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Biomedical subjects

T Ikegami

Publications and source records attributed to T Ikegami.

At least 109 records · Page 6Linked to original sources

[Clinical usefulness of myocardial iodine-123-15-(p-iodophenyl)-3(R,S)-methyl-pentadecanoic acid distribution abnormality in patients with mitochondrial encephalomyopathy based on normal data file in bull's-eye polar map].

Visual interpretation of iodine-123-beta-15-(p-iodophenyl)-3(R,S)-methyl-pentadecanoic acid (123I-BMIPP) myocardial images cannot easily detect mild reduction in tracer uptake. Objective assessment of myocardial 123I-BMIPP maldistributions at rest was attempted using a bull's-eye map and its normal data file for detecting myocardial damage in patients with mitochondrial encephalomyopathy. Six patients, two with Kearns-Sayre syndrome and four with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and 10 normal subjects were studied. Fractional myocardial uptake of 123I-BMIPP was also measured by dynamic static imaging to assess the global myocardial free fatty acid. These data were compared with the cardiothoracic ratio measured by chest radiography and left ventricular ejection fraction assessed by echocardiography. Abnormal cardiothoracic ratio and lower ejection fraction were detected in only one patient with Kearns-Sayre syndrome. Abnormal fractional myocardial uptake was detected in two patients (1.61%, 1.91%), whereas abnormal regional 123I-BMIPP uptake assessed by the bull's-eye map was detected in five patients (83%). All patients showed abnormal uptake in the anterior portion, and one showed progressive atrioventricular conduction abnormality and systolic dysfunction with extended 123I-BMIPP abnormal uptake. The results suggest that assessment based on the normal data file in a bull's-eye polar map is clinically useful for detection of myocardial damage in patients with mitochondrial encephalomyopathy.

Adult↗

The relationship between amniotic fluid interleukin-6 concentration and histologic evidence of chorioamnionitis.

BACKGROUND: Chorioamnionitis is considered to be one of the important causes of preterm labor. To investigate the relationship between inflammatory cytokines in amniotic fluid and the histologic evidence of chorioamnionitis, we studied amniotic fluid interleukin-6 (IL-6) levels in patients with preterm labor. METHODS: Between 1993 and 1996, we obtained amniotic fluid by amniocentesis from 110 patients before 32 weeks of gestation who had preterm labor on admission. We measured IL-6 levels in the amniotic fluid with an ELISA method. Histologic examination of placentae and fetal membranes after delivery was evaluated. As controls, we measured IL-6 levels in the amniotic fluid of 37 patients without preterm labor. Seventy-eight patients delivered after 35 weeks of gestation, and 32 patients delivered before 34 weeks of gestation. Analysis was conducted using Mann-Whitney U test and Scheffe's multiple comparison test. RESULTS: Amniotic fluid IL-6 levels in patients delivering before 34 weeks were significantly higher than those in patients delivering after 35 weeks (p<0.01). IL-6 levels in the amniotic fluid were significantly different among control patients, patients without chorioamnionitis and those with histologic stages I, II and III which means subchorionic intervillositis, chorionitis and amnionitis, respectively (controls vs patients with stage I, II, III: p<0.001, patients without chorioamnionitis vs those with stage II, III, stage I vs II, stage II vs III: p<0.01). The IL-6 concentration in the amniotic fluid associated with histologic stages II or III was above 3500 pg/ml (sensitivity: 87.5%, specificity: 89.5%). CONCLUSIONS: Our findings indicate that amniotic fluid IL-6 may have a sensitive diagnostic and prognostic value in the management of preterm labor and is an index of the severity of chorioamnionitis during pregnancy.

Amniotic Fluid↗

Urgent living-related liver transplantation using a graft with multiple intrahepatic arterioportal fistulae.

BACKGROUND: We describe the case of a man with intrahepatic arterioportal fistulae located in the left lobe, whose left lateral segment was transplanted into his son who was suffering from severe acute hepatitis B. METHODS: A male infant with severe acute hepatitis B was considered to be a candidate for liver transplantation. The father was willing to be the donor. Preoperative evaluation of the donor revealed intrahepatic arterioportal fistulae, however, duplex ultrasonography showed normograde portal blood flow. A living-related liver transplantation was performed. RESULTS: The postoperative course for both the donor and recipient was uneventful. The recipient is free of recurrent hepatitis B and has normograde portal blood flow. CONCLUSIONS: The present case suggests that there may be a symptomless population with intrahepatic arterioportal fistulae, which cause various degrees of disruption of the portal blood flow. Duplex ultrasonography might be helpful in the evaluation of candidates for liver donation.

Adult↗

Peripheral nerves regenerated in familial amyloid polyneuropathy after liver transplantation.

BACKGROUND: Liver transplantation holds promise as a treatment for familial amyloid polyneuropathy. OBJECTIVE: To determine whether peripheral nerves regenerate in patients with familial amyloid polyneuropathy after liver transplantation. DESIGN: Case report. SETTING: University hospital in Matsumoto, Japan. PATIENT: A 34 year-old-women with familial amyloid polyneuropathy who had liver transplantation and showed marked clinical improvement 3 years after surgery. MEASUREMENTS: Histopathologic examination and morphometric analysis of biopsy specimens taken from sural nerves. RESULTS: Diffuse fiber loss and amyloid deposits were seen in a biopsy specimen of the left sural nerve obtained before liver transplantation (total number of myelinated fibers, 1326/mm2 of the endoneurial area). In the biopsy specimen of the right sural nerve, which was obtained 3 years after transplantation, amyloid deposits remained but the number of myelinated fibers was markedly increased (total number of myelinated fibers, 4740/mm2). CONCLUSION: Peripheral nerves regenerated in a patient with familial amyloid polyneuropathy after liver transplantation.

Adult↗

Efficacy of quantitative analysis of Epstein-Barr virus-infected peripheral blood lymphocytes by in situ hybridization of EBER1 after living-related liver transplantation: a case report.

BACKGROUND: We describe a 1-year-old female who underwent living-related liver transplantation for biliary atresia and developed Epstein-Barr virus (EBV)-related posttransplant lymphoproliferative disorder. This disorder was resolved after withdrawal of immunosuppression therapy and administration of a high dose of acyclovir. METHODS: To quantify the extent of EBV activation and EBV load in peripheral blood, we measured the levels of EBV-infected peripheral lymphocytes by in situ hybridization (ISH) of EBV-encoded small mRNA 1 (EBER1). RESULTS: The decline in the number of EBER1-positive lymphocytes (from 362/50,000 mononuclear cells to 0/50,000) after treatment was in accord with the patient's clinical improvement. CONCLUSIONS: This finding showed that quantitative analysis of EBV-infected peripheral lymphocytes by ISH of EBER1 is very useful for monitoring the EBV load and response to treatment of patients with EBV-related disorders. Furthermore, ISH may become an important tool for the early diagnosis and prevention of life-threatening posttransplant lymphoproliferative disorder in posttransplant patients.

Acyclovir↗

Facilitated diagnosis of CMT1A duplication in chromosome 17p11.2-12: analysis with a CMT1A-REP repeat probe and photostimulated luminescence imaging.

Charcot-Marie-Tooth disease type 1A (CMT1A) is a common autosomal dominant demyelinating peripheral neuropathy. Most patients with CMT1A have been found to have a 1.5 megabase tandem DNA duplication in chromosome 17p11.2-12. Meiotic unequal crossover mediated by the CMT1A-REP repeat is a proposed mechanism for generation of the duplication in CMT1A and a reciprocal deletion seen in hereditary neuropathy with liability to pressure palsies. Testing for the CMT1A duplication is frequently the first step in the molecular diagnosis of patients with suspected inherited demyelinating neuropathy. We used a 1.0 kb EcoRI-PstI DNA fragment (pHK1.0P) from the proximal CMT1A-REP repeat as a probe for Southern blot analysis and detected increased gene dosage in CMT1A by determining measuring radioactivity ratios with a photostimulated luminescence imaging plate. We found that this method is useful for rapid diagnosis of the DNA duplication associated with CMT1A.

Autoradiography↗

Hepatic artery reconstruction in living donor liver transplantation from the microsurgeon's point of view.

Microvascular surgery for the reconstruction of the hepatic artery in living donor liver transplantation is discussed from the microsurgeon's point of view. A refined operative procedure to improve the safety of the anastomosis is described. In living donor liver transplantation, the hepatic artery of the graft is short and small, the operative site is deep and mobile, and the anatomic arrangement of the graft left hepatic artery may differ from that of the recipient's dilated hepatic artery. To create a safe anastomosis under these conditions, recipient arteries that were slightly smaller than the graft artery were dissected. Without the size discrepancy, and end-to-end anastomosis could be created. Some refinements to create a good operative field made the anastomosis easy. The apparatus and techniques used in free-flap transfer facilitated a clean anastomosis. We anastomosed 44 arteries in 40 patients undergoing living donor liver transplantation using microsurgical techniques. Neither a decrease in the arterial blood flow nor hepatic artery thrombosis was noted. The refined operative procedure we describe in this report can be used to overcome the problems associated with the hepatic artery anastomosis in living donor liver transplantation.

Adolescent↗

Locations of crossover breakpoints within the CMT1A-REP repeat in Japanese patients with CMT1A and HNPP.

The crossover breakpoints for Charcot-Marie-Tooth disease type 1A (CMT1A) and hereditary neuropathy with liability to pressure palsies (HNPP) are located in the CMT1A-REP repeat flanking a 1.5-Mb region of chromosome 17p11.2-12. The precise locations of the breakpoints are heterogeneous, and we analyzed the relative frequency distribution of breakpoints in 33 unrelated Japanese CMT1A and 3 unrelated HNPP families. The CMT1A-REP repeat region was divided into five regions, A, B, C, D and E, based on restriction site differences between the proximal and distal CMT1A-REP repeats. The frequency distribution of breakpoints within the CMT1A-REP repeat in the Japanese patients was 3% in region A, .78% in B/C and 19% in D, which is similar to that in Caucasian patients. This result also indicates that an 8-kb region defined by region B/C is a recombinational hotspot within the CMT1A-REP repeat in Japanese patients.

Asian People↗

Intraoperative evaluation of small-calibre arterial reconstructions.

A new hammerhead-shaped, small probe for intraoperative duplex ultrasound was devised to evaluate small-calibre arterial reconstructions. This probe was used in two patients; one with terminal liver cirrhosis who had a left hepatic lobe that had been transplanted from her mother, and a second patient with limb-threatening ischaemia who had undergone arterial reconstructions. The technique was diagnostically useful and contributed to successful clinical outcomes.

Adolescent↗

Increased biliary group II phospholipase A2 and altered gallbladder bile in patients with multiple cholesterol stones.

BACKGROUND & AIMS: Multiple cholesterol stones are associated with more biliary complications and show more rapid cholesterol nucleation than solitary stones. Group II phospholipase A2 (PLA2-II) may play a critical role in the process of mucosal inflammation, which in turn may produce pronucleating agents. PLA2-II concentrations in gallbladders and gallbladder bile from patients with different types of gallstone disease were assayed to correlate PLA2-II with alterations in biliary composition. METHODS: PLA2-II protein concentrations were assayed immunoradiometrically using monoclonal antibodies against human splenic PLA2-II. RESULTS: Immunoreactive PLA2-II levels in gallbladder bile were significantly higher in patients with multiple cholesterol stones (68.2 +/- 6.3 ng/dL, mean +/- SEM; n = 24) than in those with solitary stones (24.9 +/- 2.8; n = 20; P < 0.01), those with multiple pigment stones (24.2 +/- 3.7; n = 18; P < 0.01), or control subjects (13.4 +/- 1.7; n = 19; P < 0.01). Increased biliary immunoreactive PLA2-II levels in multiple cholesterol stones were associated with a concomitant increase in the lysophosphatidylcholine to phosphatidylcholine ratio; free arachidonate, protein, and hexosamine concentrations; and gallbladder bile viscosity. The gallbladders showed an increased PLA2-II protein mass and steady-state messenger RNA levels, which was associated with increased prostaglandin E2 levels. CONCLUSIONS: Increased biliary PLA2-II may be of pathogenetic importance in multiple cholesterol stones, probably through potentiating gallbladder mucosal inflammation with associated biliary alterations favoring cholesterol crystal formation.

Adult↗

Simultaneous determination of plasma mevalonate and 7alpha-hydroxy-4-cholesten-3-one levels in hyperlipoproteinemia: convenient indices for estimating hepatic defects of cholesterol and bile acid syntheses and biliary cholesterol supersaturation.

The high prevalence of cholesterol gallstone disease in hypertriglyceridemic patients may be associated with frequent metabolic defects in cholesterol and bile acid syntheses and in the concomitant formation of bile supersaturated with cholesterol. This study had the two aims: 1) to assess whether the defects as well as the degree of biliary cholesterol supersaturation in patients with hyperlipoproteinemia (HLP) can be estimated by the simultaneous determination of plasma mevalonate (MVL) and 7alpha-hydroxy-4-cholesten-3-one (C4); and 2) to assess the possible application of an estimated cholesterol saturation index ([CSI]E) as a means of evaluating the clinical effects of simvastatin on biliary lipid composition. Biliary cholesterol supersaturation was observed in patients with both IIa and IV HLP types. Consistent with the high activity and steady-state messenger RNA level of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) reductase, plasma MVL was significantly higher in 86 patients with HLP (38 type IIa, 44.1 +/- 2.4 nmol/L and 48 type IV, 56.7 +/- 2.3; P < .01) than in 41 normolipidemic subjects (34.2 +/- 1.5), closely correlating with the molar percentage of cholesterol in bile (r = .61, P = .0001; n = 86). On the other hand, consistent with the high activity and messenger RNA level of cholesterol 7alpha-hydroxylase, plasma C4 was significantly higher in patients with HLP (type IIa, 28.8 +/- 2.3 nmol/L and type IV, 38.3 +/- 2.7; P < .01) than in normolipidemic subjects (17.4 +/- 1.5). Plasma C4 was closely correlated with plasma MVL (r = .40, P = .0001; n = 86), but was inversely correlated with the molar percentage of bile acids in bile (r = .49, P = .0001; n = 86). Assuming that cholesterol supersaturation in patients with HLP may be governed by both an enhanced cholesterol secretion (closely reflected by plasma MVL) and a decreased secretion of bile acids (closely reflected by plasma C4), the multivariate linear regression-analyses revealed that an index defined as estimated CSI ([CSI]E) (%) in patients with HLP was given by the following equation using plasma MVL and C4 (nmol/L): [CSI]E = 1[MVL] + 0.7[C4] + 44.4. Biliary cholesterol supersaturation in patients treated with simvastatin improved in a manner parallel to the time course of decreases in plasma MVL and C4. The [CSI]E before and at the end of treatment were correlated with biliary CSI. These results indicate that defects of hepatic cholesterogenesis, and bile acid synthesis, and the degree of biliary cholesterol supersaturation in patients with HLP can be estimated exactly by the simultaneous determination of plasma MVL and C4; furthermore [CSI]E may be adopted for clinical use as a convenient index of biliary CSI.

Adult↗

Emergence of collective strategies in a prey-predator game model.

The emergence of collective strategies in a prey-predator system is studied. We use the term "collective" in the sense of the collective motion of defense or attack often found in behaviors of animal groups. In our prey-predator system, both prey and predators move around on a two-dimensional plane, interacting by playing a game; predators can score by touching the backside of a prey. Thresholds are assumed for the scores of both prey and predators. The species with the higher scores can reproduce more, and that with the lower scores will be diminished. As a result, strategies as collective motions are observed; these consist of rotating cluster motions, line formations, disordered but one-way marching, and random swarming. In particular, the strategy of random swarming encourages symbiosis in the sense that it is associated with a low extinction probability for the whole system.

Animals↗

Pressure palsy as the initial presentation in a case of late-onset Charcot-Marie-Tooth disease type 1A.

We report siblings of late-onset Charcot-Marie-Tooth disease type 1A (CMT1A) of whom the elder brother presented with drop foot. DNA analysis confirmed the 17p11.2-p12 duplication. Estimation of the age of onset is difficult in CMT1A because of the subtle and slow progress of the symptoms. These cases are unique in that the initial clinical manifestation was a pressure palsy in the brother and both siblings were quite delayed in their clinical presentations. The peripheral myelin protein-22 gene duplication is uniformly found in CMT1A patients. However, other factors influencing the disease manifestations are yet to be determined.

Aged↗