type of CD56+NK T cells existed in the liver graft showing macrochimerism at 1 month after liver transplantation. Furthermore, interleukin (IL)-10 production of Th2 type cytokines was up-regulated after transplantation. Three patients died of sepsis and infection. The 5-year survival rate was 70% by the Kaplan-Meier method. CONCLUSION: Adult ABO-incompatible liver transplantation can be performed with acceptable patient and graft survival rates with a low risk of antibody-mediated rejection using intraportal administration of DSLT. Donor type CD56+NK T cells may induce tolerance by a veto or an anti-idiotype network mechanism.