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The Nemuro Belt is a tectonic belt in the Paleo-Kuril Arc system, the NW Pacific region. The Paleo-Kuril Arc has been interpreted as an intra-oceanic arc system between the Izanagi and Pacific plates during the Late Cretaceous, suggesting that the boundary between these plates was a trench. However, this study shows it was a volcanic arc that developed atop a continental margin. To determine the nature of this arc during the Late Cretaceous, U-Pb ages of detrital zircons from the Nemuro and Urahoro groups in the Paleo-Kuril Arc were analyzed. Our results identify two distinct types of detrital zircon U-Pb age distributions. The first (Type 1) is characterized by multimodal age distributions with peaks ranging from ca. 1.8 Ga to 78 Ma. The other (Type 2) exhibits a unimodal age distribution with a peak at 60–52 Ma. These different age distributions indicate a provenance transition occurred between the Late Cretaceous and Paleogene. Precambrian zircons in Type 1 sandstones indicate that the Paleo-Kuril Arc was part of a continental plate, presumably the Okhotsk Block, in NE Asia during the Late Cretaceous. In contrast, Type 2 sandstones were supplied only from the magmatic arc region that the Izanagi-Pacific Ridge subduction could have activated. This provenance transition suggests the initially continental arc became separated from its continental source at the beginning of the Paleogene.

Cooperation is a strategy that has been adopted by groups of organisms to execute complex tasks more efficiently than single entities. Cooperation increases the robustness and flexibility of the working groups and permits sharing of the workload among individuals. However, the utilization of this strategy in artificial systems at the molecular level, which could enable substantial advances in microrobotics and nanotechnology, remains highly challenging. Here, we demonstrate molecular transportation through the cooperative action of a large number of artificial molecular machines, photoresponsive DNA-conjugated microtubules driven by kinesin motor proteins. Mechanical communication via conjugated photoresponsive DNA enables these microtubules to organize into groups upon photoirradiation. The groups of transporters load and transport cargo, and cargo unloading is achieved by dissociating the groups into single microtubules. The group formation permits the loading and transport of cargoes with larger sizes and in larger numbers over long distances compared with single transporters. We also demonstrate that cargo can be collected at user-determined locations defined by ultraviolet light exposure. This work demonstrates cooperative task performance by molecular machines, which will help to construct molecular robots with advanced functionalities in the future.

Within this study, we show that single-phase face centered cubic (fcc) Ti0.47Al0.46Ce0.02Si0.05N coatings (sputtered from Ti0.37Al0.57Ce0.02Si0.04 targets plus the addition of Ti) outperform their single-phase fcc Ti0.49Al0.51N counterparts (sputtered from Ti0.40Al0.60 targets plus the same addition of Ti). The deposition rate increases by more than 43% and also the hardness of as-deposited Ti0.47Al0.46Ce0.02Si0.05N coatings is with 39.9 ± 1.2 GPa (on sapphire) 13% higher. Furthermore, this Ce–Si alloyed coating shows a remarkably higher thermal stability, represented by a higher annealing temperature (1200 °C instead of 900 °C) after which hexagonal structured wurtzite-type AlN (w-AlN) can be detected. They also show a more parabolic like oxide growth rate (4.13·10−7 and 1.13·10−5 μm2/s at 850 and 950 °C) during the 10-h-oxidation experiment, whereas that of Ti0.49Al0.51N is close to linear already at 850 °C (especially after ∼2 h). The postponed w-AlN formation guarantees that the hardness of Ti0.47Al0.46Ce0.02Si0.05N is still 40.8 ± 1.6 GPa even after annealing at 1100 °C. Our results clearly demonstrate that the addition of 2 mol% CeSi2 to Ti–Al targets allows to increase the sputter rate and leads to Ce–Si alloyed nitride coatings with improved thermomechanical properties and oxidation resistance.

Recently we showed that Ta as well as Ce significantly increase the thermomechanical properties and oxidation resistance of Ti–Al–N coatings. Here we investigate their synergistic effect by comparing single-phase face centered cubic (fcc) structured Ti0.39Al0.61N, Ti0.40Al0.58Ce0.02N, Ti0.43Al0.51Ta0.06N, Ti0.44Al0.44Ta0.12N, Ti0.43Al0.42Ta0.14Ce0.01N, and Ti0.43Al0.35Ta0.21Ce0.01N coatings, which were prepared by reactive magnetron sputtering of corresponding powder metallurgically prepared composite targets. Especially the Ti0.43Al0.42Ta0.14Ce0.01N coating outperforms the others in hardness, thermal stability and oxidation resistance. This coating is prepared with a Ti0.44Al0.44Ta0.10Ce0.02 target, which allows for a 2.8 times higher deposition rate than the Ti0.50Al0.50 target (for the preparation of a fcc-Ti0.39Al0.61N) under the same deposition parameters (temperature, gas flow, sputtering current, bias potential). The hardness of Ti0.43Al0.42Ta0.14Ce0.01N is 35 GPa in its as-deposited single-phase fcc state, and still 34 GPa after vacuum-annealing at 1200 °C, where only a very small fraction of hexagonal phase-formation can be detected. Ti0.39Al0.61N shows 30 GPa in as-deposited state and 27 GPa after vacuum-annealing at 900 °C (peak-hardness of 32 GPa with Ta = 800 °C), where already hexagonal phases form. But even more striking is the improved oxidation resistance, which outperforms those of the individual Ta or Ce alloyed Ti–Al–N, due to the cumulative effect of Ta and Ce. With a Ta/Ti ratio of ~1/3, Ti0.43Al0.42Ta0.14Ce0.01N provides the optimum Ta content for the formation of a stable and dense TiO2-containing scale, and the additional 1 at.% Ce-metal-fraction enables the growth of a dense and well-adherent protective oxide scale. Based on our results we can conclude, that the combined alloying of Ta and Ce to Ti–Al–N improves the deposition characteristics, thermomechanical properties, as well as thermal stabilities (incl. oxidation resistance), which should provide a better performance of thereby protective machining tools.

Ti–Al–N thin films are well established due to their outstanding thermo-mechanical properties. Nevertheless, this system is still a subject of many research activities to further enhance their oxidation resistance and thermal stability. The addition of reactive elements, such as Cerium, can significantly improve especially the oxidation resistance of various materials. Therefore, we study in detail the impact of Ce (2 at.% alloyed to powder metallurgically prepared Ti 0.50 Al 0.50 targets) on growth processes, structure, mechanical properties, thermal stability, and oxidation resistance of magnetron sputtered Ti 1 − x − y Al x Ce y N coatings prepared with DC bias potentials of U bias = − 25, − 50, − 75, and − 100 V. The deposition rate is significantly increased by a factor of ~ 1.75 (U bias = − 25 V) to 1.45 (U bias = − 100 V) when using Ti 0.49 Al 0.49 Ce 0.02 instead of Ti 0.50 Al 0.50 targets. Furthermore, also the hardness of the resulting single phase face centered cubic Ti 0.43 Al 0.55 Ce 0.02 N is with ~ 35 GPa above that of Ti 0.42 Al 0.58 N with ~ 34 GPa, for coatings on polycrystalline Al 2 O 3 and U bias = − 50 V. All temperature dependent characteristics of Ti 0.42 Al 0.58 N are improved significantly by the addition of Cerium. Wurtzite-structured AlN formation within Ti 0.43 Al 0.55 Ce 0.02 N can only be detected at T a = 1100 °C, about 200 °C higher as for Ti 0.42 Al 0.58 N. Their peak-hardness, due to spinodal decomposition of the supersaturated cubic phase is ~ 37.0 GPa with T a = 900 °C, as compared to 34.6 GPa with T a = 800 °C for Ti 0.42 Al 0.58 N. Additionally, even after exposure to ambient air at 950 °C for 3 h, still > 50% of the Ti 0.43 Al 0.55 Ce 0.02 N coating is intact (below the ~ 1.2 μm thin oxide scale), whereas Ti 0.42 Al 0.58 N is already fully oxidized. Based on our results we can conclude, that Ce-doping improves the deposition characteristics and mechanical properties as well as thermal stabilities (incl. oxidation resistance) of Ti–Al–N, to be used as protective coatings for a wide range of high-demanding applications.

State-of-the-art machining applications require new developments in the field of protective coatings, to guarantee for excellent dimensional accuracy and effective processes. Recently, we showed an enormous enhancement in deposition rate, mechanical strength, and thermal stability of Ti–Al–N when using Ce-alloyed Ti–Al composite targets. Within this study, we further follow the concept of alloying lanthanides to nitride-based coatings, by sputtering Ti0.5Al0.5 composite targets alloyed with 2 mol% LaB6 in mixed Ar/N2 atmospheres. This allowed us to produce coatings that outperform not only Ti–Al–N (significantly) but also Ce-alloyed Ti–Al–N coatings. Compared with coatings prepared from non-alloyed Ti0.5Al0.5 composite targets (Ti0.43Al0.57N), we achieved an impressive increase in deposition rate from 77 to 139 nm/min. Furthermore, we observed an increase in hardness from 34 to 40 GPa (on polished polycrystalline Al2O3 substrates) in the as-deposited state, accompanied by a delayed spinodal decomposition, and an additional TiB2 precipitation, allowing for still 40 GPa after annealing at 1100 °C. Also the oxidation resistance could be significantly improved through the addition of LaB6. After exposure to ambient air at 850 °C for 10 h or 950 °C for 1 h, the oxide scale thickness is only 500 nm for the LaB6 alloyed coatings, whereas the Ti0.43Al0.57N counterpart was already fully oxidized after 10 h at 850 °C or 1 h at 950 °C.

The hydrous mineral, δ-AlOOH, is stable up to at least the core-mantle boundary, and therefore has been proposed as a water carrier to the Earth’s deep mantle. If δ-AlOOH is transported down to the core-mantle boundary by a subducting slab or the mantle convection, then the reaction between the iron alloy core and δ-AlOOH is important in the deep water/hydrogen cycle in the Earth. Here we conducted an in situ X-ray diffraction study to determine the behavior of hydrogen between Fe–Ni alloys and δ-AlOOH up to near the core-mantle boundary conditions. The obtained diffraction spectra show that fcc/dhcp Fe–Ni hydride is stable over a wide pressure range of 19–121 GPa at high temperatures. Although the temperature of formation of Fe–Ni hydride tends to increase up to 1950 K with increasing pressure to 121 GPa, this reaction temperature is well below the mantle geotherm. δ-AlOOH was confirmed to coexist stably with perovskite, suggesting that δ-AlOOH can be a major hydrous phase in the lower mantle. Therefore, when δ-AlOOH contacts with the core at the core-mantle boundary, the hydrogen is likely to dissolve into the Earth’s core. Based on the present results, the amount of hydrogen to explain the core density deficit is estimated to be 1.0–2.0 wt.%.

The pressure–volume equations of state of iron–nickel–silicon alloy Fe0.83Ni0.09Si0.08 (Fe-9.8 wt.% Ni-4.0 wt.% Si) and iron–silicon alloy Fe0.93Si0.07 (Fe-3.4 wt.% Si) have been investigated up to 374 GPa and 252 GPa, respectively. The present compression data covered pressures of the Earth's core. We confirmed that both Fe0.83Ni0.09Si0.08 and Fe0.93Si0.07 alloys remain in the hexagonal close packed structure at all pressures studied. We obtained the density of these alloys at the pressure of the inner core boundary (ICB), 330 GPa at 300 K by fitting the compression data to the third order Birch–Murnaghan equation of state. Using these density values combined with the previous data for hcp-Fe, hcp-Fe0.8Ni0.2, and hcp-Fe0.84Si0.16 alloys and comparing with the density of the PREM inner core, we estimated the Ni and Si contents of the inner core. The Si content of the inner core estimated here is slightly greater than that estimated previously based on the sound velocity measurement of the hcp-Fe–Ni–Si alloy at high pressure.

The melting temperature of Fe–18 wt% Si alloy was determined up to 119 GPa based on a change of laser heating efficiency and the texture of the recovered samples in the laser-heated diamond anvil cell experiments. We have also investigated the subsolidus phase relations of Fe–18 wt% Si alloy by the in-situ X-ray diffraction method and confirmed that the bcc phase is stable at least up to 57 GPa and high temperature. The melting curve of the alloy was fitted by the Simon’s equation, P(GPa)/a = (T m(K)/T 0) c , with parameters, T 0 = 1,473 K, a = 3.5 ± 1.1 GPa, and c = 4.5 ± 0.4. The melting temperature of bcc Fe–18 wt% Si alloy is comparable with that of pure iron in the pressure range of this work. The melting temperature of Fe–18 wt% Si alloy is estimated to be 3,300–3,500 K at 135 GPa, and 4,000–4,200 K at around 330 GPa, which may provide the lower bound of the temperatures at the core–mantle boundary and the inner core–outer core boundary if the light element in the core is silicon.

Although surfactant-secreting type II alveolar cells have been shown to be damaged during influenzavirus pneumonia, little is known about the effects of surfactant replacement therapy. We have developed a mouse influenza model, in which viral infection can be localized to the upper respiratory tract or to both the upper and lower respiratory tract depending on the volume (rather than infectious dose) of intranasal inocula of influenzavirus. In this model, only mice infected with a large inocula die with massive infection in the lung. Using this model, we unexpectedly found that intranasal administration of surfactant dramatically exacerbated influenzavirus infection causing fatal disease even in mice inoculated with a small inocula. This exacerbation resulted from enhancement of intrabronchial and intraalveolar spread of virus, as confirmed by immunohistochemical detection of viral antigen in lungs. Assuming this experimental model in mice recapitulates naturally occurring disease in humans, extreme caution is warranted in surfactant-replacement treatment of influenzavirus pneumonia in humans.

Gilbert's damping constants, alpha, of Ni-Fe and Ni-Co thin films are determined by Q-band ferromagnetic resonance (FMR) analysis. alpha is calculated from the resonance width of the FMR spectrum. alpha of Ni85 Fe15 film is found to be 0.0034, which is one-fourth of those of Ni film (alpha=0.013) and Co (alpha=0.013). alpha of the Ni100-x Cox specimens increases with decreasing the Co concentration from 100 to 68 at%, and the alpha value of Ni32 Co68 film has the maximum value of 0.0021. The alpha values of the Ni-Co specimens are nearly the same as those of the Co-Cr-Ta and the Co-Cr-Pt

The protective roles of influenza viral nucleoprotein (NP), together with the cellular mechanism of the protection in the nasal site, were examined in BALB/c mice immunized intranasally with an adjuvant (cholera toxin B subunit containing 0.2% of the whole toxin)-combined A or B virus recombinant NP. The NP-immune mice, when challenged intranasally with a sublethal dose of the virus 3 wk after immunization, had accelerated virus clearance from the nasal site in both an influenza type-specific and a nonspecific manner, as shown by the protection from high morbidity from the second day after challenge. Both type-specific and nonspecific acceleration of recovery was confirmed by the increased survival rate after challenge with a lethal dose of virus in mice immunized and boosted with adjuvant-combined NP. The acceleration of nasal virus clearance was accompanied with acceleration of type-specific systemic delayed-type hypersensitivity (DTH) and with IFN-gamma production by nasal lymphocytes. The nasal lymphocytes from the immunized and challenged mice generated a significantly high level of DTH when transferred locally, but no class I MHC-restricted CTL response. Moreover, nasal CD4+ T cells, induced by NP immunization and increased in number by the subsequent challenge, were involved in the accelerated IFN-gamma production. These results suggest that nasal Th1 cells, capable of producing IFN-gamma and mediating DTH, are involved in the type-specific acceleration of recovery from influenza after challenge in mice immunized intranasally with adjuvant-combined NP, although the nonspecific mechanism of accelerated recovery remains to be solved.

Cross-protection against influenza virus infection was examined in mice, immunized intranasally with a nasal site-restricted volume of inactivated vaccines together with cholera toxin B subunit (CTB) as an adjuvant. The mice were challenged with either a small or a large volume of mouse-adapted virus suspension, each of which gave virgin mice either a predominant upper or lower respiratory tract infection. A single dose of a monovalent influenza A H3N2 virus vaccine with CTB provided complete cross-protection against the small-volume challenge with a drift virus within the same subtype, but a slight cross-protection against the large-volume challenge. A second dose of another drift virus vaccine increased the efficacy of cross-protection against the large-volume challenge. Similar cross-protection against H1N1, H3N2, or B type drift virus challenge was provided in the mice having received a primary dose of a mixture of H1N1, H3N2, and B virus vaccines with CTB and a second dose of another trivalent vaccine. The degree of cross-protection against the small- and the large-volume infection paralleled mainly the amount of cross-reacting IgA antibodies to challenge virus hemagglutinin in the nasal wash and that of cross-reacting IgG antibodies in the bronchoalveolar wash, respectively. On the other hand, in mice immunized subcutaneously with the trivalent vaccines having no cross-reacting IgA antibodies, the efficacy of cross-protection was not so high as that of nasal vaccination. These results suggest that the nasal inoculation of trivalent vaccines with CTB provides cross-protection against a broader range of viruses than does the current parenteral vaccination.

[1] X-ray diffraction experiments were conducted to 257 GPa and high temperature in situ on an iron-silicon alloy containing 3.4 wt% silicon, a candidate for the Earth's inner core forming material. The results revealed that fcc and hcp phases coexist up to 104 GPa. A single hcp phase is stable at higher pressures at least up to 3600 K at 242 GPa and to 2400 K at 257 GPa. Dissolution of silicon in the liquid outer core following reaction with the silicate mantle during core formation strongly suggests the existence of silicon in the solid inner core. Our results revealed that the iron-3.4 wt% silicon alloy in the inner core is likely to possess an hcp structure, which can explain the inner core anisotropy observed in seismology.

This study investigates damping constant (alpha) values of soft magnetic materials employing Q-band ferromagnetic resonance (FMR) analyses. The FMR spectra for Ni alloy specimens in addition of Co elements are discussed in detail.

The authors combined the concept of the Collapsing method and multiplet analysis, and derived an algorithm that is a variation of the collapsing method (Coherence Collapsing method). In the Coherence Collapsing method, the absolute locations of the multiplets are selectively located to the simplest structure, and the whole AE/MS cloud is optimized in the same manner as in the Collapsing method. Because the multiplets are related to the multiple slip of a fracture/fault, their locations are of importance to interpret the physical phenomenon. In this paper, we describe an application of the Coherence Collapsing method to the AE events from a compression test of a salt rock specimen and compare the locations with the distribution of the fractures in the specimen.

Amlodipine increases NO levels in coronary vessels and aorta via bradykinin-dependent mechanisms in vitro. We have previously reported that a long-acting Ca channel blocker, benidipine, increases cardiac NO levels in ischemic canine hearts, suggesting that benidipine may also protect against ischemia and reperfusion injury via bradykinin- and NO-dependent mechanisms. We examined this possibility. In open chest dogs, the left anterior descending coronary artery was perfused with blood through a bypass tube and was occluded for 90 min followed by 6 hours of reperfusion. Infarct size was assessed by TTC staining at 6 hours of reperfusion. When benidipine doses of 50, 100, and 200 ng/kg/min were infused via the bypass tube between 10 min prior to the onset of ischemia and after 60 min of reperfusion, systemic blood pressure did not change significantly. Infarct size decreased with the administration of benidipine (50, 100, and 200 ng/kg/min) when compared to the untreated condition (24.8+/-2.5, 17.3+/-3.1, and 16.5+/-2.0 vs. 43.4+/-5.6%, respectively) associated with the increased release of NO and bradykinin in the coronary venous blood upon reperfusion. Myeloperoxidase activity of the myocardium increased after 6 hours of reperfusion, which was attenuated by benidipine. The limitation of infarct size and the increase in myeloperoxidase activity were completely blunted by either L-NAME or HOE140. There were no significant differences in collateral blood flow assessed by the microsphere method after 45 min of ischemia for any of the groups. Thus, we conclude that the Ca channel blocker, benidipine, limits infarct size via bradykinin- and NO-dependent mechanisms.

Although cDNA array technique has recently become available in the cardiovascular field, it has not yet been established what kind of genes in the myocardium are expressed by acute ischemia. Since many substances contribute to the pathophysiology of acute ischemic hearts, we investigated transcription responses of murine hearts to ischemia using cDNA array representing 18,376 genes.In 29 male mice, we ligated the proximal site of the left coronary artery for 60 min. In 14 mice, we performed the sham operation without the ligation of the left coronary artery. After 60 min, the hearts were excised to obtain mRNA, and we performed cDNA array analysis. In 18,376 cDNA, 2 known genes were upregulated over 10-fold, 11 known genes were upregulated 5.0- to 9.9-fold, and 32 unknown genes were upregulated over 5.0-fold compared to sham-operated controls. In contrast, 11 known genes and 7 unknown genes were downregulated to levels below 0.2-fold. For 9 of the 13 known genes of which expression was increased as analyzed by cDNA array, subsequent Northern blot analysis also revealed an increase in expression.Using cDNA array analysis we found that cardiac expression of 24 known and 39 unknown genes was modulated by acute ischemic stress, and appeared to be related to the pathophysiology of ischemic hearts. These results show that cDNA array analysis may provide a new molecular insight to the pathophysiology of acute ischemic hearts.

Advanced material systems such as actuators and/or sensors embedded materials are becoming of worldwide interest because of their new material functions, e.g., actuation, noise reduction, vibration suppression, damage detection, self recovery or repair, and fabrication process monitoring. Fabrication of these new material systems used for smart structures has been realized by embedding sophisticated sensors and/or actuators in host structural materials such as polymer matrix composites.[1,2]

Chronic inhibition of nitric oxide (NO) synthesis is reported to induce the thickening of coronary artery walls and cardiac hypertrophy in vivo via angiotensin II receptors. Increased protein synthesis is the main feature of these structural changes. Activation of 70 kD S6 kinase (p70S6K) phosphorylates the 40S ribosomal protein S6 that regulates protein synthesis. We examined the role of p70S6K in the vascular and myocardial structural changes induced by the chronic inhibition of NO synthesis. The following 5 groups were studied: untreated Wister-Kyoto rats, those treated with an inhibitor of NO synthase, Nomega-nitro-L-arginine methyl ester (L-NAME), those treated with L-NAME and an angiotensin I converting enzyme inhibitor (imidapril), those treated with L-NAME and hydralazine, and those treated with L-NAME and an inhibitor of p70S6K (rapamycin). After 8 weeks, wall-to-lumen ratio in myocardium and cardiomyocyte cross-sectional areas were quantified. L-NAME increased systolic blood pressure, wall-to-lumen ratio, and cardiomyocyte cross-sectional area compared with control animals. Imidapril or rapamycin, but not hydralazine, markedly reduced these structural changes. L-NAME increased p70S6K activity in myocardium compared with control rats. Imidapril or rapamycin prevented the activation of p70S6K activity in myocardium induced by L-NAME. These results suggest that activation of p70S6K plays an important role in coronary vascular remodeling and cardiac hypertrophy induced by the chronic inhibition of nitric oxide synthesis in vivo.

FK506, an immunosuppressant, modulates phosphorylation of nitric oxide (NO) synthase, and induces cardiac hypertrophy in clinical settings. Having recently reported that chronic treatment with an inhibitor of NO synthase induces cardiac hypertrophy associated with the activation of 70-kD S6 kinase (p70S6K), which plays an important role in cardiac hypertrophy by regulating protein synthesis, we investigated the effects of chronic administration of FK506 on NO synthase and p70S6K activities in hearts. Twenty rabbits were divided into four groups: untreated rabbits, those treated with low-dose FK506 (0.10 mg/kg), those treated with medium-dose FK506 (0.20 mg/kg), and those treated with high-dose FK506 (0.40 mg/kg). FK506 was administered intravenously twice a day. After 4 weeks of treatment with FK506, calcium-dependent NO synthase activity in myocardium in the high-dose FK506 group was lower (P0.05) than in the untreated group. p70S6K activity in myocardium in the high-dose group was higher (P0.05) than in the untreated group. There was a significant (P0.05) inverse correlation between NO synthase and p70S6K activities in myocardium. However, the endothelial-dependent vasodilation of aortic rings or plasma levels of NO metabolites during experimental protocols did not differ among the groups studied. These findings suggest that chronic treatment of FK506 activates p70S6K and reduces NO synthase activity in rabbit hearts. Reduced NO synthase and/or activated p70S6K activities in hearts might contribute to the cardiac hypertrophy observed in some patients receiving FK506.

Cellular immune responses are associated with the pathogenesis of human cytomegalovirus (HCMV) hepatitis. We investigated a patient with post-transfusion HCMV hepatitis. A 9 year-old girl was involved in a traffic accident and suffered from traumatic damage to the left kidney and diaphragm and received a pelvic bone fracture. At emergency surgery she was transfused with 1200 ml of fresh whole donor blood. Abnormal liver function was observed in the 10 days after surgery. Titers of serum anti-HCMV IgG and IgM antibodies were elevated at 11, 17 and 25 weeks after operation. We analyzed the surface markers of peripheral blood mononuclear cells obtained 21 weeks after surgery. The CD4/CD8 ratio and the number of CD16 + CD56 decreased. We detected HCMV immediate early (IE) DNA in the fractionated peripheral blood cells (polymorphonuclear leukocytes, CD2+, CD4+ and CD8+ T lymphocytes) by polymerase chain reaction. The histology of liver biopsy at 23 weeks after operation showed the findings of acute hepatitis and the absence of HCMV IE antigen. It was considered that the immunosuppressive condition associated with the trauma, operation or transfusion itself induced the reactivation of HCMV or that transfused blood cells infected with HCMV caused reinfection. It was also speculated that HCMV hepatitis was not only due to the direct damage of hepatic cells by HCMV, but also due to the cellular immune responses associated with HCMV infection.

Anti-human cytomegalovirus (HCMV) properties of povidone-iodine (PVP-I) were evaluated in vitro. The effect of PVP-I was evaluated by indirect immunofluorescence assay on HCMV-infected MRC-5 cells. Percentages of fluorescent cells positive for HCMV immediate early and early antigens in cultures inoculated with AD 169 treated with PVP-I at various concentrations and reaction times were compared with the number of fluorescent cells in the controls inoculated with the virus alone. PVP-I was found to exert some inhibitory effect at a concentration of 0.5% and complete inhibition at a concentration of 7.5% on the infection of MRC-5 cells by HCMV AD 169 strain. Entirely new approaches to the prevention of HCMV infections in infants are necessary. The adequate use of PVP-I as a disinfectant may reduce the transmission of HCMV.

We established a monoclonal antibody, 3G12 (IgG1), with antiproliferative effects on a human T-cell leukaemia cell line, SUP-T13. Among haematolymphoid cell lines, 3G12 reacted with most T-cell lines, Epstein-Barr transformed B-cell lines, some myelomonocytic cell lines and, most strongly with an anaplastic large cell lymphoma (ALCL) cell line, Karpas 299. The cell panel reactive with 3G12 was similar, but not identical, to that of the anti-CD30 antibody Ber-H2. 3G12 induced Fas-independent apoptosis in SUP-T13 and it also induced growth-inhibition in a limited number of other cell lines, but not Karpas 299. Immunohistochemical studies on paraffin-embedded tissue specimens demonstrated that 3G12 reacted with most CD30-positive ALCL cases and some T-cell lymphomas and some Hodgkin's lymphomas, but not with B-cell lymphomas or non-haematogeneic tumours. The immunoprecipitation study with 3G12 demonstrated a major band of 200 kD and a minor band of 100 kD, which were different from CD30. Thus 3G12 defines a novel antigen that shares a similarity to CD30 in terms of distribution among haemopoietic cells. The data suggest that the 3G12-defined antigen, designated Hal-1, is important as a marker for ALCL and may play a role in its pathogenesis.

Cystinuria is an autosomal recessive disorder, and primary manifestation is the repeated formation of cystine calculi. Little information is available regarding clinical course of pediatric cystinuria having followed into adulthood. We report our experience with the management and the clinical course on cystinuria in children, who have been followed up for relatively long time.We retrospectively reviewed the records of all pediatric patients with cystinuria in whom urolithiasis was treated from 1970 to 1996.A total of 15 pediatric patients with cystine calculi (9 boys, 6 girls) were treated in our hospital. Average age at diagnosis was 3 years 4 months old. Mean follow-up was 104 months. Stone location was upper urinary tract in 11 cases, bladder in 3 cases and both upper urinary tract and bladder in 1 case. Medical treatments including hydration, urine alkalization and dissolution therapy were performed in all patients. In three cases whose urinary cystine level ranged from 138 to 326 mg/gCr, cystine calculi were disappeared by medical therapy alone. In one of 3 cases vesicoureteral reflux was identified. Side effects were noticed in 30.0% of patients with tiopronin and in 85.7% of those with D-penicillamine, especially in 1 case with tiopronin nephrotic syndrome being noticed. Surgical procedures were performed in 13 patients (lithotomy: 17 calculi, endourology: 7 calculi and ESWL: 7 calculi). The stone free rate was 100% with lithotomy, 80 to 100% with endourology and 43% with ESWL at an average of 5.9 procedures. No complications were recognized after the surgical treatments. The stone events of 15 patients ranged from 0 to 1.5 (average 0.55). In all six patients followed up over the age of 20 years, stone recurrences were observed exclusively between 17 and 20 years of age.Dissolution therapy is more effective for cystinuric patients in whom urinary cystine excretion is less than 330 mg/gCr. For those cases with low urinary cystine level it is necessary to evaluate structural abnormalities of the urinary tract to avoid stone recurrence. ESWL and endourology should be tried for pediatric cystinuria except for neonates and infants, considering its safety. The patients and their parents must have adequate knowledge about the disease itself and its management. Prevention of cystine calculi recurrences depends on patient compliance to the therapeutic regimens necessitating close follow up according to the clinical conditions, especially for those in pubertic or postpubertic age.

Long-lasting potentiation of the cat motor cortex units induced by tetanic stimulation of the VL + SCx led to an increase of the motor cortex unit discharge rate. The findings suggest that co-activation of cortico-cortical and thalamo-cortical afferents modifies neuronal activity of the motor cortex at the specific site which receives convergent sensory input from the thalamus and the somatosensory cortex.

Contrast enhancement of the left heart cavity and myocardium were assessed after venous injection of the ultrasound contrast agent Albunex. Myocardial perfusion was also assessed using a drug stress and image analyzing system. The study population consisted of 46 patients with normal cardiac function and without coronary artery disease, and 38 patients with effort angina. Contrast echocardiography was performed by imaging the parasternal or apical long-axis view during pulmonary arterial injection of Albunex through a Swan-Ganz catheter. Contrast enhancement in the left ventricular cavity and ascending aorta were visually assessed. Hemodynamic, arterial blood gas and electrocardiography changes were recorded before and after the injection of Albunex. Contrast echocardiography was performed before and during intravenous infusion of dipyridamole to assess left ventricular myocardial enhancement by both visual inspection and peak background-subtracted gray level using an image analyzing system. Doppler flow signal change after the injection of Albunex was assessed in 26 patients using a Doppler guide wire located in the left anterior descending coronary artery. Good contrast enhancement was obtained in all patients in the left ventricular cavity and in 17% of patients in the ascending aorta. No significant changes were observed in hemodynamics, electrocardiograms and aortic gas analysis. Significant myocardial enhancement was not seen in any patient but gray level analysis of the echo images during dipyridamole infusion showed significant enhancement in 25% of the patients without coronary artery disease and in 34% of the patients with effort angina. Doppler flow signal in the coronary artery was significantly augmented in all patients after injection of Albunex and suggests that ultrasound contrast agent reaches coronary arteries in all patients regardless of myocardial contrast enhancement. Contrast echocardiography with pulmonary arterial injection of Albunex is safe and useful to obtain sufficient left ventricular contrast enhancement. For myocardial perfusion assessment, further refinement of the ultrasound contrast agent and echo equipment is necessary.

Little information is available regarding the correlation between Prader-Willi syndrome and urolithiasis. We report a patient with Prader-Willi syndrome with a renal uric acid (UA) stone. A 23-year-old male patient was admitted to our department with gross hematuria and left flank pain. The blood and urine examination demonstrated hyperuricemia with the presence of UA crystals in the urine. Excretory urography revealed a radiolucent stone (17 x 27 mm) in the left renal pelvis suggesting a UA stone. The stone was removed successfully using extracorporeal shockwave lithotripsy (ESWL) combined with medication for UA metabolism. The stone was thought to have formed as a result of overeating associated with Prader-Willi syndrome, and accompanying overproduction of purine.

An enzyme-linked immunosorbent assay (ELISA) has been developed for the detection of antinuclear antibodies (ANAs) previously established as diagnostic and/or prognostic marker ANAs for various connective tissue diseases. The antigen used in ELISA is a mixture of purified recombinant or natural antigens including single-and double-stranded DNA, RNP, Sm, SS-A/Ro, SS-B/La, centromere, topoisomerase I and Jo-1 antigens. Thirty hundred and fifty nine patients sera from a variety of connective tissue diseases and 113 normal human sera (NHS) were examined. ELISA ANAs were positive in 3.5% of NHS and 80.2% of patients sera at cut off index 11.5, whereas indirect immunofluorescent antinuclear antibodies (FANAs) using HEp-2 cells were positive in 9.7% of NHS and 92.5% of patients sera at 1:160 serum dilution. More than 80% of sera from systemic lupus erythematosus, mixed connective tissue disease and primary Sjögrens disease were ELISA ANAs positive. Mean value of ELISA ANAs was highest in sera of patients with MCTD. ELISA ANAs were positive in 92.5% of sera with marker ANAs for connective tissue diseases. Mean value of ELISA ANAs was higher in sera with more than two marker ANAs than in sera with a single ANA or in sera without marker ANAs. In contrast incidence and mean value of ELISA ANAs were low in sera positive for anti topoisomerase I antibody or anti Jo-1 antibody. Sensitivity, specificity and agreement (accuracy) for connective tissue diseases with marker ANAs were as follows: ELISA ANAs (at index 11.5): 92.5%, 88.3% and 90.9%: FANAs (at 1:160 serum dilution): 99.0%, 70.4% and 88.1%, respectively. ELISA ANAs, thus, are specific for connective tissue diseases when compared to FANAs and previous ELISA for the detection of total ANAs. Moreover, ELISA ANAs are able to measure precise ANAs titers and are much less labor intensive when screening a large number of clinical specimens.

Long-term potentiation (LTP) has been proposed as a model of learning and memory. There is still little evidence, however, linking LTP to cognitive processes. We have chosen to study motor learning, first, because it is relatively simpler than cognitive learning and second, because much of the circuitry involved in motor function is already known. In behavioral studies we determined that the sensory cortex is required for the acquisition of new motor skills. Once a skill is acquired, however, the sensory cortex is no longer necessary in the performance of that skill. In electrophysiological experiments we have shown that LTP can be induced in the motor cortex with stimulation of the sensory cortex (SCx) or associativly when stimulation was applied to both SCx and thalamus. We propose that motor learning involves the formation of loop circuits between the motor cortex and the periphery involving the SCx and the thalamus. At first these loop circuits are diffuse, producing contraction of unnecessary muscles, but become specific by producing LTP through practice.