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Biomedical subjects

Kentaro Motoyama

Publications and source records attributed to Kentaro Motoyama.

6 recordsLinked to original sources

Effect of synthetic protease inhibitor gabexate mesilate on the attenuation of ischemia/reperfusion injury in canine kidney autotransplantation.

BACKGROUND: Kidneys from non-heart-beating donors are associated with delayed graft function and a high rejection rate due to the long period of warm ischemia. Gabexate mesilate (GM), a synthetic serine protease inhibitor, has been shown to improve organ function by suppressing cytokine activity and neutrophil function after ischemia/reperfusion. In this study, we evaluated the effect of GM on renal function after warm ischemia in a canine kidney autotransplantation model. METHODS: After 60 minutes of warm ischemia, the left kidney was transplanted into the iliac fossa, and the right kidney was removed. The control group (n = 7) and GM group (n = 7) were evaluated for serum creatinine and blood urea nitrogen (BUN) concentrations, renal tissue blood flow, resistive index, pulsatility index, interleukin (IL)-1beta and tumor necrosis factor (TNF)-alpha mRNA expression levels in peripheral blood mononuclear cells, apoptotic index, CD10 immunolabeling as an indicator of brush border injury, and standard histopathology. RESULTS: Compared with controls, administration of GM resulted in lower serum creatinine concentrations (11.3 +/- 2.4 vs 5.2 +/- 3.3 mg/dL at 72 hours; P = .04) and BUN concentrations (188 +/- 26 mg/dL vs 98 +/- 41 mg/dL at 72 hours; P = .04), as well as better tissue blood flow, improvement of brush border injury and apoptotic index (each P < .05). The expression of IL-1beta and TNF-alpha mRNA did not change after administration of GM. CONCLUSIONS: The present study shows that GM protected renal function after warm ischemia/reperfusion by inhibition of serine proteases, maintenance of tissue blood flow, and amelioration of tubular apoptosis.

Animals↗

Recurrent nephrotic syndrome after living-related renal transplantation resistant to plasma exchange: report of two cases.

We encountered two patients of recurrent nephrotic syndrome (NS) after renal transplantation that was resistant to plasma exchange (PEX). Case 1 was a 34-year-old man with a living-related renal transplant for type-I membranoproliferative glomerulonephritis (MPGN) related end-stage renal disease (ESRD). He developed overt proteinuria 7 months post-transplant and presented with NS 5 months later. Biopsy of the transplant kidney revealed recurrent type I MPGN, but no features of acute rejection (AR) or chronic allograft nephropathy (CAN). He was treated with cyclophosphamide (CP), oral prednisolone (40 mg/d), an anti-platelet agent, heparin sulfate, and PEX, but the nephrotic state persisted and renal function was deteriorated. He recommenced hemodialysis 3 yr and 9 months after renal transplant. Case 2 was a 47-year-old male who underwent living-related renal transplant for ESRD due to focal segmental glomerulosclerosis (FSGS). He presented with proteinuria shortly after renal transplantation. He also had frequent episodes of AR. Graft biopsy revealed recurrent FSGS. Treatment of pulse methylprednisolone and PEX was transiently effective, but NS relapsed shortly after PEX. Graft biopsy at our hospital showed features of CAN with moderate interstitial fibrosis and tubular atrophy, presence of intraglomerular foam cells but no segmental sclerosis. Treatment with 12 courses of low-density lipoprotein apheresis (LDL-A) reduced proteinuria from 9.6 to 2.0 g/d, and incomplete remission has been maintained for more than 1 yr after LDL-A with slowly progressive renal dysfunction. Despite recent therapeutic advances, including the use of immunosuppressants and PEX, treatment of recurrent disease remains difficult. The LDL-A might be useful in cases with recurrent FSGS resistant to PEX.

Adult↗

DNA interference: a simple and efficient gene-silencing system for high-throughput functional analysis in the fern adiantum.

RNA interference (RNAi) has become a powerful tool for determining gene function and is used in a wide variety of organisms. Since it is necessary to generate double-stranded RNA (dsRNA) as an inducer for RNAi, preparation of RNAi-inducing constructs is somewhat cumbersome and time consuming, especially for the thousands of genes used in a genome-wide analysis. To overcome these problems, we have developed a more convenient gene-silencing method in the fern Adiantum using double-stranded DNA (dsDNA) as a model system for functional analysis in plants. Delivery of dsDNA fragments homologous to an endogenous gene into gametophytic cells can induce sequence-specific gene silencing. As it only requires dsDNA fragments homologous to a target gene, PCR-amplified fragments are enough to trigger gene silencing. Maximum gene silencing efficiencies of >90% have been achieved for transformed plants. In addition, simultaneous transfer of dsDNA fragments corresponding to multiple genes still has a silencing effect for individual genes. We term this approach 'DNA interference'.

Adiantum↗

[A case of para-aortic lymph node recurrence of gallbladder cancer completely responding to single drug (UFT) chemotherapy].

A 67-year-old man with gallbladder cancer was treated by cholecystectomy and extrahepatic bile duct resection with regional lymph node dissection. At 10 months after surgery, CT demonstrated para-aortic lymph node recurrence. Single drug chemotherapy of UFT at 400 mg was started. After one month, the lymph node recurrence could not be detected by CT. UFT may be the primary candidate for chemotherapy for lymph node recurrence of gallbladder cancer.

Adenocarcinoma↗

Focal pancreatic hemorrhage mimicking pancreas carcinoma with lymph node metastasis.

A 67-year-old man was referred to our department because of a mass in the pancreas tail. Pancreatic tail cancer with lymph node metastasis was diagnosed, based on various radiological findings. Computed tomography (CT) revealed a slightly enhanced tumor mass around the celiac plexus, and endoscopic retrograde pancreatography (ERP) showed complete obstruction of the main pancreatic duct at the tail, although magnetic resonance imaging (MRI) demonstrated no elevation of the mean pixel value of the tumor after gadolinium (Gd) injection, and tumor markers of pancreas cancer were within normal limits. At surgery, the mass around the celiac plexus was found to be blood coagulation, and the pancreas tail tumor was found to be a focal hematoma in the pancreas. Pathologically, the hematoma was not encapsulated, and it was diagnosed as hemorrhage in the pancreas parenchyma. Both hemorrhagic lesions were suspected to have developed respectively. It is difficult to distinguish pancreas hemorrhage from carcinoma in the pancreas with chronic pancreatitis, especially when the hemorrhage is small in size and there are other extrapancreatic hemorrhagic lesions. For such diagnosis, the superiority of MRI with Gd injection is indicated.

Aged↗

Benign nonepithelial fibroma in the pancreas.

This is, to our knowledge, the first report of a fibroma originating in the pancreas in which preoperative imaging findings or explicit descriptions of histopathologic observations are clearly described. A 64-year-old man was referred to our hospital for further evaluation of a pancreatic mass. Clinical examination and laboratory analysis revealed no abnormal findings, except for mild elevation of serum trypsin (550 ng/ml). Abdominal ultrasonogram, computed tomographic scan, magnetic resonance imaging, and angiography demonstrated a well-demarcated circular mass in the tail of the pancreas. A laparotomy was performed on April 26, 1995. The tumor was observed to be tan-colored and smooth, and was localized in the front of the pancreas tail, suggesting that it had arisen from the pancreatic capsule. The patient underwent enucleation of the tumor. The resected tumor presented macroscopically as a fibrous nodule measuring 5.5 x 6.0 cm. The pathological diagnosis was fibroma. Immunohistochemically, spindle cells were positive for vimentin and negative for alpha-smooth muscle actin, desmin, S-100, and neuron-specific enolase.

Fibroma↗