Recovery of renal function after living-related liver transplantation in a case of hepatitis B virus liver cirrhosis with renal failure.
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Publications and source records attributed to K Sano.
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A new photosensitizing agent 5-aminolevulinic acid (ALA)-based photodynamic therapy (PDT) has been demonstrated as a useful method for treatment of superficial neoplastic lesions. The aim of this study was to determine the effects of topically and systemically ALA-based PDT in neoplastic lesions of the oral cavity. Premalignant and malignant lesions of mouse tongue induced by 4-nitroquinoline-l-oxide (4NQO) were used in this study. At 1, 2 and 3 h after topical application of ALA or 3 h after systemic administration of ALA (250 or 1000 mg/kg), the lesions were irradiated with Nd: YAG dye laser at 630 nm (200 J/cm2). Both premalignant and early malignant lesions showed complete response to systemically ALA-based PDT. In an invasive nodular malignant lesion, however, only the superficial portion was affected. There was no apparent difference in the PDT effect between 250 and 1000 mg/kg doses of ALA. In contrast, topically ALA-based PDT had virtually no effect on most lesions. It was concluded that systemically ALA-based PDT is a useful method for treating premalignant and early malignant lesions in the oral cavity, while topically ALA-based PDT using this preparation may be unsuitable for treatment of oral lesions.
Tumour reaction and tumour cell kinetics in mouse NR-S1 carcinoma subjected to photodynamic therapy (PDT) were evaluated by percentage of necrotic area as well as by proliferating cell nuclear antigen (PCNA) immunohistochemistry, and an effective PDT fractionation interval was proposed. PDT was carried out in mouse NR-S1 carcinomas using a photosensitizer (haematoporphyrin oligomers: 20 mg kg body weight) and pulsed Nd:YAG dye laser. The percentages of tumour necrotic area and PCNA labelling indices (LIs) in the tumours were assessed at intervals of 0, 0.5, 5, 2.5, 6, 24, 48, and 72 h after PDT. It was demonstrated that maximum damage and repopulation of the tumour cells emerge at 24 and 48 h, respectively, following PDT, suggesting that subsequent light treatment should be performed within 24 h to enhance the therapeutic effect of PDT.
Adhesions of leukocytes to hepatocytes and sinusoidal endothelial cells mediates the induction and progression of hepatic injury. However, in contrast to endothelial cells, information regarding the regulation of interactions between leukocytes and hepatocytes is limited. In the present study, we investigated the effect of inflammatory mediators including lipopolysaccharide (LPS), staphylococcal enterotoxin B (SEB), interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1beta (IL-1beta) on the adhesion of polymorphonuclear leukocytes or lymphocytes to primary cultured rat hepatocytes, and on the expression of intercellular adhesion molecule-1 (ICAM-1) gene in hepatocytes. Both polymorphonuclear leukocyte and lymphocyte adhesion to hepatocytes were enhanced after exposure of hepatocytes to IFN-gamma and TNF-alpha, but not after exposure to LPS, SEB or IL-1beta. The adhesion induced by either IFN-gamma or TNF-alpha was inhibited by monoclonal antibodies against ICAM-1 or lymphocyte function-associated antigen-1 (LFA-1). Nonstimulated hepatocytes expressed faintly ICAM-1 mRNA, which increased slightly during the culture period. ICAM-1 mRNA expression was up-regulated to a greater extent by incubating hepatocytes with IFN-gamma or TNF-alpha, and peaked after 12 hr of incubation with TNF-alpha and after 24 hr with IFN-gamma. These results indicate that IFN-gamma and TNF-alpha induce the expression of ICAM-1 on parenchymal hepatocytes and that the LFA-1-ICAM-1 pathway plays an important role in the interaction between hepatocytes and neutrophils or lymphocytes.
We report a 7-year-old girl with hemophagocytic lymphohistiocytosis who received a syngeneic bone marrow transplant from her twin sister. She presented with high fever and cough. Laboratory findings revealed pancytopenia, elevation of liver enzymes, and hyperferritinemia. Bone marrow examination revealed histiocytic hemophagocytes and lymphoblastoid cells. Southern blot analysis of the bone marrow cells revealed a monoclonal proliferation of EBV-infected lymphocytes. Although she underwent combined chemotherapy according to the HLH-94 protocol, she developed severe pancytopenia. Following myeloablative conditioning with busulfan (16 mg/kg), cyclophosphamide (120 mg/kg), and etoposide (1.5 g/m2), she was transplanted with 6.6 x 10(8)/kg mononuclear cells from the twin sister. She remains in complete remission 23 months after transplantation.
The amino acid sequence predicted from a rat liver cDNA library indicated that the precursor of beta-AlaAT I (4-aminobutyrate aminotransferase, beta-alanine-oxoglutarate aminotransferase) consists of a mature enzyme of 466 amino acid residues and a 34-amino acid terminal segment, with amino acids attributed to the leader peptide. However, the mass of beta-AlaAT I from rat brain was larger than that from rat liver and kidney, as assessed by Western-blot analysis, mass spectroscopy and N-terminal sequencing. The mature form of beta-AlaAT I from the brain had an ISQAAAK- peptide on the N-terminus of the liver mature beta-AlaAT I. Brain beta-AlaAT I was cleaved to liver beta-AlaAT I when incubated with fresh mitochondrial extract from rat liver. These results imply that mature rat liver beta-AlaAT I is proteolytically cleaved in two steps. The first cleavage of the motif XRX( downward arrow)XS is performed by a mitochondrial processing peptidase, yielding an intermediate-sized protein which is the mature brain beta-AlaAT I. The second cleavage, which generates the mature liver beta-AlaAT I, is also carried out by a mitochondrial endopeptidase. The second peptidase is active in liver but lacking in brain.
Intravascular fasciitis is a very unusual variant of nodular fasciitis. A unique case of this lesion occurring in the proximal portion of the superficial vein of the forearm in an otherwise healthy 26-year-old man is reported. The intravascular polypoid lesion grew longitudinally along the vascular lumen, was loosely attached to the intimal layer, and was partly anchored beyond the internal elastic lamina into the medial smooth muscle layer. However, extravascular involvement was absent. The histological features were identical to those observed in ordinary cellular nodular fasciitis. Because of its myofibroblastic phenotype exhibited by highly proliferative spindle cells, certain intimomedial myofibroblasts are thought to be the indigenous source of this unique fibroproliferative lesion. Unless the diagnosis of intravascular fasciitis is considered and appropriate differential markers examined, it may be confused with other intravascular lesions, such as intravascular leiomyoma, intravenous pyogenic granuloma, organized thrombus and, even, fibromuscular dysplasia if it arises in the arteries. A simple excision is considered curable. Even so, two recurrent cases have been documented to date.
A case of an 8-year-old Japanese boy with a testicular large cell calcifying Sertoli cell tumor (LCCSCT) is presented. This report appears to be the first Japanese case of LCCSCT. The patient presented with left testicular swelling and gynecomastia. His family history was not contributory; however, his past history was remarkable for a benign myxoid tumor in the nasal cavity, which was removed at the age of 2 months. After removal of the testicular tumor, the gynecomastia disappeared gradually and no recurrence or metastasis developed during a 15 month follow-up period. Although the tumor was initially interpreted as a Leydig cell tumor, a review of the slides after the patient's past history of nasal myxoid tumor was revealed led us to the diagnosis of LCCSCT. An accurate diagnosis of LCCSCT is crucial because this tumor is occasionally associated with Carney complex, which can comprise various pathological conditions, including cardiac myxoma, that may be life-threatening. Myxoma of Carney complex has been described to occur in the heart, skin, oral cavity and breast in a wide age range, but there have been no reports referring to nasal myxoid tumor associated with Carney complex.
We report a 75-year-old woman with metachronous bile duct cancer who underwent curative resection twice and has survived for a decade. In 1989, she was admitted because her serum alkaline phosphatase level was elevated. Computed tomography (CT) showed a low-density mass, 2 cm in diameter, at the left hepatic duct and intrahepatic bile duct dilatation in the left lobe. We diagnosed the lesion as an intrahepatic bile duct cancer and performed extended left hepatic lobectomy with systematic lymph node dissection. The histological diagnosis was a well differentiated cholangiocellular carcinoma with hepatic hilar and celiac lymph node metastases (T1N2M0, Stage IVB). In 1996, she was re-admitted with obstructive jaundice. CT showed a slightly enhanced mass, 4 cm in diameter, in the pancreatic head. After reducing the jaundice by percutaneous transhepatic biliary drainage, pancreatoduodenectomy was performed. The histological diagnosis of this lesion was a moderately differentiated adenocarcinoma originating from the intrapancreatic bile duct. Ten years after the first operation, she is leading a normal daily life with no cancer recurrence. These findings suggest that repeated curative surgery can result in a long-term survival of patients with metachronous bile duct cancer.
OBJECTIVE: Aneurysm surgery carries considerable risk to the patient, in part because the surgical field can be so constricted that accurate placement of the aneurysm clip is impeded. In fact, most aneurysm clip appliers are so bulky that they can impair the surgeon's view, if the field is tight. We describe a system of aneurysm clips and appliers that have a very low profile and consequently allow better visualization of the operative field at critical moments during surgery. INSTRUMENTATION: A new system of clips for aneurysm surgery was developed to overcome some of the deficiencies of conventional sets. The new clip blades are opened from inside the spring, so the clip blades are clearly seen as they are applied across the base of the aneurysm. In addition, these clips can be angled in any desired direction in the applier, which makes their application easier. A third advantage is that the clip applier is used as a clip remover should adjustment or reapplication of the clip be necessary. RESULTS: Thirty aneurysms were obliterated with the new clips without any complications attributable to the clips. The new instruments allowed the safe application of clips to aneurysms in deep, confined, and anatomically complex spaces, such as aneurysms of the basilar tip and anterior communicating artery. CONCLUSION: The newly described system of aneurysm clips and appliers appears to have significant advantages over other currently available systems.
Borna disease virus (BDV), a negative nonsegmented single-stranded RNA virus, has not been fully characterized morphologically. Here we present what is to our knowledge the first data on the fine ultrastructure and morphogenesis of BDV. The supernatant of MDCK cells persistently infected with BDV treated with n-butyrate contained many virus-like particles and more BDV-specific RNA than that of untreated samples. The particles were spherical, enveloped, and approximately 130 nm in diameter; had spikes 7 nm in length; and reacted with BDV p40 antibody. A thin nucleocapsid, 4 nm in width, was present peripherally in contrast to the thick nucleocapsid of hemagglutinating virus of Japan. The BDV particles reproduced by budding on the cell surface.
We have isolated cDNA and genomic DNA encoding mouse PDNP2 (PD-Ialpha). The mouse Pdnp2 cDNA contains a 2,589-nucleotide open reading frame encoding a polypeptide of 863 amino acids. The 5' region of the mouse Pdnp2 gene contains Sp1, Max1, HNF-3B, and AP1 putative transcription factor binding sites, without typical TATA or CAAT boxes. Fluorescence in situ hybridization showed that Pdnp2 is located at Chromosome 15D2, as expected based on mouse-human conserved regions.
A recent increase in allergic disorders has coincided with a decrease in infections, including tuberculosis. Although an inverse association between tuberculin responses and atopic disorders was reported, it was not known how T-helper (Th)1-biased immune responses to Mycobacterium tuberculosis influenced Th2-dominant responses to allergens. We examined whether M. tuberculosis could modulate ovalbumin (OVA)-induced eosinophilic inflammation in the murine trachea in a manner that transcended the barrier of antigen specificity. We found that CD4(+) T cells primed with OVA in complete Freund's adjuvant (CFA) inhibited OVA-induced tracheal eosinophilia through interferon (IFN)-gamma secretion. Immunization with an irrelevant antigen in CFA or with OVA in incomplete Freund's adjuvant failed to induce suppressor cells. In vitro experiments confirmed that both M. tuberculosis and OVA (as opposed to either one alone) were necessary to evoke polarized development toward a Th1-like phenotype through interleukin-12 secretion. These results indicate that exposure to an allergen along with M. tuberculosis switches development of allergen-specific T cells toward a Th1 phenotype, which, in turn, downregulates allergic manifestations in an antigen-specific manner. The possible implications of these results are discussed in the context of the causal relationship between a decrease in tuberculosis and an increase in allergic disorders.
The induction of peripheral tolerance is one of the feasible approaches for the control of autoimmunities and allergies. Tolerance induction in the intestine has been studied extensively and therapeutic applications to autoimmunities are in progress, whereas tolerance in the respiratory tract is poorly investigated. We examined the immunoregulatory mechanisms for evading exaggerated inflammatory responses in the murine airway mucosa. Administration of an optimal dose of ovalbumin (OVA) to the trachea elicited eosinophilic inflammation in the trachea of OVA/aluminum hydroxide-sensitized BALB/c mice, whereas higher doses were unable to do so. This failure paralleled the downregulation of interleukin-4 production by mediastinal lymph node (LN) T cells. This high-dose tolerance was attributable to the mechanisms of antigen (Ag)-specific suppression, because the adoptive transfer of CD4(+) LN T cells from the OVA-tolerant mice inhibited the OVA-specific, but not irrelevant Ag KLH-specific, eosinophilic responses. The inhibitory effects were neutralized by the intratracheal administration of anti-transforming growth factor (TGF)-beta, but not that of anti-interferon (IFN)-gamma, monoclonal antibodies, indicating that the high-dose tolerance was mediated by secreted TGF-beta, but not by the dominance of transferred T helper (Th)1 cells over Th2 cells. The pivotal role of TGF-beta was reinforced by the finding that the LN cells from the OVA-tolerant mice produced TGF-beta in response to the in vitro Ag stimulation. These results demonstrate a novel regulatory mechanism in the airway: that TGF-beta secreted by T cells plays an important role in the downmodulation of the immune responses to high doses of Ag which might otherwise induce deleterious inflammation in the airway mucosal tissues.
This study was designed to test the hypothesis that Gadolinium-diethylenetriamine pentaacetic acid (Gd-DTPA)-enhanced magnetic resonance images (MRI) reflect the severity of ischemic injury during the acute and chronic phases of myocardial infarction (MI). Twenty-nine patients with their first acute MI underwent Gd-DTPA-enhanced MRI in the first week (4.2+/-0.3 days) and at 1 month after onset. Pairs of left ventriculograms were compared with Gd-DTPA-enhanced magnetic resonance images, classified into 3 pattern groups: hyper-enhancement, with and without a central hypo-enhanced region (P1 and P2, respectively), and non-enhancement (P3). In the acute phase of MI, P1 was found in 10, P2 in 11, and P3 in 8 patients. One month later, the image pattern had changed from P1 to P2 in a single patient, from P2 to P3 in 4 patients, and had remained identical in the others. Patients with P3 showed improvement of anterior wall motion in the 1-month follow-up study, and had higher TIMI flow grades and lower peak creatine kinase values than those without recovery. Thus, Gd-DTPA-enhanced magnetic resonance images, closely reflecting the severity of myocardial injury, are useful in predicting myocardial functional recovery after MI.
The objectives of this study were to establish an adult rat model for the late onset of radiation-induced cognitive dysfunction and to compare behavioural dysfunction with histopathological changes. While under anaesthesia, 30 rats (experimental group) were irradiated with a total dose of 40 Gy, given as eight fractions in 24 days. Another 30 rats (control group) underwent sham irradiation. The cognitive functions of all rats were evaluated at 6, 9 and 12 months after irradiation using the Morris water maze and passive avoidance tasks. Histopathological examination of these rats was carried out after the evaluation of cognitive functions was complete. At 6 and 9 months after irradiation there were no significant differences between the control and irradiated groups in passive avoidance and water maze tests. At 12 months after irradiation, the passive avoidance task revealed a deterioration of cognitive function in the experimental group. Histopathological observations revealed no abnormal findings in the irradiated brains at the light microscope level. Late onset cognitive dysfunction following cranial irradiation was observed in an adult rat model. Pathological investigations showed no abnormalities in the irradiated brains. These findings indicate that radiation-induced cognitive dysfunction can precede morphological changes in the brain or that they arise without them. The present model seems useful for elucidating the pathogenesis of radiation-induced cognitive dysfunction and for developing methods for therapy and prophylaxis.